=== Generating (published_papers) ===
=== Generating (teaching_experience) ===
=== Generating (education) ===
=== Generating (research_experience) ===
=== Generating (misc) ===
=== Generating (research_projects) ===
=== Generating (books_etc) ===
=== Generating (committee_memberships) ===
=== Generating (awards) ===
=== Generating (association_memberships) ===
=== Generating (presentations) ===
==== begin registerFile(/WWW/pub2/data/ERD/person/141809/researchmap/published_papers.jsonl) ====
line:1, {"insert":{"user_id":"6000008820","type":"published_papers","id":"46098810"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=406198","label":"url"}],"paper_title":{"en":"Association of non-steroidal anti-inflammatory drug use with encephalopathy development: an analysis using the United States Food and Drug Administration Adverse Event Reporting System (FAERS) and Japanese Adverse Drug Event Report (JADER) databases","ja":"Association of non-steroidal anti-inflammatory drug use with encephalopathy development: an analysis using the United States Food and Drug Administration Adverse Event Reporting System (FAERS) and Japanese Adverse Drug Event Report (JADER) databases"},"authors":{"en":[{"name":"Kawada Kei"},{"name":"Ishida Tomoaki"},{"name":"Yoshioka Toshihiko"},{"name":"Fukuda Hitoshi"},{"name":"Hayashi Toshinobu"},{"name":"Goda Mitsuhiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"川田 敬"},{"name":"Ishida Tomoaki"},{"name":"Yoshioka Toshihiko"},{"name":"Fukuda Hitoshi"},{"name":"Hayashi Toshinobu"},{"name":"合田 光寛"},{"name":"石澤 啓介"}]},"publication_date":"2024-03","publication_name":{"en":"Die Pharmazie in press","ja":"Die Pharmazie in press"},"languages":["eng"],"referee":true,"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:2, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37969096","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=406560","label":"url"}],"paper_title":{"en":"Effect of pre-treatment with EGFR-TKIs on immune checkpoint inhibitor-associated interstitial lung disease in lung cancer patients: Analysis using a Japanese claims database.","ja":"Effect of pre-treatment with EGFR-TKIs on immune checkpoint inhibitor-associated interstitial lung disease in lung cancer patients: Analysis using a Japanese claims database."},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Hamano Hirofumi"},{"name":"Yagi Kenta"},{"name":"Niimura Takahiro"},{"name":"Aizawa Fuka"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Kitahara Takashi"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"濱野 裕章"},{"name":"八木 健太"},{"name":"新村 貴博"},{"name":"相澤 風花"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"Kitahara Takashi"},{"name":"石澤 啓介"}]},"description":{"en":"Although further analyses are required to confirm our findings, this study indicated that pre-treatment with EGFR-TKI might not increase the ILD risk after ICI treatment.","ja":"A total of 353 patients were included, of which 61 were included in the ILD group. The median time to onset of ILD after ICI administration was 3 months. Multivariate logistic regression analysis revealed that pre-treatment with EGFR-TKI was not associated with ICI-associated ILD (odds ratio: 0.26, 95% confidence interval: 0.033 - 2.01)."},"publication_date":"2024-02","publication_name":{"en":"International journal of clinical pharmacology and therapeutics","ja":"International journal of clinical pharmacology and therapeutics"},"volume":"Vol.62","number":"No.2","starting_page":"69","ending_page":"76","languages":["eng"],"referee":true,"identifiers":{"doi":["10.5414/CP204491"],"issn":["0946-1965"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:3, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/38145933","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=407553","label":"url"}],"paper_title":{"en":"Concomitant Use of Multiple Nephrotoxins including Renal Hypoperfusion Medications Causes Vancomycin-Associated Nephrotoxicity: Combined Retrospective Analyses of Two Real-World Databases.","ja":"Concomitant Use of Multiple Nephrotoxins including Renal Hypoperfusion Medications Causes Vancomycin-Associated Nephrotoxicity: Combined Retrospective Analyses of Two Real-World Databases."},"authors":{"en":[{"name":"Bando Takashi"},{"name":"Chuma Masayuki"},{"name":"Hamano Hirofumi"},{"name":"Niimura Takahiro"},{"name":"Okada Naoto"},{"name":"Kondo Masateru"},{"name":"Izumi Yuki"},{"name":"Ishida Shunsuke"},{"name":"Yoshioka Toshihiko"},{"name":"Asada Mizuho"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Goda Mitsuhiro"},{"name":"Miyata Koji"},{"name":"Yagi Kenta"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Azuma Momoyo"},{"name":"Yanagawa Hiroaki"},{"name":"Tasaki Yoshikazu"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"坂東 貴司"},{"name":"中馬 真幸"},{"name":"濱野 裕章"},{"name":"新村 貴博"},{"name":"岡田 直人"},{"name":"近藤 正輝"},{"name":"泉 侑希"},{"name":"石田 俊介"},{"name":"吉岡 俊彦"},{"name":"朝田 瑞穂"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"合田 光寛"},{"name":"宮田 晃志"},{"name":"八木 健太"},{"name":"石澤 有紀"},{"name":"東 桃代"},{"name":"楊河 宏章"},{"name":"田崎 嘉一"},{"name":"石澤 啓介"}]},"description":{"en":"There is a growing concern about the relationship between vancomycin-associated nephrotoxicity (VAN) and concomitant use of nephrotoxins. We examined this relationship by combined retrospective analyses of two real-world databases. Initially, the FDA Adverse Event Reporting System (FAERS) was analyzed for the effects of concomitant use of one or more nephrotoxins on VAN and the types of combinations of nephrotoxins that exacerbate VAN. Next, electronic medical records (EMRs) of patients who received vancomycin (VCM) at Tokushima University Hospital between January 2006 and March 2019 were examined to confirm the FAERS analysis. An elevated reporting odds ratio (ROR) was observed with increases in the number of nephrotoxins administered (VCM + one nephrotoxin, adjusted ROR (95% confidence interval [CI]) 1.67 [1.51-1.85]; VCM + 2 nephrotoxins, adjusted ROR [95% CI] 1.54 [1.37-1.73]) in FAERS. EMRs analysis showed that the number of nephrotoxins was associated with higher incidences of VAN [odds ratio: 1.99; 95% CI: 1.42-2.78]. Overall, concomitant use of nephrotoxins was associated with an increased incidence of VAN, especially when at least one of those nephrotoxins was a renal hypoperfusion medication (furosemide, non-steroidal anti-inflammatory drugs, and vasopressors). The concomitant use of multiple nephrotoxins, especially including renal hypoperfusion medication, should be avoided to prevent VAN.","ja":"There is a growing concern about the relationship between vancomycin-associated nephrotoxicity (VAN) and concomitant use of nephrotoxins. We examined this relationship by combined retrospective analyses of two real-world databases. Initially, the FDA Adverse Event Reporting System (FAERS) was analyzed for the effects of concomitant use of one or more nephrotoxins on VAN and the types of combinations of nephrotoxins that exacerbate VAN. Next, electronic medical records (EMRs) of patients who received vancomycin (VCM) at Tokushima University Hospital between January 2006 and March 2019 were examined to confirm the FAERS analysis. An elevated reporting odds ratio (ROR) was observed with increases in the number of nephrotoxins administered (VCM + one nephrotoxin, adjusted ROR (95% confidence interval [CI]) 1.67 [1.51-1.85]; VCM + 2 nephrotoxins, adjusted ROR [95% CI] 1.54 [1.37-1.73]) in FAERS. EMRs analysis showed that the number of nephrotoxins was associated with higher incidences of VAN [odds ratio: 1.99; 95% CI: 1.42-2.78]. Overall, concomitant use of nephrotoxins was associated with an increased incidence of VAN, especially when at least one of those nephrotoxins was a renal hypoperfusion medication (furosemide, non-steroidal anti-inflammatory drugs, and vasopressors). The concomitant use of multiple nephrotoxins, especially including renal hypoperfusion medication, should be avoided to prevent VAN."},"publication_date":"2023-12","publication_name":{"en":"Acta Medica Okayama","ja":"Acta Medica Okayama"},"volume":"Vol.77","number":"No.6","starting_page":"595","ending_page":"605","languages":["eng"],"referee":true,"identifiers":{"doi":["10.18926/AMO/66151"],"issn":["0386-300X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:4, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/119176","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37973221","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=406137","label":"url"}],"paper_title":{"en":"CA9 and PRELID2; hypoxia-responsive potential therapeutic targets for pancreatic ductal adenocarcinoma as per bioinformatics analyses.","ja":"CA9 and PRELID2; hypoxia-responsive potential therapeutic targets for pancreatic ductal adenocarcinoma as per bioinformatics analyses."},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Inoue Takahisa"},{"name":"Fukushima Keijo"},{"name":"Yamashita Ryosuke"},{"name":"Nakayama Ryo"},{"name":"Nojima Masataka"},{"name":"Kondo Kosuke"},{"name":"Gomi Yoshiki"},{"name":"Tsunematsu Honoka"},{"name":"Goto Kohei"},{"name":"Miyamoto Licht"},{"name":"Funamoto Masafumi"},{"name":"Denda Masaya"},{"name":"Ishizawa Keisuke"},{"name":"Otaka Akira"},{"name":"Fujino Hiromichi"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"}],"ja":[{"name":"今西 正樹"},{"name":"井上 貴久"},{"name":"福島 圭穣"},{"name":"山下 竜介"},{"name":"中山 涼"},{"name":"野島 雅孝"},{"name":"Kondo Kosuke"},{"name":"五味 義輝"},{"name":"常松 保乃加"},{"name":"後藤 廣平"},{"name":"宮本 理人"},{"name":"船本 雅文"},{"name":"傳田 将也"},{"name":"石澤 啓介"},{"name":"大髙 章"},{"name":"藤野 裕道"},{"name":"池田 康将"},{"name":"土屋 浩一郎"}]},"description":{"en":"A strong hypoxic environment has been observed in pancreatic ductal adenocarcinoma (PDAC) cells, which contributes to drug resistance, tumor progression, and metastasis. Therefore, we performed bioinformatics analyses to investigate potential targets for the treatment of PDAC. To identify potential genes as effective PDAC treatment targets, we selected all genes whose expression level was related to worse overall survival (OS) in The Cancer Genome Atlas (TCGA) database and selected only the genes that matched with the genes upregulated due to hypoxia in pancreatic cancer cells in the dataset obtained from the Gene Expression Omnibus (GEO) database. Although the extracted 107 hypoxia-responsive genes included the genes that were slightly enriched in angiogenic factors, TCGA data analysis revealed that the expression level of endothelial cell (EC) markers did not affect OS. Finally, we selected CA9 and PRELID2 as potential targets for PDAC treatment and elucidated that a CA9 inhibitor, U-104, suppressed pancreatic cancer cell growth more effectively than 5-fluorouracil (5-FU) and PRELID2 siRNA treatment suppressed the cell growth stronger than CA9 siRNA treatment. Thus, we elucidated that specific inhibition of PRELID2 as well as CA9, extracted via exhaustive bioinformatic analyses of clinical datasets, could be a more effective strategy for PDAC treatment.","ja":"A strong hypoxic environment has been observed in pancreatic ductal adenocarcinoma (PDAC) cells, which contributes to drug resistance, tumor progression, and metastasis. Therefore, we performed bioinformatics analyses to investigate potential targets for the treatment of PDAC. To identify potential genes as effective PDAC treatment targets, we selected all genes whose expression level was related to worse overall survival (OS) in The Cancer Genome Atlas (TCGA) database and selected only the genes that matched with the genes upregulated due to hypoxia in pancreatic cancer cells in the dataset obtained from the Gene Expression Omnibus (GEO) database. Although the extracted 107 hypoxia-responsive genes included the genes that were slightly enriched in angiogenic factors, TCGA data analysis revealed that the expression level of endothelial cell (EC) markers did not affect OS. Finally, we selected CA9 and PRELID2 as potential targets for PDAC treatment and elucidated that a CA9 inhibitor, U-104, suppressed pancreatic cancer cell growth more effectively than 5-fluorouracil (5-FU) and PRELID2 siRNA treatment suppressed the cell growth stronger than CA9 siRNA treatment. Thus, we elucidated that specific inhibition of PRELID2 as well as CA9, extracted via exhaustive bioinformatic analyses of clinical datasets, could be a more effective strategy for PDAC treatment."},"publication_date":"2023-10-17","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.153","number":"No.4","starting_page":"232","ending_page":"242","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.jphs.2023.10.003"],"issn":["1347-8648"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:5, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37700528","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=407554","label":"url"}],"paper_title":{"en":"Valproic acid treatment attenuates cisplatin-induced kidney injury by suppressing proximal tubular cell damage.","ja":"Valproic acid treatment attenuates cisplatin-induced kidney injury by suppressing proximal tubular cell damage."},"authors":{"en":[{"name":"Yoshioka Toshihiko"},{"name":"Goda Mitsuhiro"},{"name":"Kanda Masaya"},{"name":"Itobayashi Sayuri"},{"name":"Sugimoto Yugo"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yagi Kenta"},{"name":"Aizawa Fuka"},{"name":"Miyata Koji"},{"name":"Niimura Takahiro"},{"name":"Hamano Hirofumi"},{"name":"Sakurada Takumi"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"吉岡 俊彦"},{"name":"合田 光寛"},{"name":"神田 将哉"},{"name":"糸林 小友理"},{"name":"杉本 祐悟"},{"name":"石澤 有紀"},{"name":"八木 健太"},{"name":"相澤 風花"},{"name":"宮田 晃志"},{"name":"新村 貴博"},{"name":"濱野 裕章"},{"name":"櫻田 巧"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Cisplatin treatment is effective against several types of carcinomas. However, it frequently leads to kidney injury, which warrants effective prevention methods. Sodium valproic acid is a prophylactic drug candidate with a high potential for clinical application against cisplatin-induced kidney injury. Therefore, in this study, we aimed to elucidate the mechanism underlying the prophylactic effect of valproic acid on cisplatin-induced kidney injury in a mouse model and HK2 and PODO cells with cisplatin-induced toxicity. In the mouse model of cisplatin-induced kidney injury, various renal function parameters and tubular damage scores were worsened by cisplatin, but they were significantly improved upon combination with valproic acid. No difference was observed in cisplatin accumulation between the cisplatin-treated and valproic acid-treated groups in whole blood and the kidneys. The mRNA expression levels of proximal tubular damage markers, apoptosis markers, and inflammatory cytokines significantly increased in the cisplatin group 72 h after cisplatin administration but significantly decreased upon combination with valproic acid. In HK2 cells, a human proximal tubular cell line, the cisplatin-induced decrease in cell viability was significantly suppressed by co-treatment with valproic acid. Valproic acid may inhibit cisplatin-induced kidney injury by suppressing apoptosis, inflammatory responses, and glomerular damage throughout the kidneys by suppressing proximal tubular cell damage. However, prospective controlled trials need to evaluate these findings before their practical application.","ja":"Cisplatin treatment is effective against several types of carcinomas. However, it frequently leads to kidney injury, which warrants effective prevention methods. Sodium valproic acid is a prophylactic drug candidate with a high potential for clinical application against cisplatin-induced kidney injury. Therefore, in this study, we aimed to elucidate the mechanism underlying the prophylactic effect of valproic acid on cisplatin-induced kidney injury in a mouse model and HK2 and PODO cells with cisplatin-induced toxicity. In the mouse model of cisplatin-induced kidney injury, various renal function parameters and tubular damage scores were worsened by cisplatin, but they were significantly improved upon combination with valproic acid. No difference was observed in cisplatin accumulation between the cisplatin-treated and valproic acid-treated groups in whole blood and the kidneys. The mRNA expression levels of proximal tubular damage markers, apoptosis markers, and inflammatory cytokines significantly increased in the cisplatin group 72 h after cisplatin administration but significantly decreased upon combination with valproic acid. In HK2 cells, a human proximal tubular cell line, the cisplatin-induced decrease in cell viability was significantly suppressed by co-treatment with valproic acid. Valproic acid may inhibit cisplatin-induced kidney injury by suppressing apoptosis, inflammatory responses, and glomerular damage throughout the kidneys by suppressing proximal tubular cell damage. However, prospective controlled trials need to evaluate these findings before their practical application."},"publication_date":"2023-09-25","publication_name":{"en":"Clinical and Translational Science","ja":"Clinical and Translational Science"},"volume":"Vol.16","number":"No.11","starting_page":"2369","ending_page":"2381","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/cts.13638"],"issn":["1752-8062"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:6, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37722188","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=406562","label":"url"}],"paper_title":{"en":"Angiogenesis inhibitor-specific hypertension increases the risk of developing aortic dissection.","ja":"Angiogenesis inhibitor-specific hypertension increases the risk of developing aortic dissection."},"authors":{"en":[{"name":"Tsujinaka Kaito"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyata Koji"},{"name":"Yoshioka Toshihiko"},{"name":"Oomine Kohei"},{"name":"Nishi Honoka"},{"name":"Kondo Masateru"},{"name":"Itokazu Syuto"},{"name":"Miyata Tatsumi"},{"name":"Niimura Takahiro"},{"name":"Sato Maki"},{"name":"Aizawa Fuka"},{"name":"Yagi Kenta"},{"name":"Chuma Masayuki"},{"name":"Zamami Yoshito"},{"name":"Goda Mitsuhiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Tsujinaka Kaito"},{"name":"石澤 有紀"},{"name":"Miyata Koji"},{"name":"Yoshioka Toshihiko"},{"name":"Oomine Kohei"},{"name":"Nishi Honoka"},{"name":"Kondo Masateru"},{"name":"Itokazu Syuto"},{"name":"Miyata Tatsumi"},{"name":"新村 貴博"},{"name":"Sato Maki"},{"name":"相澤 風花"},{"name":"八木 健太"},{"name":"中馬 真幸"},{"name":"座間味 義人"},{"name":"合田 光寛"},{"name":"石澤 啓介"}]},"description":{"en":"Aortic dissection is an adverse event of angiogenesis inhibitors; however, the association between the drugs and aortic dissection is unclear. Therefore, we investigated if and how angiogenesis inhibitors increase the onset of aortic dissection using pharmacologically-induced aortic dissection-prone model (LAB) mice, cultured endothelial cells, and real-world databases, which is a novel integrated research approach. Disproportionality analysis was performed and calculated using the reporting odds ratio as a risk signal using a worldwide database of spontaneous adverse events to estimate the risk of adverse events. Angiogenesis inhibitors, but not other hypertension-inducing drugs, showed significant risk signals for aortic aneurysms and dissection. A retrospective cohort analysis using JMDC, a medical receipt database in Japan, showed that the history of atherosclerosis and dyslipidemia, but not hypertension, were significantly associated with the onset of aortic dissection during angiogenesis inhibitor medication administration. For in vivo studies, sunitinib (100 mg/kg/day) was administered to LAB mice. Sunitinib increased systolic blood pressure (182 mmHg vs. 288 mmHg with sunitinib; p<0.01) and the incidence of aortic dissection (40% vs. 59% with sunitinib; p = 0.34) in mice. In vivo and in vitro studies revealed that sunitinib increased endothelin-1 expression and induced endothelial cell damage evaluated by intracellular- and vascular cell adhesion molecule-1 expressions. The increased risk of developing aortic dissection with angiogenesis inhibitors is associated with the development of drug-specific hypertension via endothelial cell damage and endothelin-1 expression. Our findings are invaluable in establishing safer anticancer therapies and strategies to prevent the development of vascular toxicity in high-risk patients.","ja":"Aortic dissection is an adverse event of angiogenesis inhibitors; however, the association between the drugs and aortic dissection is unclear. Therefore, we investigated if and how angiogenesis inhibitors increase the onset of aortic dissection using pharmacologically-induced aortic dissection-prone model (LAB) mice, cultured endothelial cells, and real-world databases, which is a novel integrated research approach. Disproportionality analysis was performed and calculated using the reporting odds ratio as a risk signal using a worldwide database of spontaneous adverse events to estimate the risk of adverse events. Angiogenesis inhibitors, but not other hypertension-inducing drugs, showed significant risk signals for aortic aneurysms and dissection. A retrospective cohort analysis using JMDC, a medical receipt database in Japan, showed that the history of atherosclerosis and dyslipidemia, but not hypertension, were significantly associated with the onset of aortic dissection during angiogenesis inhibitor medication administration. For in vivo studies, sunitinib (100 mg/kg/day) was administered to LAB mice. Sunitinib increased systolic blood pressure (182 mmHg vs. 288 mmHg with sunitinib; p<0.01) and the incidence of aortic dissection (40% vs. 59% with sunitinib; p = 0.34) in mice. In vivo and in vitro studies revealed that sunitinib increased endothelin-1 expression and induced endothelial cell damage evaluated by intracellular- and vascular cell adhesion molecule-1 expressions. The increased risk of developing aortic dissection with angiogenesis inhibitors is associated with the development of drug-specific hypertension via endothelial cell damage and endothelin-1 expression. Our findings are invaluable in establishing safer anticancer therapies and strategies to prevent the development of vascular toxicity in high-risk patients."},"publication_date":"2023-09-16","publication_name":{"en":"Biomedicine & Pharmacotherapy","ja":"Biomedicine & Pharmacotherapy"},"volume":"Vol.167","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.biopha.2023.115504"],"issn":["1950-6007"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:7, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37482254","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85165980754&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=399017","label":"url"}],"paper_title":{"en":"Structural characterization of the optical isomers esomeprazole and omeprazole using the JADER and FAERS databases","ja":"Structural characterization of the optical isomers esomeprazole and omeprazole using the JADER and FAERS databases"},"authors":{"en":[{"name":"Neishi Mami"},{"name":"Hamano Hirofumi"},{"name":"Niimura Takahiro"},{"name":"Denda Masaya"},{"name":"Yagi Kenta"},{"name":"Miyata Koji"},{"name":"Lin Tsung-Jen"},{"name":"Higashionna Tsukasa"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"},{"name":"Nawa Hideki"}],"ja":[{"name":"Neishi Mami"},{"name":"濱野 裕章"},{"name":"新村 貴博"},{"name":"傳田 将也"},{"name":"八木 健太"},{"name":"宮田 晃志"},{"name":"Lin Tsung-Jen"},{"name":"Higashionna Tsukasa"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"石澤 啓介"},{"name":"Nawa Hideki"}]},"description":{"en":"It is unclear whether the s (-) form of esomeprazole (EPZ) has an improved safety profile when compared with its racemic form omeprazole (OPZ). We assessed the potential complications of these optical isomers when combined with cilostazol, clopidogrel, and prasugrel, which are frequently used concomitant medications. Using two adverse event spontaneous reporting databases, Japanese Adverse Drug Event Report (JADER) and FDA Adverse Event Reporting System (FAERS), adverse event names for hemorrhage, venous/arterial embolization, and thrombus were obtained from the Medical Dictionary for Regulatory Activities. Reported odds ratios were calculated using a 2 × 2 contingency table, and a signal was considered present if the lower limit of the 95% confidence interval was >1. In combination with cilostazol, a hemorrhagic signal for OPZ in JADER and arterial emboli and thrombus signals for EPZ were detected in both databases. In combination with clopidogrel, OPZ showed arterial emboli and thrombus signals in JADER and venous/arterial emboli and thrombus signals in FAERS, while EPZ displayed arterial emboli and thrombus signals in FAERS. In contrast, when in combination with prasugrel, there were no adverse event signals in either database. This study has confirmed using big data, that EPZ, the optical isomer and racemic form of omeprazole, has the beneficial characteristics of being less sensitive to CYP, as was intended by its design.","ja":"It is unclear whether the s (-) form of esomeprazole (EPZ) has an improved safety profile when compared with its racemic form omeprazole (OPZ). We assessed the potential complications of these optical isomers when combined with cilostazol, clopidogrel, and prasugrel, which are frequently used concomitant medications. Using two adverse event spontaneous reporting databases, Japanese Adverse Drug Event Report (JADER) and FDA Adverse Event Reporting System (FAERS), adverse event names for hemorrhage, venous/arterial embolization, and thrombus were obtained from the Medical Dictionary for Regulatory Activities. Reported odds ratios were calculated using a 2 × 2 contingency table, and a signal was considered present if the lower limit of the 95% confidence interval was >1. In combination with cilostazol, a hemorrhagic signal for OPZ in JADER and arterial emboli and thrombus signals for EPZ were detected in both databases. In combination with clopidogrel, OPZ showed arterial emboli and thrombus signals in JADER and venous/arterial emboli and thrombus signals in FAERS, while EPZ displayed arterial emboli and thrombus signals in FAERS. In contrast, when in combination with prasugrel, there were no adverse event signals in either database. This study has confirmed using big data, that EPZ, the optical isomer and racemic form of omeprazole, has the beneficial characteristics of being less sensitive to CYP, as was intended by its design."},"publication_date":"2023-09-15","publication_name":{"en":"Toxicology and Applied Pharmacology","ja":"Toxicology and Applied Pharmacology"},"volume":"Vol.475","starting_page":"116632","ending_page":"116632","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.taap.2023.116632"],"issn":["1096-0333"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:8, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37601729","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=406563","label":"url"}],"paper_title":{"en":"Pharmacovigilance Study on Eosinophilic Pneumonia Induced by Anti-MRSA Agents: Analysis Based on the FDA Adverse Event Reporting System.","ja":"Pharmacovigilance Study on Eosinophilic Pneumonia Induced by Anti-MRSA Agents: Analysis Based on the FDA Adverse Event Reporting System."},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Niimura Takahiro"},{"name":"Saisyo Atsuyuki"},{"name":"Kawaguchi Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Kitahara Takashi"}],"ja":[{"name":"岡田 直人"},{"name":"新村 貴博"},{"name":"Saisyo Atsuyuki"},{"name":"Kawaguchi Yoshitaka"},{"name":"石澤 啓介"},{"name":"Kitahara Takashi"}]},"description":{"en":"This study revealed that among the anti-MRSA agents, disproportionality in the occurrence of EP was observed only with DAP. Our results suggest that sex, age, and treatment duration may affect the occurrence of DAP-induced EP. Clinicians should exercise caution regarding EP during DAP administration.","ja":"This study revealed that among the anti-MRSA agents, disproportionality in the occurrence of EP was observed only with DAP. Our results suggest that sex, age, and treatment duration may affect the occurrence of DAP-induced EP. Clinicians should exercise caution regarding EP during DAP administration."},"publication_date":"2023-08-02","publication_name":{"en":"Open forum infectious diseases","ja":"Open forum infectious diseases"},"volume":"Vol.10","number":"No.8","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/ofid/ofad414"],"issn":["2328-8957"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:9, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/118887","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37568602","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=402960","label":"url"}],"paper_title":{"en":"Trends in Head and Neck Cancer Mortality from 1999 to 2019 in Japan: An Observational Analysis.","ja":"Trends in Head and Neck Cancer Mortality from 1999 to 2019 in Japan: An Observational Analysis."},"authors":{"en":[{"name":"Higashionna Tsukasa"},{"name":"Harada Keisaku"},{"name":"Maruo Akinari"},{"name":"Niimura Takahiro"},{"name":"Tan Elizabeth"},{"name":"Vu Quynh Thi"},{"name":"Kawabata Takayoshi"},{"name":"Ushio Soichiro"},{"name":"Hamano Hirofumi"},{"name":"Kajizono Makoto"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"},{"name":"Harada Ko"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"},{"name":"Hagiya Hideharu"},{"name":"Koyama Toshihiro"}],"ja":[{"name":"Higashionna Tsukasa"},{"name":"Harada Keisaku"},{"name":"Maruo Akinari"},{"name":"新村 貴博"},{"name":"Tan Elizabeth"},{"name":"Vu Quynh Thi"},{"name":"Kawabata Takayoshi"},{"name":"Ushio Soichiro"},{"name":"濱野 裕章"},{"name":"Kajizono Makoto"},{"name":"座間味 義人"},{"name":"石澤 啓介"},{"name":"Harada Ko"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"},{"name":"Hagiya Hideharu"},{"name":"Koyama Toshihiro"}]},"description":{"en":"= 156,742). HNC mortality trends were analysed using joinpoint regression models to estimate annual percentage change (APC) and average APC (AAPC). Among men, no significant change was observed in the age-adjusted death rate trend from 1999 to 2014; however, a marked decrease was observed from 2014 to 2019. No changing point was observed in women. Age-adjusted mortality rates continuously decreased over the 21-year period, with an AAPC of -0.7% in men and -0.6% in women. In conclusion, the overall trend in age-adjusted rates of HNC-associated deaths decreased, particularly among men, in the past 5 years. These results will contribute to the formulation of medical policies to develop targeted screening and prevention programmes for HNC in Japan and determine the direction of treatment strategies.","ja":"= 156,742). HNC mortality trends were analysed using joinpoint regression models to estimate annual percentage change (APC) and average APC (AAPC). Among men, no significant change was observed in the age-adjusted death rate trend from 1999 to 2014; however, a marked decrease was observed from 2014 to 2019. No changing point was observed in women. Age-adjusted mortality rates continuously decreased over the 21-year period, with an AAPC of -0.7% in men and -0.6% in women. In conclusion, the overall trend in age-adjusted rates of HNC-associated deaths decreased, particularly among men, in the past 5 years. These results will contribute to the formulation of medical policies to develop targeted screening and prevention programmes for HNC in Japan and determine the direction of treatment strategies."},"publication_date":"2023-07-26","publication_name":{"en":"Cancers","ja":"Cancers"},"volume":"Vol.15","number":"No.15","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3390/cancers15153786"],"issn":["2072-6694"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:10, {"insert":{"user_id":"6000008820","type":"published_papers","id":"42506359"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/119057","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37269004","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=397854","label":"url"}],"paper_title":{"en":"A polo-like kinase inhibitor identified by computational repositioning attenuates pulmonary fibrosis.","ja":"A polo-like kinase inhibitor identified by computational repositioning attenuates pulmonary fibrosis."},"authors":{"en":[{"name":"Imakura Takeshi"},{"name":"Satou Seidai"},{"name":"Koyama Kazuya"},{"name":"Ogawa Hirohisa"},{"name":"Niimura Takahiro"},{"name":"Murakami Kojin"},{"name":"Yamashita Yuya"},{"name":"Haji Keiko"},{"name":"Naito Nobuhito"},{"name":"Kagawa Kozo"},{"name":"Kawano Hiroshi"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"},{"name":"Nishioka Yasuhiko"}],"ja":[{"name":"Imakura Takeshi"},{"name":"佐藤 正大"},{"name":"小山 壱也"},{"name":"小川 博久"},{"name":"新村 貴博"},{"name":"Murakami Kojin"},{"name":"山下 雄也"},{"name":"土師 恵子"},{"name":"内藤 伸仁"},{"name":"香川 耕造"},{"name":"河野 弘"},{"name":"座間味 義人"},{"name":"石澤 啓介"},{"name":"西岡 安彦"}]},"description":{"en":"These findings suggest that targeting PLK1 may be a novel therapeutic approach for pulmonary fibrosis by inhibiting lung fibroblast proliferation without affecting lung epithelial cells. In addition, while in silico screening is useful, it is essential to fully determine the biological activities of candidates by wet-lab validation studies.","ja":"These findings suggest that targeting PLK1 may be a novel therapeutic approach for pulmonary fibrosis by inhibiting lung fibroblast proliferation without affecting lung epithelial cells. In addition, while in silico screening is useful, it is essential to fully determine the biological activities of candidates by wet-lab validation studies."},"publication_date":"2023-06-02","publication_name":{"en":"Respiratory Research","ja":"Respiratory Research"},"volume":"Vol.24","number":"No.1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1186/s12931-023-02446-x"],"issn":["1465-993X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:11, {"insert":{"user_id":"6000008820","type":"published_papers","id":"42309244"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37106270","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=396451","label":"url"}],"paper_title":{"en":"Cardiovascular Toxicities Associated with Anaplastic Lymphoma Kinase Inhibitors: A Disproportionality Analysis of the WHO Pharmacovigilance Database (VigiBase).","ja":"Cardiovascular Toxicities Associated with Anaplastic Lymphoma Kinase Inhibitors: A Disproportionality Analysis of the WHO Pharmacovigilance Database (VigiBase)."},"authors":{"en":[{"name":"Niimura Takahiro"},{"name":"Miyata Koji"},{"name":"Hamano Hirofumi"},{"name":"Nounin Yuuki"},{"name":"Unten Hiroto"},{"name":"Yoshino Masaki"},{"name":"Mitsuboshi Satoru"},{"name":"Aizawa Fuka"},{"name":"Yagi Kenta"},{"name":"Koyama Toshihiro"},{"name":"Goda Mitsuhiro"},{"name":"Kanda Yasunari"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"新村 貴博"},{"name":"宮田 晃志"},{"name":"濱野 裕章"},{"name":"Nounin Yuuki"},{"name":"運天 拡人"},{"name":"Yoshino Masaki"},{"name":"Mitsuboshi Satoru"},{"name":"相澤 風花"},{"name":"八木 健太"},{"name":"Koyama Toshihiro"},{"name":"合田 光寛"},{"name":"Kanda Yasunari"},{"name":"石澤 有紀"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Systematic evaluation of ALK inhibitor-associated adverse events revealed differences in the cardiotoxicity profiles among ALK inhibitors. Understanding the differences in the cardiovascular toxicity profile of each ALK inhibitor will contribute to safe drug therapy when switching between ALK inhibitors.","ja":"Systematic evaluation of ALK inhibitor-associated adverse events revealed differences in the cardiotoxicity profiles among ALK inhibitors. Understanding the differences in the cardiovascular toxicity profile of each ALK inhibitor will contribute to safe drug therapy when switching between ALK inhibitors."},"publication_date":"2023-04-27","publication_name":{"en":"Drug Safety","ja":"Drug Safety"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s40264-023-01300-9"],"issn":["1179-1942"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:12, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36847276","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=402956","label":"url"}],"paper_title":{"en":"Proton Pump Inhibitors and Rhabdomyolysis: Analysis of Two Different Cross-Sectional Databases.","ja":"Proton Pump Inhibitors and Rhabdomyolysis: Analysis of Two Different Cross-Sectional Databases."},"authors":{"en":[{"name":"Mitsuboshi Satoru"},{"name":"Hamano Hirofumi"},{"name":"Kuniki Yurika"},{"name":"Niimura Takahiro"},{"name":"Chuma Masayuki"},{"name":"Ushio Soichiro"},{"name":"Lin Tsung-Jen"},{"name":"Matsumoto Jun"},{"name":"Takeda Tatsuaki"},{"name":"Kajizono Makoto"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Mitsuboshi Satoru"},{"name":"濱野 裕章"},{"name":"Kuniki Yurika"},{"name":"新村 貴博"},{"name":"中馬 真幸"},{"name":"Ushio Soichiro"},{"name":"Lin Tsung-Jen"},{"name":"Matsumoto Jun"},{"name":"Takeda Tatsuaki"},{"name":"Kajizono Makoto"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"The data in 2 separate databases consistently suggest that PPIs may increase the risk of rhabdomyolysis. The evidence for this association should be assessed in further drug safety studies.","ja":"The data in 2 separate databases consistently suggest that PPIs may increase the risk of rhabdomyolysis. The evidence for this association should be assessed in further drug safety studies."},"publication_date":"2023-02-27","publication_name":{"en":"The Annals of Pharmacotherapy","ja":"The Annals of Pharmacotherapy"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1177/10600280231156270"],"issn":["1542-6270"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:13, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36738305","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394581","label":"url"}],"paper_title":{"en":"Effects of vonoprazan and proton pump inhibitors on the efficacy of bevacizumab: a multicentre retrospective study.","ja":"Effects of vonoprazan and proton pump inhibitors on the efficacy of bevacizumab: a multicentre retrospective study."},"authors":{"en":[{"name":"Yagi Kenta"},{"name":"Maruo Akinori"},{"name":"Ishida Shunsuke"},{"name":"Aizawa Fuka"},{"name":"Ushio Soichiro"},{"name":"Sakaguchi Satoshi"},{"name":"Kajizono Makoto"},{"name":"Niimura Takahiro"},{"name":"Goda Mitsuhiro"},{"name":"Hamano Hirofumi"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"八木 健太"},{"name":"Maruo Akinori"},{"name":"Ishida Shunsuke"},{"name":"相澤 風花"},{"name":"Ushio Soichiro"},{"name":"坂口 暁"},{"name":"Kajizono Makoto"},{"name":"新村 貴博"},{"name":"合田 光寛"},{"name":"濱野 裕章"},{"name":"石澤 有紀"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Gastric acid secretion inhibitors such as proton pump inhibitors (PPIs) and vonoprazan may change the duration of treatment with bevacizumab, a vascular endothelial growth factor (VEGF) inhibitor, for cancer. However, there are no data on this prolongation effect. Here, we aimed to determine whether the use of PPIs or vonoprazan in patients with cancer receiving bevacizumab affected the duration of bevacizumab treatment. This observational study was conducted at two national university hospitals in Japan and involved 222 patients using oral PPIs (N = 190) or vonoprazan (N = 32) at the start of bevacizumab treatment between January 2015 and December 2018. Patients who received only one course of bevacizumab were excluded. The primary endpoint was the duration of bevacizumab treatment. The duration of bevacizumab treatment varied significantly between the PPI and vonoprazan groups. For cancer types other than colorectal cancer (breast, lung, brain, and ovarian cancers), the median duration of treatment was 217 days (p < 0.05) and was longer in the vonoprazan group than in the PPI group. However, for colorectal cancer, the median duration of bevacizumab treatment was 147 days longer in the PPI group than in the vonoprazan group. Selection of appropriate gastric acid secretion inhibitors may improve the therapeutic efficacy of anti-VEGF drugs, including bevacizumab. Oestrogen is a key regulator of this effect and may be responsible for the varying association between PPI or vonoprazan administration and the difference in bevacizumab treatment duration between colon cancer and other cancer types.","ja":"Gastric acid secretion inhibitors such as proton pump inhibitors (PPIs) and vonoprazan may change the duration of treatment with bevacizumab, a vascular endothelial growth factor (VEGF) inhibitor, for cancer. However, there are no data on this prolongation effect. Here, we aimed to determine whether the use of PPIs or vonoprazan in patients with cancer receiving bevacizumab affected the duration of bevacizumab treatment. This observational study was conducted at two national university hospitals in Japan and involved 222 patients using oral PPIs (N = 190) or vonoprazan (N = 32) at the start of bevacizumab treatment between January 2015 and December 2018. Patients who received only one course of bevacizumab were excluded. The primary endpoint was the duration of bevacizumab treatment. The duration of bevacizumab treatment varied significantly between the PPI and vonoprazan groups. For cancer types other than colorectal cancer (breast, lung, brain, and ovarian cancers), the median duration of treatment was 217 days (p < 0.05) and was longer in the vonoprazan group than in the PPI group. However, for colorectal cancer, the median duration of bevacizumab treatment was 147 days longer in the PPI group than in the vonoprazan group. Selection of appropriate gastric acid secretion inhibitors may improve the therapeutic efficacy of anti-VEGF drugs, including bevacizumab. Oestrogen is a key regulator of this effect and may be responsible for the varying association between PPI or vonoprazan administration and the difference in bevacizumab treatment duration between colon cancer and other cancer types."},"publication_date":"2023-02-04","publication_name":{"en":"Clinical and Experimental Medicine","ja":"Clinical and Experimental Medicine"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10238-023-01008-1"],"issn":["1591-9528"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:14, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36453166","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=396493","label":"url"}],"paper_title":{"en":"Characterization of Immune Checkpoint Inhibitor-Induced Myasthenia Gravis Using the US Food and Drug Administration Adverse Event Reporting System.","ja":"Characterization of Immune Checkpoint Inhibitor-Induced Myasthenia Gravis Using the US Food and Drug Administration Adverse Event Reporting System."},"authors":{"en":[{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Miyata Koji"},{"name":"Mikami Takahisa"},{"name":"Asada Mizuho"},{"name":"Fukushima Keijo"},{"name":"Yoshino Masaki"},{"name":"Mitsuboshi Satoru"},{"name":"Okada Naoto"},{"name":"Hamano Hirofumi"},{"name":"Sakurada Takumi"},{"name":"Matsuoka-Ando Rie"},{"name":"Aizawa Fuka"},{"name":"Yagi Kenta"},{"name":"Goda Mitsuhiro"},{"name":"Chuma Masayuki"},{"name":"Koyama Toshihiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yanagawa Hiroaki"},{"name":"Fujino Hiromichi"},{"name":"Yamanishi Yoshihiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"宮田 晃志"},{"name":"Mikami Takahisa"},{"name":"Asada Mizuho"},{"name":"福島 圭穣"},{"name":"Yoshino Masaki"},{"name":"Mitsuboshi Satoru"},{"name":"岡田 直人"},{"name":"濱野 裕章"},{"name":"櫻田 巧"},{"name":"Matsuoka-Ando Rie"},{"name":"相澤 風花"},{"name":"八木 健太"},{"name":"合田 光寛"},{"name":"中馬 真幸"},{"name":"Koyama Toshihiro"},{"name":"石澤 有紀"},{"name":"楊河 宏章"},{"name":"藤野 裕道"},{"name":"Yamanishi Yoshihiro"},{"name":"石澤 啓介"}]},"description":{"en":"Myasthenia gravis (MG) is a rare but fatal adverse event of immune checkpoint inhibitors (ICIs). We assessed whether patient characteristics differed between those with ICI-related myasthenia gravis and those with idiopathic myasthenia gravis. Reports from the US Food and Drug Administration Adverse Event Reporting System were analyzed. Multivariate analyses were conducted to evaluate the associations between age, sex, and ICI treatment and the reporting rate of myasthenia gravis. Among 5 464 099 cases between 2011 and 2019, 53 447 were treated with ICIs. Myasthenia gravis was reported more often in ICI users. Multiple logistic regression analyses showed that the reporting rate of ICI-related myasthenia gravis did not differ significantly between men and women; however, it was higher in older people than in younger people (adjusted odds ratio, 2.4 [95%CI, 1.84-3.13]). We also investigated useful signs for the early detection of myositis and myocarditis, which are fatal when overlapping with ICI-related myasthenia gravis. Patients with elevated serum creatine kinase or troponin levels were more likely to have concurrent myositis and myocarditis. Unlike idiopathic myasthenia gravis, there was no sex difference in the development of ICI-related myasthenia gravis, which may be more common in older people. Considering the physiological muscle weakness that occurs in the elderly, it may be necessary to monitor ICI-related myasthenia gravis more closely in older people.","ja":"Myasthenia gravis (MG) is a rare but fatal adverse event of immune checkpoint inhibitors (ICIs). We assessed whether patient characteristics differed between those with ICI-related myasthenia gravis and those with idiopathic myasthenia gravis. Reports from the US Food and Drug Administration Adverse Event Reporting System were analyzed. Multivariate analyses were conducted to evaluate the associations between age, sex, and ICI treatment and the reporting rate of myasthenia gravis. Among 5 464 099 cases between 2011 and 2019, 53 447 were treated with ICIs. Myasthenia gravis was reported more often in ICI users. Multiple logistic regression analyses showed that the reporting rate of ICI-related myasthenia gravis did not differ significantly between men and women; however, it was higher in older people than in younger people (adjusted odds ratio, 2.4 [95%CI, 1.84-3.13]). We also investigated useful signs for the early detection of myositis and myocarditis, which are fatal when overlapping with ICI-related myasthenia gravis. Patients with elevated serum creatine kinase or troponin levels were more likely to have concurrent myositis and myocarditis. Unlike idiopathic myasthenia gravis, there was no sex difference in the development of ICI-related myasthenia gravis, which may be more common in older people. Considering the physiological muscle weakness that occurs in the elderly, it may be necessary to monitor ICI-related myasthenia gravis more closely in older people."},"publication_date":"2022-12-21","publication_name":{"en":"Journal of Clinical Pharmacology","ja":"Journal of Clinical Pharmacology"},"volume":"Vol.63","number":"No.4","starting_page":"473","ending_page":"479","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/jcph.2187"],"issn":["1552-4604"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:15, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/118289","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36484282","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394580","label":"url"}],"paper_title":{"en":"Differential effects of proton pump inhibitors and vonoprazan on vascular endothelial growth factor expression in cancer cells.","ja":"Differential effects of proton pump inhibitors and vonoprazan on vascular endothelial growth factor expression in cancer cells."},"authors":{"en":[{"name":"Ando-Matsuoka Rie"},{"name":"Yagi Kenta"},{"name":"Takaoka Mayu"},{"name":"Sakajiri Yuko"},{"name":"Shibata Tomokazu"},{"name":"Sawada Ryusuke"},{"name":"Maruo Akinori"},{"name":"Miyata Koji"},{"name":"Aizawa Fuka"},{"name":"Hamano Hirofumi"},{"name":"Niimura Takahiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Goda Mitsuhiro"},{"name":"Sakaguchi Satoshi"},{"name":"Zamami Yoshito"},{"name":"Yamanishi Yoshihiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Ando-Matsuoka Rie"},{"name":"八木 健太"},{"name":"Takaoka Mayu"},{"name":"Sakajiri Yuko"},{"name":"Shibata Tomokazu"},{"name":"Sawada Ryusuke"},{"name":"Maruo Akinori"},{"name":"Miyata Koji"},{"name":"相澤 風花"},{"name":"濱野 裕章"},{"name":"新村 貴博"},{"name":"石澤 有紀"},{"name":"合田 光寛"},{"name":"坂口 暁"},{"name":"座間味 義人"},{"name":"Yamanishi Yoshihiro"},{"name":"石澤 啓介"}]},"description":{"en":"Proton pump inhibitors (PPIs) are potent inhibitors of gastric acid secretion, used as first-line agents in treating peptic ulcers. However, we have previously reported that PPIs may diminish the therapeutic effect of anti-vascular endothelial growth factor (VEGF) drugs in patients with cancer. In this study, we explored the effects of vonoprazan, a novel gastric acid secretion inhibitor used for the treatment of peptic ulcers, on the secretion of VEGF in cancer cells and attempted to propose it as an alternative PPI for cancer chemotherapy. The effects of PPI and vonoprazan on VEGF expression in cancer cells were compared by real-time reverse transcription-polymerase chain reaction and ELISA. The interaction of vonoprazan and PPIs with transcriptional regulators by docking simulation analysis. In various cancer cell lines, including the human colorectal cancer cell line (LS174T), PPI increased VEGF messenger RNA expression and VEGF protein secretion, while this effect was not observed with vonoprazan. Molecular docking simulation analysis showed that vonoprazan had a lower binding affinity for estrogen receptor alpha (ER-α), one of the transcriptional regulators of VEGF, compared to PPI. Although the PPI-induced increase in VEGF expression was counteracted by pharmacological ER-α inhibition, the effect of vonoprazan on VEGF expression was unchanged. Vonoprazan does not affect VEGF expression in cancer cells, which suggests that vonoprazan might be an alternative to PPIs, with no interference with the therapeutic effects of anti-VEGF cancer chemotherapy.","ja":"Proton pump inhibitors (PPIs) are potent inhibitors of gastric acid secretion, used as first-line agents in treating peptic ulcers. However, we have previously reported that PPIs may diminish the therapeutic effect of anti-vascular endothelial growth factor (VEGF) drugs in patients with cancer. In this study, we explored the effects of vonoprazan, a novel gastric acid secretion inhibitor used for the treatment of peptic ulcers, on the secretion of VEGF in cancer cells and attempted to propose it as an alternative PPI for cancer chemotherapy. The effects of PPI and vonoprazan on VEGF expression in cancer cells were compared by real-time reverse transcription-polymerase chain reaction and ELISA. The interaction of vonoprazan and PPIs with transcriptional regulators by docking simulation analysis. In various cancer cell lines, including the human colorectal cancer cell line (LS174T), PPI increased VEGF messenger RNA expression and VEGF protein secretion, while this effect was not observed with vonoprazan. Molecular docking simulation analysis showed that vonoprazan had a lower binding affinity for estrogen receptor alpha (ER-α), one of the transcriptional regulators of VEGF, compared to PPI. Although the PPI-induced increase in VEGF expression was counteracted by pharmacological ER-α inhibition, the effect of vonoprazan on VEGF expression was unchanged. Vonoprazan does not affect VEGF expression in cancer cells, which suggests that vonoprazan might be an alternative to PPIs, with no interference with the therapeutic effects of anti-VEGF cancer chemotherapy."},"publication_date":"2022-12-09","publication_name":{"en":"Drug Development Research","ja":"Drug Development Research"},"volume":"Vol.84","number":"No.1","starting_page":"75","ending_page":"83","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/ddr.22013"],"issn":["1098-2299"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:16, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36169161","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394582","label":"url"}],"paper_title":{"en":"Non-recovery of vancomycin-associated nephrotoxicity is related to worsening survival outcomes: Combined retrospective analyses of two real-world databases.","ja":"Non-recovery of vancomycin-associated nephrotoxicity is related to worsening survival outcomes: Combined retrospective analyses of two real-world databases."},"authors":{"en":[{"name":"Chuma Masayuki"},{"name":"Hamano Hirofumi"},{"name":"Bando Takashi"},{"name":"Kondo Masateru"},{"name":"Okada Naoto"},{"name":"Izumi Yuki"},{"name":"Ishida Shunsuke"},{"name":"Yoshioka Toshihiko"},{"name":"Asada Mizuho"},{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Goda Mitsuhiro"},{"name":"Miyata Koji"},{"name":"Yagi Kenta"},{"name":"Kasamo Sachiko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Azuma Momoyo"},{"name":"Yanagawa Hiroaki"},{"name":"Tasaki Yoshikazu"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"中馬 真幸"},{"name":"濱野 裕章"},{"name":"Bando Takashi"},{"name":"Kondo Masateru"},{"name":"岡田 直人"},{"name":"Izumi Yuki"},{"name":"Ishida Shunsuke"},{"name":"Yoshioka Toshihiko"},{"name":"Asada Mizuho"},{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"合田 光寛"},{"name":"Miyata Koji"},{"name":"八木 健太"},{"name":"Kasamo Sachiko"},{"name":"石澤 有紀"},{"name":"東 桃代"},{"name":"楊河 宏章"},{"name":"Tasaki Yoshikazu"},{"name":"石澤 啓介"}]},"description":{"en":"There has been growing concern in worsening survival and renal outcomes following vancomycin-associated nephrotoxicity (VAN) onset, but the factors associated with these phenomena remain unclear. To examine these factors, we performed a retrospective study combining the analysis of two real-world databases. Initially, the FDA Adverse Event Reporting System (FAERS) was used to evaluate the relationship between VAN and mortality using odds ratios (ORs) and 95% confidence intervals (CIs). Next, electronic medical records (EMRs) were examined in a more robust cohort for evaluation of the association between renal outcomes and worsening survival using Cox proportional hazards regression models. FAERS analysis revealed a significant correlation between VAN occurrence and increased mortality (OR: 1.30; 95% CI: 1.17-1.46). EMR analysis showed that non-recovery of VAN was associated with increased hospital mortality (hazard ratio [HR]: 4.05; 95% CI: 2.42-6.77) and 1-year mortality (HR: 3.03, 95% CI: 1.98-4.64). The HR for VAN recovery was lower for patients with acute kidney injury (AKI) stage 2 (HR: 0.09; 95% CI: 0.02-0.40). Thus, worsening survival outcomes were associated with non-recovery of VAN, whereby AKI stage 2 was a significant risk factor. Progression to severe VAN should be prevented for better survival outcomes.","ja":"There has been growing concern in worsening survival and renal outcomes following vancomycin-associated nephrotoxicity (VAN) onset, but the factors associated with these phenomena remain unclear. To examine these factors, we performed a retrospective study combining the analysis of two real-world databases. Initially, the FDA Adverse Event Reporting System (FAERS) was used to evaluate the relationship between VAN and mortality using odds ratios (ORs) and 95% confidence intervals (CIs). Next, electronic medical records (EMRs) were examined in a more robust cohort for evaluation of the association between renal outcomes and worsening survival using Cox proportional hazards regression models. FAERS analysis revealed a significant correlation between VAN occurrence and increased mortality (OR: 1.30; 95% CI: 1.17-1.46). EMR analysis showed that non-recovery of VAN was associated with increased hospital mortality (hazard ratio [HR]: 4.05; 95% CI: 2.42-6.77) and 1-year mortality (HR: 3.03, 95% CI: 1.98-4.64). The HR for VAN recovery was lower for patients with acute kidney injury (AKI) stage 2 (HR: 0.09; 95% CI: 0.02-0.40). Thus, worsening survival outcomes were associated with non-recovery of VAN, whereby AKI stage 2 was a significant risk factor. Progression to severe VAN should be prevented for better survival outcomes."},"publication_date":"2022-10-07","publication_name":{"en":"Basic & Clinical Pharmacology & Toxicology","ja":"Basic & Clinical Pharmacology & Toxicology"},"volume":"Vol.131","number":"No.6","starting_page":"525","ending_page":"535","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/bcpt.13799"],"issn":["1742-7843"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:17, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/118179","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36128688","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394583","label":"url"}],"paper_title":{"en":"Evaluation of the potential complication of interstitial lung disease associated with antifibrotic drugs using data from databases reporting spontaneous adverse effects.","ja":"Evaluation of the potential complication of interstitial lung disease associated with antifibrotic drugs using data from databases reporting spontaneous adverse effects."},"authors":{"en":[{"name":"Nawa Hideki"},{"name":"Hamano Hirofumi"},{"name":"Niimura Takahiro"},{"name":"Miyata Koji"},{"name":"Yagi Kenta"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Nawa Hideki"},{"name":"濱野 裕章"},{"name":"新村 貴博"},{"name":"Miyata Koji"},{"name":"八木 健太"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Interstitial lung disease (ILD), as an adverse effect of certain drugs, leads to inflammation and damage in the walls of the alveoli, making it difficult for the alveoli to take up oxygen. Interstitial pneumonia with no identifiable cause is called idiopathic interstitial pneumonia (IIP), and, among the major IIPs, idiopathic pulmonary fibrosis (IPF) is diagnosed in about half of patients. Current treatment options are limited, among which the antifibrotic drugs nintedanib (Ofev) and pirfenidone (Pirespa) are the first-line drugs. In this study, we investigated the incidence of ILD possibly caused by antifibrotic agents using data from the Japanese Adverse Drug Event Report (JADER) database, a database of spontaneous adverse event reports published by the Pharmaceuticals and Medical Devices Agency (PMDA), and the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS), published by the FDA. We used the FAERS and JADER to detect the signals of adverse events on the basis of reporting odds ratios. The relationship between indications and adverse events was clarified by separating indications and adverse events using the spontaneous adverse event reporting database with novel drug involvement. Regarding the involvement of nintedanib and pirfenidone in the development of ILD, JADER and FAERS showed signals for both nintedanib and pirfenidone as suspect drugs, and no signals for nintedanib or pirfenidone as concomitant drug interactions were detected. We highlight this because there are only a few effective drugs for IPF, and effective and safe drug therapies should be implemented by taking into consideration drug-induced ILD.","ja":"Interstitial lung disease (ILD), as an adverse effect of certain drugs, leads to inflammation and damage in the walls of the alveoli, making it difficult for the alveoli to take up oxygen. Interstitial pneumonia with no identifiable cause is called idiopathic interstitial pneumonia (IIP), and, among the major IIPs, idiopathic pulmonary fibrosis (IPF) is diagnosed in about half of patients. Current treatment options are limited, among which the antifibrotic drugs nintedanib (Ofev) and pirfenidone (Pirespa) are the first-line drugs. In this study, we investigated the incidence of ILD possibly caused by antifibrotic agents using data from the Japanese Adverse Drug Event Report (JADER) database, a database of spontaneous adverse event reports published by the Pharmaceuticals and Medical Devices Agency (PMDA), and the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS), published by the FDA. We used the FAERS and JADER to detect the signals of adverse events on the basis of reporting odds ratios. The relationship between indications and adverse events was clarified by separating indications and adverse events using the spontaneous adverse event reporting database with novel drug involvement. Regarding the involvement of nintedanib and pirfenidone in the development of ILD, JADER and FAERS showed signals for both nintedanib and pirfenidone as suspect drugs, and no signals for nintedanib or pirfenidone as concomitant drug interactions were detected. We highlight this because there are only a few effective drugs for IPF, and effective and safe drug therapies should be implemented by taking into consideration drug-induced ILD."},"publication_date":"2022-09-27","publication_name":{"en":"Clinical and Translational Science","ja":"Clinical and Translational Science"},"volume":"Vol.15","number":"No.12","starting_page":"2982","ending_page":"2988","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/cts.13419"],"issn":["1752-8062"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:18, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35811059","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=388295","label":"url"}],"paper_title":{"en":"First reported case of Lachnoanaerobaculum gingivalis bacteremia in an acute myeloid leukemia patient with oral mucositis during high dose chemotherapy.","ja":"First reported case of Lachnoanaerobaculum gingivalis bacteremia in an acute myeloid leukemia patient with oral mucositis during high dose chemotherapy."},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Murakami Akikazu"},{"name":"Satou Masami"},{"name":"Nakamura Shingen"},{"name":"Fujii Shiroh"},{"name":"Sogabe Kimiko"},{"name":"Takahashi Mamiko"},{"name":"Okada Asami"},{"name":"Abe Akane"},{"name":"Fujii Hideki"},{"name":"Abe Masahiro"},{"name":"Azuma Momoyo"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"村上 明一"},{"name":"Satou Masami"},{"name":"中村 信元"},{"name":"藤井 志朗"},{"name":"曽我部 公子"},{"name":"Takahashi Mamiko"},{"name":"Okada Asami"},{"name":"阿部 あかね"},{"name":"藤猪 英樹"},{"name":"安倍 正博"},{"name":"東 桃代"},{"name":"石澤 啓介"}]},"description":{"en":"During chemotherapy in patients with oral mucositis, we should consider the possibility of L. gingivalis bacteremia.","ja":"During chemotherapy in patients with oral mucositis, we should consider the possibility of L. gingivalis bacteremia."},"publication_date":"2022-07-08","publication_name":{"en":"Anaerobe","ja":"Anaerobe"},"volume":"Vol.76","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.anaerobe.2022.102610"],"issn":["1095-8274"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:19, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117391","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35325241","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=387316","label":"url"}],"paper_title":{"en":"Prevention of Pemetrexed-Induced Rash Using Low-Dose Corticosteroids: A Phase II Study.","ja":"Prevention of Pemetrexed-Induced Rash Using Low-Dose Corticosteroids: A Phase II Study."},"authors":{"en":[{"name":"Sakurada Takumi"},{"name":"Nokihara Hiroshi"},{"name":"Koga Tadashi"},{"name":"Zamami Yoshito"},{"name":"Goda Mitsuhiro"},{"name":"Yagi Kenta"},{"name":"Hamano Hirofumi"},{"name":"Aizawa Fuka"},{"name":"Ogino Hirokazu"},{"name":"Satou Seidai"},{"name":"Kirino Yasushi"},{"name":"Goto Hisatsugu"},{"name":"Nishioka Yasuhiko"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Sakurada Takumi"},{"name":"軒原 浩"},{"name":"Koga Tadashi"},{"name":"座間味 義人"},{"name":"合田 光寛"},{"name":"Yagi Kenta"},{"name":"Hamano Hirofumi"},{"name":"相澤 風花"},{"name":"荻野 広和"},{"name":"佐藤 正大"},{"name":"Kirino Yasushi"},{"name":"後東 久嗣"},{"name":"西岡 安彦"},{"name":"石澤 啓介"}]},"description":{"en":"Prophylactic administration of low-dose dexamethasone for 5 days from the day after pemetrexed administration resulted in a milder incidence and severity of rash. These findings may provide a standard preventative strategy for pemetrexed-induced rashes. (Trial identifier: UMIN000025666).","ja":"This single-arm, phase II study recruited patients with non-squamous non-small cell lung cancer and malignant pleural mesothelioma scheduled to receive chemotherapy including pemetrexed. Patients received 2 mg of dexamethasone daily from days 2 to 6 after chemotherapy with pemetrexed. The primary endpoint was the 3-week incidence of rash eruptions."},"publication_date":"2022-07-05","publication_name":{"en":"The Oncologist","ja":"The Oncologist"},"volume":"Vol.27","number":"No.7","starting_page":"e554","ending_page":"e560","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/oncolo/oyab077"],"issn":["1549-490X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:20, {"insert":{"user_id":"6000008820","type":"published_papers","id":"38890553"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117583","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35752658","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=386499","label":"url"}],"paper_title":{"en":"A machine learning model using SNPs obtained from a genome-wide association study predicts the onset of vincristine-induced peripheral neuropathy","ja":"A machine learning model using SNPs obtained from a genome-wide association study predicts the onset of vincristine-induced peripheral neuropathy"},"authors":{"en":[{"name":"Yamada Hiroki"},{"name":"Ohmori Rio"},{"name":"Okada Naoto"},{"name":"Nakamura Shingen"},{"name":"Kagawa Kumiko"},{"name":"Fujii Shiroh"},{"name":"Miki Hirokazu"},{"name":"Ishizawa Keisuke"},{"name":"Abe Masahiro"},{"name":"Sato Youichi"}],"ja":[{"name":"山田 博貴"},{"name":"大森 理央"},{"name":"Okada Naoto"},{"name":"中村 信元"},{"name":"Kagawa Kumiko"},{"name":"藤井 志朗"},{"name":"三木 浩和"},{"name":"石澤 啓介"},{"name":"安倍 正博"},{"name":"佐藤 陽一"}]},"description":{"en":"Vincristine treatment may cause peripheral neuropathy. In this study, we identified the genes associated with the development of peripheral neuropathy due to vincristine therapy using a genome-wide association study (GWAS) and constructed a predictive model for the development of peripheral neuropathy using genetic information-based machine learning. The study included 72 patients admitted to the Department of Hematology, Tokushima University Hospital, who received vincristine. Of these, 56 were genotyped using the Illumina Asian Screening Array-24 Kit, and a GWAS for the onset of peripheral neuropathy caused by vincristine was conducted. Using Sanger sequencing for 16 validation samples, the top three single nucleotide polymorphisms (SNPs) associated with the onset of peripheral neuropathy were determined. Machine learning was performed using the statistical software R package \"caret\". The 56 GWAS and 16 validation samples were used as the training and test sets, respectively. Predictive models were constructed using random forest, support vector machine, naive Bayes, and neural network algorithms. According to the GWAS, rs2110179, rs7126100, and rs2076549 were associated with the development of peripheral neuropathy on vincristine administration. Machine learning was performed using these three SNPs to construct a prediction model. A high accuracy of 93.8% was obtained with the support vector machine and neural network using rs2110179 and rs2076549. Thus, peripheral neuropathy development due to vincristine therapy can be effectively predicted by a machine learning prediction model using SNPs associated with it.","ja":"Vincristine treatment may cause peripheral neuropathy. In this study, we identified the genes associated with the development of peripheral neuropathy due to vincristine therapy using a genome-wide association study (GWAS) and constructed a predictive model for the development of peripheral neuropathy using genetic information-based machine learning. The study included 72 patients admitted to the Department of Hematology, Tokushima University Hospital, who received vincristine. Of these, 56 were genotyped using the Illumina Asian Screening Array-24 Kit, and a GWAS for the onset of peripheral neuropathy caused by vincristine was conducted. Using Sanger sequencing for 16 validation samples, the top three single nucleotide polymorphisms (SNPs) associated with the onset of peripheral neuropathy were determined. Machine learning was performed using the statistical software R package \"caret\". The 56 GWAS and 16 validation samples were used as the training and test sets, respectively. Predictive models were constructed using random forest, support vector machine, naive Bayes, and neural network algorithms. According to the GWAS, rs2110179, rs7126100, and rs2076549 were associated with the development of peripheral neuropathy on vincristine administration. Machine learning was performed using these three SNPs to construct a prediction model. A high accuracy of 93.8% was obtained with the support vector machine and neural network using rs2110179 and rs2076549. Thus, peripheral neuropathy development due to vincristine therapy can be effectively predicted by a machine learning prediction model using SNPs associated with it."},"publication_date":"2022-06-25","publication_name":{"en":"The Pharmacogenomics Journal","ja":"The Pharmacogenomics Journal"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41397-022-00282-8"],"issn":["1473-1150"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:21, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117365","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35659512","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390279","label":"url"}],"paper_title":{"en":"Investigation of drugs for the prevention of doxorubicin-induced cardiac events using big data analysis.","ja":"Investigation of drugs for the prevention of doxorubicin-induced cardiac events using big data analysis."},"authors":{"en":[{"name":"Nishiuchi Shiori"},{"name":"Yagi Kenta"},{"name":"Saito Hiroumi"},{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Miyata Koji"},{"name":"Sakamoto Yoshika"},{"name":"Fukunaga Kimiko"},{"name":"Ishida Shunsuke"},{"name":"Hamano Hirofumi"},{"name":"Aizawa Fuka"},{"name":"Goda Mitsuhiro"},{"name":"Chuma Masayuki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Nawa Hideki"},{"name":"Yanagawa Hiroaki"},{"name":"Kanda Yasunari"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"西内 栞"},{"name":"八木 健太"},{"name":"齊藤 広海"},{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"宮田 晃志"},{"name":"阪本 淑華"},{"name":"Fukunaga Kimiko"},{"name":"Ishida Shunsuke"},{"name":"濱野 裕章"},{"name":"相澤 風花"},{"name":"合田 光寛"},{"name":"中馬 真幸"},{"name":"石澤 有紀"},{"name":"Nawa Hideki"},{"name":"楊河 宏章"},{"name":"Kanda Yasunari"},{"name":"石澤 啓介"}]},"description":{"en":"These findings suggest that doxorubicin-induced cardiac events are suppressed by the administration of mosapride and sirolimus.","ja":"The Gene Expression Omnibus (GEO), Library of Integrated Network-based Cellular Signatures (LINCS), and Food and Drug Administration Adverse Events Reporting System (FAERS) databases were used to extract candidate prophylactic drugs. Mouse models of doxorubicin-induced cardiac events were generated by intraperitoneal administration of 20 mg/kg of doxorubicin on Day 1 and oral administration of prophylactic candidate drugs for 6 consecutive days beginning the day before doxorubicin administration. On Day 6, mouse hearts were extracted and examined for mRNA expression of apoptosis-related genes."},"publication_date":"2022-05","publication_name":{"en":"European Journal of Pharmacology","ja":"European Journal of Pharmacology"},"volume":"Vol.928","number":"No.175083","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.ejphar.2022.175083"],"issn":["1879-0712"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:22, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117366","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35445533","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390280","label":"url"}],"paper_title":{"en":"Discovery of preventive drugs for cisplatin-induced acute kidney injury using big data analysis.","ja":"Discovery of preventive drugs for cisplatin-induced acute kidney injury using big data analysis."},"authors":{"en":[{"name":"Kanda Masaya"},{"name":"Goda Mitsuhiro"},{"name":"Maegawa Akiko"},{"name":"Yoshioka Toshihiko"},{"name":"Yoshida Ami"},{"name":"Miyata Koji"},{"name":"Aizawa Fuka"},{"name":"Niimura Takahiro"},{"name":"Hamano Hirofumi"},{"name":"Okada Naoto"},{"name":"Sakurada Takumi"},{"name":"Chuma Masayuki"},{"name":"Yagi Kenta"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yanagawa Hiroaki"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Kanda Masaya"},{"name":"合田 光寛"},{"name":"Maegawa Akiko"},{"name":"Yoshioka Toshihiko"},{"name":"Yoshida Ami"},{"name":"Miyata Koji"},{"name":"相澤 風花"},{"name":"新村 貴博"},{"name":"濱野 裕章"},{"name":"岡田 直人"},{"name":"Sakurada Takumi"},{"name":"中馬 真幸"},{"name":"八木 健太"},{"name":"石澤 有紀"},{"name":"楊河 宏章"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Cisplatin is effective against many types of carcinoma. However, a high rate of renal damage is a clinical problem. Thus, there is a need to establish a method to prevent it. Although various compounds have been reported to be effective against cisplatin-induced renal injury, there are no examples of their clinical application. Therefore, we attempted to search for prophylactic agents with a high potential for clinical application. We used Cascade Eye to identify genes that are altered during cisplatin-induced renal injury, Library of Integrated Network-based Cellular Signatures (LINCS) to identify drugs that inhibit changes in gene expression, and a large database of spontaneous adverse drug reaction reports to identify drugs that could prevent cisplatin-induced kidney injury in clinical practice. In total, 10 candidate drugs were identified. Using the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS), we identified drugs that reduce cisplatin-induced kidney injury. Fenofibrate was selected as a candidate drug to prevent cisplatin-induced kidney injury based on the FAERS analysis. A model was used to evaluate the efficacy of fenofibrate against cisplatin-induced renal injury. Studies using HK2 cells and mouse models showed that fenofibrate significantly inhibited cisplatin-induced renal injury but did not inhibit the antitumor effect of cisplatin. Fenofibrate is a candidate prophylactic drug with high clinical applicability for cisplatin-induced renal injury. Analysis of data from multiple big databases will improve the search for novel prophylactic drugs with high clinical applicability. For the practical application of these findings, evaluation in prospective controlled trials is necessary.","ja":"Cisplatin is effective against many types of carcinoma. However, a high rate of renal damage is a clinical problem. Thus, there is a need to establish a method to prevent it. Although various compounds have been reported to be effective against cisplatin-induced renal injury, there are no examples of their clinical application. Therefore, we attempted to search for prophylactic agents with a high potential for clinical application. We used Cascade Eye to identify genes that are altered during cisplatin-induced renal injury, Library of Integrated Network-based Cellular Signatures (LINCS) to identify drugs that inhibit changes in gene expression, and a large database of spontaneous adverse drug reaction reports to identify drugs that could prevent cisplatin-induced kidney injury in clinical practice. In total, 10 candidate drugs were identified. Using the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS), we identified drugs that reduce cisplatin-induced kidney injury. Fenofibrate was selected as a candidate drug to prevent cisplatin-induced kidney injury based on the FAERS analysis. A model was used to evaluate the efficacy of fenofibrate against cisplatin-induced renal injury. Studies using HK2 cells and mouse models showed that fenofibrate significantly inhibited cisplatin-induced renal injury but did not inhibit the antitumor effect of cisplatin. Fenofibrate is a candidate prophylactic drug with high clinical applicability for cisplatin-induced renal injury. Analysis of data from multiple big databases will improve the search for novel prophylactic drugs with high clinical applicability. For the practical application of these findings, evaluation in prospective controlled trials is necessary."},"publication_date":"2022-04-30","publication_name":{"en":"Clinical and Translational Science","ja":"Clinical and Translational Science"},"volume":"Vol.15","number":"No.7","starting_page":"1664","ending_page":"1675","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/cts.13282"],"issn":["1752-8062"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:23, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35464114","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390276","label":"url"}],"paper_title":{"en":"A web-based survey of educational opportunities of medical professionals based on changes in conference design during the COVID-19 pandemic.","ja":"A web-based survey of educational opportunities of medical professionals based on changes in conference design during the COVID-19 pandemic."},"authors":{"en":[{"name":"Yagi Kenta"},{"name":"Sato Yasutaka"},{"name":"Sakaguchi Satoshi"},{"name":"Goda Mitsuhiro"},{"name":"Hamano Hirofumi"},{"name":"Aizawa Fuka"},{"name":"Shimizu Mayuko"},{"name":"Inoue-Hamano Arisa"},{"name":"Nishimori Toshihide"},{"name":"Tagi Masato"},{"name":"Kanno Marina"},{"name":"Matsuoka-Ando Rie"},{"name":"Yoshioka Toshihiko"},{"name":"Matstubara Yoshiko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Shimizu Rieko"},{"name":"Maruo Akinori"},{"name":"Kuniki Yurika"},{"name":"Sakamoto Yoshika"},{"name":"Itobayashi Sayuri"},{"name":"Zamami Yoshito"},{"name":"Yanagawa Hiroaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"八木 健太"},{"name":"Sato Yasutaka"},{"name":"坂口 暁"},{"name":"合田 光寛"},{"name":"濱野 裕章"},{"name":"相澤 風花"},{"name":"清水 真祐子"},{"name":"Inoue-Hamano Arisa"},{"name":"Nishimori Toshihide"},{"name":"田木 真和"},{"name":"Kanno Marina"},{"name":"Matsuoka-Ando Rie"},{"name":"吉岡 俊彦"},{"name":"Matstubara Yoshiko"},{"name":"石澤 有紀"},{"name":"Shimizu Rieko"},{"name":"Maruo Akinori"},{"name":"國木 悠理香"},{"name":"阪本 淑華"},{"name":"糸林 小友理"},{"name":"座間味 義人"},{"name":"楊河 宏章"},{"name":"石澤 啓介"}]},"description":{"en":"The online version contains supplementary material available at 10.1007/s10639-022-11032-5.","ja":"The online version contains supplementary material available at 10.1007/s10639-022-11032-5."},"publication_date":"2022-04-18","publication_name":{"en":"Education and Information Technologies","ja":"Education and Information Technologies"},"volume":"Vol.27","starting_page":"10371","ending_page":"10386","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10639-022-11032-5"],"issn":["1360-2357"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:24, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117810","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35262686","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390814","label":"url"}],"paper_title":{"en":"Association between statin use and daptomycin-related musculoskeletal adverse events: A mixed approach combining a meta-analysis and a disproportionality analysis.","ja":"Association between statin use and daptomycin-related musculoskeletal adverse events: A mixed approach combining a meta-analysis and a disproportionality analysis."},"authors":{"en":[{"name":"Chuma Masayuki"},{"name":"Nakamoto Aki"},{"name":"Bando Takashi"},{"name":"Niimura Takahiro"},{"name":"Kondo Yutaka"},{"name":"Hamano Hirofumi"},{"name":"Okada Naoto"},{"name":"Asada Mizuho"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Goda Mitsuhiro"},{"name":"Miyata Koji"},{"name":"Yagi Kenta"},{"name":"Yoshioka Toshihiko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yanagawa Hiroaki"},{"name":"Tasaki Yoshikazu"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"中馬 真幸"},{"name":"中本 亜樹"},{"name":"坂東 貴司"},{"name":"新村 貴博"},{"name":"Kondo Yutaka"},{"name":"濱野 裕章"},{"name":"岡田 直人"},{"name":"Asada Mizuho"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"合田 光寛"},{"name":"宮田 晃志"},{"name":"八木 健太"},{"name":"吉岡 俊彦"},{"name":"石澤 有紀"},{"name":"楊河 宏章"},{"name":"Tasaki Yoshikazu"},{"name":"石澤 啓介"}]},"description":{"en":"There is a growing concern about the association between the combined use of daptomycin (DAP) and statins and the occurrence of musculoskeletal adverse events (MAEs), but this remains controversial. This study aimed to clarify the association between statin use and DAP-related MAEs. We used a mixed approach that combines two methodologies. First, we conducted a meta-analysis to examine the effects of statin use on DAP-related MAEs. Second, we conducted a disproportionality analysis using the FDA Adverse Events Reporting System (FAERS) to further confirm the results of the meta-analysis and to examine the effect of each type of statin on DAP-related MAEs in a large population. In the meta-analysis, statin use significantly increased the incidence of DAP-related rhabdomyolysis (odds ratio [OR]: 3.83, 95% confidence interval [CI]: 1.43-10.26) but not DAP-related myopathy (OR: 1.72, 95% CI: 0.95-3.12). In the disproportionality analysis using the FAERS, the use of statin significantly increased the reporting OR (ROR) for DAP-related myopathy (ROR: 5.69, 95% CI: 4.31-7.51) and rhabdomyolysis (ROR: 5.77, 95% CI: 4.33-7.68). Atorvastatin, rosuvastatin, and simvastatin all increased the incidence of DAP-related myopathy and rhabdomyolysis. The mixed approach combining a meta-analysis and disproportionality analysis showed that statin use was associated with the occurrence of DAP-related rhabdomyolysis. The appropriate use of statins and DAP should be performed with careful consideration of its safety.","ja":"There is a growing concern about the association between the combined use of daptomycin (DAP) and statins and the occurrence of musculoskeletal adverse events (MAEs), but this remains controversial. This study aimed to clarify the association between statin use and DAP-related MAEs. We used a mixed approach that combines two methodologies. First, we conducted a meta-analysis to examine the effects of statin use on DAP-related MAEs. Second, we conducted a disproportionality analysis using the FDA Adverse Events Reporting System (FAERS) to further confirm the results of the meta-analysis and to examine the effect of each type of statin on DAP-related MAEs in a large population. In the meta-analysis, statin use significantly increased the incidence of DAP-related rhabdomyolysis (odds ratio [OR]: 3.83, 95% confidence interval [CI]: 1.43-10.26) but not DAP-related myopathy (OR: 1.72, 95% CI: 0.95-3.12). In the disproportionality analysis using the FAERS, the use of statin significantly increased the reporting OR (ROR) for DAP-related myopathy (ROR: 5.69, 95% CI: 4.31-7.51) and rhabdomyolysis (ROR: 5.77, 95% CI: 4.33-7.68). Atorvastatin, rosuvastatin, and simvastatin all increased the incidence of DAP-related myopathy and rhabdomyolysis. The mixed approach combining a meta-analysis and disproportionality analysis showed that statin use was associated with the occurrence of DAP-related rhabdomyolysis. The appropriate use of statins and DAP should be performed with careful consideration of its safety."},"publication_date":"2022-03-09","publication_name":{"en":"Clinical Infectious Diseases","ja":"Clinical Infectious Diseases"},"volume":"Vol.75","number":"No.8","starting_page":"1416","ending_page":"1422","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/cid/ciac128"],"issn":["1537-6591"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:25, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117414","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35240525","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=388515","label":"url"}],"paper_title":{"en":"Identification of prophylactic drugs for oxaliplatin-induced peripheral neuropathy using big data.","ja":"Identification of prophylactic drugs for oxaliplatin-induced peripheral neuropathy using big data."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Kawashiri Takehiro"},{"name":"Goda Mitsuhiro"},{"name":"Naito Yutaro"},{"name":"Fukushima Keijo"},{"name":"Ushio Soichiro"},{"name":"Aizawa Fuka"},{"name":"Hamano Hirofumi"},{"name":"Okada Naoto"},{"name":"Yagi Kenta"},{"name":"Miyata Koji"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Koyama Toshihiro"},{"name":"Kobayashi Daisuke"},{"name":"Shimazoe Takao"},{"name":"Fujino Hiromichi"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"Kawashiri Takehiro"},{"name":"合田 光寛"},{"name":"Naito Yutaro"},{"name":"福島 圭穣"},{"name":"Ushio Soichiro"},{"name":"相澤 風花"},{"name":"濱野 裕章"},{"name":"岡田 直人"},{"name":"八木 健太"},{"name":"Miyata Koji"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"Koyama Toshihiro"},{"name":"Kobayashi Daisuke"},{"name":"Shimazoe Takao"},{"name":"藤野 裕道"},{"name":"石澤 有紀"},{"name":"石澤 啓介"}]},"description":{"en":"Thus, drug repositioning using data from large-scale basic and clinical databases enables the discovery of new indications for approved drugs with a high probability of success.","ja":"Thus, drug repositioning using data from large-scale basic and clinical databases enables the discovery of new indications for approved drugs with a high probability of success."},"publication_date":"2022-02-28","publication_name":{"en":"Biomedicine & Pharmacotherapy","ja":"Biomedicine & Pharmacotherapy"},"volume":"Vol.148","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.biopha.2022.112744"],"issn":["1950-6007"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:26, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117584","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/34657909","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=383649","label":"url"}],"paper_title":{"en":"A genome-wide association study predicts the onset of dysgeusia due to anti-cancer drug treatment","ja":"A genome-wide association study predicts the onset of dysgeusia due to anti-cancer drug treatment"},"authors":{"en":[{"name":"Takei Minori"},{"name":"Okada Naoto"},{"name":"Nakamura Shingen"},{"name":"Kagawa Kumiko"},{"name":"Fujii Shiroh"},{"name":"Miki Hirokazu"},{"name":"Ishizawa Keisuke"},{"name":"Abe Masahiro"},{"name":"Sato Youichi"}],"ja":[{"name":"武井 みのり"},{"name":"Okada Naoto"},{"name":"中村 信元"},{"name":"賀川 久美子"},{"name":"藤井 志朗"},{"name":"三木 浩和"},{"name":"石澤 啓介"},{"name":"安倍 正博"},{"name":"佐藤 陽一"}]},"description":{"en":"Dysgeusia is a major side effect of anti-cancer drug treatment. Since dysgeusia significantly lowers the patient's QOL, predicting and avoiding its onset in advance is desirable. Accordingly, aims of the present study were to use a genome-wide association study (GWAS) to identify genes associated with the development of dysgeusia in patients taking anti-cancer drugs and to predict the development of dysgeusia using associated single nucleotide polymorphisms (SNPs). GWAS was conducted on 76 patients admitted to the Department of Hematology, Tokushima University Hospital. Using Sanger sequencing for 23 separately collected validation samples, the top two SNPs associated with the development of dysgeusia were determined. GWAS identified rs73049478 and rs41396146 SNPs on the retinoic acid receptor beta (RARB) gene associated with dysgeusia development due to the administration of anti-cancer drugs. Evaluation of the two SNPs using 23 validation samples indicated that the accuracy rate of rs73049478 was relatively high (87.0%). Thus, the findings of the present study suggest that the rs73049478 SNP of RARB can be used to predict the onset of dysgeusia caused by the administration of anti-cancer drugs.","ja":"Dysgeusia is a major side effect of anti-cancer drug treatment. Since dysgeusia significantly lowers the patient's QOL, predicting and avoiding its onset in advance is desirable. Accordingly, aims of the present study were to use a genome-wide association study (GWAS) to identify genes associated with the development of dysgeusia in patients taking anti-cancer drugs and to predict the development of dysgeusia using associated single nucleotide polymorphisms (SNPs). GWAS was conducted on 76 patients admitted to the Department of Hematology, Tokushima University Hospital. Using Sanger sequencing for 23 separately collected validation samples, the top two SNPs associated with the development of dysgeusia were determined. GWAS identified rs73049478 and rs41396146 SNPs on the retinoic acid receptor beta (RARB) gene associated with dysgeusia development due to the administration of anti-cancer drugs. Evaluation of the two SNPs using 23 validation samples indicated that the accuracy rate of rs73049478 was relatively high (87.0%). Thus, the findings of the present study suggest that the rs73049478 SNP of RARB can be used to predict the onset of dysgeusia caused by the administration of anti-cancer drugs."},"publication_date":"2022-01-01","publication_name":{"en":"Biological & Pharmaceutical Bulletin","ja":"Biological & Pharmaceutical Bulletin"},"volume":"Vol.45","number":"No.1","starting_page":"114","ending_page":"117","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1248/bpb.b21-00745"],"issn":["1347-5215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:27, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/34803077","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390812","label":"url"}],"paper_title":{"en":"Renin-Angiotensin-Aldosterone System Inhibitors Prevent the Onset of Oxaliplatin-Induced Peripheral Neuropathy: A Retrospective Multicenter Study and in Vitro Evaluation.","ja":"Renin-Angiotensin-Aldosterone System Inhibitors Prevent the Onset of Oxaliplatin-Induced Peripheral Neuropathy: A Retrospective Multicenter Study and in Vitro Evaluation."},"authors":{"en":[{"name":"Uchida Mami"},{"name":"Ushio Soichiro"},{"name":"Niimura Takahiro"},{"name":"Takechi Kenshi"},{"name":"Kawazoe Hitoshi"},{"name":"Hidaka Noriaki"},{"name":"Tanaka Akihiro"},{"name":"Araki Hiroaki"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"},{"name":"Kitamura Yoshihisa"},{"name":"Sendou Toshiaki"},{"name":"Kawasaki Hiromu"},{"name":"Namba Hiroyuki"},{"name":"Shibata Kazuhiko"},{"name":"Tanaka Mamoru"},{"name":"Takatori Shingo"}],"ja":[{"name":"Uchida Mami"},{"name":"Ushio Soichiro"},{"name":"新村 貴博"},{"name":"Takechi Kenshi"},{"name":"Kawazoe Hitoshi"},{"name":"Hidaka Noriaki"},{"name":"Tanaka Akihiro"},{"name":"Araki Hiroaki"},{"name":"座間味 義人"},{"name":"石澤 啓介"},{"name":"Kitamura Yoshihisa"},{"name":"Sendou Toshiaki"},{"name":"Kawasaki Hiromu"},{"name":"Namba Hiroyuki"},{"name":"Shibata Kazuhiko"},{"name":"Tanaka Mamoru"},{"name":"Takatori Shingo"}]},"description":{"en":"Oxaliplatin (OXA) is used in chemotherapy for various cancer types and is associated with acute and chronic neurotoxicity. However, a preventive strategy for OXA-induced peripheral neuropathy (OIPN) and its underlying mechanism remain unclear. We examined the effects of renin-angiotensin-aldosterone system inhibitors (RAASIs) on OIPN by performing a retrospective multicenter study and an in vitro assay. We retrospectively evaluated electronic medical records of 976 patients who underwent one or more courses of OXA-containing regimens at Ehime, Okayama, and Tokushima University Hospitals. The primary endpoint was the incidence of OIPN during or after OXA administration. The effects of RAASIs and OXA on the neurite length in PC12 cells were determined. The combined administration of an OXA-containing regimen and RAASI significantly inhibited the cumulative incidence grade-2 or higher OIPN (log-rank test; p = 0.0001). RAASIs markedly suppressed the development of both acute and chronic OIPN (multivariate analysis; p = 0.017 and p = 0.011). In an in vitro assay, 10 µM OXA suppressed the neurite length; treatment with 1 µM aliskiren, spironolactone, 10 µM candesartan, and enalapril significantly restored neurite length to the control level. Moreover, 1 µM SCH772984 (a selective inhibitor of extracellular signal-regulated kinase, ERK1/2) and 500 µM SQ22536 (a cell-permeable adenylate cyclase (AC) inhibitor) markedly abolished neurite-extending effects of candesartan and enalapril. These results indicate that RAASIs possess preventive or therapeutic effects in acute and chronic OIPN, candesartan and enalapril may increase in the activity of ERK1/2 and AC in PC12 cells.","ja":"Oxaliplatin (OXA) is used in chemotherapy for various cancer types and is associated with acute and chronic neurotoxicity. However, a preventive strategy for OXA-induced peripheral neuropathy (OIPN) and its underlying mechanism remain unclear. We examined the effects of renin-angiotensin-aldosterone system inhibitors (RAASIs) on OIPN by performing a retrospective multicenter study and an in vitro assay. We retrospectively evaluated electronic medical records of 976 patients who underwent one or more courses of OXA-containing regimens at Ehime, Okayama, and Tokushima University Hospitals. The primary endpoint was the incidence of OIPN during or after OXA administration. The effects of RAASIs and OXA on the neurite length in PC12 cells were determined. The combined administration of an OXA-containing regimen and RAASI significantly inhibited the cumulative incidence grade-2 or higher OIPN (log-rank test; p = 0.0001). RAASIs markedly suppressed the development of both acute and chronic OIPN (multivariate analysis; p = 0.017 and p = 0.011). In an in vitro assay, 10 µM OXA suppressed the neurite length; treatment with 1 µM aliskiren, spironolactone, 10 µM candesartan, and enalapril significantly restored neurite length to the control level. Moreover, 1 µM SCH772984 (a selective inhibitor of extracellular signal-regulated kinase, ERK1/2) and 500 µM SQ22536 (a cell-permeable adenylate cyclase (AC) inhibitor) markedly abolished neurite-extending effects of candesartan and enalapril. These results indicate that RAASIs possess preventive or therapeutic effects in acute and chronic OIPN, candesartan and enalapril may increase in the activity of ERK1/2 and AC in PC12 cells."},"publication_date":"2021-11-20","publication_name":{"en":"Biological & Pharmaceutical Bulletin","ja":"Biological & Pharmaceutical Bulletin"},"volume":"Vol.45","number":"No.2","starting_page":"226","ending_page":"234","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1248/bpb.b21-00852"],"issn":["1347-5215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:28, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/34726078","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390804","label":"url"}],"paper_title":{"en":"Risk of Hematologic Events With Coadministration of Methotrexate and the Breast Cancer Resistance Protein Inhibitor Febuxostat.","ja":"Risk of Hematologic Events With Coadministration of Methotrexate and the Breast Cancer Resistance Protein Inhibitor Febuxostat."},"authors":{"en":[{"name":"Mitsuboshi Satoru"},{"name":"Niimura Takahiro"},{"name":"Kanda Masaya"},{"name":"Ishida Shunsuke"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Mitsuboshi Satoru"},{"name":"新村 貴博"},{"name":"Kanda Masaya"},{"name":"Ishida Shunsuke"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"The breast cancer resistance protein (BCRP) is a key drug transporter found in the liver, kidney, central nervous system, and gastrointestinal tract. Due to the wide expression of BCRP, interactions of other drugs with methotrexate (MTX) may differ in oral and intravenous MTX users, and understanding of these interactions may be useful in preventing severe adverse events. Febuxostat, a urate-lowering drug, inhibits BCRP. The objective of this study was to clarify the differences in the drug-drug interaction profiles of oral and intravenous methotrexate, associated with BCRP. We analyzed the Japanese Adverse Drug Event Report database and compared the frequency of hematologic events in patients taking oral and intravenous MTX, with or without the concomitant use of febuxostat or allopurinol. Hematologic events were defined as pancytopenia and neutropenia. Multiple logistic regression analysis was then used to identify the risk factors for hematologic events in oral and intravenous MTX users. We identified 8 453 oral and 810 intravenous MTX users with 546 and 126 cases of hematologic events, respectively. Compared with those not using febuxostat, a disproportionate number of hematologic events was observed in intravenous MTX users concomitantly using febuxostat ( < 0.01). The multivariate logistic analysis of intravenous MTX users showed that hematologic events were significantly associated with febuxostat use ( < 0.01) and age ≥ 60 years ( < 0.01). Our findings suggest that patients being treated with intravenous MTX who concomitantly use febuxostat may be at an increased risk of hematologic events, presumably due to BCRP-mediated drug-drug interaction.","ja":"The breast cancer resistance protein (BCRP) is a key drug transporter found in the liver, kidney, central nervous system, and gastrointestinal tract. Due to the wide expression of BCRP, interactions of other drugs with methotrexate (MTX) may differ in oral and intravenous MTX users, and understanding of these interactions may be useful in preventing severe adverse events. Febuxostat, a urate-lowering drug, inhibits BCRP. The objective of this study was to clarify the differences in the drug-drug interaction profiles of oral and intravenous methotrexate, associated with BCRP. We analyzed the Japanese Adverse Drug Event Report database and compared the frequency of hematologic events in patients taking oral and intravenous MTX, with or without the concomitant use of febuxostat or allopurinol. Hematologic events were defined as pancytopenia and neutropenia. Multiple logistic regression analysis was then used to identify the risk factors for hematologic events in oral and intravenous MTX users. We identified 8 453 oral and 810 intravenous MTX users with 546 and 126 cases of hematologic events, respectively. Compared with those not using febuxostat, a disproportionate number of hematologic events was observed in intravenous MTX users concomitantly using febuxostat ( < 0.01). The multivariate logistic analysis of intravenous MTX users showed that hematologic events were significantly associated with febuxostat use ( < 0.01) and age ≥ 60 years ( < 0.01). Our findings suggest that patients being treated with intravenous MTX who concomitantly use febuxostat may be at an increased risk of hematologic events, presumably due to BCRP-mediated drug-drug interaction."},"publication_date":"2021-11-02","publication_name":{"en":"The Annals of Pharmacotherapy","ja":"The Annals of Pharmacotherapy"},"volume":"Vol.56","number":"No.8","starting_page":"910","ending_page":"915","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1177/10600280211055794"],"issn":["1542-6270"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:29, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/34642081","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390281","label":"url"}],"paper_title":{"en":"Impact of Area Under the Concentration-Time Curve on the Prevalence of Vancomycin-Induced Nephrotoxicity in Combination With Tazobactam/Piperacillin or Cefepime: A Single-Institution Retrospective Study.","ja":"Impact of Area Under the Concentration-Time Curve on the Prevalence of Vancomycin-Induced Nephrotoxicity in Combination With Tazobactam/Piperacillin or Cefepime: A Single-Institution Retrospective Study."},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Izumi Yuki"},{"name":"Nakamoto Aki"},{"name":"Chuma Masayuki"},{"name":"Goda Mitsuhiro"},{"name":"Yagi Kenta"},{"name":"Aizawa Fuka"},{"name":"Hamano Hirofumi"},{"name":"Zamami Yoshito"},{"name":"Azuma Momoyo"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"Izumi Yuki"},{"name":"Nakamoto Aki"},{"name":"中馬 真幸"},{"name":"合田 光寛"},{"name":"八木 健太"},{"name":"相澤 風花"},{"name":"濱野 裕章"},{"name":"座間味 義人"},{"name":"東 桃代"},{"name":"石澤 啓介"}]},"description":{"en":"VIN risk was higher with VT than with VC, even when the AUC was controlled to the guideline-recommended range. These results strongly suggest that VIN prevention may be difficult with AUC-guided vancomycin dosing in patients receiving VT.","ja":"The prevalences of VIN were 29.5% (18/61) and 7.1% (3/42) in the VT and VC groups, respectively. Multivariate logistic regression analysis of data from all patients revealed concurrent use of tazobactam/piperacillin (odds ratio [OR] = 4.59; P = 0.039) and AUC increase (OR = 1.01; P < 0.01) as risk factors for VIN, but only concurrent use of tazobactam/piperacillin was identified as a risk factor in patients with an AUC of <600 μg · h/mL, the guideline-recommended value (OR = 9.52; P = 0.041). Moreover, the vancomycin exposure-toxicity curve showed that in the guideline-recommended AUC range, VIN probability was consistently higher and the slope of VIN probability was greater in the VT group than in the VC group."},"publication_date":"2021-10-09","publication_name":{"en":"Clinical Therapeutics","ja":"Clinical Therapeutics"},"volume":"Vol.43","number":"No.11","starting_page":"1910","ending_page":"1920.e3","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.clinthera.2021.09.007"],"issn":["1879-114X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:30, {"insert":{"user_id":"6000008820","type":"published_papers","id":"32939291"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/34177574","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=376605","label":"url"}],"paper_title":{"en":"Evaluation of Potential Complications of Interstitial Lung Disease Associated With Antiandrogens Using Data From Databases Reporting Spontaneous Adverse Effects.","ja":"Evaluation of Potential Complications of Interstitial Lung Disease Associated With Antiandrogens Using Data From Databases Reporting Spontaneous Adverse Effects."},"authors":{"en":[{"name":"Nawa Hideki"},{"name":"Niimura Takahiro"},{"name":"Hamano Hirofumi"},{"name":"Yagi Kenta"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Nawa Hideki"},{"name":"新村 貴博"},{"name":"濱野 裕章"},{"name":"八木 健太"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"From 2002 to 2018, the number of patients with prostate cancer significantly increased from 679,023 to 1276,106 worldwide. Total prostatectomy (including robot-assisted prostatectomy), radiation therapy, and pharmacological treatment are commonly used to treat prostate cancer. The Chief of the Pharmaceutical Safety Division, that is, the Federation of Pharmaceutical Manufacturers' Associations of Japan (FPMAJ), recently called for the revision of package inserts for ethical drugs. However, the pathogenesis of interstitial lung disease (ILD), a serious drug-induced adverse effect, remains unclear. Moreover, there have been no large-scale evaluations of potential complications associated with currently used antiandrogens, which are commonly employed to treat prostate cancer. Hence, ILD, as an adverse event, remains poorly understood. Therefore, we conducted a survey of reports in the Japanese Adverse Drug Event Report (JADER) database to investigate the potential association between the reporting of ILD and antiandrogen drug use in clinical practice. The occurrence of ILD was investigated by evaluating the relationship between antiandrogen drug use and ILD. Adverse event signals were detected with reporting odds ratios (RORs), using data from the JADER and FDA Adverse Event Reporting System (FAERS) databases, for the analysis of post-marketing adverse event reports. The JADER was used to examine the time profile of adverse event occurrence for each drug, whereas the FAERS was used to screen cases of unknown adverse events and analyze their trends of occurrence. The analysis of data from both databases revealed the 95% confidence interval lower limits of ROR for bicalutamide and flutamide to be > 1, and adverse event signals were detected following the use of either drug. While caution should be exercised for drugs that are new to the market, we conclude that drugs with similar therapeutic effects that have been in use for a long period should also be re-examined for potential adverse events.","ja":"From 2002 to 2018, the number of patients with prostate cancer significantly increased from 679,023 to 1276,106 worldwide. Total prostatectomy (including robot-assisted prostatectomy), radiation therapy, and pharmacological treatment are commonly used to treat prostate cancer. The Chief of the Pharmaceutical Safety Division, that is, the Federation of Pharmaceutical Manufacturers' Associations of Japan (FPMAJ), recently called for the revision of package inserts for ethical drugs. However, the pathogenesis of interstitial lung disease (ILD), a serious drug-induced adverse effect, remains unclear. Moreover, there have been no large-scale evaluations of potential complications associated with currently used antiandrogens, which are commonly employed to treat prostate cancer. Hence, ILD, as an adverse event, remains poorly understood. Therefore, we conducted a survey of reports in the Japanese Adverse Drug Event Report (JADER) database to investigate the potential association between the reporting of ILD and antiandrogen drug use in clinical practice. The occurrence of ILD was investigated by evaluating the relationship between antiandrogen drug use and ILD. Adverse event signals were detected with reporting odds ratios (RORs), using data from the JADER and FDA Adverse Event Reporting System (FAERS) databases, for the analysis of post-marketing adverse event reports. The JADER was used to examine the time profile of adverse event occurrence for each drug, whereas the FAERS was used to screen cases of unknown adverse events and analyze their trends of occurrence. The analysis of data from both databases revealed the 95% confidence interval lower limits of ROR for bicalutamide and flutamide to be > 1, and adverse event signals were detected following the use of either drug. While caution should be exercised for drugs that are new to the market, we conclude that drugs with similar therapeutic effects that have been in use for a long period should also be re-examined for potential adverse events."},"publication_date":"2021-06-09","publication_name":{"en":"Frontiers in Pharmacology","ja":"Frontiers in Pharmacology"},"volume":"Vol.12","number":"No.655605","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3389/fphar.2021.655605"],"issn":["1663-9812"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:31, {"insert":{"user_id":"6000008820","type":"published_papers","id":"32553170"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116008","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33982438","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=375733","label":"url"}],"paper_title":{"en":"Effects of 5-HT3 receptor antagonists on cisplatin-induced kidney injury.","ja":"Effects of 5-HT3 receptor antagonists on cisplatin-induced kidney injury."},"authors":{"en":[{"name":"Goda Mitsuhiro"},{"name":"Kanda Masaya"},{"name":"Yoshioka Toshihiko"},{"name":"Yoshida Ami"},{"name":"Murai Yoichi"},{"name":"Zamami Yoshito"},{"name":"Aizawa Fuka"},{"name":"Niimura Takahiro"},{"name":"Hamano Hirofumi"},{"name":"Okada Naoto"},{"name":"Yagi Kenta"},{"name":"Chuma Masayuki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"合田 光寛"},{"name":"Kanda Masaya"},{"name":"Yoshioka Toshihiko"},{"name":"Yoshida Ami"},{"name":"Murai Yoichi"},{"name":"座間味 義人"},{"name":"相澤 風花"},{"name":"新村 貴博"},{"name":"濱野 裕章"},{"name":"岡田 直人"},{"name":"八木 健太"},{"name":"中馬 真幸"},{"name":"石澤 有紀"},{"name":"石澤 啓介"}]},"description":{"en":"receptor antagonists do not worsen cisplatin-induced acute kidney injury. The findings should be validated in a prospective controlled trial before implementation in clinical practice.","ja":"receptor antagonists do not worsen cisplatin-induced acute kidney injury. The findings should be validated in a prospective controlled trial before implementation in clinical practice."},"publication_date":"2021-05-13","publication_name":{"en":"Clinical and Translational Science","ja":"Clinical and Translational Science"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/cts.13045"],"issn":["1752-8062"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:32, {"insert":{"user_id":"6000008820","type":"published_papers","id":"32553171"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116289","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33939324","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=375759","label":"url"}],"paper_title":{"en":"Evaluation of potential complication of interstitial lung disease with abemaciclib and palbociclib treatments.","ja":"Evaluation of potential complication of interstitial lung disease with abemaciclib and palbociclib treatments."},"authors":{"en":[{"name":"Nawa Hideki"},{"name":"Niimura Takahiro"},{"name":"Yagi Kenta"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Nawa Hideki"},{"name":"新村 貴博"},{"name":"八木 健太"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Treatment with abemaciclib and palbociclib is associated with a potential complication of interstitial lung disease, regardless of age.","ja":"We evaluated the relationship between the CDK4/6 inhibitors (abemaciclib and palbociclib) and interstitial lung disease in clinical practice using data from the Japanese Adverse Drug Event Report (JADER) database and FDA Adverse Event Reporting System (FAERS) to detect adverse event signals with reported odds ratios (RORs). Furthermore, we performed an adverse event-time analysis for each drug using data from the JADER database to examine the time of onset of the adverse events. The analysis of the reports in the JADER database showed that the lower limit of the 95% confidence interval (CI) of ROR for abemaciclib was >1 regardless of age, and a signal was detected. Interstitial lung disease associated with abemaciclib and palbociclib use has been reported, with an average onset period from treatment initiation [median (25th-75th quartile)] of 65.1 [56.0 days (25.3-98.3 days)] and 53.1 days [38.0 days (10.8-76.0 days)], respectively. The analysis of the reports in the FAERS showed that the lower limit of the 95% CI of the ROR for the two drugs was >1, and a signal was detected."},"publication_date":"2021-05-03","publication_name":{"en":"Cancer Reports","ja":"Cancer Reports"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/cnr2.1402"],"issn":["2573-8348"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:33, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://repo.lib.tokushima-u.ac.jp/116038","label":"url"},{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116038","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1050851320431028352/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390121","label":"url"}],"paper_title":{"en":"薬剤誘発性大動脈解離易発症モデルマウスを用いた薬効評価","ja":"薬剤誘発性大動脈解離易発症モデルマウスを用いた薬効評価"},"authors":{"en":[{"name":"Izawa-Ishizawa Yuki"},{"name":"Goda Mitsuhiro"},{"name":"Aizawa Fuka"},{"name":"Zamami Yoshito"},{"name":"Hamano Hirofumi"},{"name":"Yagi Kenta"},{"name":"Ikeda Yasumasa"},{"name":"Ishizawa Keisuke"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 有紀"},{"name":"合田 光寛"},{"name":"相澤 風花"},{"name":"座間味 義人"},{"name":"濱野 裕章"},{"name":"八木 健太"},{"name":"池田 康将"},{"name":"石澤 啓介"},{"name":"玉置 俊晃"}]},"description":{"en":"Aortic dissection (or dissecting aortic aneurysm) is a condition in which the aortic wall is separated into two layers at the medial level to form a pseudocavity. The intima crack, called the ``entry'', allows blood to tear through the medial layer and flow in. The location of the ``entry'' and the extent of the dissection can cause a variety of serious complications, including rupture, cardiac tamponade, and obstruction of branched vessels. According to the Guideline on Diagnosis and Treatment of Aortic Aneurysm and Aortic Dissection 2020, it is estimated that 61.4% of the onset of dissection die before arrival at the hospital, and 93% will die within 24 hours after the onset. It has been suggested that the morbidity rate has been increasing in recent years. Since many of them have a fatal prognosis, it is an important issue to prevent the onset itself. However, no effective therapeutic agent or preventive strategy has been established so far. The first reason is that it is extremely difficult to design clinical studies because aortic dissection traced the rapid onset and progression. The second is that the pathophysiology and preventive drug search are not sufficiently conducted even at the basic research level. Epidemiologically, the results of the International Registry of Aortic Dissection (IRAD) revealed that aging, hypertension, atherosclerosis, and hereditary connective tissue diseases are risk factors. The aortic aneurysm also shows similar pathological conditions caused by these risk factors. However, one of the major differences between aneurysm and dissection is the presence of aortic intima rupture. Therefore, we attempted to establish a mouse model developing dissection at a high rate by adding the endothelial dysfunction to a pharmacologically induced aortic aneurysm model mouse. Furthermore, we evaluated the efficacy of pitavastatin and several nutrients using our novel model mice and verified its usefulness as a model animal.","ja":"Aortic dissection (or dissecting aortic aneurysm) is a condition in which the aortic wall is separated into two layers at the medial level to form a pseudocavity. The intima crack, called the ``entry'', allows blood to tear through the medial layer and flow in. The location of the ``entry'' and the extent of the dissection can cause a variety of serious complications, including rupture, cardiac tamponade, and obstruction of branched vessels. According to the Guideline on Diagnosis and Treatment of Aortic Aneurysm and Aortic Dissection 2020, it is estimated that 61.4% of the onset of dissection die before arrival at the hospital, and 93% will die within 24 hours after the onset. It has been suggested that the morbidity rate has been increasing in recent years. Since many of them have a fatal prognosis, it is an important issue to prevent the onset itself. However, no effective therapeutic agent or preventive strategy has been established so far. The first reason is that it is extremely difficult to design clinical studies because aortic dissection traced the rapid onset and progression. The second is that the pathophysiology and preventive drug search are not sufficiently conducted even at the basic research level. Epidemiologically, the results of the International Registry of Aortic Dissection (IRAD) revealed that aging, hypertension, atherosclerosis, and hereditary connective tissue diseases are risk factors. The aortic aneurysm also shows similar pathological conditions caused by these risk factors. However, one of the major differences between aneurysm and dissection is the presence of aortic intima rupture. Therefore, we attempted to establish a mouse model developing dissection at a high rate by adding the endothelial dysfunction to a pharmacologically induced aortic aneurysm model mouse. Furthermore, we evaluated the efficacy of pitavastatin and several nutrients using our novel model mice and verified its usefulness as a model animal."},"publication_date":"2021-04-25","publication_name":{"en":"Shikoku Acta Medica","ja":"四国医学雑誌"},"volume":"Vol.77","number":"No.1,2","starting_page":"57","ending_page":"62","languages":["jpn"],"referee":true,"identifiers":{"issn":["0037-3699"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:34, {"insert":{"user_id":"6000008820","type":"published_papers","id":"32553173"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116301","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33910036","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=375760","label":"url"}],"paper_title":{"en":"Examination of the antiepileptic effects of valacyclovir using kindling mice- search for novel antiepileptic agents by drug repositioning using a large medical information database.","ja":"Examination of the antiepileptic effects of valacyclovir using kindling mice- search for novel antiepileptic agents by drug repositioning using a large medical information database."},"authors":{"en":[{"name":"Takahashi Shimon"},{"name":"Takechi Kenshi"},{"name":"Jozukuri Natsumi"},{"name":"Niimura Takahiro"},{"name":"Chuma Masayuki"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Imanishi Masaki"},{"name":"Horinouchi Yuya"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Yanagawa Hiroaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Takahashi Shimon"},{"name":"武智 研志"},{"name":"Jozukuri Natsumi"},{"name":"新村 貴博"},{"name":"中馬 真幸"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"石澤 有紀"},{"name":"今西 正樹"},{"name":"堀ノ内 裕也"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"楊河 宏章"},{"name":"石澤 啓介"}]},"description":{"en":"Despite the availability of more than 20 clinical antiepileptic drugs, approximately 30% of patients with epilepsy do not respond to antiepileptic drug treatment. Therefore, it is important to develop antiepileptic products that function via novel mechanisms. In the present study, we evaluated data from one of the largest global databases to identify drugs with antiepileptic effects, and subsequently attempted to understand the effect of the combination of antiepileptic drugs and valacyclovir in epileptic seizures using a kindling model. To induce kindling in mice, pentylenetetrazol at a dose of 40 mg/kg was administered once every 48 h. Valacyclovir was orally administered 30 min before antiepileptic drug injection in kindled mice, and behavioral seizures were monitored for 20 min following pentylenetetrazol administration. Additionally, c-Fos expression in the hippocampal dentate gyrus was measured in kindled mice. Valacyclovir showed inhibitory effects on pentylenetetrazol-induced kindled seizures. In addition, simultaneous use of levetiracetam and valacyclovir caused more potent inhibition of seizure activity, and neither valproic acid nor diazepam augmented the anti-seizure effect in kindled mice. Furthermore, kindled mice showed increased c-Fos levels in the dentate gyrus. The increase in c-Fos expression was significantly inhibited by the simultaneous use of levetiracetam and valacyclovir. The findings of the present study indicate that a combination of levetiracetam and valacyclovir had possible anticonvulsive effects on pentylenetetrazol-induced kindled epileptic seizures. These results suggest that valacyclovir may have an antiseizure effect in patients with epilepsy.","ja":"Despite the availability of more than 20 clinical antiepileptic drugs, approximately 30% of patients with epilepsy do not respond to antiepileptic drug treatment. Therefore, it is important to develop antiepileptic products that function via novel mechanisms. In the present study, we evaluated data from one of the largest global databases to identify drugs with antiepileptic effects, and subsequently attempted to understand the effect of the combination of antiepileptic drugs and valacyclovir in epileptic seizures using a kindling model. To induce kindling in mice, pentylenetetrazol at a dose of 40 mg/kg was administered once every 48 h. Valacyclovir was orally administered 30 min before antiepileptic drug injection in kindled mice, and behavioral seizures were monitored for 20 min following pentylenetetrazol administration. Additionally, c-Fos expression in the hippocampal dentate gyrus was measured in kindled mice. Valacyclovir showed inhibitory effects on pentylenetetrazol-induced kindled seizures. In addition, simultaneous use of levetiracetam and valacyclovir caused more potent inhibition of seizure activity, and neither valproic acid nor diazepam augmented the anti-seizure effect in kindled mice. Furthermore, kindled mice showed increased c-Fos levels in the dentate gyrus. The increase in c-Fos expression was significantly inhibited by the simultaneous use of levetiracetam and valacyclovir. The findings of the present study indicate that a combination of levetiracetam and valacyclovir had possible anticonvulsive effects on pentylenetetrazol-induced kindled epileptic seizures. These results suggest that valacyclovir may have an antiseizure effect in patients with epilepsy."},"publication_date":"2021-04-25","publication_name":{"en":"European Journal of Pharmacology","ja":"European Journal of Pharmacology"},"volume":"Vol.902","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.ejphar.2021.174099"],"issn":["1879-0712"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:35, {"insert":{"user_id":"6000008820","type":"published_papers","id":"32234595"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33826081","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=374839","label":"url"}],"paper_title":{"en":"Population-Based Observational Study of Adverse Drug Event-Related Mortality in the Super-Aged Society of Japan.","ja":"Population-Based Observational Study of Adverse Drug Event-Related Mortality in the Super-Aged Society of Japan."},"authors":{"en":[{"name":"Funahashi Tomoko"},{"name":"Koyama Toshihiro"},{"name":"Hagiya Hideharu"},{"name":"Harada Ko"},{"name":"Iinuma Syunya"},{"name":"Ushio Soichiro"},{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Shinomiya Kazuaki"},{"name":"Ishizawa Keisuke"},{"name":"Sendo Toshiaki"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"}],"ja":[{"name":"Funahashi Tomoko"},{"name":"Koyama Toshihiro"},{"name":"Hagiya Hideharu"},{"name":"Harada Ko"},{"name":"Iinuma Syunya"},{"name":"Ushio Soichiro"},{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"Shinomiya Kazuaki"},{"name":"石澤 啓介"},{"name":"Sendo Toshiaki"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"}]},"description":{"en":"The number of and trend in ADE-related deaths increased in Japan from 1999 to 2016, particularly in the older population.","ja":"The number of and trend in ADE-related deaths increased in Japan from 1999 to 2016, particularly in the older population."},"publication_date":"2021-04-07","publication_name":{"en":"Drug Safety","ja":"Drug Safety"},"volume":"Vol.44","number":"No.5","starting_page":"531","ending_page":"539","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s40264-020-01037-9"],"issn":["1179-1942"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:36, {"insert":{"user_id":"6000008820","type":"published_papers","id":"31510813"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33477139","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=373335","label":"url"}],"paper_title":{"en":"The Risk Factors Associated with Immune Checkpoint Inhibitor-Related Pneumonitis.","ja":"The Risk Factors Associated with Immune Checkpoint Inhibitor-Related Pneumonitis."},"authors":{"en":[{"name":"Asada Mizuho"},{"name":"Mikami Takahisa"},{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Uesawa Yoshihiro"},{"name":"Chuma Masayuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Asada Mizuho"},{"name":"Mikami Takahisa"},{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"Uesawa Yoshihiro"},{"name":"中馬 真幸"},{"name":"石澤 啓介"}]},"description":{"en":"Our data suggest that the risk of ICI-related pneumonitis may increase in certain populations, including younger age (age <60 years) and ICIs users. These patients require careful monitoring.","ja":"Our data suggest that the risk of ICI-related pneumonitis may increase in certain populations, including younger age (age <60 years) and ICIs users. These patients require careful monitoring."},"publication_date":"2021-01-21","publication_name":{"en":"Oncology","ja":"Oncology"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1159/000512633"],"issn":["1423-0232"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:37, {"insert":{"user_id":"6000008820","type":"published_papers","id":"36183953"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117585","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=383725","label":"url"}],"paper_title":{"en":"Association analysis between adverse drug reactions to cytarabine therapy and single nucleotide polymorphisms in cytarabine metabolic genes in patients with hematopoietic tumor","ja":"Association analysis between adverse drug reactions to cytarabine therapy and single nucleotide polymorphisms in cytarabine metabolic genes in patients with hematopoietic tumor"},"authors":{"en":[{"name":"Hozumi Tashima"},{"name":"Yuka Endo"},{"name":"Okada Naoto"},{"name":"Nakamura Shingen"},{"name":"Kagawa Kumiko"},{"name":"Fujii Shiroh"},{"name":"Miki Hirokazu"},{"name":"Ishizawa Keisuke"},{"name":"Abe Masahiro"},{"name":"Sato Youichi"}],"ja":[{"name":"田島 穂澄"},{"name":"遠藤 優香"},{"name":"岡田 直人"},{"name":"中村 信元"},{"name":"賀川 久美子"},{"name":"藤井 志朗"},{"name":"三木 浩和"},{"name":"石澤 啓介"},{"name":"安倍 正博"},{"name":"佐藤 陽一"}]},"publication_date":"2021","publication_name":{"en":"Personalized Medicine Universe","ja":"Personalized Medicine Universe"},"volume":"Vol.10","starting_page":"1","ending_page":"6","languages":["eng"],"referee":true,"identifiers":{"doi":["10.46459/pmu.2021002"],"issn":["2186-4950"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:38, {"insert":{"user_id":"6000008820","type":"published_papers","id":"32553172"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115987","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33994483","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=375761","label":"url"}],"paper_title":{"en":"Academic investigators' interest in promoting specified clinical trials : Questionnaire survey before and after implementation of the Clinical Trial Act","ja":"Academic investigators' interest in promoting specified clinical trials : Questionnaire survey before and after implementation of the Clinical Trial Act"},"authors":{"en":[{"name":"Chuma Masayuki"},{"name":"Takechi Kenshi"},{"name":"Yagi Kenta"},{"name":"Sakaguchi Satoshi"},{"name":"Nokihara Hiroshi"},{"name":"Kane Chikako"},{"name":"Sato Yasutaka"},{"name":"Niimura Takahiro"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"},{"name":"Yanagawa Hiroaki"}],"ja":[{"name":"中馬 真幸"},{"name":"武智 研志"},{"name":"八木 健太"},{"name":"坂口 暁"},{"name":"軒原 浩"},{"name":"加根 千賀子"},{"name":"佐藤 康敬"},{"name":"新村 貴博"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"石澤 啓介"},{"name":"楊河 宏章"}]},"description":{"en":"Background : Enforcement of the 2018 Clinical Trials Act (CTA) in Japan resulted in strict and complicated regulations surrounding intervention studies. Few Japan-specific measures have been developed to promote intervention studies in Japan despite concerns about CTA's negative influence on such studies. Therefore, this study examined the changes in academic investigators' interest in conducting clinical studies before and after enforcement of the CTA to determine measures to promote specified clinical trials. Methods : We conducted a questionnaire survey with investigators belonging to the Institute of Biomedical Sciences, Tokushima University Graduate School, before and after enforcement of the CTA. Results : Investigators had lesser interest in intervention studies in the post-questionnaire survey (post) group than in the pre-questionnaire survey (pre) group. Their desire for \"project management\" was significantly higher in the post-group than in the pre-group. Their desire for \"support for preparing documents when conducting specified clinical trials\" was significantly higher in the group interested in conducting specified clinical trials than that in the not-interested group. Conclusion : We revealed that investigators were highly interested in \"project management\" and \"support for preparing documents when conducting specified clinical trials\" after enforcement of the CTA. Measures for these desires may promote specified clinical trials. J. Med. Invest. 68 : 71-75, February, 2021.","ja":"Background : Enforcement of the 2018 Clinical Trials Act (CTA) in Japan resulted in strict and complicated regulations surrounding intervention studies. Few Japan-specific measures have been developed to promote intervention studies in Japan despite concerns about CTA's negative influence on such studies. Therefore, this study examined the changes in academic investigators' interest in conducting clinical studies before and after enforcement of the CTA to determine measures to promote specified clinical trials. Methods : We conducted a questionnaire survey with investigators belonging to the Institute of Biomedical Sciences, Tokushima University Graduate School, before and after enforcement of the CTA. Results : Investigators had lesser interest in intervention studies in the post-questionnaire survey (post) group than in the pre-questionnaire survey (pre) group. Their desire for \"project management\" was significantly higher in the post-group than in the pre-group. Their desire for \"support for preparing documents when conducting specified clinical trials\" was significantly higher in the group interested in conducting specified clinical trials than that in the not-interested group. Conclusion : We revealed that investigators were highly interested in \"project management\" and \"support for preparing documents when conducting specified clinical trials\" after enforcement of the CTA. Measures for these desires may promote specified clinical trials. J. Med. Invest. 68 : 71-75, February, 2021."},"publication_date":"2021","publication_name":{"en":"The Journal of Medical Investigation : JMI","ja":"The Journal of Medical Investigation : JMI"},"volume":"Vol.68","number":"No.1.2","starting_page":"71","ending_page":"75","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2152/jmi.68.71"],"issn":["1349-6867"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:39, {"insert":{"user_id":"6000008820","type":"published_papers","id":"39705155"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117446","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33424555","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390675","label":"url"}],"paper_title":{"en":"Chronic Tear Deficiency Sensitizes Transient Receptor Potential Vanilloid 1-Mediated Responses in Corneal Sensory Nerves.","ja":"Chronic Tear Deficiency Sensitizes Transient Receptor Potential Vanilloid 1-Mediated Responses in Corneal Sensory Nerves."},"authors":{"en":[{"name":"Masuoka Takayoshi"},{"name":"Yamashita Yuka"},{"name":"Nakano Katsuya"},{"name":"Takechi Kenshi"},{"name":"Niimura Takahiro"},{"name":"Tawa Masashi"},{"name":"He Qiang"},{"name":"Ishizawa Keisuke"},{"name":"Ishibashi Takaharu"}],"ja":[{"name":"Masuoka Takayoshi"},{"name":"Yamashita Yuka"},{"name":"Nakano Katsuya"},{"name":"Takechi Kenshi"},{"name":"新村 貴博"},{"name":"Tawa Masashi"},{"name":"He Qiang"},{"name":"石澤 啓介"},{"name":"Ishibashi Takaharu"}]},"description":{"en":"Chronic tear deficiency enhances the excitability of corneal cold-sensitive nerves that detect ocular dryness, which can lead to discomfort in patients with dry eye disease (DED). However, changes in corneal nerve excitations through the polymodal nociceptor \"transient receptor potential vanilloid 1\" (TRPV1) and the potential link between this receptor and symptoms of DED remain unclear. In this study, we examined the firing properties of corneal cold-sensitive nerves expressing TRPV1 and possible contributions of chronic tear deficiency to corneal nerve excitability by TRPV1 activation. The bilateral excision of lacrimal glands in guinea pigs decreased the tear volume and increased the frequency of spontaneous eyeblinks 1-4 weeks after surgery. An analysis of the firing properties of the cold-sensitive nerves was performed by single-unit recordings of corneal preparations 4 weeks after surgery in both the sham-operated and gland-excised groups. Perfusion of the TRPV1 agonist, capsaicin (1 μM), transiently increased the firing frequency in approximately 46-48% of the cold-sensitive nerves characterized by low-background activity and high threshold (LB-HT) cold thermoreceptors in both groups. Gland excision significantly decreased the latency of capsaicin-induced firing in cold-sensitive nerves; however, its magnitude was unchanged. Calcium imaging of cultured trigeminal ganglion neurons from both groups showed that intracellular calcium elevation of corneal neurons induced by a low concentration of capsaicin (0.03 μM) was significantly larger in the gland excision group, regardless of responsiveness to cold. An immunohistochemical study of the trigeminal ganglion revealed that gland excision significantly increased the proportion of corneal neurons enclosed by glial fibrillary acidic protein (GFAP)-immunopositive satellite glial cells. Topical application of the TRPV1 antagonist, A784168 (30 μM), on the ocular surface attenuated eye-blink frequency after gland excision. Furthermore, gland excision enhanced blink behavior induced by a low concentration of capsaicin (0.1 μM). These results suggest that chronic tear deficiency sensitizes the TRPV1-mediated response in the corneal LB-HT cold thermoreceptors and cold-insensitive polymodal nociceptors, which may be linked to dry eye discomfort and hyperalgesia resulting from nociceptive stimuli in aqueous-deficient dry eyes.","ja":"Chronic tear deficiency enhances the excitability of corneal cold-sensitive nerves that detect ocular dryness, which can lead to discomfort in patients with dry eye disease (DED). However, changes in corneal nerve excitations through the polymodal nociceptor \"transient receptor potential vanilloid 1\" (TRPV1) and the potential link between this receptor and symptoms of DED remain unclear. In this study, we examined the firing properties of corneal cold-sensitive nerves expressing TRPV1 and possible contributions of chronic tear deficiency to corneal nerve excitability by TRPV1 activation. The bilateral excision of lacrimal glands in guinea pigs decreased the tear volume and increased the frequency of spontaneous eyeblinks 1-4 weeks after surgery. An analysis of the firing properties of the cold-sensitive nerves was performed by single-unit recordings of corneal preparations 4 weeks after surgery in both the sham-operated and gland-excised groups. Perfusion of the TRPV1 agonist, capsaicin (1 μM), transiently increased the firing frequency in approximately 46-48% of the cold-sensitive nerves characterized by low-background activity and high threshold (LB-HT) cold thermoreceptors in both groups. Gland excision significantly decreased the latency of capsaicin-induced firing in cold-sensitive nerves; however, its magnitude was unchanged. Calcium imaging of cultured trigeminal ganglion neurons from both groups showed that intracellular calcium elevation of corneal neurons induced by a low concentration of capsaicin (0.03 μM) was significantly larger in the gland excision group, regardless of responsiveness to cold. An immunohistochemical study of the trigeminal ganglion revealed that gland excision significantly increased the proportion of corneal neurons enclosed by glial fibrillary acidic protein (GFAP)-immunopositive satellite glial cells. Topical application of the TRPV1 antagonist, A784168 (30 μM), on the ocular surface attenuated eye-blink frequency after gland excision. Furthermore, gland excision enhanced blink behavior induced by a low concentration of capsaicin (0.1 μM). These results suggest that chronic tear deficiency sensitizes the TRPV1-mediated response in the corneal LB-HT cold thermoreceptors and cold-insensitive polymodal nociceptors, which may be linked to dry eye discomfort and hyperalgesia resulting from nociceptive stimuli in aqueous-deficient dry eyes."},"publication_date":"2020-12-23","publication_name":{"en":"Frontiers in Cellular Neuroscience","ja":"Frontiers in Cellular Neuroscience"},"volume":"Vol.14","starting_page":"598678","ending_page":"598678","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3389/fncel.2020.598678"],"issn":["1662-5102"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:40, {"insert":{"user_id":"6000008820","type":"published_papers","id":"31136375"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33270271","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=372619","label":"url"}],"paper_title":{"en":"Differences in risk factors for anticoagulant-related nephropathy between warfarin and direct oral anticoagulants: analysis of the Japanese Adverse Drug Event Report database.","ja":"Differences in risk factors for anticoagulant-related nephropathy between warfarin and direct oral anticoagulants: analysis of the Japanese Adverse Drug Event Report database."},"authors":{"en":[{"name":"Mitsuboshi Satoru"},{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Mitsuboshi Satoru"},{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Limited information is available on anticoagulant-related nephropathy (ARN). We therefore reviewed the Japanese Adverse Drug Event Report database to investigate kidney injury (KI) in patients administered warfarin or direct oral anticoagulants (DOACs) and sought to clarify the risk factors for ARN. KI risk in warfarin users was associated with male sex (odds ratio [OR], 1.70; 95% confidence interval [CI], 1.35-2.13; P < 0.01) and age 80 years (OR, 1.35; 95% CI, 1.07-1.72; P = 0.01). KI risk in DOAC users was associated with body weight 80 kg (OR, 1.60; 95% CI, 1.01-2.53; P = 0.04) and use of dabigatran (OR, 1.61; 95% CI, 1.09-2.37; P < 0.01). Our findings suggest that risk factors for ARN differ between warfarin and DOACs, and that these risk factors may be associated with bleeding risk. Therefore, the risk of ARN may be decreased by better managing bleeding risk in patients taking anticoagulants.","ja":"Limited information is available on anticoagulant-related nephropathy (ARN). We therefore reviewed the Japanese Adverse Drug Event Report database to investigate kidney injury (KI) in patients administered warfarin or direct oral anticoagulants (DOACs) and sought to clarify the risk factors for ARN. KI risk in warfarin users was associated with male sex (odds ratio [OR], 1.70; 95% confidence interval [CI], 1.35-2.13; P < 0.01) and age 80 years (OR, 1.35; 95% CI, 1.07-1.72; P = 0.01). KI risk in DOAC users was associated with body weight 80 kg (OR, 1.60; 95% CI, 1.01-2.53; P = 0.04) and use of dabigatran (OR, 1.61; 95% CI, 1.09-2.37; P < 0.01). Our findings suggest that risk factors for ARN differ between warfarin and DOACs, and that these risk factors may be associated with bleeding risk. Therefore, the risk of ARN may be decreased by better managing bleeding risk in patients taking anticoagulants."},"publication_date":"2020-12-03","publication_name":{"en":"British Journal of Clinical Pharmacology","ja":"British Journal of Clinical Pharmacology"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/bcp.14688"],"issn":["1365-2125"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:41, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116288","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33231381","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=372620","label":"url"}],"paper_title":{"en":"Investigation of drugs affecting hypertension in bevacizumab-treated patients and examination of the impact on the therapeutic effect.","ja":"Investigation of drugs affecting hypertension in bevacizumab-treated patients and examination of the impact on the therapeutic effect."},"authors":{"en":[{"name":"Yagi Kenta"},{"name":"Mitstui Marin"},{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Goda Mitsuhiro"},{"name":"Chuma Masayuki"},{"name":"Fukunaga Kimiko"},{"name":"Shibata Takahiro"},{"name":"Ishida Shunsuke"},{"name":"Sakurada Takumi"},{"name":"Okada Naoto"},{"name":"Hamano Hirofumi"},{"name":"Horinouchi Yuya"},{"name":"Ikeda Yasumasa"},{"name":"Yanagawa Hiroaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"八木 健太"},{"name":"Mitstui Marin"},{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"石澤 有紀"},{"name":"合田 光寛"},{"name":"中馬 真幸"},{"name":"Fukunaga Kimiko"},{"name":"Shibata Takahiro"},{"name":"Ishida Shunsuke"},{"name":"Sakurada Takumi"},{"name":"岡田 直人"},{"name":"Hamano Hirofumi"},{"name":"堀ノ内 裕也"},{"name":"池田 康将"},{"name":"楊河 宏章"},{"name":"石澤 啓介"}]},"description":{"en":"PPIs prevent hypertension in bevacizumab-treated patients but may reduce bevacizumab's anti-tumoral effects by inducing VEGF expression.","ja":"PPIs prevent hypertension in bevacizumab-treated patients but may reduce bevacizumab's anti-tumoral effects by inducing VEGF expression."},"publication_date":"2020-11-24","publication_name":{"en":"Cancer Medicine","ja":"Cancer Medicine"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/cam4.3587"],"issn":["2045-7634"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:42, {"insert":{"user_id":"6000008820","type":"published_papers","id":"32680489"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/34074484","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=375996","label":"url"}],"paper_title":{"en":"A comparison of the safety and effectiveness of prasugrel and clopidogrel in younger population undergoing percutaneous coronary intervention: A retrospective study using a Japanese claims database.","ja":"A comparison of the safety and effectiveness of prasugrel and clopidogrel in younger population undergoing percutaneous coronary intervention: A retrospective study using a Japanese claims database."},"authors":{"en":[{"name":"Hagiwara Hiromi"},{"name":"Fukuta Hidekatsu"},{"name":"Hashimoto Hiroya"},{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"},{"name":"Kamiya Takeshi"},{"name":"Ohte Nobuyuki"}],"ja":[{"name":"Hagiwara Hiromi"},{"name":"Fukuta Hidekatsu"},{"name":"Hashimoto Hiroya"},{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"石澤 啓介"},{"name":"Kamiya Takeshi"},{"name":"Ohte Nobuyuki"}]},"description":{"en":"The safety and effectiveness of prasugrel was comparable to that of clopidogrel in real-world Japanese patients scheduled to undergo PCI.","ja":"The safety and effectiveness of prasugrel was comparable to that of clopidogrel in real-world Japanese patients scheduled to undergo PCI."},"publication_date":"2020-10-21","publication_name":{"en":"Journal of Cardiology","ja":"Journal of Cardiology"},"volume":"Vol.77","number":"No.3","starting_page":"285","ending_page":"291","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.jjcc.2020.10.001"],"issn":["1876-4738"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:43, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115332","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85091999803&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=371707","label":"url"}],"paper_title":{"en":"Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice","ja":"Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice"},"authors":{"en":[{"name":"Masateru Kondo"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Goda Mitsuhiro"},{"name":"Mayuko Hosooka"},{"name":"Yuu Kagimoto"},{"name":"Naoko Saito"},{"name":"Rie Matsuoka"},{"name":"Zamami Yoshito"},{"name":"Chuma Masayuki"},{"name":"Yagi Kenta"},{"name":"Takechi Kenshi"},{"name":"Tsuneyama Koichi"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"近藤 正輝"},{"name":"石澤 有紀"},{"name":"合田 光寛"},{"name":"細岡 真由子"},{"name":"鍵本 優有"},{"name":"齋藤 尚子"},{"name":"松岡 里英"},{"name":"座間味 義人"},{"name":"中馬 真幸"},{"name":"八木 健太"},{"name":"武智 研志"},{"name":"常山 幸一"},{"name":"石澤 啓介"}]},"publication_date":"2020-09-30","publication_name":{"en":"International Journal of Molecular Sciences","ja":"International Journal of Molecular Sciences"},"volume":"Vol.21","number":"No.19","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3390/ijms21197226"],"issn":["1422-0067"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:44, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116635","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32792640","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=377435","label":"url"}],"paper_title":{"en":"Risk factors of immune checkpoint inhibitor-related interstitial lung disease in patients with lung cancer: a single-institution retrospective study.","ja":"Risk factors of immune checkpoint inhibitor-related interstitial lung disease in patients with lung cancer: a single-institution retrospective study."},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Matsuoka Rie"},{"name":"Sakurada Takumi"},{"name":"Goda Mitsuhiro"},{"name":"Chuma Masayuki"},{"name":"Yagi Kenta"},{"name":"Zamami Yoshito"},{"name":"Nishioka Yasuhiko"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Okada Naoto"},{"name":"Matsuoka Rie"},{"name":"Sakurada Takumi"},{"name":"Goda Mitsuhiro"},{"name":"Chuma Masayuki"},{"name":"Yagi Kenta"},{"name":"Zamami Yoshito"},{"name":"西岡 安彦"},{"name":"石澤 啓介"}]},"description":{"en":"Immune checkpoint inhibitors (ICIs) elicit antitumour effects by activating the host immunity and cause immune-related adverse events (irAEs). ICI-related interstitial lung disease (ICI-ILD) is a fatal irAE that is difficult to treat; moreover, its incidence is relatively higher in patients with lung cancer. Therefore, early ICI-ILD detection and intervention are important for patient safety. However, a risk assessment method for ICI-ILD has not been established and the prediction of ICI-ILD occurrence is difficult. The aim of our study was to identify the risk factors associated with ICI-ILD. To this end, we retrospectively analysed 102 patients with lung cancer who first received ICI and completed the treatment between April 2016 and December 2019 at Tokushima University Hospital. Nineteen patients had all grades of ICI-ILD and 10 had grade ≥ 3 ICI-ILD. The 30-day mortality rate of patients with grade ≥ 3 ICI-ILD was the highest among all patients (P < 0.01). The multivariate logistic analysis indicated that the performance status ≥ 2 alone and both performance status ≥ 2 and ≥ 50 pack-year were independent risk factors of ICI-ILD of grade ≥ 3 and all grades, respectively. Overall, our study provides insights to predict ICI-ILD occurrence.","ja":"Immune checkpoint inhibitors (ICIs) elicit antitumour effects by activating the host immunity and cause immune-related adverse events (irAEs). ICI-related interstitial lung disease (ICI-ILD) is a fatal irAE that is difficult to treat; moreover, its incidence is relatively higher in patients with lung cancer. Therefore, early ICI-ILD detection and intervention are important for patient safety. However, a risk assessment method for ICI-ILD has not been established and the prediction of ICI-ILD occurrence is difficult. The aim of our study was to identify the risk factors associated with ICI-ILD. To this end, we retrospectively analysed 102 patients with lung cancer who first received ICI and completed the treatment between April 2016 and December 2019 at Tokushima University Hospital. Nineteen patients had all grades of ICI-ILD and 10 had grade ≥ 3 ICI-ILD. The 30-day mortality rate of patients with grade ≥ 3 ICI-ILD was the highest among all patients (P < 0.01). The multivariate logistic analysis indicated that the performance status ≥ 2 alone and both performance status ≥ 2 and ≥ 50 pack-year were independent risk factors of ICI-ILD of grade ≥ 3 and all grades, respectively. Overall, our study provides insights to predict ICI-ILD occurrence."},"publication_date":"2020-08-13","publication_name":{"en":"Scientific Reports","ja":"Scientific Reports"},"volume":"Vol.10","number":"No.1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41598-020-70743-2"],"issn":["2045-2322"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:45, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/114409","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32430665","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85085484596&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=363775","label":"url"}],"paper_title":{"en":"Deletion of H-ferritin in macrophages alleviates obesity and diabetes induced by high-fat diet in mice","ja":"Deletion of H-ferritin in macrophages alleviates obesity and diabetes induced by high-fat diet in mice"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Watanabe Hiroaki"},{"name":"Shiuchi Tetsuya"},{"name":"Hamano Hirofumi"},{"name":"Horinouchi Yuya"},{"name":"Imanishi Masaki"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Aihara Ken-ichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"渡邊 大晃"},{"name":"志内 哲也"},{"name":"濱野 裕章"},{"name":"堀ノ内 裕也"},{"name":"今西 正樹"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"石澤 有紀"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"粟飯原 賢一"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Iron accumulation affects obesity and diabetes, both of which are ameliorated by iron reduction. Ferritin, an iron-storage protein, plays a crucial role in iron metabolism. H-ferritin exerts its cytoprotective action by reducing toxicity via its ferroxidase activity. We investigated the role of macrophage H-ferritin in obesity and diabetes. Conditional macrophage-specific H-ferritin (Fth, also known as Fth1) knockout (LysM-Cre Fth KO) mice were used and divided into four groups: wild-type (WT) and LysM-Cre Fth KO mice with normal diet (ND), and WT and LysM-Cre Fth KO mice with high-fat diet (HFD). These mice were analysed for characteristics of obesity and diabetes, tissue iron content, inflammation, oxidative stress, insulin sensitivity and metabolic measurements. RAW264.7 macrophage cells were used for in vitro experiments. Iron concentration reduced, and mRNA expression of ferroportin increased, in macrophages from LysM-Cre Fth KO mice. HFD-induced obesity was lower in LysM-Cre Fth KO mice than in WT mice at 12 weeks (body weight: KO 34.6 ± 5.6 g vs WT 40.1 ± 5.2 g). mRNA expression of inflammatory cytokines and infiltrated macrophages and oxidative stress increased in the adipose tissue of HFD-fed WT mice, but was not elevated in HFD-fed LysM-Cre Fth KO mice. However, WT mice fed an HFD had elevated iron concentration in adipose tissue and spleen, which was not observed in LysM-Cre Fth KO mice fed an HFD (adipose tissue [μmol Fe/g protein]: KO 1496 ± 479 vs WT 2316 ± 866; spleen [μmol Fe/g protein]: KO 218 ± 54 vs WT 334 ± 83). Moreover, HFD administration impaired both glucose tolerance and insulin sensitivity in WT mice, which was ameliorated in LysM-Cre Fth KO mice. In addition, energy expenditure, mRNA expression of thermogenic genes, and body temperature were higher in KO mice with HFD than WT mice with HFD. In vitro experiments showed that iron content was reduced, and lipopolysaccharide-induced Tnf-α (also known as Tnf) mRNA upregulation was inhibited in a macrophage cell line transfected with Fth siRNA. Deletion of macrophage H-ferritin suppresses the inflammatory response by reducing intracellular iron levels, resulting in the prevention of HFD-induced obesity and diabetes. The findings from this study highlight macrophage iron levels as a potential therapeutic target for obesity and diabetes.","ja":"Iron accumulation affects obesity and diabetes, both of which are ameliorated by iron reduction. Ferritin, an iron-storage protein, plays a crucial role in iron metabolism. H-ferritin exerts its cytoprotective action by reducing toxicity via its ferroxidase activity. We investigated the role of macrophage H-ferritin in obesity and diabetes. Conditional macrophage-specific H-ferritin (Fth, also known as Fth1) knockout (LysM-Cre Fth KO) mice were used and divided into four groups: wild-type (WT) and LysM-Cre Fth KO mice with normal diet (ND), and WT and LysM-Cre Fth KO mice with high-fat diet (HFD). These mice were analysed for characteristics of obesity and diabetes, tissue iron content, inflammation, oxidative stress, insulin sensitivity and metabolic measurements. RAW264.7 macrophage cells were used for in vitro experiments. Iron concentration reduced, and mRNA expression of ferroportin increased, in macrophages from LysM-Cre Fth KO mice. HFD-induced obesity was lower in LysM-Cre Fth KO mice than in WT mice at 12 weeks (body weight: KO 34.6 ± 5.6 g vs WT 40.1 ± 5.2 g). mRNA expression of inflammatory cytokines and infiltrated macrophages and oxidative stress increased in the adipose tissue of HFD-fed WT mice, but was not elevated in HFD-fed LysM-Cre Fth KO mice. However, WT mice fed an HFD had elevated iron concentration in adipose tissue and spleen, which was not observed in LysM-Cre Fth KO mice fed an HFD (adipose tissue [μmol Fe/g protein]: KO 1496 ± 479 vs WT 2316 ± 866; spleen [μmol Fe/g protein]: KO 218 ± 54 vs WT 334 ± 83). Moreover, HFD administration impaired both glucose tolerance and insulin sensitivity in WT mice, which was ameliorated in LysM-Cre Fth KO mice. In addition, energy expenditure, mRNA expression of thermogenic genes, and body temperature were higher in KO mice with HFD than WT mice with HFD. In vitro experiments showed that iron content was reduced, and lipopolysaccharide-induced Tnf-α (also known as Tnf) mRNA upregulation was inhibited in a macrophage cell line transfected with Fth siRNA. Deletion of macrophage H-ferritin suppresses the inflammatory response by reducing intracellular iron levels, resulting in the prevention of HFD-induced obesity and diabetes. The findings from this study highlight macrophage iron levels as a potential therapeutic target for obesity and diabetes."},"publication_date":"2020-07-11","publication_name":{"en":"Diabetologia","ja":"Diabetologia"},"volume":"Vol.63","number":"No.8","starting_page":"1588","ending_page":"1602","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00125-020-05153-0"],"issn":["1432-0428"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:46, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115324","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32526602","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=377432","label":"url"}],"paper_title":{"en":"Anti-PD-1 antibody combined with chemotherapy suppresses the growth of mesothelioma by reducing myeloid-derived suppressor cells.","ja":"Anti-PD-1 antibody combined with chemotherapy suppresses the growth of mesothelioma by reducing myeloid-derived suppressor cells."},"authors":{"en":[{"name":"Otsuka Kenji"},{"name":"Mitsuhashi Atsushi"},{"name":"Goto Hisatsugu"},{"name":"Hanibuchi Masaki"},{"name":"Koyama Kazuya"},{"name":"Ogawa Hirohisa"},{"name":"Ogino Hirokazu"},{"name":"Saijo Atsuro"},{"name":"Kozai Hiroyuki"},{"name":"Yoneda Hiroto"},{"name":"Tobiume Makoto"},{"name":"Kishuku Masatoshi"},{"name":"Ishizawa Keisuke"},{"name":"Nishioka Yasuhiko"}],"ja":[{"name":"大塚 憲司"},{"name":"三橋 惇志"},{"name":"後東 久嗣"},{"name":"埴淵 昌毅"},{"name":"小山 壱也"},{"name":"小川 博久"},{"name":"荻野 広和"},{"name":"西條 敦郎"},{"name":"香西 博之"},{"name":"米田 浩人"},{"name":"飛梅 亮"},{"name":"Kishuku Masatoshi"},{"name":"石澤 啓介"},{"name":"西岡 安彦"}]},"description":{"en":"T cells in tumors, the number of Foxp3","ja":"The combination of anti-PD-1 antibody with CDDP + PEM may be a promising therapy for MPM via inhibiting the accumulation of MDSCs and vessels in tumors."},"publication_date":"2020-05-21","publication_name":{"en":"Lung Cancer","ja":"Lung Cancer"},"volume":"Vol.146","starting_page":"86","ending_page":"96","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.lungcan.2020.05.023"],"issn":["1872-8332"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:47, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32307577","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=366414","label":"url"}],"paper_title":{"en":"Fibroblast-specific ERK5 deficiency changes tumor vasculature and exacerbates tumor progression in a mouse model.","ja":"Fibroblast-specific ERK5 deficiency changes tumor vasculature and exacerbates tumor progression in a mouse model."},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Yamakawa Yusuke"},{"name":"Fukushima Keijo"},{"name":"Ikuto Raiki"},{"name":"Maegawa Akiko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Horinouchi Yuya"},{"name":"Kondo Masateru"},{"name":"Kishuku Masatoshi"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Fujino Hiromichi"},{"name":"Tsuneyama Koichi"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"今西 正樹"},{"name":"Yamakawa Yusuke"},{"name":"福島 圭穣"},{"name":"生藤 来希"},{"name":"前川 晃子"},{"name":"石澤 有紀"},{"name":"堀ノ内 裕也"},{"name":"近藤 正輝"},{"name":"木宿 昌俊"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"藤野 裕道"},{"name":"常山 幸一"},{"name":"石澤 啓介"}]},"description":{"en":"The roles of cancer-associated fibroblasts (CAFs) have been studied in the tumor progression, and CAFs are expected to become the new targets for cancer pharmacotherapies. CAFs contribute to tumor cell survival and proliferation, tumor angiogenesis, immune suppression, tumor inflammation, tumor cell invasion and metastasis, and extracellular matrix remodeling. However, detailed mechanisms of how CAFs function in the living system remain unclear. CAFs include α-smooth muscle actin, expressing activated fibroblasts similar to myofibroblasts, and are highly capable of producing collagen. Several reports have demonstrated the contributions of extracellular-signal-regulated kinase 5 (ERK5) in fibroblasts to the fibrotic processes; however, the roles of CAF-derived ERK5 remain unclear. To investigate the roles of CAF-derived ERK5 in the tumor progression, we created mice lacking the ERK5 gene specifically in fibroblasts. Colon-26 mouse colon cancer cells were implanted into the mice subcutaneously, and the histological analyses of the tumor tissue were performed after 2 weeks. Immunofluorescence analyses showed that recipient-derived fibroblasts existed within the tumor tissue. The present study demonstrated that fibroblast-specific ERK5 deficiency exacerbated tumor progression and it was accompanied with thicker tumor vessel formation and the increase in the number of activated fibroblasts. We combined the results of The Cancer Genome Atlas (TCGA) database analysis with our animal studies, and indicated that regulating ERK5 activity in CAFs or CAF invasion into the tumor tissue can be important strategies for the development of new targets in cancer pharmacotherapies.","ja":"The roles of cancer-associated fibroblasts (CAFs) have been studied in the tumor progression, and CAFs are expected to become the new targets for cancer pharmacotherapies. CAFs contribute to tumor cell survival and proliferation, tumor angiogenesis, immune suppression, tumor inflammation, tumor cell invasion and metastasis, and extracellular matrix remodeling. However, detailed mechanisms of how CAFs function in the living system remain unclear. CAFs include α-smooth muscle actin, expressing activated fibroblasts similar to myofibroblasts, and are highly capable of producing collagen. Several reports have demonstrated the contributions of extracellular-signal-regulated kinase 5 (ERK5) in fibroblasts to the fibrotic processes; however, the roles of CAF-derived ERK5 remain unclear. To investigate the roles of CAF-derived ERK5 in the tumor progression, we created mice lacking the ERK5 gene specifically in fibroblasts. Colon-26 mouse colon cancer cells were implanted into the mice subcutaneously, and the histological analyses of the tumor tissue were performed after 2 weeks. Immunofluorescence analyses showed that recipient-derived fibroblasts existed within the tumor tissue. The present study demonstrated that fibroblast-specific ERK5 deficiency exacerbated tumor progression and it was accompanied with thicker tumor vessel formation and the increase in the number of activated fibroblasts. We combined the results of The Cancer Genome Atlas (TCGA) database analysis with our animal studies, and indicated that regulating ERK5 activity in CAFs or CAF invasion into the tumor tissue can be important strategies for the development of new targets in cancer pharmacotherapies."},"publication_date":"2020-04-19","publication_name":{"en":"Naunyn-Schmiedeberg's Archives of Pharmacology","ja":"Naunyn-Schmiedeberg's Archives of Pharmacology"},"volume":"Vol.393","number":"No.7","starting_page":"1239","ending_page":"1250","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00210-020-01859-5"],"issn":["1432-1912"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:48, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115153","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32218694","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85081614223&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=364188","label":"url"}],"paper_title":{"en":"Comparison of Hemorrhagic Risk between Prasugrel and Clopidogrel: a Retrospective Study using Adverse Drug Event Reporting Databases.","ja":"Comparison of Hemorrhagic Risk between Prasugrel and Clopidogrel: a Retrospective Study using Adverse Drug Event Reporting Databases."},"authors":{"en":[{"name":"Hagiwara Hiromi"},{"name":"Fukuta Hidekatsu"},{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"},{"name":"Kimura Kazunori"},{"name":"Kamiya Takeshi"},{"name":"Ohte Nobuyuki"}],"ja":[{"name":"Hagiwara Hiromi"},{"name":"Fukuta Hidekatsu"},{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"石澤 啓介"},{"name":"Kimura Kazunori"},{"name":"Kamiya Takeshi"},{"name":"Ohte Nobuyuki"}]},"description":{"en":": The hemorrhagic risk was found to be greater with prasugrel than clopidogrel in real-world patients, including Japanese patients.","ja":": The hemorrhagic risk was found to be greater with prasugrel than clopidogrel in real-world patients, including Japanese patients."},"publication_date":"2020-03-05","publication_name":{"en":"International Journal of Medical Sciences","ja":"International Journal of Medical Sciences"},"volume":"Vol.17","number":"No.6","starting_page":"728","ending_page":"733","languages":["eng"],"referee":true,"identifiers":{"doi":["10.7150/ijms.43168"],"issn":["1449-1907"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:49, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115530","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31882204","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=366415","label":"url"}],"paper_title":{"en":"Rho-associated protein kinase and cyclophilin a are involved in inorganic phosphate-induced calcification signaling in vascular smooth muscle cells.","ja":"Rho-associated protein kinase and cyclophilin a are involved in inorganic phosphate-induced calcification signaling in vascular smooth muscle cells."},"authors":{"en":[{"name":"Tsuda Tatsuya"},{"name":"Imanishi Masaki"},{"name":"Oogoshi Mizuho"},{"name":"Goda Mitsuhiro"},{"name":"Kihira Yoshitaka"},{"name":"Horinouchi Yuya"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Hashimoto Ichiro"},{"name":"Tamaki Toshiaki"},{"name":"Izawa-Ishizawa Yuki"}],"ja":[{"name":"津田 達也"},{"name":"今西 正樹"},{"name":"Oogoshi Mizuho"},{"name":"合田 光寛"},{"name":"木平 孝高"},{"name":"堀ノ内 裕也"},{"name":"座間味 義人"},{"name":"石澤 啓介"},{"name":"池田 康将"},{"name":"橋本 一郎"},{"name":"玉置 俊晃"},{"name":"石澤 有紀"}]},"description":{"en":"Arterial calcification, a risk factor of cardiovascular events, develops with differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. Cyclophilin A (CypA) is a peptidyl-prolyl isomerase involved in cardiovascular diseases such as atherosclerosis and aortic aneurysms, and rho-associated protein kinase (ROCK) is involved in the pathogenesis of vascular calcification. CypA is secreted in a ROCK activity-dependent manner and works as a mitogen via autocrine or paracrine mechanisms in VSMCs. We examined the involvement of the ROCK-CypA axis in VSMC calcification induced by inorganic phosphate (Pi), a potent cell mineralization initiator. We found that Pi stimulated ROCK activity, CypA secretion, extracellular signal-regulated protein kinase (ERK) 1/2 phosphorylation, and runt-related transcription factor 2 expression, resulting in calcium accumulation in rat aortic smooth muscle cells (RASMCs). The ROCK inhibitor Y-27632 significantly suppressed Pi-induced CypA secretion, ERK1/2 phosphorylation, and calcium accumulation. Recombinant CypA was found to be associated with increased calcium accumulation in RASMCs. Based on these results, we suggest that autocrine CypA is mediated by ROCK activity and is involved in Pi-induced ERK1/2 phosphorylation following calcification signaling in RASMCs.","ja":"Arterial calcification, a risk factor of cardiovascular events, develops with differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. Cyclophilin A (CypA) is a peptidyl-prolyl isomerase involved in cardiovascular diseases such as atherosclerosis and aortic aneurysms, and rho-associated protein kinase (ROCK) is involved in the pathogenesis of vascular calcification. CypA is secreted in a ROCK activity-dependent manner and works as a mitogen via autocrine or paracrine mechanisms in VSMCs. We examined the involvement of the ROCK-CypA axis in VSMC calcification induced by inorganic phosphate (Pi), a potent cell mineralization initiator. We found that Pi stimulated ROCK activity, CypA secretion, extracellular signal-regulated protein kinase (ERK) 1/2 phosphorylation, and runt-related transcription factor 2 expression, resulting in calcium accumulation in rat aortic smooth muscle cells (RASMCs). The ROCK inhibitor Y-27632 significantly suppressed Pi-induced CypA secretion, ERK1/2 phosphorylation, and calcium accumulation. Recombinant CypA was found to be associated with increased calcium accumulation in RASMCs. Based on these results, we suggest that autocrine CypA is mediated by ROCK activity and is involved in Pi-induced ERK1/2 phosphorylation following calcification signaling in RASMCs."},"publication_date":"2020-03","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.142","number":"No.3","starting_page":"109","ending_page":"115","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.jphs.2019.12.005"],"issn":["1347-8648"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:50, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612696"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113812","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31669099","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=360423","label":"url"}],"paper_title":{"en":"Proton pump inhibitors block iron absorption through direct regulation of hepcidin via the aryl hydrocarbon receptor-mediated pathway","ja":"Proton pump inhibitors block iron absorption through direct regulation of hepcidin via the aryl hydrocarbon receptor-mediated pathway"},"authors":{"en":[{"name":"Hamano Hirofumi"},{"name":"Niimura Takahiro"},{"name":"Horinouchi Yuya"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Goda Mitsuhiro"},{"name":"Imanishi Masaki"},{"name":"Chuma Masayuki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyamoto Licht"},{"name":"Fukushima Keijo"},{"name":"Fujino Hiromichi"},{"name":"Tsuchiya Koichiro"},{"name":"Ishizawa Keisuke"},{"name":"Tamaki Toshiaki"},{"name":"Ikeda Yasumasa"}],"ja":[{"name":"濱野 裕章"},{"name":"新村 貴博"},{"name":"堀ノ内 裕也"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"合田 光寛"},{"name":"今西 正樹"},{"name":"中馬 真幸"},{"name":"石澤 有紀"},{"name":"宮本 理人"},{"name":"福島 圭穣"},{"name":"藤野 裕道"},{"name":"土屋 浩一郎"},{"name":"石澤 啓介"},{"name":"玉置 俊晃"},{"name":"池田 康将"}]},"description":{"en":"Proton pump inhibitors (PPIs) have been used worldwide to treat gastrointestinal disorders. A recent study showed that long-term use of PPIs caused iron deficiency; however, it is unclear whether PPIs affect iron metabolism directly. We investigated the effect of PPIs on the peptide hepcidin, an important iron regulatory hormone. First, we used the FDA Adverse Event Reporting System database and analyzed the influence of PPIs. We found that PPIs, as well as H2 blockers, increased the odds ratio of iron-deficient anemia. Next, HepG2 cells were used to examine the action of PPIs and H2 blockers on hepcidin. PPIs augmented hepcidin expression, while H2 blockers did not. In fact, the PPI omeprazole increased hepcidin secretion, and omeprazole-induced hepcidin upregulation was inhibited by gene silencing or the pharmacological inhibition of the aryl hydrocarbon receptor. In mouse experiments, omeprazole also increased hepatic hepcidin mRNA expression and blood hepcidin levels. In mice treated with omeprazole, protein levels of duodenal and splenic ferroportin decreased. Taken together, PPIs directly affect iron metabolism by suppressing iron absorption through the inhibition of duodenal ferroportin via hepcidin upregulation. These findings provide a new insight into the molecular mechanism of PPI-induced iron deficiency.","ja":"Proton pump inhibitors (PPIs) have been used worldwide to treat gastrointestinal disorders. A recent study showed that long-term use of PPIs caused iron deficiency; however, it is unclear whether PPIs affect iron metabolism directly. We investigated the effect of PPIs on the peptide hepcidin, an important iron regulatory hormone. First, we used the FDA Adverse Event Reporting System database and analyzed the influence of PPIs. We found that PPIs, as well as H2 blockers, increased the odds ratio of iron-deficient anemia. Next, HepG2 cells were used to examine the action of PPIs and H2 blockers on hepcidin. PPIs augmented hepcidin expression, while H2 blockers did not. In fact, the PPI omeprazole increased hepcidin secretion, and omeprazole-induced hepcidin upregulation was inhibited by gene silencing or the pharmacological inhibition of the aryl hydrocarbon receptor. In mouse experiments, omeprazole also increased hepatic hepcidin mRNA expression and blood hepcidin levels. In mice treated with omeprazole, protein levels of duodenal and splenic ferroportin decreased. Taken together, PPIs directly affect iron metabolism by suppressing iron absorption through the inhibition of duodenal ferroportin via hepcidin upregulation. These findings provide a new insight into the molecular mechanism of PPI-induced iron deficiency."},"publication_date":"2020-01","publication_name":{"en":"Toxicology Letters","ja":"Toxicology Letters"},"volume":"Vol.318","starting_page":"86","ending_page":"91","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.toxlet.2019.10.016"],"issn":["1879-3169"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:51, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/114461","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31780928","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85075592155&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=361105","label":"url"}],"paper_title":{"en":"Search for Therapeutic Agents for Cardiac Arrest Using a Drug Discovery Tool and Large-Scale Medical Information Database.","ja":"Search for Therapeutic Agents for Cardiac Arrest Using a Drug Discovery Tool and Large-Scale Medical Information Database."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Koyama Toshihiro"},{"name":"Shigemi Yuta"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Morita Mizuki"},{"name":"Ohshima Ayako"},{"name":"Harada Keisaku"},{"name":"Imai Toru"},{"name":"Hagiwara Hiromi"},{"name":"Okada Naoto"},{"name":"Goda Mitsuhiro"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Kondo Yutaka"},{"name":"Tsuchiya Koichiro"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"Koyama Toshihiro"},{"name":"Shigemi Yuta"},{"name":"石澤 有紀"},{"name":"Morita Mizuki"},{"name":"Ohshima Ayako"},{"name":"Harada Keisaku"},{"name":"Imai Toru"},{"name":"Hagiwara Hiromi"},{"name":"岡田 直人"},{"name":"合田 光寛"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"Kondo Yutaka"},{"name":"土屋 浩一郎"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"},{"name":"石澤 啓介"}]},"description":{"en":"The survival rate of cardiac arrest patients is less than 10%; therefore, development of a therapeutic strategy that improves their prognosis is necessary. Herein, we searched data collected from medical facilities throughout Japan for drugs that improve the survival rate of cardiac arrest patients. Candidate drugs, which could improve the prognosis of cardiac arrest patients, were extracted using \"TargetMine,\" a drug discovery tool. We investigated whether the candidate drugs were among the drugs administered within 1 month after cardiac arrest in data of cardiac arrest cases obtained from the Japan Medical Data Center. Logistic regression analysis was performed, with the explanatory variables being the presence or absence of the administration of those candidate drugs that were administered to 10 patients and the objective variable being the \"survival discharge.\" Adjusted odds ratios for survival discharge were calculated using propensity scores for drugs that significantly improved the proportion of survival discharge; the influence of covariates, such as patient background, medical history, and treatment factors, was excluded by the inverse probability-of-treatment weighted method. Using the search strategy, we extracted 165 drugs with vasodilator activity as candidate drugs. Drugs not approved in Japan, oral medicines, and external medicines were excluded. Then, we investigated whether the candidate drugs were administered to the 2,227 cardiac arrest patients included in this study. The results of the logistic regression analysis showed that three (isosorbide dinitrate, nitroglycerin, and nicardipine) of seven drugs that were administered to 10 patients showed significant association with improvement in the proportion of survival discharge. Further analyses using propensity scores revealed that the adjusted odds ratios for survival discharge for patients administered isosorbide dinitrate, nitroglycerin, and nicardipine were 3.35, 5.44, and 4.58, respectively. Thus, it can be suggested that isosorbide dinitrate, nitroglycerin, and nicardipine could be novel therapeutic agents for improving the prognosis of cardiac arrest patients.","ja":"The survival rate of cardiac arrest patients is less than 10%; therefore, development of a therapeutic strategy that improves their prognosis is necessary. Herein, we searched data collected from medical facilities throughout Japan for drugs that improve the survival rate of cardiac arrest patients. Candidate drugs, which could improve the prognosis of cardiac arrest patients, were extracted using \"TargetMine,\" a drug discovery tool. We investigated whether the candidate drugs were among the drugs administered within 1 month after cardiac arrest in data of cardiac arrest cases obtained from the Japan Medical Data Center. Logistic regression analysis was performed, with the explanatory variables being the presence or absence of the administration of those candidate drugs that were administered to 10 patients and the objective variable being the \"survival discharge.\" Adjusted odds ratios for survival discharge were calculated using propensity scores for drugs that significantly improved the proportion of survival discharge; the influence of covariates, such as patient background, medical history, and treatment factors, was excluded by the inverse probability-of-treatment weighted method. Using the search strategy, we extracted 165 drugs with vasodilator activity as candidate drugs. Drugs not approved in Japan, oral medicines, and external medicines were excluded. Then, we investigated whether the candidate drugs were administered to the 2,227 cardiac arrest patients included in this study. The results of the logistic regression analysis showed that three (isosorbide dinitrate, nitroglycerin, and nicardipine) of seven drugs that were administered to 10 patients showed significant association with improvement in the proportion of survival discharge. Further analyses using propensity scores revealed that the adjusted odds ratios for survival discharge for patients administered isosorbide dinitrate, nitroglycerin, and nicardipine were 3.35, 5.44, and 4.58, respectively. Thus, it can be suggested that isosorbide dinitrate, nitroglycerin, and nicardipine could be novel therapeutic agents for improving the prognosis of cardiac arrest patients."},"publication_date":"2019-11-08","publication_name":{"en":"Frontiers in Pharmacology","ja":"Frontiers in Pharmacology"},"volume":"Vol.10","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3389/fphar.2019.01257"],"issn":["1663-9812"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:52, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612697"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31511938","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=361040","label":"url"}],"paper_title":{"en":"Effect of serum concentration and concomitant drugs on vancomycin-induced acute kidney injury in haematologic patients: a single-centre retrospective study.","ja":"Effect of serum concentration and concomitant drugs on vancomycin-induced acute kidney injury in haematologic patients: a single-centre retrospective study."},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Chuma Masayuki"},{"name":"Azuma Momoyo"},{"name":"Nakamura Shingen"},{"name":"Miki Hirokazu"},{"name":"Hamano Hirofumi"},{"name":"Goda Mitsuhiro"},{"name":"Takechi Kenshi"},{"name":"Zamami Yoshito"},{"name":"Abe Masahiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"中馬 真幸"},{"name":"東 桃代"},{"name":"中村 信元"},{"name":"三木 浩和"},{"name":"Hamano Hirofumi"},{"name":"合田 光寛"},{"name":"武智 研志"},{"name":"座間味 義人"},{"name":"安倍 正博"},{"name":"石澤 啓介"}]},"description":{"en":"We retrospectively analysed 150 haematologic patients to whom VCM was administered between April 2010 and March 2018 at Tokushima University Hospital. VCM-induced AKI was defined according to Kidney Disease Improving Global Outcomes (KDIGO) criteria. Multivariate logistic regression analyses were performed to identify risk factors for VCM-induced AKI.","ja":"The optimal initial VCM trough concentration was 10-15 mg/L in haematologic patients, considering safety and effectiveness. There were differences in the effect of VCM-induced AKI between nephrotoxic drugs."},"publication_date":"2019-09-11","publication_name":{"en":"European Journal of Clinical Pharmacology","ja":"European Journal of Clinical Pharmacology"},"volume":"Vol.75","number":"No.12","starting_page":"1695","ending_page":"1704","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00228-019-02756-4"],"issn":["1432-1041"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:53, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612698"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31502114","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=361009","label":"url"}],"paper_title":{"en":"Prophylactic administration of granulocyte colony-stimulating factor in epirubicin and cyclophosphamide chemotherapy for Japanese breast cancer patients: a retrospective study.","ja":"Prophylactic administration of granulocyte colony-stimulating factor in epirubicin and cyclophosphamide chemotherapy for Japanese breast cancer patients: a retrospective study."},"authors":{"en":[{"name":"Sakurada Takumi"},{"name":"Bando Sanako"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Goda Mitsuhiro"},{"name":"Kirino Yasushi"},{"name":"Nakamura Toshimi"},{"name":"Teraoka Kazuhiko"},{"name":"Morimoto Masami"},{"name":"Tangoku Akira"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"櫻田 巧"},{"name":"Bando Sanako"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"合田 光寛"},{"name":"Kirino Yasushi"},{"name":"Nakamura Toshimi"},{"name":"寺岡 和彦"},{"name":"森本 雅美"},{"name":"丹黒 章"},{"name":"石澤 啓介"}]},"description":{"en":"The incidence of FN in EC therapy among Japanese patients was higher than expected, EC therapy appears to be a high-risk chemotherapy for FN, and prophylactic administration of G-CSF is recommended. Maintaining high therapeutic intensity is associated with a positive prognosis for patients with early breast cancer, and prophylactic administration of G-CSF is likely to be beneficial in treatment involving EC therapy.","ja":"The incidence rate of FN was 23.9%. In patients who received G-CSF as primary prophylaxis, FN expression was completely suppressed. The incidence rate of severe leucopenia/neutropenia, emergency hospitalization, and the use of antimicrobial agents were low in patients receiving primary prophylaxis with G-CSF compared with those not receiving G-CSF (27.3% vs. 64.8%, 9.1% vs. 27.3%, and 27.3% vs. 71.6%, respectively). Furthermore, in all patients who received primary prophylaxis with G-CSF, a relative dose intensity > 85% using EC therapy was maintained."},"publication_date":"2019-09-09","publication_name":{"en":"Cancer Chemotherapy and Pharmacology","ja":"Cancer Chemotherapy and Pharmacology"},"volume":"Vol.84","number":"No.5","starting_page":"1107","ending_page":"1114","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00280-019-03948-6"],"issn":["1432-0843"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:54, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612699"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31436802","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=358249","label":"url"}],"paper_title":{"en":"Factors Associated With Immune Checkpoint Inhibitor-Related Myocarditis.","ja":"Factors Associated With Immune Checkpoint Inhibitor-Related Myocarditis."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Okada Naoto"},{"name":"Koyama Toshihiro"},{"name":"Fukushima Keijo"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"岡田 直人"},{"name":"Koyama Toshihiro"},{"name":"福島 圭穣"},{"name":"石澤 有紀"},{"name":"石澤 啓介"}]},"publication_date":"2019-08-22","publication_name":{"en":"JAMA Oncology","ja":"JAMA Oncology"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1001/jamaoncol.2019.3113"],"issn":["2374-2445"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:55, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612700"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113746","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31145863","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=351099","label":"url"}],"paper_title":{"en":"Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress","ja":"Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Satoh Akiho"},{"name":"Horinouchi Yuya"},{"name":"Hamano Hirofumi"},{"name":"Watanabe Hiroaki"},{"name":"Imao Mizuki"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyamoto Licht"},{"name":"Tasuku Hirayama"},{"name":"Nagasawa Hideko"},{"name":"Ishizawa Keisuke"},{"name":"Aihara Ken-ichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"佐藤 明穂"},{"name":"堀ノ内 裕也"},{"name":"濱野 裕章"},{"name":"渡邉 大晃"},{"name":"今尾 瑞季"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"石澤 有紀"},{"name":"宮本 理人"},{"name":"Tasuku Hirayama"},{"name":"永澤 秀子"},{"name":"石澤 啓介"},{"name":"粟飯原 賢一"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Skeletal muscle atrophy is caused by disruption in the homeostatic balance of muscle degeneration and regeneration under various pathophysiological conditions. We have previously reported that iron accumulation induces skeletal muscle atrophy a ubiquitin ligase-dependent pathway. However, the potential effect of iron accumulation on muscle regeneration remains unclear. To examine the effect of iron accumulation on myogenesis, we used a mouse model with cardiotoxin (CTX)-induced muscle regeneration and C2C12 mouse myoblast cells . In mice with iron overload, the skeletal muscles exhibited increased oxidative stress and decreased expression of satellite cell markers. Following CTX-induced muscle injury, these mice also displayed delayed muscle regeneration with a decrease in the size of regenerating myofibers, reduced expression of myoblast differentiation markers, and decreased phosphorylation of MAPK signaling pathways. , iron overload also suppressed the differentiation of C2C12 myoblast cells but the suppression could be reversed by superoxide scavenging using tempol. Excess iron inhibits myogenesis oxidative stress, leading to an imbalance in skeletal muscle homeostasis.-Ikeda, Y., Satoh, A., Horinouchi, Y., Hamano, H., Watanabe, H., Imao, M., Imanishi, M., Zamami, Y., Takechi, K., Izawa-Ishizawa, Y., Miyamoto, L., Hirayama, T., Nagasawa, H., Ishizawa, K., Aihara, K.-I., Tsuchiya, K., Tamaki, T. Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress.","ja":"Skeletal muscle atrophy is caused by disruption in the homeostatic balance of muscle degeneration and regeneration under various pathophysiological conditions. We have previously reported that iron accumulation induces skeletal muscle atrophy a ubiquitin ligase-dependent pathway. However, the potential effect of iron accumulation on muscle regeneration remains unclear. To examine the effect of iron accumulation on myogenesis, we used a mouse model with cardiotoxin (CTX)-induced muscle regeneration and C2C12 mouse myoblast cells . In mice with iron overload, the skeletal muscles exhibited increased oxidative stress and decreased expression of satellite cell markers. Following CTX-induced muscle injury, these mice also displayed delayed muscle regeneration with a decrease in the size of regenerating myofibers, reduced expression of myoblast differentiation markers, and decreased phosphorylation of MAPK signaling pathways. , iron overload also suppressed the differentiation of C2C12 myoblast cells but the suppression could be reversed by superoxide scavenging using tempol. Excess iron inhibits myogenesis oxidative stress, leading to an imbalance in skeletal muscle homeostasis.-Ikeda, Y., Satoh, A., Horinouchi, Y., Hamano, H., Watanabe, H., Imao, M., Imanishi, M., Zamami, Y., Takechi, K., Izawa-Ishizawa, Y., Miyamoto, L., Hirayama, T., Nagasawa, H., Ishizawa, K., Aihara, K.-I., Tsuchiya, K., Tamaki, T. Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress."},"publication_date":"2019-08-01","publication_name":{"en":"The FASEB journal","ja":"The FASEB journal"},"volume":"Vol.33","number":"No.8","starting_page":"9551","ending_page":"9564","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1096/fj.201802724RR"],"issn":["1530-6860"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:56, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612701"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30062585","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=341569","label":"url"}],"paper_title":{"en":"Irinotecan-induced neutropenia is reduced by oral alkalization drugs: analysis using retrospective chart reviews and the spontaneous reporting database.","ja":"Irinotecan-induced neutropenia is reduced by oral alkalization drugs: analysis using retrospective chart reviews and the spontaneous reporting database."},"authors":{"en":[{"name":"Hamano Hirofumi"},{"name":"Mitsui Marin"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Nimura Takahiro"},{"name":"Okada Naoto"},{"name":"Fukushima Keijo"},{"name":"Imanishi Masaki"},{"name":"Chuma Masayuki"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kirino Yasushi"},{"name":"Nakamura Toshimi"},{"name":"Teraoka Kazuhiko"},{"name":"Ikeda Yasumasa"},{"name":"Fujino Hiromichi"},{"name":"Yanagawa Hiroaki"},{"name":"Tamaki Toshiaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"濱野 裕章"},{"name":"三井 茉綸"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"Nimura Takahiro"},{"name":"岡田 直人"},{"name":"福島 圭穣"},{"name":"今西 正樹"},{"name":"中馬 真幸"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"Kirino Yasushi"},{"name":"Nakamura Toshimi"},{"name":"寺岡 和彦"},{"name":"池田 康将"},{"name":"藤野 裕道"},{"name":"楊河 宏章"},{"name":"玉置 俊晃"},{"name":"石澤 啓介"}]},"description":{"en":"These data indicate that oral alkalization drugs may reduce the frequency of neutropenia caused by irinotecan administration, making it possible to increase the dose safely.","ja":"These data indicate that oral alkalization drugs may reduce the frequency of neutropenia caused by irinotecan administration, making it possible to increase the dose safely."},"publication_date":"2019-03","publication_name":{"en":"Supportive Care in Cancer","ja":"Supportive Care in Cancer"},"volume":"Vol.27","number":"No.3","starting_page":"849","ending_page":"856","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00520-018-4367-y"],"issn":["1433-7339"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:57, {"insert":{"user_id":"6000008820","type":"published_papers","id":"12877869"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30351343","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=347373","label":"url"}],"paper_title":{"en":"Xanthine Oxidase Inhibition by Febuxostat in Macrophages Suppresses Angiotensin II-induced Aortic Fibrosis.","ja":"Xanthine Oxidase Inhibition by Febuxostat in Macrophages Suppresses Angiotensin II-induced Aortic Fibrosis."},"authors":{"en":[{"name":"Kondo Masateru"},{"name":"Imanishi Masaki"},{"name":"Fukushima Keijo"},{"name":"Ikuto Raiki"},{"name":"Murai Yoichi"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Ikeda Yasumasa"},{"name":"Fujino Hiromichi"},{"name":"Tsuchiya Koichiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"近藤 正輝"},{"name":"今西 正樹"},{"name":"福島 圭穣"},{"name":"生藤 来希"},{"name":"村井 陽一"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"池田 康将"},{"name":"藤野 裕道"},{"name":"土屋 浩一郎"},{"name":"石澤 啓介"}]},"description":{"en":"Our results suggested that FEB ameliorates Ang II-induced aortic fibrosis via suppressing macrophage-derived TGF-1 expression.","ja":"Our results suggested that FEB ameliorates Ang II-induced aortic fibrosis via suppressing macrophage-derived TGF-1 expression."},"publication_date":"2019-02-12","publication_name":{"en":"American Journal of Hypertension","ja":"American Journal of Hypertension"},"volume":"Vol.32","number":"No.3","starting_page":"249","ending_page":"256","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/ajh/hpy157"],"issn":["1941-7225"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:58, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612703"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113264","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30303488","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=347382","label":"url"}],"paper_title":{"en":"Development of a novel aortic dissection mouse model and evaluation of drug efficacy using in-vivo assays and database analyses.","ja":"Development of a novel aortic dissection mouse model and evaluation of drug efficacy using in-vivo assays and database analyses."},"authors":{"en":[{"name":"Izawa-Ishizawa Yuki"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Hiroki Toya"},{"name":"Tomoko Nagao"},{"name":"Morishita Marin"},{"name":"Tsuneyama Koichi"},{"name":"Horinouchi Yuya"},{"name":"Kihira Yoshitaka"},{"name":"Takechi Kenshi"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Yoshizumi Masanori"},{"name":"Tamaki Toshiaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"石澤 有紀"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"戸谷 紘基"},{"name":"長尾 朋子"},{"name":"Morishita Marin"},{"name":"常山 幸一"},{"name":"堀ノ内 裕也"},{"name":"木平 孝高"},{"name":"武智 研志"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"吉栖 正典"},{"name":"玉置 俊晃"},{"name":"石澤 啓介"}]},"description":{"en":"Aortic dissection is a life-threatening disease. At present, the only therapeutic strategies available are surgery and antihypertensive drugs. Moreover, the molecular mechanisms underlying the onset of aortic dissection are still unclear. We established a novel aortic dissection model in mice using pharmacologically induced endothelial dysfunction. We then used the Japanese Adverse Drug Event Report database to investigate the role of pitavastatin in preventing the onset of aortic dissection. To induce endothelial dysfunction, Nω-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, was administered to C57BL/6 mice. Three weeks later, angiotensin II (Ang II) and β-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, were administered with osmotic mini-pumps. False lumen formation was used as the pathological determinant of aortic dissection. The incidences of aortic dissection and death from aneurysmal rupture were significantly higher in the Nω-nitro-L-arginine methyl ester, Ang II, and BAPN (LAB) group than they were in the Ang II and BAPN (AB) group.Pitavastatin was administered orally to LAB mice. It significantly lowered the incidences of dissection and rupture. It also decreased inflammation and medial degradation, both of which were exacerbated in the LAB group. The Japanese Adverse Drug Event Report database analysis indicated that there were 113 cases of aortic dissection out of 95 090 patients (0.12%) not receiving statins but only six cases out of 16 668 patients receiving statins (0.04%) (odds ratio: 0.30; P = 0.0043). Our results suggest that endothelial dysfunction is associated with the onset of aortic dissection and pitavastatin can help prevent this condition.","ja":"Aortic dissection is a life-threatening disease. At present, the only therapeutic strategies available are surgery and antihypertensive drugs. Moreover, the molecular mechanisms underlying the onset of aortic dissection are still unclear. We established a novel aortic dissection model in mice using pharmacologically induced endothelial dysfunction. We then used the Japanese Adverse Drug Event Report database to investigate the role of pitavastatin in preventing the onset of aortic dissection. To induce endothelial dysfunction, Nω-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, was administered to C57BL/6 mice. Three weeks later, angiotensin II (Ang II) and β-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, were administered with osmotic mini-pumps. False lumen formation was used as the pathological determinant of aortic dissection. The incidences of aortic dissection and death from aneurysmal rupture were significantly higher in the Nω-nitro-L-arginine methyl ester, Ang II, and BAPN (LAB) group than they were in the Ang II and BAPN (AB) group.Pitavastatin was administered orally to LAB mice. It significantly lowered the incidences of dissection and rupture. It also decreased inflammation and medial degradation, both of which were exacerbated in the LAB group. The Japanese Adverse Drug Event Report database analysis indicated that there were 113 cases of aortic dissection out of 95 090 patients (0.12%) not receiving statins but only six cases out of 16 668 patients receiving statins (0.04%) (odds ratio: 0.30; P = 0.0043). Our results suggest that endothelial dysfunction is associated with the onset of aortic dissection and pitavastatin can help prevent this condition."},"publication_date":"2019-01","publication_name":{"en":"Journal of Hypertension","ja":"Journal of Hypertension"},"volume":"Vol.37","number":"No.1","starting_page":"73","ending_page":"83","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1097/HJH.0000000000001898"],"issn":["1473-5598"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:59, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31685767","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=397037","label":"url"}],"paper_title":{"en":"Study on the Optimal Dose of Irinotecan for Patients with Heterozygous Uridine Diphosphate-Glucuronosyltransferase 1A1 (UGT1A1).","ja":"Study on the Optimal Dose of Irinotecan for Patients with Heterozygous Uridine Diphosphate-Glucuronosyltransferase 1A1 (UGT1A1)."},"authors":{"en":[{"name":"Konaka Ken"},{"name":"Sakurada Takumi"},{"name":"Saito Tatsuhiko"},{"name":"Mori Sachiko"},{"name":"Imanishi Masaki"},{"name":"Kakiuchi Soji"},{"name":"Fushitani Shuji"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Konaka Ken"},{"name":"Sakurada Takumi"},{"name":"Saito Tatsuhiko"},{"name":"Mori Sachiko"},{"name":"今西 正樹"},{"name":"Kakiuchi Soji"},{"name":"Fushitani Shuji"},{"name":"石澤 啓介"}]},"description":{"en":"Uridine 5'-diphospho-glucuronosyltransferase (UGT), a metabolic enzyme of irinotecan active metabolite, has two genetic polymorphisms (UGT1A1*6 and UGT1A1*28). In UGT1A1 homozygous or heterozygous patients, metabolism is delayed and the risk of developing adverse effects is increased, and therefore, dose reduction of irinotecan is considered. However, the specific dose reduction rate of irinotecan for heterozygous patients is uncertain. We studied the necessity of irinotecan dose reduction and its optimal dose in UGT1A1 heterozygous patients with lung cancer. Patients with lung cancer treated with irinotecan in the Tokushima University Hospital or Tokushima Municipal Hospital were included in this study. The dose of irinotecan was evaluated based on the relative dose intensity (RDI). The time to treatment failure (TTF) was defined as the period until treatment change, death, or progressive disease based on response evaluation criteria of solid tumors. We targeted 31 patients treated with irinotecan: 12 wild types (WT), 14 heterozygotes, and 1 complex heterozygote and 4 homozygotes. There was no significant difference in the TTF, but the mean RDI during the entire treatment period was significantly different in the wild type (79%), heterozygous (62%), and complex heterozygous and homozygous groups (46%). In addition, the proportion of patients who completed treatment without dose reduction in the WT group tended to be higher than that in the other groups. For lung cancer patients with UGT1A1 heterozygote types who start irinotecan therapy, reducing the initial dose by approximately 20% might be a safer chemotherapy without decreasing the therapeutic effect.","ja":"Uridine 5'-diphospho-glucuronosyltransferase (UGT), a metabolic enzyme of irinotecan active metabolite, has two genetic polymorphisms (UGT1A1*6 and UGT1A1*28). In UGT1A1 homozygous or heterozygous patients, metabolism is delayed and the risk of developing adverse effects is increased, and therefore, dose reduction of irinotecan is considered. However, the specific dose reduction rate of irinotecan for heterozygous patients is uncertain. We studied the necessity of irinotecan dose reduction and its optimal dose in UGT1A1 heterozygous patients with lung cancer. Patients with lung cancer treated with irinotecan in the Tokushima University Hospital or Tokushima Municipal Hospital were included in this study. The dose of irinotecan was evaluated based on the relative dose intensity (RDI). The time to treatment failure (TTF) was defined as the period until treatment change, death, or progressive disease based on response evaluation criteria of solid tumors. We targeted 31 patients treated with irinotecan: 12 wild types (WT), 14 heterozygotes, and 1 complex heterozygote and 4 homozygotes. There was no significant difference in the TTF, but the mean RDI during the entire treatment period was significantly different in the wild type (79%), heterozygous (62%), and complex heterozygous and homozygous groups (46%). In addition, the proportion of patients who completed treatment without dose reduction in the WT group tended to be higher than that in the other groups. For lung cancer patients with UGT1A1 heterozygote types who start irinotecan therapy, reducing the initial dose by approximately 20% might be a safer chemotherapy without decreasing the therapeutic effect."},"publication_date":"2019","publication_name":{"en":"Biological & Pharmaceutical Bulletin","ja":"Biological & Pharmaceutical Bulletin"},"volume":"Vol.42","number":"No.11","starting_page":"1839","ending_page":"1845","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1248/bpb.b19-00357"],"issn":["1347-5215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:60, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115037","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30561126","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=348788","label":"url"}],"paper_title":{"en":"Pharmacovigilance evaluation of the relationship between impaired glucose metabolism and BCR-ABL inhibitor use by using an adverse drug event reporting database.","ja":"Pharmacovigilance evaluation of the relationship between impaired glucose metabolism and BCR-ABL inhibitor use by using an adverse drug event reporting database."},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Hamano Hirofumi"},{"name":"Ishida Shunsuke"},{"name":"Goda Mitsuhiro"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Imanishi Masaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"Hamano Hirofumi"},{"name":"Ishida Shunsuke"},{"name":"合田 光寛"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"今西 正樹"},{"name":"石澤 啓介"}]},"description":{"en":"Breakpoint cluster region-Abelson murine leukemia (BCR-ABL) inhibitors markedly improve the prognosis of chronic myeloid leukemia. However, high treatment adherence is necessary for successful treatment with BCR-ABL inhibitors. Therefore, an adequate understanding of the adverse event profiles of BCR-ABL inhibitors is essential. Although many adverse events are observed in trials, an accurate identification of adverse events based only on clinical trial results is difficult because of strict entry criteria or limited follow-up durations. In particular, BCR-ABL inhibitor-induced impaired glucose metabolism remains controversial. Pharmacovigilance evaluations using spontaneous reporting systems are useful for analyzing drug-related adverse events in clinical settings. Therefore, we conducted signal detection analyses for BCR-ABL inhibitor-induced impaired glucose metabolism by using the FDA Adverse Event Reporting System (FAERS) and Japanese Adverse Drug Event Report (JADER) database. Signals for an increased reporting rate of impaired glucose metabolism were detected only for nilotinib use, whereas these signals were not detected for other BCR-ABL inhibitors. Subgroup analyses showed a clearly increased nilotinib-associated reporting rate of impaired glucose metabolism in male and younger patients. Although FAERS- and JADER-based signal detection analyses cannot determine causality perfectly, our study suggests the effects on glucose metabolism are different between BCR-ABL inhibitors and provides useful information for the selection of appropriate BCR-ABL inhibitors.","ja":"Breakpoint cluster region-Abelson murine leukemia (BCR-ABL) inhibitors markedly improve the prognosis of chronic myeloid leukemia. However, high treatment adherence is necessary for successful treatment with BCR-ABL inhibitors. Therefore, an adequate understanding of the adverse event profiles of BCR-ABL inhibitors is essential. Although many adverse events are observed in trials, an accurate identification of adverse events based only on clinical trial results is difficult because of strict entry criteria or limited follow-up durations. In particular, BCR-ABL inhibitor-induced impaired glucose metabolism remains controversial. Pharmacovigilance evaluations using spontaneous reporting systems are useful for analyzing drug-related adverse events in clinical settings. Therefore, we conducted signal detection analyses for BCR-ABL inhibitor-induced impaired glucose metabolism by using the FDA Adverse Event Reporting System (FAERS) and Japanese Adverse Drug Event Report (JADER) database. Signals for an increased reporting rate of impaired glucose metabolism were detected only for nilotinib use, whereas these signals were not detected for other BCR-ABL inhibitors. Subgroup analyses showed a clearly increased nilotinib-associated reporting rate of impaired glucose metabolism in male and younger patients. Although FAERS- and JADER-based signal detection analyses cannot determine causality perfectly, our study suggests the effects on glucose metabolism are different between BCR-ABL inhibitors and provides useful information for the selection of appropriate BCR-ABL inhibitors."},"publication_date":"2018-12-18","publication_name":{"en":"Cancer Medicine","ja":"Cancer Medicine"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/cam4.1920"],"issn":["2045-7634"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:61, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612704"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30528047","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85057595502&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=368977","label":"url"}],"paper_title":{"en":"Association Between Immune-Related Adverse Events and Clinical Efficacy in Patients with Melanoma Treated With Nivolumab: A Multicenter Retrospective Study.","ja":"Association Between Immune-Related Adverse Events and Clinical Efficacy in Patients with Melanoma Treated With Nivolumab: A Multicenter Retrospective Study."},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Kawazoe Hitoshi"},{"name":"Takechi Kenshi"},{"name":"Matsudate Yoshihiro"},{"name":"Utsunomiya Ryo"},{"name":"Zamami Yoshito"},{"name":"Goda Mitsuhiro"},{"name":"Imanishi Masaki"},{"name":"Chuma Masayuki"},{"name":"Hidaka Noriaki"},{"name":"Sayama Koji"},{"name":"Kubo Yoshiaki"},{"name":"Tanaka Akihiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"Kawazoe Hitoshi"},{"name":"武智 研志"},{"name":"松立 吉弘"},{"name":"Utsunomiya Ryo"},{"name":"座間味 義人"},{"name":"合田 光寛"},{"name":"今西 正樹"},{"name":"中馬 真幸"},{"name":"Hidaka Noriaki"},{"name":"Sayama Koji"},{"name":"久保 宜明"},{"name":"Tanaka Akihiro"},{"name":"石澤 啓介"}]},"description":{"en":"Our study indicated that clinical response with nivolumab treatment improves with irAE occurrence in patients with melanoma. Moreover, the early increase in peripheral lymphocyte count may act as a biomarker for predicting the occurrence of irAEs induced by nivolumab.","ja":"After a median of 4 cycles of nivolumab treatment, irAEs occurred. The DCRs were 75% and 14% in the irAEs-positive and irAEs-negative groups, respectively (p < 0.05). OS in the irAEs-positive group was higher than that in the irAEs-negative group (p < 0.05). Multivariable Cox proportional hazards regression analysis revealed that irAE occurrence affected OS with nivolumab treatment. Moreover, the increase in baseline peripheral lymphocyte count at the time of onset of irAEs was significantly greater in the irAEs-positive group than in the irAEs-negative group after 4 cycles of nivolumab treatment (p < 0.05)."},"publication_date":"2018-12-06","publication_name":{"en":"Clinical Therapeutics","ja":"Clinical Therapeutics"},"volume":"Vol.41","number":"No.1","starting_page":"59","ending_page":"67","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.clinthera.2018.11.004"],"issn":["1879-114X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:62, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30522561","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=348706","label":"url"}],"paper_title":{"en":"Relationship between the administration of nicardipine hydrochloride and the development of delirium in patients on mechanical ventilation.","ja":"Relationship between the administration of nicardipine hydrochloride and the development of delirium in patients on mechanical ventilation."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Kouno Y"},{"name":"Niimura T"},{"name":"Chuma Masayuki"},{"name":"Imai T"},{"name":"Mitsui M"},{"name":"Koyama T"},{"name":"Kayano M"},{"name":"Okada Naoto"},{"name":"Hamano H"},{"name":"Goda Mitsuhiro"},{"name":"Imanishi Masaki"},{"name":"Takechi Kenshi"},{"name":"Horinouchi Yuya"},{"name":"Kondo Y"},{"name":"Yanagawa Hiroaki"},{"name":"Kitamura Y"},{"name":"Sendo T"},{"name":"Ujike Y"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"Kouno Y"},{"name":"Niimura T"},{"name":"中馬 真幸"},{"name":"Imai T"},{"name":"Mitsui M"},{"name":"Koyama T"},{"name":"Kayano M"},{"name":"岡田 直人"},{"name":"Hamano H"},{"name":"合田 光寛"},{"name":"今西 正樹"},{"name":"武智 研志"},{"name":"堀ノ内 裕也"},{"name":"Kondo Y"},{"name":"楊河 宏章"},{"name":"Kitamura Y"},{"name":"Sendo T"},{"name":"Ujike Y"},{"name":"石澤 啓介"}]},"description":{"en":"A history of hypertension is a known risk factor for delirium in patients in intensive care units, but the effect of antihypertensive agents on delirium development is unclear. Nicardipine, a calcium channel blocker, is widely used in ICU as a treatment agent for hypertensive emergency. This study investigated the relationship between the administration of nicardipine hydrochloride and delirium development in patients under mechanical ventilation. We conducted a medical chart review of 103 patients, who were divided into two groups according to the use of nicardipine hydrochloride. The prevalence of delirium was compared with respect to factors such as age, sex, laboratory data, and medical history, by multivariate analysis. 21 patients (20.4 %) were treated with nicardipine hydrochloride in 103 patients. The treatment and non-treatment groups differed significantly in age (72 vs. 65 years) and history of high blood pressure (57% vs. 11%). Multivariate analysis revealed that patients in the treatment group developed delirium significantly less often than those in the non-treatment group (19% vs. 48%). These results suggested that treatment of high blood pressure with nicardipine hydrochloride is a possible method for preventing the development of delirium.","ja":"A history of hypertension is a known risk factor for delirium in patients in intensive care units, but the effect of antihypertensive agents on delirium development is unclear. Nicardipine, a calcium channel blocker, is widely used in ICU as a treatment agent for hypertensive emergency. This study investigated the relationship between the administration of nicardipine hydrochloride and delirium development in patients under mechanical ventilation. We conducted a medical chart review of 103 patients, who were divided into two groups according to the use of nicardipine hydrochloride. The prevalence of delirium was compared with respect to factors such as age, sex, laboratory data, and medical history, by multivariate analysis. 21 patients (20.4 %) were treated with nicardipine hydrochloride in 103 patients. The treatment and non-treatment groups differed significantly in age (72 vs. 65 years) and history of high blood pressure (57% vs. 11%). Multivariate analysis revealed that patients in the treatment group developed delirium significantly less often than those in the non-treatment group (19% vs. 48%). These results suggested that treatment of high blood pressure with nicardipine hydrochloride is a possible method for preventing the development of delirium."},"publication_date":"2018-12-01","publication_name":{"en":"Die Pharmazie","ja":"Die Pharmazie"},"volume":"Vol.73","number":"No.12","starting_page":"740","ending_page":"743","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1691/ph.2018.8711"],"issn":["0031-7144"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:63, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612705"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30253416","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85054191604&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=354050","label":"url"}],"paper_title":{"en":"Nitrosonifedipine, a Photodegradation Product of Nifedipine, Suppresses Pharmacologically Induced Aortic Aneurysm Formation.","ja":"Nitrosonifedipine, a Photodegradation Product of Nifedipine, Suppresses Pharmacologically Induced Aortic Aneurysm Formation."},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Sakurada T"},{"name":"Kohara Y"},{"name":"Horinouchi Yuya"},{"name":"Sairyo E"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Fukushima Keijo"},{"name":"Ikeda Yasumasa"},{"name":"Fujino Hiromichi"},{"name":"Yoshizumi M"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"今西 正樹"},{"name":"石澤 有紀"},{"name":"Sakurada T"},{"name":"Kohara Y"},{"name":"堀ノ内 裕也"},{"name":"Sairyo E"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"福島 圭穣"},{"name":"池田 康将"},{"name":"藤野 裕道"},{"name":"Yoshizumi M"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"},{"name":"石澤 啓介"}]},"description":{"en":"We have reported that nitrosonifedipine (NO-NIF), a photodegradation product of nifedipine, has strong antioxidant and endothelial protective effects, and can suppress several cardiovascular diseases in animal models. The objective of the present study was to investigate the effects of NO-NIF on aortic aneurysm formation. The mice were infused with β-aminopropionitrile for 2 weeks and angiotensin II for 6 weeks to induce aortic aneurysm formation. The oxidative stress was measured by dihydroethidium staining and nitrotyrosine staining. The expressions of inflammation-related genes were assessed by quantitative real-time PCR and immunohistochemical staining. To clarify the mechanisms of how NO-NIF suppresses vascular cell adhesion molecule (VCAM)-1, endothelial cells were used in in vitro system. NO-NIF suppressed pharmacologically induced the aortic aneurysm formation and aortic expansion without blood pressure changes. NO-NIF suppressed elastin degradation and matrix metalloproteinase-2 mRNA expression. NO-NIF suppressed the reactive oxygen species-cyclophilin A positive feedback loop. Upregulated mRNA expressions of inflammation-related genes and endothelial VCAM-1 were suppressed by NO-NIF co-treatment in aortae. NO-NIF has the potential to be a new, nifedipine-derived therapeutic drug for suppressing aortic aneurysm formation by directly improving aortic structure with its strong ability to reduce oxidative stress and inflammation.","ja":"We have reported that nitrosonifedipine (NO-NIF), a photodegradation product of nifedipine, has strong antioxidant and endothelial protective effects, and can suppress several cardiovascular diseases in animal models. The objective of the present study was to investigate the effects of NO-NIF on aortic aneurysm formation. The mice were infused with β-aminopropionitrile for 2 weeks and angiotensin II for 6 weeks to induce aortic aneurysm formation. The oxidative stress was measured by dihydroethidium staining and nitrotyrosine staining. The expressions of inflammation-related genes were assessed by quantitative real-time PCR and immunohistochemical staining. To clarify the mechanisms of how NO-NIF suppresses vascular cell adhesion molecule (VCAM)-1, endothelial cells were used in in vitro system. NO-NIF suppressed pharmacologically induced the aortic aneurysm formation and aortic expansion without blood pressure changes. NO-NIF suppressed elastin degradation and matrix metalloproteinase-2 mRNA expression. NO-NIF suppressed the reactive oxygen species-cyclophilin A positive feedback loop. Upregulated mRNA expressions of inflammation-related genes and endothelial VCAM-1 were suppressed by NO-NIF co-treatment in aortae. NO-NIF has the potential to be a new, nifedipine-derived therapeutic drug for suppressing aortic aneurysm formation by directly improving aortic structure with its strong ability to reduce oxidative stress and inflammation."},"publication_date":"2018-09-25","publication_name":{"en":"Pharmacology","ja":"Pharmacology"},"volume":"Vol.102","number":"No.5-6","starting_page":"281","ending_page":"286","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1159/000492577"],"issn":["1423-0313"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:64, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/112203","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30221424","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=346269","label":"url"}],"paper_title":{"en":"Development and pharmacist-mediated use of tools for monitoring atypical antipsychotic-induced side effects related to blood glucose levels.","ja":"Development and pharmacist-mediated use of tools for monitoring atypical antipsychotic-induced side effects related to blood glucose levels."},"authors":{"en":[{"name":"Ishida Shunsuke"},{"name":"Takechi Kenshi"},{"name":"Bando Hiroshi"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Chuma Masayuki"},{"name":"Yanagawa Hiroaki"},{"name":"Kirino Yasushi"},{"name":"Nakamura Toshimi"},{"name":"Teraoka Kazuhiko"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Ishida Shunsuke"},{"name":"武智 研志"},{"name":"Bando Hiroshi"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"中馬 真幸"},{"name":"楊河 宏章"},{"name":"Kirino Yasushi"},{"name":"Nakamura Toshimi"},{"name":"Teraoka Kazuhiko"},{"name":"石澤 啓介"}]},"description":{"en":"The results suggested that regardless of pharmacists' experience or skill, the introduction of this tool enables centralization of side effect monitoring and can contribute to proper drug use.","ja":"The results suggested that regardless of pharmacists' experience or skill, the introduction of this tool enables centralization of side effect monitoring and can contribute to proper drug use."},"publication_date":"2018-09-17","publication_name":{"en":"Pharmacoepidemiology and Drug Safety","ja":"Pharmacoepidemiology and Drug Safety"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/pds.4656"],"issn":["1099-1557"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:65, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/112445","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30022146","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=342025","label":"url"}],"paper_title":{"en":"Renoprotective effects of a factor Xa inhibitor: fusion of basic research and a database analysis.","ja":"Renoprotective effects of a factor Xa inhibitor: fusion of basic research and a database analysis."},"authors":{"en":[{"name":"Horinouchi Yuya"},{"name":"Ikeda Yasumasa"},{"name":"Fukushima Keijo"},{"name":"Imanishi Masaki"},{"name":"Hamano Hirofumi"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Miyamoto Licht"},{"name":"Fujino Hiromichi"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"堀ノ内 裕也"},{"name":"池田 康将"},{"name":"福島 圭穣"},{"name":"今西 正樹"},{"name":"Hamano Hirofumi"},{"name":"石澤 有紀"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"宮本 理人"},{"name":"藤野 裕道"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Renal tubulointerstitial injury, an inflammation-associated condition, is a major cause of chronic kidney disease (CKD). Levels of activated factor X (FXa), a blood coagulation factor, are increased in various inflammatory diseases. Therefore, we investigated the protective effects of an FXa inhibitor against renal tubulointerstitial injury using unilateral ureteral obstruction (UUO) mice (a renal tubulointerstitial fibrosis model) and the Food and Drug Administration Adverse Events Reporting System (FAERS) database. The renal expression levels of FX and the FXa receptors protease-activated receptor (PAR)-1 and PAR-2 were significantly higher in UUO mice than in sham-operated mice. UUO-induced tubulointerstitial fibrosis and extracellular matrix expression were suppressed in UUO mice treated with the FXa inhibitor edoxaban. Additionally, edoxaban attenuated UUO-induced macrophage infiltration and inflammatory molecule upregulation. In an analysis of the FAERS database, there were significantly fewer reports of tubulointerstitial nephritis for patients treated with FXa inhibitors than for patients not treated with inhibitors. These results suggest that FXa inhibitors exert protective effects against CKD by inhibiting tubulointerstitial fibrosis.","ja":"Renal tubulointerstitial injury, an inflammation-associated condition, is a major cause of chronic kidney disease (CKD). Levels of activated factor X (FXa), a blood coagulation factor, are increased in various inflammatory diseases. Therefore, we investigated the protective effects of an FXa inhibitor against renal tubulointerstitial injury using unilateral ureteral obstruction (UUO) mice (a renal tubulointerstitial fibrosis model) and the Food and Drug Administration Adverse Events Reporting System (FAERS) database. The renal expression levels of FX and the FXa receptors protease-activated receptor (PAR)-1 and PAR-2 were significantly higher in UUO mice than in sham-operated mice. UUO-induced tubulointerstitial fibrosis and extracellular matrix expression were suppressed in UUO mice treated with the FXa inhibitor edoxaban. Additionally, edoxaban attenuated UUO-induced macrophage infiltration and inflammatory molecule upregulation. In an analysis of the FAERS database, there were significantly fewer reports of tubulointerstitial nephritis for patients treated with FXa inhibitors than for patients not treated with inhibitors. These results suggest that FXa inhibitors exert protective effects against CKD by inhibiting tubulointerstitial fibrosis."},"publication_date":"2018-07-18","publication_name":{"en":"Scientific Reports","ja":"Scientific Reports"},"volume":"Vol.8","number":"No.1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41598-018-29008-2"],"issn":["2045-2322"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:66, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612706"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/110922","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28992067","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=325682","label":"url"}],"paper_title":{"en":"The uremic toxin indoxyl sulfate interferes with iron metabolism by regulating hepcidin in chronic kidney disease","ja":"The uremic toxin indoxyl sulfate interferes with iron metabolism by regulating hepcidin in chronic kidney disease"},"authors":{"en":[{"name":"Hamano Hirofumi"},{"name":"Ikeda Yasumasa"},{"name":"Watanabe Hiroaki"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"濱野 裕章"},{"name":"池田 康将"},{"name":"渡邉 大晃"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"publication_date":"2018-04","publication_name":{"en":"Nephrology, Dialysis, Transplantation","ja":"Nephrology, Dialysis, Transplantation"},"volume":"Vol.33","number":"No.4","starting_page":"586","ending_page":"597","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/ndt/gfx252"],"issn":["1460-2385"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:67, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612707"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/29305017","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=336420","label":"url"}],"paper_title":{"en":"Potential Usefulness of Early Potassium Supplementation for Preventing Severe Hypokalemia Induced by Liposomal Amphotericin B in Hematologic Patients: A Retrospective Study.","ja":"Potential Usefulness of Early Potassium Supplementation for Preventing Severe Hypokalemia Induced by Liposomal Amphotericin B in Hematologic Patients: A Retrospective Study."},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Azuma Momoyo"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Kirino Yasushi"},{"name":"Nakamura Toshimi"},{"name":"Teraoka Kazuhiko"},{"name":"Abe Masahiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"東 桃代"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"Kirino Yasushi"},{"name":"Nakamura Toshimi"},{"name":"寺岡 和彦"},{"name":"Abe Masahiro"},{"name":"石澤 啓介"}]},"description":{"en":"This study showed that starting administration of a potassium formulation within 2 days from the start of L-AMB administration was a risk reduction factor for L-AMB-induced hypokalemia. This finding indicates that early potassium supplementation should be incorporated into the regimen of hypokalemia management when L-AMB is used.","ja":"This study showed that starting administration of a potassium formulation within 2 days from the start of L-AMB administration was a risk reduction factor for L-AMB-induced hypokalemia. This finding indicates that early potassium supplementation should be incorporated into the regimen of hypokalemia management when L-AMB is used."},"publication_date":"2018-01-02","publication_name":{"en":"Clinical Therapeutics","ja":"Clinical Therapeutics"},"volume":"Vol.40","number":"No.2","starting_page":"252","ending_page":"260","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.clinthera.2017.12.006"],"issn":["1879-114X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:68, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612708"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/111388","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/29593190","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=337283","label":"url"}],"paper_title":{"en":"Administration of Kampo medicine through a tube at an advanced critical care center.","ja":"Administration of Kampo medicine through a tube at an advanced critical care center."},"authors":{"en":[{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Imai Toru"},{"name":"Ito Tsuyoshi"},{"name":"Sagara Hidenori"},{"name":"Hiroyuki Hichiya"},{"name":"Esumi Satoru"},{"name":"Takechi Kenshi"},{"name":"Imanishi Masaki"},{"name":"Koyama Toshihiro"},{"name":"Amano Manabu"},{"name":"Kurata Naomi"},{"name":"Kitamura Yoshihisa"},{"name":"Nakura Hironori"},{"name":"Sendo Toshiaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"Imai Toru"},{"name":"Ito Tsuyoshi"},{"name":"Sagara Hidenori"},{"name":"Hiroyuki Hichiya"},{"name":"Esumi Satoru"},{"name":"武智 研志"},{"name":"今西 正樹"},{"name":"Koyama Toshihiro"},{"name":"Amano Manabu"},{"name":"Kurata Naomi"},{"name":"Kitamura Yoshihisa"},{"name":"Nakura Hironori"},{"name":"Sendo Toshiaki"},{"name":"石澤 啓介"}]},"description":{"en":"n emergency and critical care medical centers, tube administration is employed for patients who have difficulty swallowing oral drugs owing to decreased consciousness or mechanical ventilation. However, tube clogging due to drug injection is a concern. We compared the crushing method with the simple suspension method for the passage of amlodipine, an antihypertensive drug, in combination with rikkunshito, which has been used to treat upper gastrointestinal disorders such as functional dyspepsia and gastroesophageal reflux in emergency and critical care medical centers, to ascertain the effect of Kampo products on the passage of other drugs during tube administration. When the crushing method was employed, poorly water-soluble solid products were formed, while a uniformly dispersed suspension was obtained using the simple suspension method. In addition, the passage rate of amlodipine through the tube was 64% and 93% in the crushing and simple suspension methods, respectively, thereby indicating that the simple suspension method provided more favorable than the crushing method. The results of this study suggested that the passage rate of amlodipine for patients who received Kampo products concurrently was higher when the simple suspension method was used, and an appropriate drug amount might well be able to administered to patients using this method. J. Med. Invest. 65:32-36, February, 2018.","ja":"n emergency and critical care medical centers, tube administration is employed for patients who have difficulty swallowing oral drugs owing to decreased consciousness or mechanical ventilation. However, tube clogging due to drug injection is a concern. We compared the crushing method with the simple suspension method for the passage of amlodipine, an antihypertensive drug, in combination with rikkunshito, which has been used to treat upper gastrointestinal disorders such as functional dyspepsia and gastroesophageal reflux in emergency and critical care medical centers, to ascertain the effect of Kampo products on the passage of other drugs during tube administration. When the crushing method was employed, poorly water-soluble solid products were formed, while a uniformly dispersed suspension was obtained using the simple suspension method. In addition, the passage rate of amlodipine through the tube was 64% and 93% in the crushing and simple suspension methods, respectively, thereby indicating that the simple suspension method provided more favorable than the crushing method. The results of this study suggested that the passage rate of amlodipine for patients who received Kampo products concurrently was higher when the simple suspension method was used, and an appropriate drug amount might well be able to administered to patients using this method. J. Med. Invest. 65:32-36, February, 2018."},"publication_date":"2018","publication_name":{"en":"The Journal of Medical Investigation : JMI","ja":"The Journal of Medical Investigation : JMI"},"volume":"Vol.65","number":"No.1.2","starting_page":"32","ending_page":"36","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2152/jmi.65.32"],"issn":["1349-6867"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:69, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/29455711","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85044119660&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=336419","label":"url"}],"paper_title":{"en":"Evaluation of the Benefits of De-Escalation for Patients with Sepsis in the Emergency Intensive Care Unit.","ja":"Evaluation of the Benefits of De-Escalation for Patients with Sepsis in the Emergency Intensive Care Unit."},"authors":{"en":[{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Imai Toru"},{"name":"Nagao Kanako"},{"name":"Kayano Masafumi"},{"name":"Sagara Hidenori"},{"name":"Goda Mitsuhiro"},{"name":"Okada Naoto"},{"name":"Chuma Masayuki"},{"name":"Takechi Kenshi"},{"name":"Imanishi Masaki"},{"name":"Koyama Toshihiro"},{"name":"Koga Tadashi"},{"name":"Nakura Hironori"},{"name":"Sendo Toshiaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"Imai Toru"},{"name":"Nagao Kanako"},{"name":"Kayano Masafumi"},{"name":"Sagara Hidenori"},{"name":"Goda Mitsuhiro"},{"name":"岡田 直人"},{"name":"中馬 真幸"},{"name":"武智 研志"},{"name":"今西 正樹"},{"name":"Koyama Toshihiro"},{"name":"Koga Tadashi"},{"name":"Nakura Hironori"},{"name":"Sendo Toshiaki"},{"name":"石澤 啓介"}]},"description":{"en":"The length of hospital stay after diagnosis was significantly shorter for the de-escalation group than for the non-de-escalation group. In the subgroup analysis, de-escalation for blood culture-positive patients was beneficial in terms of the length of hospital stay and length of antibiotic administration.","ja":"The findings of this study suggest that sepsis treatment de-escalation is beneficial for treatment efficacy and appropriate use of antibiotics. This article is open to POST-PUBLICATION REVIEW. Registered readers (see \"For Readers\") may comment by clicking on ABSTRACT on the issue's contents page."},"publication_date":"2018","publication_name":{"en":"Journal of Pharmacy & Pharmaceutical Sciences","ja":"Journal of Pharmacy & Pharmaceutical Sciences"},"volume":"Vol.21","number":"No.1","starting_page":"54","ending_page":"59","languages":["eng"],"referee":true,"identifiers":{"doi":["10.18433/jpps29737"],"issn":["1482-1826"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:70, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/112397","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/29263333","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=335442","label":"url"}],"paper_title":{"en":"Hydrocortisone administration was associated with improved survival in Japanese patients with cardiac arrest.","ja":"Hydrocortisone administration was associated with improved survival in Japanese patients with cardiac arrest."},"authors":{"en":[{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Koyama Toshihiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyake Masashi"},{"name":"Koga Tadashi"},{"name":"Harada Keisaku"},{"name":"Ohshima Ayako"},{"name":"Imai Toru"},{"name":"Kondo Yutaka"},{"name":"Imanishi Masaki"},{"name":"Takechi Kenshi"},{"name":"Fukushima Keijo"},{"name":"Horinouchi Yuya"},{"name":"Ikeda Yasumasa"},{"name":"Fujino Hiromichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"Koyama Toshihiro"},{"name":"石澤 有紀"},{"name":"Miyake Masashi"},{"name":"Koga Tadashi"},{"name":"Harada Keisaku"},{"name":"Ohshima Ayako"},{"name":"Imai Toru"},{"name":"Kondo Yutaka"},{"name":"今西 正樹"},{"name":"武智 研志"},{"name":"福島 圭穣"},{"name":"堀ノ内 裕也"},{"name":"池田 康将"},{"name":"藤野 裕道"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"},{"name":"石澤 啓介"}]},"description":{"en":"There are few reports on hydrocortisone administration after cardiac arrest, and those that have been published included few subjects. This study aimed to evaluate the effect of hydrocortisone administration on the outcomes of patients who experienced cardiac arrest. We investigated the survival discharge rates and the length of hospital stay from cardiac arrest to discharge, stratified by use of hydrocortisone, using a Japanese health-insurance claims dataset that covers approximately 2% of the Japanese population. The study included the data of 2233 subjects who experienced either in-hospital or out-of-hospital cardiac arrest between January 2005 and May 2014. These patients were divided into two groups, based on the administration of hydrocortisone. We adjusted the baseline characteristics, medical treatment, and drug administration data of the two groups using propensity scores obtained via the inverse probability of treatment weighted method. The hydrocortisone group had a significantly higher survival discharge rate (13/61 [21.1%] vs. 240/2172 [11.0%], adjusted odds ratio: 4.2, 95% CI: 1.60-10.98, p = 0.004). In addition, the administration of hydrocortisone was independent predictor of survival to discharge (hazard ratio: 4.6, p < 0.001). The results demonstrate a correlation between hydrocortisone administration and the high rates of survival to discharge.","ja":"There are few reports on hydrocortisone administration after cardiac arrest, and those that have been published included few subjects. This study aimed to evaluate the effect of hydrocortisone administration on the outcomes of patients who experienced cardiac arrest. We investigated the survival discharge rates and the length of hospital stay from cardiac arrest to discharge, stratified by use of hydrocortisone, using a Japanese health-insurance claims dataset that covers approximately 2% of the Japanese population. The study included the data of 2233 subjects who experienced either in-hospital or out-of-hospital cardiac arrest between January 2005 and May 2014. These patients were divided into two groups, based on the administration of hydrocortisone. We adjusted the baseline characteristics, medical treatment, and drug administration data of the two groups using propensity scores obtained via the inverse probability of treatment weighted method. The hydrocortisone group had a significantly higher survival discharge rate (13/61 [21.1%] vs. 240/2172 [11.0%], adjusted odds ratio: 4.2, 95% CI: 1.60-10.98, p = 0.004). In addition, the administration of hydrocortisone was independent predictor of survival to discharge (hazard ratio: 4.6, p < 0.001). The results demonstrate a correlation between hydrocortisone administration and the high rates of survival to discharge."},"publication_date":"2017-12-20","publication_name":{"en":"Scientific Reports","ja":"Scientific Reports"},"volume":"Vol.7","number":"No.1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41598-017-17686-3"],"issn":["2045-2322"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:71, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/112393","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28978927","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85030715238&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=334079","label":"url"}],"paper_title":{"en":"Meta-analysis of the efficacies of amiodarone and nifekalant in shock-resistant ventricular fibrillation and pulseless ventricular tachycardia.","ja":"Meta-analysis of the efficacies of amiodarone and nifekalant in shock-resistant ventricular fibrillation and pulseless ventricular tachycardia."},"authors":{"en":[{"name":"Sato Shiho"},{"name":"Zamami Yoshito"},{"name":"Imai Toru"},{"name":"Tanaka Satoshi"},{"name":"Koyama Toshihiro"},{"name":"Niimura Takahiro"},{"name":"Chuma Masayuki"},{"name":"Koga Tadashi"},{"name":"Takechi Kenshi"},{"name":"Kurata Yasuko"},{"name":"Kondo Yutaka"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Sendo Toshiaki"},{"name":"Nakura Hironori"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Sato Shiho"},{"name":"座間味 義人"},{"name":"Imai Toru"},{"name":"Tanaka Satoshi"},{"name":"Koyama Toshihiro"},{"name":"新村 貴博"},{"name":"中馬 真幸"},{"name":"Koga Tadashi"},{"name":"武智 研志"},{"name":"Kurata Yasuko"},{"name":"Kondo Yutaka"},{"name":"石澤 有紀"},{"name":"Sendo Toshiaki"},{"name":"Nakura Hironori"},{"name":"石澤 啓介"}]},"description":{"en":"Amiodarone (AMD) and nifekalant (NIF) are used in the treatment of ventricular fibrillation or tachycardia; however, only few studies have been conducted on their efficacies. Therefore, a meta-analysis was conducted. Relevant sources were identified from PubMed, Cochrane Central Register of Controlled Trials, and Igaku Chuo Zasshi. The outcomes were short-term and long-term survival in patients with shock-resistant ventricular fibrillation /pulseless ventricular tachycardia. Thirty-three studies were analysed. The results showed that, compared to the control treatment, AMD did not improve short-term survival (odds ratio (OR): 1.25, 95% confidence interval (CI): 0.91-1.71) or long-term survival (OR: 1.00, 95% CI: 0.63-1.57). However, compared to the control treatment, NIF significantly improved short-term survival (OR: 3.23, 95% CI: 2.21-4.72) and long-term survival (OR: 1.88, 95% CI: 1.36-2.59). No significant difference was observed in short-term survival (OR: 0.85, 95% CI: 0.63-1.15) or long-term survival (OR: 1.25, 95% CI: 0.67-2.31) between AMD- and NIF-treated patients. The results suggest that NIF is beneficial for short-term and long-term survival in shock-resistant ventricular fibrillation/pulseless ventricular tachycardia; however, the efficacy of AMD in either outcome is not clear.","ja":"Amiodarone (AMD) and nifekalant (NIF) are used in the treatment of ventricular fibrillation or tachycardia; however, only few studies have been conducted on their efficacies. Therefore, a meta-analysis was conducted. Relevant sources were identified from PubMed, Cochrane Central Register of Controlled Trials, and Igaku Chuo Zasshi. The outcomes were short-term and long-term survival in patients with shock-resistant ventricular fibrillation /pulseless ventricular tachycardia. Thirty-three studies were analysed. The results showed that, compared to the control treatment, AMD did not improve short-term survival (odds ratio (OR): 1.25, 95% confidence interval (CI): 0.91-1.71) or long-term survival (OR: 1.00, 95% CI: 0.63-1.57). However, compared to the control treatment, NIF significantly improved short-term survival (OR: 3.23, 95% CI: 2.21-4.72) and long-term survival (OR: 1.88, 95% CI: 1.36-2.59). No significant difference was observed in short-term survival (OR: 0.85, 95% CI: 0.63-1.15) or long-term survival (OR: 1.25, 95% CI: 0.67-2.31) between AMD- and NIF-treated patients. The results suggest that NIF is beneficial for short-term and long-term survival in shock-resistant ventricular fibrillation/pulseless ventricular tachycardia; however, the efficacy of AMD in either outcome is not clear."},"publication_date":"2017-10-04","publication_name":{"en":"Scientific Reports","ja":"Scientific Reports"},"volume":"Vol.7","number":"No.1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41598-017-13073-0"],"issn":["2045-2322"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:72, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/112368","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28878231","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=329173","label":"url"}],"paper_title":{"en":"Dietary iron restriction alleviates renal tubulointerstitial injury induced by protein overload in mice","ja":"Dietary iron restriction alleviates renal tubulointerstitial injury induced by protein overload in mice"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Horinouchi Yuya"},{"name":"Hirofumi Hamano"},{"name":"Tasuku Hirayama"},{"name":"Kishi Seiji"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Aihara Ken-ichi"},{"name":"Nagasawa Hideko"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"堀ノ内 裕也"},{"name":"濱野 裕章"},{"name":"Tasuku Hirayama"},{"name":"岸 誠司"},{"name":"石澤 有紀"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"粟飯原 賢一"},{"name":"永澤 秀子"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Increased proteinuria causes tubulointerstitial injury due to inflammation in chronic kidney disease (CKD). Iron restriction exhibits protective effects against renal dysfunction; however, its effects against protein overload-induced tubulointerstitial damage remain unclear. Here, we investigated dietary iron restriction effect on tubulointerstitial damage in mice with protein-overload tubulointerstitial injury. Renal tubulointerstitial injury in animal model was induced by intraperitoneal injection of an overdose of bovine serum albumin (BSA). We divided mice into three groups: normal saline + normal diet (ND), BSA + ND, and BSA + iron-restricted diet (IRD). BSA overload induced renal tubulointerstitial injury in the ND mice, which was ameliorated in the IRD mice. Inflammatory cytokines and extracellular matrix mRNA expression was upregulated in BSA + ND mice kidneys and was inhibited by IRD. BSA-induced increase in renal superoxide production, NADPH oxidase activity, and p22(phox) expression was diminished in the IRD mice. IRD suppression increased BSA-induced renal macrophage infiltration. Moreover, BSA mice exhibited nucleotide-binding oligomerisation domain-like receptor pyrin domain-containing protein (NLRP) inflammasome activation, which was inhibited by IRD. Ferrous iron increased in kidneys with BSA overload and was inhibited by IRD. Thus, iron restriction inhibited oxidative stress and inflammatory changes, contributing to the protective effect against BSA overload-induced tubulointerstitial injury.","ja":"Increased proteinuria causes tubulointerstitial injury due to inflammation in chronic kidney disease (CKD). Iron restriction exhibits protective effects against renal dysfunction; however, its effects against protein overload-induced tubulointerstitial damage remain unclear. Here, we investigated dietary iron restriction effect on tubulointerstitial damage in mice with protein-overload tubulointerstitial injury. Renal tubulointerstitial injury in animal model was induced by intraperitoneal injection of an overdose of bovine serum albumin (BSA). We divided mice into three groups: normal saline + normal diet (ND), BSA + ND, and BSA + iron-restricted diet (IRD). BSA overload induced renal tubulointerstitial injury in the ND mice, which was ameliorated in the IRD mice. Inflammatory cytokines and extracellular matrix mRNA expression was upregulated in BSA + ND mice kidneys and was inhibited by IRD. BSA-induced increase in renal superoxide production, NADPH oxidase activity, and p22(phox) expression was diminished in the IRD mice. IRD suppression increased BSA-induced renal macrophage infiltration. Moreover, BSA mice exhibited nucleotide-binding oligomerisation domain-like receptor pyrin domain-containing protein (NLRP) inflammasome activation, which was inhibited by IRD. Ferrous iron increased in kidneys with BSA overload and was inhibited by IRD. Thus, iron restriction inhibited oxidative stress and inflammatory changes, contributing to the protective effect against BSA overload-induced tubulointerstitial injury."},"publication_date":"2017-09-06","publication_name":{"en":"Scientific Reports","ja":"Scientific Reports"},"volume":"Vol.7","number":"No.1","starting_page":"10621","ending_page":"10621","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41598-017-11089-0"],"issn":["2045-2322"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:73, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/114522","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28748102","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=332490","label":"url"}],"paper_title":{"en":"Kamishoyosan and Shakuyakukanzoto promote recovery from paclitaxel-induced neurite retraction in PC12 cells","ja":"Kamishoyosan and Shakuyakukanzoto promote recovery from paclitaxel-induced neurite retraction in PC12 cells"},"authors":{"en":[{"name":"Konaka Ken"},{"name":"Moriyama Kota"},{"name":"Sakurada Takumi"},{"name":"Okada Naoto"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Kawazoe Kazuyoshi"},{"name":"Fushitani Shuji"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Konaka Ken"},{"name":"Moriyama Kota"},{"name":"Sakurada Takumi"},{"name":"岡田 直人"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"川添 和義"},{"name":"Fushitani Shuji"},{"name":"石澤 啓介"}]},"description":{"en":"In chemotherapy, the full round of treatment must be completed as scheduled to achieve the strongest therapeutic effect. However, peripheral neuropathy, a severe side effect of the chemotherapeutic agent paclitaxel, can force the premature discontinuation of treatment. As some kampo practitioners have suggested that it may be possible to counteract such side effects, we analyzed the effects of Kamishoyosan, Shakuyakukanzoto, and Goshajinkigan in an in vitro model of paclitaxel-induced peripheral neuropathy. Paclitaxel-treated PC12 cells were assessed for neurite length and performed Western blot analysis for growth-associated protein-43 (GAP-43) and light neurofilament protein (NF-L) levels in the presence of nerve growth factor (NGF); they were re-assessed, with additional testing for acetylcholinesterase levels, after application of one of the kampo. We also compared phosphorylation of extracellular signal-regulated kinase (Erk)1/2 and Akt via Western blot analysis. About effect of kampo to anticancer efficacy, we confirmed cell cytotoxicity in A549 cells using MTT assay. Addition of Kamishoyosan or Shakuyakukanzoto, but not Goshajinkigan, significantly improved neurite length and GAP-43 and NF-L levels from paclitaxel-treated PC12 cells, relative to those of only NGF-treated PC12 cells. The promoting effect of Kamishoyosan and Shakuyakukanzoto in neurite outgrowth is confirmed when NGF promoted neurite outgrowth, and it was inhibited partially when Erk1/2 and Akt were blocked by Erk1/2 inhibitor or Akt inhibitor alone. Furthermore, neurite outgrowth induced by TJ24 and TJ68 was inhibited more strongly when Erk1/2 inhibitor and Akt inhibitor were treated at the same time. NGF with Kamishoyosan or Shakuyakukanzoto promoted the proportion of phosphorylated Erk1/2 and phosphorylated Akt compare with NGF only. On the other hand, Kamishoyosan or Shakuyakukanzoto didn't influence cytotoxicity of paclitaxel in A549 cells. Kamishoyosan or Shakuyakukanzoto promotes neurite outgrowth with NGF via increasing the proportion of phosphorylated Erk1/2 and phosphorylated Akt in PC12 cells. The effect applies to recovery from paclitaxel-induced axonal involvement and might promote recovery from paclitaxel-induced neuropathy without influence of anticancer effect of paclitaxel.","ja":"In chemotherapy, the full round of treatment must be completed as scheduled to achieve the strongest therapeutic effect. However, peripheral neuropathy, a severe side effect of the chemotherapeutic agent paclitaxel, can force the premature discontinuation of treatment. As some kampo practitioners have suggested that it may be possible to counteract such side effects, we analyzed the effects of Kamishoyosan, Shakuyakukanzoto, and Goshajinkigan in an in vitro model of paclitaxel-induced peripheral neuropathy. Paclitaxel-treated PC12 cells were assessed for neurite length and performed Western blot analysis for growth-associated protein-43 (GAP-43) and light neurofilament protein (NF-L) levels in the presence of nerve growth factor (NGF); they were re-assessed, with additional testing for acetylcholinesterase levels, after application of one of the kampo. We also compared phosphorylation of extracellular signal-regulated kinase (Erk)1/2 and Akt via Western blot analysis. About effect of kampo to anticancer efficacy, we confirmed cell cytotoxicity in A549 cells using MTT assay. Addition of Kamishoyosan or Shakuyakukanzoto, but not Goshajinkigan, significantly improved neurite length and GAP-43 and NF-L levels from paclitaxel-treated PC12 cells, relative to those of only NGF-treated PC12 cells. The promoting effect of Kamishoyosan and Shakuyakukanzoto in neurite outgrowth is confirmed when NGF promoted neurite outgrowth, and it was inhibited partially when Erk1/2 and Akt were blocked by Erk1/2 inhibitor or Akt inhibitor alone. Furthermore, neurite outgrowth induced by TJ24 and TJ68 was inhibited more strongly when Erk1/2 inhibitor and Akt inhibitor were treated at the same time. NGF with Kamishoyosan or Shakuyakukanzoto promoted the proportion of phosphorylated Erk1/2 and phosphorylated Akt compare with NGF only. On the other hand, Kamishoyosan or Shakuyakukanzoto didn't influence cytotoxicity of paclitaxel in A549 cells. Kamishoyosan or Shakuyakukanzoto promotes neurite outgrowth with NGF via increasing the proportion of phosphorylated Erk1/2 and phosphorylated Akt in PC12 cells. The effect applies to recovery from paclitaxel-induced axonal involvement and might promote recovery from paclitaxel-induced neuropathy without influence of anticancer effect of paclitaxel."},"publication_date":"2017-07-21","publication_name":{"en":"Journal of Pharmaceutical Health Care and Sciences","ja":"Journal of Pharmaceutical Health Care and Sciences"},"volume":"Vol.3","starting_page":"20","ending_page":"20","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1186/s40780-017-0090-y"],"issn":["2055-0294"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:74, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28655381","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=325349","label":"url"}],"paper_title":{"en":"Evaluation of factors associated with the achievement of an optimal teicoplanin trough concentration .","ja":"Evaluation of factors associated with the achievement of an optimal teicoplanin trough concentration ."},"authors":{"en":[{"name":"Takechi Kenshi"},{"name":"Yanagawa Hiroaki"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"},{"name":"Tanaka Akihiro"},{"name":"Araki Hiroaki"}],"ja":[{"name":"武智 研志"},{"name":"楊河 宏章"},{"name":"座間味 義人"},{"name":"石澤 啓介"},{"name":"Tanaka Akihiro"},{"name":"荒木 博陽"}]},"description":{"en":"These results suggested that patients with decreased renal function (eGFR.","ja":"Approximately 32% (31/97) of patients achieved the trough concentration target (≥ 15 µg/mL) on the 3rd or 4th day. Multivariate analysis showed that loading doses and body surface area (BSA) were associated with trough concentration > 15 µg/mL on the 3rd or 4th day. Moreover, patients treated with the 2-day loading dose (1,600 mg group: 800 mg/day on 2 days) promptly achieved a trough concentration > 15 µg/mL on the 3rd or 4th day compared with those receiving a 1-day loading dose (1,200 mg group: 800 mg/day on only 1 day). The receiver operating characteristic curve showed that the optimal cut-off point of estimated glomerular filtration rate (eGFR) was 56 mL/min with 1-day loading dose to achieve a trough concentration target > 15 µg/mL."},"publication_date":"2017-06-28","publication_name":{"en":"International Journal of Clinical Pharmacology and Therapeutics","ja":"International Journal of Clinical Pharmacology and Therapeutics"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.5414/CP203009"],"issn":["0946-1965"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:75, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612709"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113749","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28263291","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=322994","label":"url"}],"paper_title":{"en":"Iron suppresses erythropoietin expression via oxidative stress-dependent hypoxia-inducible factor-2 alpha inactivation","ja":"Iron suppresses erythropoietin expression via oxidative stress-dependent hypoxia-inducible factor-2 alpha inactivation"},"authors":{"en":[{"name":"Oshima Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Horinouchi Yuya"},{"name":"Watanabe Hiroaki"},{"name":"Hamano Hirofumi"},{"name":"Kihira Yoshitaka"},{"name":"Kishi Seiji"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyamoto Licht"},{"name":"Hirayama Tasuku"},{"name":"Nagasawa Hideko"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"大島 啓亮"},{"name":"池田 康将"},{"name":"堀ノ内 裕也"},{"name":"Watanabe Hiroaki"},{"name":"Hamano Hirofumi"},{"name":"木平 孝高"},{"name":"岸 誠司"},{"name":"石澤 有紀"},{"name":"宮本 理人"},{"name":"Hirayama Tasuku"},{"name":"永澤 秀子"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Renal anemia is a major complication in chronic kidney disease (CKD). Iron supplementation, as well as erythropoiesis-stimulating agents, are widely used for treatment of renal anemia. However, excess iron causes oxidative stress via the Fenton reaction, and iron supplementation might damage remnant renal function including erythropoietin (EPO) production in CKD. EPO gene expression was suppressed in mice following direct iron treatment. Hypoxia-inducible factor-2 alpha (HIF-2α), a positive regulator of the EPO gene, was also diminished in the kidney of mice following iron treatment. Anemia-induced increase in renal EPO and HIF-2α expression was inhibited by iron treatment. In in vitro experiments using EPO-producing HepG2 cells, iron stimulation reduced the expression of the EPO gene, as well as HIF-2α. Moreover, iron treatment augmented oxidative stress, and iron-induced reduction of EPO and HIF-2α expression was restored by tempol, an antioxidant compound. HIF-2α interaction with the Epo promoter was inhibited by iron treatment, and was restored by tempol. These findings suggested that iron supplementation reduced EPO gene expression via an oxidative stress-HIF-2α-dependent signaling pathway.","ja":"Renal anemia is a major complication in chronic kidney disease (CKD). Iron supplementation, as well as erythropoiesis-stimulating agents, are widely used for treatment of renal anemia. However, excess iron causes oxidative stress via the Fenton reaction, and iron supplementation might damage remnant renal function including erythropoietin (EPO) production in CKD. EPO gene expression was suppressed in mice following direct iron treatment. Hypoxia-inducible factor-2 alpha (HIF-2α), a positive regulator of the EPO gene, was also diminished in the kidney of mice following iron treatment. Anemia-induced increase in renal EPO and HIF-2α expression was inhibited by iron treatment. In in vitro experiments using EPO-producing HepG2 cells, iron stimulation reduced the expression of the EPO gene, as well as HIF-2α. Moreover, iron treatment augmented oxidative stress, and iron-induced reduction of EPO and HIF-2α expression was restored by tempol, an antioxidant compound. HIF-2α interaction with the Epo promoter was inhibited by iron treatment, and was restored by tempol. These findings suggested that iron supplementation reduced EPO gene expression via an oxidative stress-HIF-2α-dependent signaling pathway."},"publication_date":"2017-03-06","publication_name":{"en":"Laboratory Investigation; a Journal of Technical Methods and Pathology","ja":"Laboratory Investigation; a Journal of Technical Methods and Pathology"},"volume":"Vol.97","number":"No.5","starting_page":"555","ending_page":"566","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/labinvest.2017.11"],"issn":["1530-0307"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:76, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612710"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/110118","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28090711","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=323552","label":"url"}],"paper_title":{"en":"Topical Application of Nitrosonifedipine, a Novel Radical Scavenger, Ameliorates Ischemic Skin Flap Necrosis in a Mouse Model.","ja":"Topical Application of Nitrosonifedipine, a Novel Radical Scavenger, Ameliorates Ischemic Skin Flap Necrosis in a Mouse Model."},"authors":{"en":[{"name":"Fukunaga Yutaka"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Horinouchi Yuya"},{"name":"Sairyo Eriko"},{"name":"Ikeda Yasumasa"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Abe Yoshiro"},{"name":"Hashimoto Ichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"福永 豊"},{"name":"石澤 有紀"},{"name":"堀ノ内 裕也"},{"name":"Sairyo Eriko"},{"name":"池田 康将"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"安倍 吉郎"},{"name":"橋本 一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO-NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO-NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO-NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO-NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO-NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p < 0.01). NO-NIF reduced oxidative stress, apoptosis and endothelial dysfunction, which were evidenced by the decrease of malondialdehyde, p22phox protein expression, number of apoptotic cells, phosphorylated p38 MAPK protein expression, and vascular cell adhesion molecule-1 protein expression while endothelial nitric oxide synthase protein expression was increased. In conclusion, they demonstrated that NO-NIF ameliorated ischemic skin flap necrosis by reducing oxidative stress, apoptosis, and endothelial dysfunction. NO-NIF is considered to be a candidate for the treatment of ischemic flap necrosis.","ja":"Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO-NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO-NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO-NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO-NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO-NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p < 0.01). NO-NIF reduced oxidative stress, apoptosis and endothelial dysfunction, which were evidenced by the decrease of malondialdehyde, p22phox protein expression, number of apoptotic cells, phosphorylated p38 MAPK protein expression, and vascular cell adhesion molecule-1 protein expression while endothelial nitric oxide synthase protein expression was increased. In conclusion, they demonstrated that NO-NIF ameliorated ischemic skin flap necrosis by reducing oxidative stress, apoptosis, and endothelial dysfunction. NO-NIF is considered to be a candidate for the treatment of ischemic flap necrosis."},"publication_date":"2017-02-17","publication_name":{"en":"Wound Repair and Regeneration","ja":"Wound Repair and Regeneration"},"volume":"Vol.25","number":"No.2","starting_page":"217","ending_page":"223","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/wrr.12510"],"issn":["1524-475X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:77, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612711"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28966250","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85030761013&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=329187","label":"url"}],"paper_title":{"en":"Psychiatric patients with antipsychotic drug-induced hyperprolactinemia and menstruation disorders","ja":"Psychiatric patients with antipsychotic drug-induced hyperprolactinemia and menstruation disorders"},"authors":{"en":[{"name":"Takechi Kenshi"},{"name":"Yoshioka Yurika"},{"name":"Kawazoe Hitoshi"},{"name":"Tanaka Mamoru"},{"name":"Takatori Shingo"},{"name":"Kobayashi Miwako"},{"name":"Matsuoka Ichiro"},{"name":"Yanagawa Hiroaki"},{"name":"Zamami Yoshito"},{"name":"Imanishi Masaki"},{"name":"Ishizawa Keisuke"},{"name":"Tanaka Akihiro"},{"name":"Araki Hiroaki"}],"ja":[{"name":"武智 研志"},{"name":"Yoshioka Yurika"},{"name":"Kawazoe Hitoshi"},{"name":"Tanaka Mamoru"},{"name":"Takatori Shingo"},{"name":"Kobayashi Miwako"},{"name":"Matsuoka Ichiro"},{"name":"楊河 宏章"},{"name":"座間味 義人"},{"name":"今西 正樹"},{"name":"石澤 啓介"},{"name":"Tanaka Akihiro"},{"name":"荒木 博陽"}]},"description":{"en":"Treatment with antipsychotic drugs has been associated with hyperprolactinemia. The same antipsychotic drugs have also been associated with side effects such as menstruation disorders. The aim of this study was to evaluate the prevalence of hyperprolactinemia and menstruation disorders in women undergoing antipsychotic treatment. We performed a retrospective chart review study of psychiatric patients who underwent laboratory testing for serum prolactin (PRL) level between March 2011 and March 2015 in Ehime University Hospital. Patients presenting with and without menstruation disorders were evaluated to determine if they presented concomitant hyperprolactinemia. Patients with menstrual disorders had a significant increase in serum PRL level with a mean of approximately 90 ng/mL. Those with menstrual disorders presented increased PRL levels by 2-fold that of patients without menstrual disorder. However, there was no significant difference in the equivalent dose of chlorpromazine between these two groups. Additionally, about 70% of patients with menstrual disorders received risperidone treatment. The receiver operating characteristic curve showed that the optimal cutoff point of serum PRL level associated with the development of menstrual disorders was 60 ng/mL. Based on these results, we concluded that patients with menstrual disorders presented increased serum PRL, and that most of them underwent treatment with risperidone.","ja":"Treatment with antipsychotic drugs has been associated with hyperprolactinemia. The same antipsychotic drugs have also been associated with side effects such as menstruation disorders. The aim of this study was to evaluate the prevalence of hyperprolactinemia and menstruation disorders in women undergoing antipsychotic treatment. We performed a retrospective chart review study of psychiatric patients who underwent laboratory testing for serum prolactin (PRL) level between March 2011 and March 2015 in Ehime University Hospital. Patients presenting with and without menstruation disorders were evaluated to determine if they presented concomitant hyperprolactinemia. Patients with menstrual disorders had a significant increase in serum PRL level with a mean of approximately 90 ng/mL. Those with menstrual disorders presented increased PRL levels by 2-fold that of patients without menstrual disorder. However, there was no significant difference in the equivalent dose of chlorpromazine between these two groups. Additionally, about 70% of patients with menstrual disorders received risperidone treatment. The receiver operating characteristic curve showed that the optimal cutoff point of serum PRL level associated with the development of menstrual disorders was 60 ng/mL. Based on these results, we concluded that patients with menstrual disorders presented increased serum PRL, and that most of them underwent treatment with risperidone."},"publication_date":"2017","publication_name":{"en":"Biological & Pharmaceutical Bulletin","ja":"Biological & Pharmaceutical Bulletin"},"volume":"Vol.40","number":"No.10","starting_page":"1775","ending_page":"1778","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1248/bpb.b17-00053"],"issn":["1347-5215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:78, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/114521","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/27606071","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=320506","label":"url"}],"paper_title":{"en":"Evaluation of pharmaceutical lifesaving skills training oriented pharmaceutical intervention.","ja":"Evaluation of pharmaceutical lifesaving skills training oriented pharmaceutical intervention."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Imai Toru"},{"name":"Imanishi Masaki"},{"name":"Takechi Kenshi"},{"name":"Shiraishi Naoko"},{"name":"Koyama Toshihiro"},{"name":"Sagara Hidenori"},{"name":"Shiino Yasukazu"},{"name":"Sendo Toshiaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"Imai Toru"},{"name":"今西 正樹"},{"name":"武智 研志"},{"name":"Shiraishi Naoko"},{"name":"Koyama Toshihiro"},{"name":"Sagara Hidenori"},{"name":"Shiino Yasukazu"},{"name":"Sendo Toshiaki"},{"name":"石澤 啓介"}]},"description":{"en":"Our high-performance patient simulator-based lifesaving skills training program not only increased the participants' understanding of the training content but also increased their confidence in their ability to perform pharmaceutical interventions. Therefore, the pharmaceutical lifesaving skills training program we developed will contribute to the education of emergency care pharmacists who can perform pharmaceutical interventions for emergency patients.","ja":"Our high-performance patient simulator-based lifesaving skills training program not only increased the participants' understanding of the training content but also increased their confidence in their ability to perform pharmaceutical interventions. Therefore, the pharmaceutical lifesaving skills training program we developed will contribute to the education of emergency care pharmacists who can perform pharmaceutical interventions for emergency patients."},"publication_date":"2016-09-07","publication_name":{"en":"Journal of Pharmaceutical Health Care and Sciences","ja":"Journal of Pharmaceutical Health Care and Sciences"},"volume":"Vol.2","number":"No.1","starting_page":"21","ending_page":"21","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1186/s40780-016-0054-7"],"issn":["2055-0294"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:79, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612712"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113750","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/27049128","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=306466","label":"url"}],"paper_title":{"en":"Iron-induced skeletal muscle atrophy involves an Akt-forkhead box O3-E3 ubiquitin ligase-dependent pathway","ja":"Iron-induced skeletal muscle atrophy involves an Akt-forkhead box O3-E3 ubiquitin ligase-dependent pathway"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Imao Mizuki"},{"name":"Satoh Akiho"},{"name":"Watanabe Hiroaki"},{"name":"Hamano Hirofumi"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"今尾 瑞季"},{"name":"佐藤 明穂"},{"name":"渡邉 大晃"},{"name":"濱野 裕章"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Skeletal muscle wasting or sarcopenia is a critical health problem. Skeletal muscle atrophy is induced by an excess of iron, which is an essential trace metal for all living organisms. Excessive amounts of iron catalyze the formation of highly toxic hydroxyl radicals via the Fenton reaction. However, the molecular mechanism of iron-induced skeletal muscle atrophy has remained unclear. In this study, 8-weeks-old C57BL6/J mice were divided into 2 groups: vehicle-treated group and the iron-injected group (10 mg iron·day-1·mouse-1) during 2 weeks. Mice in the iron-injected group showed an increase in the iron content of the skeletal muscle and serum and ferritin levels in the muscle, along with reduced skeletal muscle mass. The skeletal muscle showed elevated mRNA expression of the muscle atrophy-related E3 ubiquitin ligases, atrogin-1 and muscle ring finger-1(MuRF1), on days 7 and 14 of iron treatment. Moreover, iron-treated mice showed reduced phosphorylation of Akt and forkhead box O3 (FOXO3a) in skeletal muscles. Inhibition of FOXO3a using siRNA in vitro in C2C12 myotube cells inhibited iron-induced upregulation of atrogin-1 and MuRF1 and reversed the reduction in myotube diameters. Iron-load caused oxidative stress, and an oxidative stress inhibitor abrogated iron-induced muscle atrophy by reactivating the Akt-FOXO3 pathway. Iron-induced skeletal muscle atrophy is suggested to involve the E3 ubiquitin ligase mediated by the reduction of Akt-FOXO3a signaling by oxidative stress.","ja":"Skeletal muscle wasting or sarcopenia is a critical health problem. Skeletal muscle atrophy is induced by an excess of iron, which is an essential trace metal for all living organisms. Excessive amounts of iron catalyze the formation of highly toxic hydroxyl radicals via the Fenton reaction. However, the molecular mechanism of iron-induced skeletal muscle atrophy has remained unclear. In this study, 8-weeks-old C57BL6/J mice were divided into 2 groups: vehicle-treated group and the iron-injected group (10 mg iron·day-1·mouse-1) during 2 weeks. Mice in the iron-injected group showed an increase in the iron content of the skeletal muscle and serum and ferritin levels in the muscle, along with reduced skeletal muscle mass. The skeletal muscle showed elevated mRNA expression of the muscle atrophy-related E3 ubiquitin ligases, atrogin-1 and muscle ring finger-1(MuRF1), on days 7 and 14 of iron treatment. Moreover, iron-treated mice showed reduced phosphorylation of Akt and forkhead box O3 (FOXO3a) in skeletal muscles. Inhibition of FOXO3a using siRNA in vitro in C2C12 myotube cells inhibited iron-induced upregulation of atrogin-1 and MuRF1 and reversed the reduction in myotube diameters. Iron-load caused oxidative stress, and an oxidative stress inhibitor abrogated iron-induced muscle atrophy by reactivating the Akt-FOXO3 pathway. Iron-induced skeletal muscle atrophy is suggested to involve the E3 ubiquitin ligase mediated by the reduction of Akt-FOXO3a signaling by oxidative stress."},"publication_date":"2016-05","publication_name":{"en":"Journal of Trace Elements in Medicine and Biology","ja":"Journal of Trace Elements in Medicine and Biology"},"volume":"Vol.35","number":"No.5","starting_page":"66","ending_page":"76","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.jtemb.2016.01.011"],"issn":["1878-3252"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:80, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612713"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/27129837","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=312093","label":"url"}],"paper_title":{"en":"Evaluation of the risk factors associated with high-dose chemotherapyinduced dysgeusia in patients undergoing autologous hematopoietic stem cell transplantation: Possible usefulness of cryotherapy in dysgeusia prevention","ja":"Evaluation of the risk factors associated with high-dose chemotherapyinduced dysgeusia in patients undergoing autologous hematopoietic stem cell transplantation: Possible usefulness of cryotherapy in dysgeusia prevention"},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Hanafusa Takeshi"},{"name":"Abe Shinji"},{"name":"Sato Chiemi"},{"name":"Nakamura Toshimi"},{"name":"Teraoka Kazuhiko"},{"name":"Abe Masahiro"},{"name":"Kawazoe Kazuyoshi"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"花房 剛志"},{"name":"阿部 真治"},{"name":"佐藤 智恵美"},{"name":"中村 敏己"},{"name":"寺岡 和彦"},{"name":"安倍 正博"},{"name":"川添 和義"},{"name":"石澤 啓介"}]},"description":{"en":"Dysgeusia is one of the sporadic adverse effects induced by chemotherapy, but it remains poorly understood. The aim of this study was to retrospectively identify the risk factors related with dysgeusia in patients undergoing autologous hematopoietic stem cell transplantation (AHSCT). Forty-eight patients with myeloma or lymphoma undergoing AHSCT were enrolled in this study. Data regarding dysgeusia and symptoms were collected by interviews conducted by medical workers. Patient characteristics and unfavorable effects induced by dysgeusia were obtained from medical records and analyzed. Logistic regression analysis was performed to identify the risk factors related with dysgeusia. Of the 48 patients, 20 (42 %) had dysgeusia after AHSCT. The total period of parenteral nutrition (TPN) administration and period of decreased oral intake in the dysgeusia group were statistically longer than those in the non-dysgeusia group. Multivariate analyses revealed that oral mucositis (odds ratio: 30.3; p < 0.01) and the type of chemotherapy prior to AHSCT (odds ratio: 6.56; p < 0.05) were independent risk factors, while oral cryotherapy was the independent suppressive factor of dysgeusia (odds ratio: 0.14; p < 0.05). Our study showed that dysgeusia after AHSCT led to the decrease in oral intake and extended the TPN administration period. Moreover, MEAM or LEED chemotherapy and oral mucositis were independent risk factors for dysgeusia in patients undergoing AHSCT, while oral cryotherapy was an independent suppressive factor for dysgeusia. Therefore, oral cryotherapy should be implemented into the regimen of supportive care management in patients undergoing AHSCT.","ja":"Dysgeusia is one of the sporadic adverse effects induced by chemotherapy, but it remains poorly understood. The aim of this study was to retrospectively identify the risk factors related with dysgeusia in patients undergoing autologous hematopoietic stem cell transplantation (AHSCT). Forty-eight patients with myeloma or lymphoma undergoing AHSCT were enrolled in this study. Data regarding dysgeusia and symptoms were collected by interviews conducted by medical workers. Patient characteristics and unfavorable effects induced by dysgeusia were obtained from medical records and analyzed. Logistic regression analysis was performed to identify the risk factors related with dysgeusia. Of the 48 patients, 20 (42 %) had dysgeusia after AHSCT. The total period of parenteral nutrition (TPN) administration and period of decreased oral intake in the dysgeusia group were statistically longer than those in the non-dysgeusia group. Multivariate analyses revealed that oral mucositis (odds ratio: 30.3; p < 0.01) and the type of chemotherapy prior to AHSCT (odds ratio: 6.56; p < 0.05) were independent risk factors, while oral cryotherapy was the independent suppressive factor of dysgeusia (odds ratio: 0.14; p < 0.05). Our study showed that dysgeusia after AHSCT led to the decrease in oral intake and extended the TPN administration period. Moreover, MEAM or LEED chemotherapy and oral mucositis were independent risk factors for dysgeusia in patients undergoing AHSCT, while oral cryotherapy was an independent suppressive factor for dysgeusia. Therefore, oral cryotherapy should be implemented into the regimen of supportive care management in patients undergoing AHSCT."},"publication_date":"2016-04-29","publication_name":{"en":"Supportive Care in Cancer","ja":"Supportive Care in Cancer"},"volume":"Vol.24","number":"No.9","starting_page":"3979","ending_page":"3985","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00520-016-3244-9"],"issn":["1433-7339"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:81, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/26830489","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=305591","label":"url"}],"paper_title":{"en":"Clinical evaluation of pharmacist interventions in patients treated with anti-methicillin-resistant Staphylococcus aureus agents in a hematological ward","ja":"Clinical evaluation of pharmacist interventions in patients treated with anti-methicillin-resistant Staphylococcus aureus agents in a hematological ward"},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Fushitani Shuji"},{"name":"Azuma Momoyo"},{"name":"Nakamura Shingen"},{"name":"Nakamura Toshimi"},{"name":"Teraoka Kazuhiko"},{"name":"Watanabe Hiroyoshi"},{"name":"Abe Masahiro"},{"name":"Kawazoe Kazuyoshi"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"伏谷 秀治"},{"name":"東 桃代"},{"name":"中村 信元"},{"name":"中村 敏己"},{"name":"寺岡 和彦"},{"name":"渡邊 浩良"},{"name":"安倍 正博"},{"name":"川添 和義"},{"name":"石澤 啓介"}]},"description":{"en":"The therapeutic effects of anti-methicillin-resistant Staphylococcus aureus (MRSA) agents, vancomycin (VCM), teicoplanin (TEIC), and arbekacin (ABK), depend on their concentrations in blood. Therefore, therapeutic drug monitoring (TDM) is important when these antibiotics are used. In the hematological ward at Tokushima University Hospital, pharmacists have ordered the measurement of blood VCM, TEIC, and ABK concentrations to promote the use of TDM in accordance with an agreed protocol since 2013. Moreover, the infection control team includes several medical disciplines and has advised on the optimal treatment using VCM, TEIC, and ABK since 2013. This study aimed to investigate the clinical effectiveness of these pharmacist interventions. We retrospectively studied 145 cases in which patients were treated with VCM, TEIC, or ABK between January 2012 and December 2013 in the hematological ward at Tokushima University Hospital. The patients were divided into a control group (71 cases) and an intervention group (74 cases), and their clinical outcomes were compared. The rate of achievement of effective drug concentrations significantly increased in the intervention group (74%), compared to the rate in the control group (55%). Moreover, univariate and multivariate Cox proportional hazard regression revealed that pharmacist intervention and appropriate concentrations of anti-MRSA agents were independent factors associated with reduced hospitalization periods in patients with lymphoma. Our study revealed that proactive pharmacist intervention may improve the therapeutic effect of anti-MRSA agents in hematology ward patients.","ja":"The therapeutic effects of anti-methicillin-resistant Staphylococcus aureus (MRSA) agents, vancomycin (VCM), teicoplanin (TEIC), and arbekacin (ABK), depend on their concentrations in blood. Therefore, therapeutic drug monitoring (TDM) is important when these antibiotics are used. In the hematological ward at Tokushima University Hospital, pharmacists have ordered the measurement of blood VCM, TEIC, and ABK concentrations to promote the use of TDM in accordance with an agreed protocol since 2013. Moreover, the infection control team includes several medical disciplines and has advised on the optimal treatment using VCM, TEIC, and ABK since 2013. This study aimed to investigate the clinical effectiveness of these pharmacist interventions. We retrospectively studied 145 cases in which patients were treated with VCM, TEIC, or ABK between January 2012 and December 2013 in the hematological ward at Tokushima University Hospital. The patients were divided into a control group (71 cases) and an intervention group (74 cases), and their clinical outcomes were compared. The rate of achievement of effective drug concentrations significantly increased in the intervention group (74%), compared to the rate in the control group (55%). Moreover, univariate and multivariate Cox proportional hazard regression revealed that pharmacist intervention and appropriate concentrations of anti-MRSA agents were independent factors associated with reduced hospitalization periods in patients with lymphoma. Our study revealed that proactive pharmacist intervention may improve the therapeutic effect of anti-MRSA agents in hematology ward patients."},"publication_date":"2015","publication_name":{"en":"Biological & Pharmaceutical Bulletin","ja":"Biological & Pharmaceutical Bulletin"},"volume":"Vol.39","number":"No.2","starting_page":"295","ending_page":"300","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1248/bpb.b15-00774"],"issn":["1347-5215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:82, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/26587904","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=295688","label":"url"}],"paper_title":{"en":"Ifosfamide and etoposide chemotherapy may interact with warfarin, enhancing the warfarin-induced anticoagulant response","ja":"Ifosfamide and etoposide chemotherapy may interact with warfarin, enhancing the warfarin-induced anticoagulant response"},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Watanabe Hiroyoshi"},{"name":"Kagami Shoji"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"渡邊 浩良"},{"name":"香美 祥二"},{"name":"石澤 啓介"}]},"description":{"en":"To report a case of warfarin-response enhancement during administration of ifosfamide and etoposide chemotherapy. A 15-yearold boy with rhabdomyosarcoma was treated with a regimen of alternating cycles of vincristine, doxorubicin, and cyclophosphamide (VDC) chemotherapy and ifosfamide and etoposide (IE) chemotherapy. During VDC chemotherapy, occlusion of the left middle cerebral artery occurred, and warfarin was started. On day 3 of IE chemotherapy, the patient's international normalized ratio (INR) transiently increased from baseline 2.61 to 5.45. The INR returned to normal within 3 days after warfarin discontinuation. An increase in INR was observed between days 1 and 3 of subsequent cycles of IE chemotherapy but not during VDC chemotherapy. This INR increase was also observed during concomitant use of aprepitant, an inducer of the CYP2C9. There are no reports describing the interaction between warfarin and IE chemotherapy because coadministration of warfarin and IE chemotherapy is unusual. The Drug Interaction Probability Scale score of this interaction was 7, and it is probable that the enhancement of the warfarin response was caused by an interaction with IE chemotherapy. Moreover, in the present case, the enhancement of warfarin response was observed during concomitant use of aprepitant, which has been reported to weaken the warfarin response. Therefore, this interaction may be quite powerful and may increase the risk of warfarin toxicity. A patient who was administered both warfarin and IE chemotherapy experienced a rapid increase in INR, suggesting that INR should be closely monitored in patients receiving warfarin with IE chemotherapy.","ja":"To report a case of warfarin-response enhancement during administration of ifosfamide and etoposide chemotherapy. A 15-yearold boy with rhabdomyosarcoma was treated with a regimen of alternating cycles of vincristine, doxorubicin, and cyclophosphamide (VDC) chemotherapy and ifosfamide and etoposide (IE) chemotherapy. During VDC chemotherapy, occlusion of the left middle cerebral artery occurred, and warfarin was started. On day 3 of IE chemotherapy, the patient's international normalized ratio (INR) transiently increased from baseline 2.61 to 5.45. The INR returned to normal within 3 days after warfarin discontinuation. An increase in INR was observed between days 1 and 3 of subsequent cycles of IE chemotherapy but not during VDC chemotherapy. This INR increase was also observed during concomitant use of aprepitant, an inducer of the CYP2C9. There are no reports describing the interaction between warfarin and IE chemotherapy because coadministration of warfarin and IE chemotherapy is unusual. The Drug Interaction Probability Scale score of this interaction was 7, and it is probable that the enhancement of the warfarin response was caused by an interaction with IE chemotherapy. Moreover, in the present case, the enhancement of warfarin response was observed during concomitant use of aprepitant, which has been reported to weaken the warfarin response. Therefore, this interaction may be quite powerful and may increase the risk of warfarin toxicity. A patient who was administered both warfarin and IE chemotherapy experienced a rapid increase in INR, suggesting that INR should be closely monitored in patients receiving warfarin with IE chemotherapy."},"publication_date":"2015","publication_name":{"en":"International Journal of Clinical Pharmacology and Therapeutics","ja":"International Journal of Clinical Pharmacology and Therapeutics"},"volume":"Vol.54","number":"No.1","starting_page":"58","ending_page":"61","languages":["eng"],"referee":true,"identifiers":{"doi":["10.5414/CP202426"],"issn":["0946-1965"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:83, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612714"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=295196","label":"url"}],"paper_title":{"en":"Ephedra protects vascular endothelium cells from vinorelbine-induced cytotoxicity by preserving endothelial nitric oxide synthase activity","ja":"Ephedra protects vascular endothelium cells from vinorelbine-induced cytotoxicity by preserving endothelial nitric oxide synthase activity"},"authors":{"en":[{"name":"Konaka Ken"},{"name":"Moriyama Kouta"},{"name":"Okada Naoto"},{"name":"Nishisako Takahiro"},{"name":"Shono Masayuki"},{"name":"Kawazoe Kazuyoshi"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Konaka Ken"},{"name":"Moriyama Kouta"},{"name":"岡田 直人"},{"name":"Nishisako Takahiro"},{"name":"庄野 正行"},{"name":"川添 和義"},{"name":"石澤 啓介"}]},"publication_date":"2015","publication_name":{"en":"Traditional & Kampo Medicine","ja":"Traditional & Kampo Medicine"},"volume":"Vol.2","number":"No.2","starting_page":"74","ending_page":"80","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/tkm2.1024"],"issn":["2053-4515"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:84, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612715"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/26521826","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84946902360&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=299156","label":"url"}],"paper_title":{"en":"Pemetrexed-induced rash may be prevented by supplementary corticosteroids","ja":"Pemetrexed-induced rash may be prevented by supplementary corticosteroids"},"authors":{"en":[{"name":"Sakurada Takumi"},{"name":"Kakiuchi Souji"},{"name":"Tajima Soichiro"},{"name":"Horinouchi Yuya"},{"name":"Konaka Ken"},{"name":"Okada Naoto"},{"name":"Nishisako Hirotaka"},{"name":"Nakamura Toshimi"},{"name":"Teraoka Kazuhiko"},{"name":"Kawazoe Kazuyoshi"},{"name":"Yanagawa Hiroaki"},{"name":"Nishioka Yasuhiko"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Sakurada Takumi"},{"name":"柿内 聡司"},{"name":"Tajima Soichiro"},{"name":"堀ノ内 裕也"},{"name":"Konaka Ken"},{"name":"岡田 直人"},{"name":"Nishisako Hirotaka"},{"name":"Nakamura Toshimi"},{"name":"寺岡 和彦"},{"name":"川添 和義"},{"name":"楊河 宏章"},{"name":"西岡 安彦"},{"name":"石澤 啓介"}]},"description":{"en":"Pemetrexed, a chemotherapeutic drug, is highly active in non-small cell lung cancer and malignant pleural mesothelioma. Unfortunately, rashes are more commonly associated with pemetrexed than other chemotherapies, and it is recommended that patients receive corticosteroids (8 mg/d of dexamethasone) for 3 d, including the day of pemetrexed administration (day 1). However, the efficacy of corticosteroids in this context has not been fully verified. In this retrospective study, we evaluated the medical records of 78 patients who received pemetrexed between April 2009 and March 2014, to confirm whether supplementary corticosteroids prevented rash development. The incidence of rash was lower in the 47 patients who received supplementary corticosteroids (after day 1) compared with the incidence among the 31 patients who did not receive supplementary corticosteroids (19.1% vs. 38.7%). The average cutoff dosage of supplementary corticosteroids on day 2 and day 3 was 1.5 mg/d of dexamethasone, as calculated using the receiver operating characteristic curve, and the odds ratio was 0.33 (95% confidence interval: 0.12-0.94). Administration of ≥1.5 mg of corticosteroids on day 2 and day 3 significantly reduced the severity of the rash compared to no supplementary treatment (grades 2/3, 13.3% vs. 33.3%, p<0.05). However, increasing the dose of corticosteroids had no additional effect on rash development. These results suggest that ≥1.5 mg of supplementary dexamethasone on day 2 and day 3 (in addition to day 1) may be necessary for preventing pemetrexed-induced rash, but high doses of dexamethasone (e.g., 8 mg/d) are unnecessary.","ja":"Pemetrexed, a chemotherapeutic drug, is highly active in non-small cell lung cancer and malignant pleural mesothelioma. Unfortunately, rashes are more commonly associated with pemetrexed than other chemotherapies, and it is recommended that patients receive corticosteroids (8 mg/d of dexamethasone) for 3 d, including the day of pemetrexed administration (day 1). However, the efficacy of corticosteroids in this context has not been fully verified. In this retrospective study, we evaluated the medical records of 78 patients who received pemetrexed between April 2009 and March 2014, to confirm whether supplementary corticosteroids prevented rash development. The incidence of rash was lower in the 47 patients who received supplementary corticosteroids (after day 1) compared with the incidence among the 31 patients who did not receive supplementary corticosteroids (19.1% vs. 38.7%). The average cutoff dosage of supplementary corticosteroids on day 2 and day 3 was 1.5 mg/d of dexamethasone, as calculated using the receiver operating characteristic curve, and the odds ratio was 0.33 (95% confidence interval: 0.12-0.94). Administration of ≥1.5 mg of corticosteroids on day 2 and day 3 significantly reduced the severity of the rash compared to no supplementary treatment (grades 2/3, 13.3% vs. 33.3%, p<0.05). However, increasing the dose of corticosteroids had no additional effect on rash development. These results suggest that ≥1.5 mg of supplementary dexamethasone on day 2 and day 3 (in addition to day 1) may be necessary for preventing pemetrexed-induced rash, but high doses of dexamethasone (e.g., 8 mg/d) are unnecessary."},"publication_date":"2015-11","publication_name":{"en":"Biological & Pharmaceutical Bulletin","ja":"Biological & Pharmaceutical Bulletin"},"volume":"Vol.38","number":"No.11","starting_page":"1752","ending_page":"1756","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1248/bpb.b15-00435"],"issn":["1347-5215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:85, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/26566409","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=317069","label":"url"}],"paper_title":{"en":"Japanese Physicians' Views on Drug Post-Marketing Surveillance.","ja":"Japanese Physicians' Views on Drug Post-Marketing Surveillance."},"authors":{"en":[{"name":"Maeda Kazuki"},{"name":"Katashima Rumi"},{"name":"Ishizawa Keisuke"},{"name":"Yanagawa Hiroaki"}],"ja":[{"name":"Maeda Kazuki"},{"name":"Katashima Rumi"},{"name":"石澤 啓介"},{"name":"楊河 宏章"}]},"description":{"en":"Registration trials leading to the approval of drugs are paramount in drug development. After approval, continuous efforts are necessary to ensure proper use of the approved drugs. In Japan, post-marketing surveillance (PMS) by drug companies is conducted in accordance with good post-marketing study practice (GPSP). Although the global standard for pharmacovigilance is incorporated into GPSP, attention has recently been focused on disassociating them. In this study, we examined physicians' views on PMS with the aim of conducting PMS more effectively. We retrospectively reviewed records between 2009 and 2013 from the institutional review board of Tokushima University Hospital, an academic hospital in rural Japan. The annual number of times PMS was performed was then determined. Next, we assessed physicians' attitudes toward drug PMS, including ethical issues, in a cross-sectional study using a questionnaire designed for this study. Five- and two-point scales were used. The questionnaire was distributed in 2014 to 221 physicians listed as investigators in PMS contracts. Of the 221 physicians, 103 (46.6%) responded to the questionnaire. About 50% of the respondents had experience writing PMS reports. Many of the physicians considered PMS to be important but burdensome. Furthermore, from the viewpoint of research ethics, many physicians considered it improper within the present PMS framework to collect and provide data beyond the scope of routine clinical practice without obtaining informed consent in the case of extra blood sampling, provision of images, monitoring and controlled studies. Beyond practical factors such as workload, attention should be given to establishing an ethical infrastructure and globally harmonized system with regard to the Japanese PMS system. Given the limitations of this single-institution study, further research is needed to collect information for developing a suitable infrastructure.","ja":"Registration trials leading to the approval of drugs are paramount in drug development. After approval, continuous efforts are necessary to ensure proper use of the approved drugs. In Japan, post-marketing surveillance (PMS) by drug companies is conducted in accordance with good post-marketing study practice (GPSP). Although the global standard for pharmacovigilance is incorporated into GPSP, attention has recently been focused on disassociating them. In this study, we examined physicians' views on PMS with the aim of conducting PMS more effectively. We retrospectively reviewed records between 2009 and 2013 from the institutional review board of Tokushima University Hospital, an academic hospital in rural Japan. The annual number of times PMS was performed was then determined. Next, we assessed physicians' attitudes toward drug PMS, including ethical issues, in a cross-sectional study using a questionnaire designed for this study. Five- and two-point scales were used. The questionnaire was distributed in 2014 to 221 physicians listed as investigators in PMS contracts. Of the 221 physicians, 103 (46.6%) responded to the questionnaire. About 50% of the respondents had experience writing PMS reports. Many of the physicians considered PMS to be important but burdensome. Furthermore, from the viewpoint of research ethics, many physicians considered it improper within the present PMS framework to collect and provide data beyond the scope of routine clinical practice without obtaining informed consent in the case of extra blood sampling, provision of images, monitoring and controlled studies. Beyond practical factors such as workload, attention should be given to establishing an ethical infrastructure and globally harmonized system with regard to the Japanese PMS system. Given the limitations of this single-institution study, further research is needed to collect information for developing a suitable infrastructure."},"publication_date":"2015-10-23","publication_name":{"en":"Journal of Clinical Medicine Research","ja":"Journal of Clinical Medicine Research"},"volume":"Vol.7","number":"No.12","starting_page":"956","ending_page":"960","languages":["eng"],"referee":true,"identifiers":{"doi":["10.14740/jocmr2328w"],"issn":["1918-3003"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:86, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113751","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/26134126","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84946558014&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=294522","label":"url"}],"paper_title":{"en":"Bilirubin exerts pro-angiogenic effects through an Akt-eNOS-dependent pathway","ja":"Bilirubin exerts pro-angiogenic effects through an Akt-eNOS-dependent pathway"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Hamano Hirofumi"},{"name":"Satoh Akiho"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Aihara Ken-ichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"濱野 裕章"},{"name":"佐藤 明穂"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"粟飯原 賢一"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Low serum bilirubin levels are associated with the risk of cardiovascular diseases including peripheral artery disease. Bilirubin is known to exert its property such as antioxidant effect or the enhancement of flow-mediated vasodilation, however, bilirubin action on angiogenesis remains unclear. To investigate the molecular mechanism of bilirubin on angiogenic effect, we first employed C57BL/6J mice with unilateral hindlimb ischemia surgery and divided the mice into two groups (vehicle-treated group and bilirubin-treated group). The analysis of laser speckle blood flow demonstrated the enhancement of blood flow recovery in response to ischemia of mice with bilirubin treatment. The density of capillaries was significantly higher in ischemic-adductor muscles of bilirubin-treated mice. The phosphorylated levels of endothelial nitric oxide synthase (eNOS) and Akt were increased in ischemic skeletal muscles of mice with bilirubin treatment compared with vehicle treatment. In in vitro experiments by using human aortic endothelial cells, bilirubin augmented eNOS and Akt phosphorylation, cell proliferation, cell migration and tube formation. These bilirubin actions on endothelial cell activation were inhibited by LY294002, a phosphatidylinositol 3-kinase inhibitor. In conclusion, bilirubin promotes angiogenesis through endothelial cells activation via Akt-eNOS-dependent manner.","ja":"Low serum bilirubin levels are associated with the risk of cardiovascular diseases including peripheral artery disease. Bilirubin is known to exert its property such as antioxidant effect or the enhancement of flow-mediated vasodilation, however, bilirubin action on angiogenesis remains unclear. To investigate the molecular mechanism of bilirubin on angiogenic effect, we first employed C57BL/6J mice with unilateral hindlimb ischemia surgery and divided the mice into two groups (vehicle-treated group and bilirubin-treated group). The analysis of laser speckle blood flow demonstrated the enhancement of blood flow recovery in response to ischemia of mice with bilirubin treatment. The density of capillaries was significantly higher in ischemic-adductor muscles of bilirubin-treated mice. The phosphorylated levels of endothelial nitric oxide synthase (eNOS) and Akt were increased in ischemic skeletal muscles of mice with bilirubin treatment compared with vehicle treatment. In in vitro experiments by using human aortic endothelial cells, bilirubin augmented eNOS and Akt phosphorylation, cell proliferation, cell migration and tube formation. These bilirubin actions on endothelial cell activation were inhibited by LY294002, a phosphatidylinositol 3-kinase inhibitor. In conclusion, bilirubin promotes angiogenesis through endothelial cells activation via Akt-eNOS-dependent manner."},"publication_date":"2015-07-02","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.38","number":"No.11","starting_page":"733","ending_page":"740","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/hr.2015.74"],"issn":["1348-4214"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:87, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113753","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25096756","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84937513465&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=280180","label":"url"}],"paper_title":{"en":"Angiotensin II alters the expression of duodenal iron transporters, hepatic hepcidin, and body iron distribution in mice","ja":"Angiotensin II alters the expression of duodenal iron transporters, hepatic hepcidin, and body iron distribution in mice"},"authors":{"en":[{"name":"Tajima Soichiro"},{"name":"Ikeda Yasumasa"},{"name":"Enomoto Hideaki"},{"name":"Imao Mizuki"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Tajima Soichiro"},{"name":"池田 康将"},{"name":"榎本 英明"},{"name":"今尾 瑞季"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Angiotensin II (ANG II) has been shown to affect iron metabolism through alteration of iron transporters, leading to increased cellular and tissue iron contents. Serum ferritin, a marker of body iron storage, is elevated in various cardiovascular diseases, including hypertension. However, the associated changes in iron absorption and the mechanism underlying increased iron content in a hypertensive state remain unclear. The C57BL6/J mice were treated with ANG II to generate a model of hypertension. Mice were divided into three groups: (1) control, (2) ANG II-treated, and (3) ANG II-treated and ANG II receptor blocker (ARB)-administered (ANG II-ARB) groups. Mice treated with ANG II showed increased serum ferritin levels compared to vehicle-treated control mice. In ANG II-treated mice, duodenal divalent metal transporter-1 and ferroportin (FPN) expression levels were increased and hepatic hepcidin mRNA expression and serum hepcidin concentration were reduced. The mRNA expression of bone morphogenetic protein 6 and CCAAT/enhancer-binding protein alpha, which are regulators of hepcidin, was also down-regulated in the livers of ANG II-treated mice. In terms of tissue iron content, macrophage iron content and renal iron content were increased by ANG II treatment, and these increases were associated with reduced expression of transferrin receptor 1 and FPN and increased expression of ferritin. These changes induced by ANG II treatment were ameliorated by the administration of an ARB. Angiotensin II (ANG II) altered the expression of duodenal iron transporters and reduced hepcidin levels, contributing to the alteration of body iron distribution.","ja":"Angiotensin II (ANG II) has been shown to affect iron metabolism through alteration of iron transporters, leading to increased cellular and tissue iron contents. Serum ferritin, a marker of body iron storage, is elevated in various cardiovascular diseases, including hypertension. However, the associated changes in iron absorption and the mechanism underlying increased iron content in a hypertensive state remain unclear. The C57BL6/J mice were treated with ANG II to generate a model of hypertension. Mice were divided into three groups: (1) control, (2) ANG II-treated, and (3) ANG II-treated and ANG II receptor blocker (ARB)-administered (ANG II-ARB) groups. Mice treated with ANG II showed increased serum ferritin levels compared to vehicle-treated control mice. In ANG II-treated mice, duodenal divalent metal transporter-1 and ferroportin (FPN) expression levels were increased and hepatic hepcidin mRNA expression and serum hepcidin concentration were reduced. The mRNA expression of bone morphogenetic protein 6 and CCAAT/enhancer-binding protein alpha, which are regulators of hepcidin, was also down-regulated in the livers of ANG II-treated mice. In terms of tissue iron content, macrophage iron content and renal iron content were increased by ANG II treatment, and these increases were associated with reduced expression of transferrin receptor 1 and FPN and increased expression of ferritin. These changes induced by ANG II treatment were ameliorated by the administration of an ARB. Angiotensin II (ANG II) altered the expression of duodenal iron transporters and reduced hepcidin levels, contributing to the alteration of body iron distribution."},"publication_date":"2015-07","publication_name":{"en":"European Journal of Nutrition","ja":"European Journal of Nutrition"},"volume":"Vol.54","number":"No.5","starting_page":"709","ending_page":"719","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00394-014-0749-1"],"issn":["1436-6215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:88, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/109948","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25832631","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390001204631777920/","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84928951796&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=289231","label":"url"}],"paper_title":{"en":"Hypoxia decreases glucagon-like peptide-1 secretion from GLUTag cell line","ja":"Hypoxia decreases glucagon-like peptide-1 secretion from GLUTag cell line"},"authors":{"en":[{"name":"Kihira Yoshitaka"},{"name":"Burentogtokh Ariunzaya"},{"name":"Itoh Mari"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"木平 孝高"},{"name":"Burentogtokh Ariunzaya"},{"name":"Itoh Mari"},{"name":"石澤 有紀"},{"name":"石澤 啓介"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Glucagon-like peptide-1 (GLP-1), an incretin hormone, is secreted from L cells located in the intestinal epithelium. It is known that intestinal oxygen tension is decreased postprandially. In addition, we found that the expression of hypoxia-inducible factor-1α (HIF-1α), which accumulates in cells under hypoxic conditions, was significantly increased in the colons of mice with food intake, indicating that the oxygen concentration is likely reduced in the colon after eating. Therefore, we hypothesized that GLP-1 secretion is affected by oxygen tension. We found that forskolin-stimulated GLP-1 secretion from GLUTag cells, a model of intestinal L cells, is suppressed in hypoxia (1% O2). Forskolin-stimulated elevations of preproglucagon (ppGCG) and proprotein convertase 1/3 (PC1/3) mRNA expression were decreased under hypoxic conditions. The finding that H89, a protein kinase A (PKA) inhibitor, inhibited the forskolin-stimulated increase of ppGCG and PC1/3 indicated that the cAMP-PKA pathway is involved in the hypoxia-induced suppression of the genes. Hypoxia decreased hexokinase 2 mRNA and protein expression and increased lactate dehydrogenase A mRNA and protein expression. Concomitantly, lactate production was increased and ATP production was decreased. Together, the results indicate that hypoxia decreases glucose utilization for ATP production, which probably causes a decrease in cAMP production and in subsequent GLP-1 production. Our findings suggest that the postprandial decrease in oxygen tension in the intestine attenuates GLP-1 secretion.","ja":"Glucagon-like peptide-1 (GLP-1), an incretin hormone, is secreted from L cells located in the intestinal epithelium. It is known that intestinal oxygen tension is decreased postprandially. In addition, we found that the expression of hypoxia-inducible factor-1α (HIF-1α), which accumulates in cells under hypoxic conditions, was significantly increased in the colons of mice with food intake, indicating that the oxygen concentration is likely reduced in the colon after eating. Therefore, we hypothesized that GLP-1 secretion is affected by oxygen tension. We found that forskolin-stimulated GLP-1 secretion from GLUTag cells, a model of intestinal L cells, is suppressed in hypoxia (1% O2). Forskolin-stimulated elevations of preproglucagon (ppGCG) and proprotein convertase 1/3 (PC1/3) mRNA expression were decreased under hypoxic conditions. The finding that H89, a protein kinase A (PKA) inhibitor, inhibited the forskolin-stimulated increase of ppGCG and PC1/3 indicated that the cAMP-PKA pathway is involved in the hypoxia-induced suppression of the genes. Hypoxia decreased hexokinase 2 mRNA and protein expression and increased lactate dehydrogenase A mRNA and protein expression. Concomitantly, lactate production was increased and ATP production was decreased. Together, the results indicate that hypoxia decreases glucose utilization for ATP production, which probably causes a decrease in cAMP production and in subsequent GLP-1 production. Our findings suggest that the postprandial decrease in oxygen tension in the intestine attenuates GLP-1 secretion."},"publication_date":"2015-04","publication_name":{"en":"Biological & Pharmaceutical Bulletin","ja":"Biological & Pharmaceutical Bulletin"},"volume":"Vol.38","number":"No.4","starting_page":"514","ending_page":"521","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1248/bpb.b14-00612"],"issn":["1347-5215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:89, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612716"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25565405","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84924872993&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=288750","label":"url"}],"paper_title":{"en":"Characteristics and risk factors of interstitial lung disease induced by chemotherapy for lung cancer","ja":"Characteristics and risk factors of interstitial lung disease induced by chemotherapy for lung cancer"},"authors":{"en":[{"name":"Sakurada Takumi"},{"name":"Kakiuchi Souji"},{"name":"Tajima Soichiro"},{"name":"Horinouchi Yuya"},{"name":"Okada Naoto"},{"name":"Nishisako Hirotaka"},{"name":"Nakamura Toshimi"},{"name":"Teraoka Kazuhiko"},{"name":"Kawazoe Kazuyoshi"},{"name":"Yanagawa Hiroaki"},{"name":"Nishioka Yasuhiko"},{"name":"Minakuchi Kazuo"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Sakurada Takumi"},{"name":"柿内 聡司"},{"name":"Tajima Soichiro"},{"name":"堀ノ内 裕也"},{"name":"岡田 直人"},{"name":"Nishisako Hirotaka"},{"name":"Nakamura Toshimi"},{"name":"寺岡 和彦"},{"name":"川添 和義"},{"name":"楊河 宏章"},{"name":"西岡 安彦"},{"name":"水口 和生"},{"name":"石澤 啓介"}]},"description":{"en":"Drug-induced interstitial lung disease (DILD) is generally a serious adverse effect and almost always necessitates the discontinuation of the offending drug. Cancer pharmacotherapy is strongly associated with DILD, and the risk of DILD has been suggested to be higher in patients with lung cancer because of preexisting pneumonic disease. The aim of this retrospective study was to identify the risk factors and prognostic factors for early death from interstitial lung disease (ILD) induced by chemotherapy for lung cancer. The medical records of 459 patients who underwent chemotherapy for lung cancer between April 2007 and March 2013 were analyzed with regard to patient background and DILD development, initial symptoms, and prognosis. A total of 33 patients (7.2%) developed chemotherapy-induced ILD. The most frequently observed initial symptom was dyspnea (94.3%). Preexisting ILD was identified as a risk factor for DILD (odds ratio [OR] = 5.38; 95% CI = 2.47-11.73; P < 0.01). Among the 33 patients who developed DILD, 10 patients suffered an early death despite steroid therapy. Poor prognostic factors included epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) use (OR = 9.26; 95% CI = 1.05-82.0; P < 0.05) and 2 or more prior chemotherapy regimens (OR = 6.95; 95% CI = 1.14-42.3; P < 0.05). Many lung cancer patients have coexisting ILD, and these patients have a high risk of developing chemotherapy-induced ILD. In addition, patients with DILD who underwent EGFR-TKI therapy and 2 or more prior chemotherapy regimens had a higher risk of fatal outcome.","ja":"Drug-induced interstitial lung disease (DILD) is generally a serious adverse effect and almost always necessitates the discontinuation of the offending drug. Cancer pharmacotherapy is strongly associated with DILD, and the risk of DILD has been suggested to be higher in patients with lung cancer because of preexisting pneumonic disease. The aim of this retrospective study was to identify the risk factors and prognostic factors for early death from interstitial lung disease (ILD) induced by chemotherapy for lung cancer. The medical records of 459 patients who underwent chemotherapy for lung cancer between April 2007 and March 2013 were analyzed with regard to patient background and DILD development, initial symptoms, and prognosis. A total of 33 patients (7.2%) developed chemotherapy-induced ILD. The most frequently observed initial symptom was dyspnea (94.3%). Preexisting ILD was identified as a risk factor for DILD (odds ratio [OR] = 5.38; 95% CI = 2.47-11.73; P < 0.01). Among the 33 patients who developed DILD, 10 patients suffered an early death despite steroid therapy. Poor prognostic factors included epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) use (OR = 9.26; 95% CI = 1.05-82.0; P < 0.05) and 2 or more prior chemotherapy regimens (OR = 6.95; 95% CI = 1.14-42.3; P < 0.05). Many lung cancer patients have coexisting ILD, and these patients have a high risk of developing chemotherapy-induced ILD. In addition, patients with DILD who underwent EGFR-TKI therapy and 2 or more prior chemotherapy regimens had a higher risk of fatal outcome."},"publication_date":"2015-04","publication_name":{"en":"The Annals of Pharmacotherapy","ja":"The Annals of Pharmacotherapy"},"volume":"Vol.49","number":"No.4","starting_page":"398","ending_page":"404","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1177/1060028014566446"],"issn":["1542-6270"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:90, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25497211","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84921044624&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=288749","label":"url"}],"paper_title":{"en":"Spontaneously hyperactive MEK-Erk pathway mediates paradoxical facilitation of cell proliferation in mild hypoxia","ja":"Spontaneously hyperactive MEK-Erk pathway mediates paradoxical facilitation of cell proliferation in mild hypoxia"},"authors":{"en":[{"name":"Miyamoto Licht"},{"name":"Yagi Yuko"},{"name":"Hatano Aya"},{"name":"Kawazoe Kazuyoshi"},{"name":"Ishizawa Keisuke"},{"name":"Minakuchi Kazuo"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"}],"ja":[{"name":"宮本 理人"},{"name":"Yagi Yuko"},{"name":"Hatano Aya"},{"name":"川添 和義"},{"name":"石澤 啓介"},{"name":"水口 和生"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"}]},"description":{"en":"Oxygen is important for common eukaryotic cells to generate ATP. Pathophysiological conditions such as ischemic diseases cause tissue hypoxia. In addition, oxygen availability in deep tissues is supposed to be far lower than surrounding atmosphere even in healthy animals, and the oxygen partial pressures in most normal tissues are estimated to be around 40-50mmHg, so-called mild hypoxia. Recent studies have demonstrated that mild hypoxia has distinct effects on living cells from severe hypoxia. For instance, mild hypoxia was reported to promote cell reprogramming. Although severe hypoxia is known to inhibit cell proliferation, mild hypoxia has been paradoxically demonstrated to increase cell proliferation. However, it has not been clarified by which molecular mechanisms mild hypoxia evokes the discontinuous increment of cell proliferation. We established experimental conditions showing the opposite influences of mild and severe hypoxia on cell proliferation using undifferentiated Caco2 human colon carcinoma cells in order to clarify the underlying molecular mechanism. The basal activity of Erk, which is a typical mediator of mitogenic signals, is spontaneously increased specifically in cells exposed to mild hypoxia, and inhibition of MEK, an upstream kinase of the Erk, completely inhibited the mild hypoxia-induced enhancement of cell proliferation. Spontaneous hyperactivation of the MEK-Erk pathway by mild hypoxia should be the plausible molecular mechanism of the paradoxical promotion of cell proliferation. Our findings will provide clues to the molecular basis of mild hypoxia-evoked phenomena such as cell reprogramming.","ja":"Oxygen is important for common eukaryotic cells to generate ATP. Pathophysiological conditions such as ischemic diseases cause tissue hypoxia. In addition, oxygen availability in deep tissues is supposed to be far lower than surrounding atmosphere even in healthy animals, and the oxygen partial pressures in most normal tissues are estimated to be around 40-50mmHg, so-called mild hypoxia. Recent studies have demonstrated that mild hypoxia has distinct effects on living cells from severe hypoxia. For instance, mild hypoxia was reported to promote cell reprogramming. Although severe hypoxia is known to inhibit cell proliferation, mild hypoxia has been paradoxically demonstrated to increase cell proliferation. However, it has not been clarified by which molecular mechanisms mild hypoxia evokes the discontinuous increment of cell proliferation. We established experimental conditions showing the opposite influences of mild and severe hypoxia on cell proliferation using undifferentiated Caco2 human colon carcinoma cells in order to clarify the underlying molecular mechanism. The basal activity of Erk, which is a typical mediator of mitogenic signals, is spontaneously increased specifically in cells exposed to mild hypoxia, and inhibition of MEK, an upstream kinase of the Erk, completely inhibited the mild hypoxia-induced enhancement of cell proliferation. Spontaneous hyperactivation of the MEK-Erk pathway by mild hypoxia should be the plausible molecular mechanism of the paradoxical promotion of cell proliferation. Our findings will provide clues to the molecular basis of mild hypoxia-evoked phenomena such as cell reprogramming."},"publication_date":"2015-04","publication_name":{"en":"Biochimica et Biophysica Acta (BBA) - General Subjects","ja":"Biochimica et Biophysica Acta (BBA) - General Subjects"},"volume":"Vol.1850","number":"No.4","starting_page":"640","ending_page":"646","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.bbagen.2014.12.006"],"issn":["0304-4165"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:91, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/40020377946/","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25994136","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282681302013696/","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84929747372&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=288751","label":"url"}],"paper_title":{"en":"A Long-Term High-Fat Diet Changes Iron Distribution in Body, Increasing Iron Accumulation Specifically in the Mouse Spleen","ja":"A Long-Term High-Fat Diet Changes Iron Distribution in Body, Increasing Iron Accumulation Specifically in the Mouse Spleen"},"authors":{"en":[{"name":"Yamano Noriko"},{"name":"Ikeda Yasumasa"},{"name":"Sakama Minoru"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Miyamoto Licht"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"山野 範子"},{"name":"池田 康将"},{"name":"阪間 稔"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"宮本 理人"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Although iron is an essential trace metal, its presence in excess causes oxidative stress in the human body. Recent studies have indicated that iron storage is a risk factor for type 2 diabetes mellitus. Dietary iron restriction or iron chelation ameliorates symptoms of type 2 diabetes in mouse models. However, whether iron content in the body changes with the development of diabetes is unknown. Here, we investigated the dynamics of iron accumulation and changes in iron absorption-related genes in mice that developed obesity and diabetes by consuming a high-fat diet (HFD-fed mice). HFD-fed mice (18-20 wk) were compared with control mice for hematologic features, serum ferritin levels, and iron contents in the gastrocnemius muscle, heart, epididymal fat, testis, liver, duodenum, and spleen. In addition, the spleen was examined histologically. Iron absorption-related gene expression in the liver and duodenum was also examined. Hemoglobin and serum ferritin levels were increased in HFD-fed mice. The HFD-fed mice showed iron accumulation in the spleen, but not in the heart or liver. Increased percentages of the splenic red pulp and macrophages were observed in HFD-fed mice and iron accumulation in the spleen was found mainly in the splenic red pulp. The HFD-fed mice also showed decreased iron content in the duodenum. The mRNA expression of divalent metal transporter-1 (DMT-1), an iron absorption-related gene, was elevated in the duodenum of HFD-fed mice. These results indicate that iron accumulation (specifically accumulation in the spleen) is enhanced by the development of type 2 diabetes induced by HFD.","ja":"Although iron is an essential trace metal, its presence in excess causes oxidative stress in the human body. Recent studies have indicated that iron storage is a risk factor for type 2 diabetes mellitus. Dietary iron restriction or iron chelation ameliorates symptoms of type 2 diabetes in mouse models. However, whether iron content in the body changes with the development of diabetes is unknown. Here, we investigated the dynamics of iron accumulation and changes in iron absorption-related genes in mice that developed obesity and diabetes by consuming a high-fat diet (HFD-fed mice). HFD-fed mice (18-20 wk) were compared with control mice for hematologic features, serum ferritin levels, and iron contents in the gastrocnemius muscle, heart, epididymal fat, testis, liver, duodenum, and spleen. In addition, the spleen was examined histologically. Iron absorption-related gene expression in the liver and duodenum was also examined. Hemoglobin and serum ferritin levels were increased in HFD-fed mice. The HFD-fed mice showed iron accumulation in the spleen, but not in the heart or liver. Increased percentages of the splenic red pulp and macrophages were observed in HFD-fed mice and iron accumulation in the spleen was found mainly in the splenic red pulp. The HFD-fed mice also showed decreased iron content in the duodenum. The mRNA expression of divalent metal transporter-1 (DMT-1), an iron absorption-related gene, was elevated in the duodenum of HFD-fed mice. These results indicate that iron accumulation (specifically accumulation in the spleen) is enhanced by the development of type 2 diabetes induced by HFD."},"publication_date":"2015-03","publication_name":{"en":"Journal of Nutritional Science and Vitaminology","ja":"Journal of Nutritional Science and Vitaminology"},"volume":"Vol.61","number":"No.1","starting_page":"20","ending_page":"27","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3177/jnsv.61.20"],"issn":["0301-4800"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:92, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/106145","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24623277","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84901457818&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=275488","label":"url"}],"paper_title":{"en":"Smooth muscle cell specific Hif-1 deficiency suppresses angiotensin II-induced vascular remodeling in mice","ja":"Smooth muscle cell specific Hif-1 deficiency suppresses angiotensin II-induced vascular remodeling in mice"},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Tomita Shuhei"},{"name":"Ishizawa Keisuke"},{"name":"Kihira Yoshitaka"},{"name":"Ueno Masaki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ikeda Yasumasa"},{"name":"Yamano Noriko"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"今西 正樹"},{"name":"冨田 修平"},{"name":"石澤 啓介"},{"name":"木平 孝高"},{"name":"Ueno Masaki"},{"name":"石澤 有紀"},{"name":"池田 康将"},{"name":"山野 範子"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Vascular remodelling is mediated by vascular smooth muscle cell (VSMC) proliferation and hypertrophy, both processes of which are linked to medial thickening and fibrosis. Here, we show that hypoxia-inducible factor-1α (Hif-1α) expressed in smooth muscle cells (SMCs) is involved in angiotensin II (Ang II)-induced vascular remodelling in an in vivo model. To clarify the role of Hif-1α in vascular remodelling, we created mice lacking the Hif-1α gene in SMCs (SMKO mice). Ang II infusion induced medial thickening and vascular fibrosis, accompanied by Hif-1α up-regulation, in the aortae of control mice, but not in those of SMKO mice. In accordance with those results, our in vitro studies showed that the deletion of SMC-derived Hif-1α suppressed the Ang II-induced hypertrophy of VSMCs, and our in vivo studies showed that the Ang II-induced expression of fibrosis-related genes in aortae was suppressed by SMC-specific Hif-1α deficiency. In addition, the SMC-specific Hif-1α deficiency suppressed Ang II-induced macrophage infiltration and Ang II-induced expression of inflammation-related genes in aortae. The superoxide production observed in the aortae of control mice with Ang II was suppressed in those of SMKO mice with Ang II, and this finding was consistent with the results of little Ang II-induced c-Src phosphorylation in SMKO mouse aortae. Loss- and gain-of-function analysis in in vitro experiments confirmed that VSMC-derived Hif-1α functions as an intrinsic modulator of vascular remodelling-related gene expression. Our results revealed that SMC-derived Hif-1α is a crucial mediator of Ang II-induced vascular remodelling.","ja":"Vascular remodelling is mediated by vascular smooth muscle cell (VSMC) proliferation and hypertrophy, both processes of which are linked to medial thickening and fibrosis. Here, we show that hypoxia-inducible factor-1α (Hif-1α) expressed in smooth muscle cells (SMCs) is involved in angiotensin II (Ang II)-induced vascular remodelling in an in vivo model. To clarify the role of Hif-1α in vascular remodelling, we created mice lacking the Hif-1α gene in SMCs (SMKO mice). Ang II infusion induced medial thickening and vascular fibrosis, accompanied by Hif-1α up-regulation, in the aortae of control mice, but not in those of SMKO mice. In accordance with those results, our in vitro studies showed that the deletion of SMC-derived Hif-1α suppressed the Ang II-induced hypertrophy of VSMCs, and our in vivo studies showed that the Ang II-induced expression of fibrosis-related genes in aortae was suppressed by SMC-specific Hif-1α deficiency. In addition, the SMC-specific Hif-1α deficiency suppressed Ang II-induced macrophage infiltration and Ang II-induced expression of inflammation-related genes in aortae. The superoxide production observed in the aortae of control mice with Ang II was suppressed in those of SMKO mice with Ang II, and this finding was consistent with the results of little Ang II-induced c-Src phosphorylation in SMKO mouse aortae. Loss- and gain-of-function analysis in in vitro experiments confirmed that VSMC-derived Hif-1α functions as an intrinsic modulator of vascular remodelling-related gene expression. Our results revealed that SMC-derived Hif-1α is a crucial mediator of Ang II-induced vascular remodelling."},"publication_date":"2014-06","publication_name":{"en":"Cardiovascular Research","ja":"Cardiovascular Research"},"volume":"Vol.102","number":"No.3","starting_page":"460","ending_page":"468","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/cvr/cvu061"],"issn":["0008-6363"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:93, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24599965","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84901845393&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=273735","label":"url"}],"paper_title":{"en":"HIF-2α/ARNT complex regulates hair development via induction of p21Waf1/Cip1 and p27Kip1","ja":"HIF-2α/ARNT complex regulates hair development via induction of p21Waf1/Cip1 and p27Kip1"},"authors":{"en":[{"name":"Imamura Yuko"},{"name":"Tomita Shuhei"},{"name":"Imanishi Masaki"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Imamura Yuko"},{"name":"冨田 修平"},{"name":"今西 正樹"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"The hypoxia-inducible factors HIF-1α or HIF-2α form heterodimeric complexes with the aryl hydrocarbon receptor nuclear translocator (ARNT). HIF-1α/ARNT and HIF-2α/ARNT complexes activate hypoxia-inducible genes that play critical roles in angiogenesis, anaerobic metabolism, and other processes in response to O2 deprivation. HIF-2α is known to regulate the function and/or differentiation of stem cells by activating the POU domain transcription factor Oct4; however, the precise underlying mechanism is unknown. This study examined the role of HIF-2α/ARNT in hair development using conditional-knockout mice, in which Arnt was specifically deleted in keratinocytes. In wild-type mice, HIF-2α and ARNT were highly expressed in the precortex above the hair matrix, an area containing differentiating stem cells. An analysis of hair size and type in these mice showed that loss of ARNT decreased the production of zigzag hairs, corresponding to reduced expression of HIF-2α and induction of the mammalian cyclin-dependent kinase inhibitors p21(Waf1/Cip1) and p27 (Kip1). The results suggest that the HIF-2α/ARNT complex regulates hair follicle differentiation via induction of p21(Waf1/Cip1) and possibly p27(Kip1), as p27(Kip1) expression was not altered in ARNT knockout mice. The findings provide insight into a possible mechanism underlying hair growth disorders and can be useful for future studies on hair follicle response to insults, such as chemotherapy and ionizing radiation.-Imamura, Y., Tomita, S., Imanishi, M., Kihira, Y., Ikeda, Y., Ishizawa, K., Tsuchiya, K., Tamaki, T. HIF-2α/ARNT complex regulates hair development via induction of p21(Waf1/Cip1) and p27(Kip1).","ja":"The hypoxia-inducible factors HIF-1α or HIF-2α form heterodimeric complexes with the aryl hydrocarbon receptor nuclear translocator (ARNT). HIF-1α/ARNT and HIF-2α/ARNT complexes activate hypoxia-inducible genes that play critical roles in angiogenesis, anaerobic metabolism, and other processes in response to O2 deprivation. HIF-2α is known to regulate the function and/or differentiation of stem cells by activating the POU domain transcription factor Oct4; however, the precise underlying mechanism is unknown. This study examined the role of HIF-2α/ARNT in hair development using conditional-knockout mice, in which Arnt was specifically deleted in keratinocytes. In wild-type mice, HIF-2α and ARNT were highly expressed in the precortex above the hair matrix, an area containing differentiating stem cells. An analysis of hair size and type in these mice showed that loss of ARNT decreased the production of zigzag hairs, corresponding to reduced expression of HIF-2α and induction of the mammalian cyclin-dependent kinase inhibitors p21(Waf1/Cip1) and p27 (Kip1). The results suggest that the HIF-2α/ARNT complex regulates hair follicle differentiation via induction of p21(Waf1/Cip1) and possibly p27(Kip1), as p27(Kip1) expression was not altered in ARNT knockout mice. The findings provide insight into a possible mechanism underlying hair growth disorders and can be useful for future studies on hair follicle response to insults, such as chemotherapy and ionizing radiation.-Imamura, Y., Tomita, S., Imanishi, M., Kihira, Y., Ikeda, Y., Ishizawa, K., Tsuchiya, K., Tamaki, T. HIF-2α/ARNT complex regulates hair development via induction of p21(Waf1/Cip1) and p27(Kip1)."},"publication_date":"2014-06","publication_name":{"en":"The FASEB journal","ja":"The FASEB journal"},"volume":"Vol.28","number":"No.6","starting_page":"2517","ending_page":"2524","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1096/fj.13-244079"],"issn":["0892-6638"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:94, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24705496","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84899440448&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=276331","label":"url"}],"paper_title":{"en":"Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation.","ja":"Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation."},"authors":{"en":[{"name":"Kihira Yoshitaka"},{"name":"Miyake Mariko"},{"name":"Hirata Manami"},{"name":"Hoshina Yoji"},{"name":"Kato Kana"},{"name":"Shirakawa Hitoshi"},{"name":"Sakaue Hiroshi"},{"name":"Yamano Noriko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"},{"name":"Tomita Shuhei"}],"ja":[{"name":"木平 孝高"},{"name":"Miyake Mariko"},{"name":"Hirata Manami"},{"name":"Hoshina Yoji"},{"name":"Kato Kana"},{"name":"Shirakawa Hitoshi"},{"name":"阪上 浩"},{"name":"山野 範子"},{"name":"石澤 有紀"},{"name":"石澤 啓介"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"},{"name":"冨田 修平"}]},"description":{"en":"It is known that obese adipose tissues are hypoxic and express hypoxia-inducible factor (HIF)-1α. Although some studies have shown that the expression of HIF-1α in adipocytes induces glucose intolerance, the mechanisms are still not clear. In this study, we examined its effects on the development of type 2 diabetes by using adipocyte-specific HIF-1α knockout (ahKO) mice. ahKO mice showed improved glucose tolerance compared with wild type (WT) mice. Macrophage infiltration and mRNA levels of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor α (TNFα) were decreased in the epididymal adipose tissues of high fat diet induced obese ahKO mice. The results indicated that the obesity-induced adipose tissue inflammation was suppressed in ahKO mice. In addition, in the ahKO mice, serum insulin levels were increased under the free-feeding but not the fasting condition, indicating that postprandial insulin secretion was enhanced. Serum glucagon-like peptide-1 (GLP-1) levels were also increased in the ahKO mice. Interestingly, adiponectin, whose serum levels were increased in the obese ahKO mice compared with the obese WT mice, stimulated GLP-1 secretion from cultured intestinal L cells. Therefore, insulin secretion may have been enhanced through the adiponectin-GLP-1 pathway in the ahKO mice. Our results suggest that the deletion of HIF-1α in adipocytes improves glucose tolerance by enhancing insulin secretion through the GLP-1 pathway and by reducing macrophage infiltration and inflammation in adipose tissue.","ja":"It is known that obese adipose tissues are hypoxic and express hypoxia-inducible factor (HIF)-1α. Although some studies have shown that the expression of HIF-1α in adipocytes induces glucose intolerance, the mechanisms are still not clear. In this study, we examined its effects on the development of type 2 diabetes by using adipocyte-specific HIF-1α knockout (ahKO) mice. ahKO mice showed improved glucose tolerance compared with wild type (WT) mice. Macrophage infiltration and mRNA levels of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor α (TNFα) were decreased in the epididymal adipose tissues of high fat diet induced obese ahKO mice. The results indicated that the obesity-induced adipose tissue inflammation was suppressed in ahKO mice. In addition, in the ahKO mice, serum insulin levels were increased under the free-feeding but not the fasting condition, indicating that postprandial insulin secretion was enhanced. Serum glucagon-like peptide-1 (GLP-1) levels were also increased in the ahKO mice. Interestingly, adiponectin, whose serum levels were increased in the obese ahKO mice compared with the obese WT mice, stimulated GLP-1 secretion from cultured intestinal L cells. Therefore, insulin secretion may have been enhanced through the adiponectin-GLP-1 pathway in the ahKO mice. Our results suggest that the deletion of HIF-1α in adipocytes improves glucose tolerance by enhancing insulin secretion through the GLP-1 pathway and by reducing macrophage infiltration and inflammation in adipose tissue."},"publication_date":"2014-04-04","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.9","number":"No.4","starting_page":"e93856","ending_page":"e93856","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0093856"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:95, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113752","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24586712","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84897786390&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=274493","label":"url"}],"paper_title":{"en":"Iron chelation by deferoxamine prevents renal interstitial fibrosis in mice with unilateral ureteral obstruction","ja":"Iron chelation by deferoxamine prevents renal interstitial fibrosis in mice with unilateral ureteral obstruction"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Ozono Iori"},{"name":"Tajima Soichro"},{"name":"Imao Mizuki"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"大園 伊織"},{"name":"Tajima Soichro"},{"name":"今尾 瑞季"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Renal fibrosis plays an important role in the onset and progression of chronic kidney diseases (CKD). Although several mechanisms underlying renal fibrosis and candidate drugs for its treatment have been identified, the effect of iron chelator on renal fibrosis remains unclear. In the present study, we examined the effect of an iron chelator, deferoxamine (DFO), on renal fibrosis in mice with surgically induced unilateral ureter obstruction (UUO). Mice were divided into 4 groups: UUO with vehicle, UUO with DFO, sham with vehicle, and sham with DFO. One week after surgery, augmented renal tubulointerstitial fibrosis and the expression of collagen I, III, and IV increased in mice with UUO; these changes were suppressed by DFO treatment. Similarly, UUO-induced macrophage infiltration of renal interstitial tubules was reduced in UUO mice treated with DFO. UUO-induced expression of inflammatory cytokines and extracellular matrix proteins was abrogated by DFO treatment. DFO inhibited the activation of the transforming growth factor-β1 (TGF-β1)-Smad3 pathway in UUO mice. UUO-induced NADPH oxidase activity and p22(phox) expression were attenuated by DFO. In the kidneys of UUO mice, divalent metal transporter 1, ferroportin, and ferritin expression was higher and transferrin receptor expression was lower than in sham-operated mice. Increased renal iron content was observed in UUO mice, which was reduced by DFO treatment. These results suggest that iron reduction by DFO prevents renal tubulointerstitial fibrosis by regulating TGF-β-Smad signaling, oxidative stress, and inflammatory responses.","ja":"Renal fibrosis plays an important role in the onset and progression of chronic kidney diseases (CKD). Although several mechanisms underlying renal fibrosis and candidate drugs for its treatment have been identified, the effect of iron chelator on renal fibrosis remains unclear. In the present study, we examined the effect of an iron chelator, deferoxamine (DFO), on renal fibrosis in mice with surgically induced unilateral ureter obstruction (UUO). Mice were divided into 4 groups: UUO with vehicle, UUO with DFO, sham with vehicle, and sham with DFO. One week after surgery, augmented renal tubulointerstitial fibrosis and the expression of collagen I, III, and IV increased in mice with UUO; these changes were suppressed by DFO treatment. Similarly, UUO-induced macrophage infiltration of renal interstitial tubules was reduced in UUO mice treated with DFO. UUO-induced expression of inflammatory cytokines and extracellular matrix proteins was abrogated by DFO treatment. DFO inhibited the activation of the transforming growth factor-β1 (TGF-β1)-Smad3 pathway in UUO mice. UUO-induced NADPH oxidase activity and p22(phox) expression were attenuated by DFO. In the kidneys of UUO mice, divalent metal transporter 1, ferroportin, and ferritin expression was higher and transferrin receptor expression was lower than in sham-operated mice. Increased renal iron content was observed in UUO mice, which was reduced by DFO treatment. These results suggest that iron reduction by DFO prevents renal tubulointerstitial fibrosis by regulating TGF-β-Smad signaling, oxidative stress, and inflammatory responses."},"publication_date":"2014-02-19","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.9","number":"No.2","starting_page":"e89355","ending_page":"e89355","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0089355"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:96, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24489716","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84900332178&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=275165","label":"url"}],"paper_title":{"en":"Nitrosonifedipine ameliorates the progression of type 2 diabetic nephropathy by exerting antioxidative effects","ja":"Nitrosonifedipine ameliorates the progression of type 2 diabetic nephropathy by exerting antioxidative effects"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yamano Noriko"},{"name":"Urushihara Maki"},{"name":"Sakurada Takumi"},{"name":"Imanishi Masaki"},{"name":"Fujii Shoko"},{"name":"Nuno Asami"},{"name":"Miyamoto Licht"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Kagami Shoji"},{"name":"Kobori Hiroyuki"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"石澤 有紀"},{"name":"山野 範子"},{"name":"漆原 真樹"},{"name":"Sakurada Takumi"},{"name":"今西 正樹"},{"name":"Fujii Shoko"},{"name":"Nuno Asami"},{"name":"宮本 理人"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"香美 祥二"},{"name":"Kobori Hiroyuki"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Diabetic nephropathy (DN) is the major cause of end-stage renal failure. Oxidative stress is implicated in the pathogenesis of DN. Nitrosonifedipine (NO-NIF) is a weak calcium channel blocker that is converted from nifedipine under light exposure. Recently, we reported that NO-NIF has potential as a novel antioxidant with radical scavenging abilities and has the capacity to treat vascular dysfunction by exerting an endothelial protective effect. In the present study, we extended these findings by evaluating the efficacy of NO-NIF against DN and by clarifying the mechanisms of its antioxidative effect. In a model of type 2 DN (established in KKAy mice), NO-NIF administration reduced albuminuria and proteinuria as well as glomerular expansion without affecting glucose metabolism or systolic blood pressure. NO-NIF also suppressed renal and systemic oxidative stress and decreased the expression of intercellular adhesion molecule (ICAM)-1, a marker of endothelial cell injury, in the glomeruli of the KKAy mice. Similarly, NO-NIF reduced albuminuria, oxidative stress, and ICAM-1 expression in endothelial nitric oxide synthase (eNOS) knockout mice. Moreover, NO-NIF suppressed urinary angiotensinogen (AGT) excretion and intrarenal AGT protein expression in proximal tubular cells in the KKAy mice. On the other hand, hyperglycemia-induced mitochondrial superoxide production was not attenuated by NO-NIF in cultured endothelial cells. These findings suggest that NO-NIF prevents the progression of type 2 DN associated with endothelial dysfunction through selective antioxidative effects.","ja":"Diabetic nephropathy (DN) is the major cause of end-stage renal failure. Oxidative stress is implicated in the pathogenesis of DN. Nitrosonifedipine (NO-NIF) is a weak calcium channel blocker that is converted from nifedipine under light exposure. Recently, we reported that NO-NIF has potential as a novel antioxidant with radical scavenging abilities and has the capacity to treat vascular dysfunction by exerting an endothelial protective effect. In the present study, we extended these findings by evaluating the efficacy of NO-NIF against DN and by clarifying the mechanisms of its antioxidative effect. In a model of type 2 DN (established in KKAy mice), NO-NIF administration reduced albuminuria and proteinuria as well as glomerular expansion without affecting glucose metabolism or systolic blood pressure. NO-NIF also suppressed renal and systemic oxidative stress and decreased the expression of intercellular adhesion molecule (ICAM)-1, a marker of endothelial cell injury, in the glomeruli of the KKAy mice. Similarly, NO-NIF reduced albuminuria, oxidative stress, and ICAM-1 expression in endothelial nitric oxide synthase (eNOS) knockout mice. Moreover, NO-NIF suppressed urinary angiotensinogen (AGT) excretion and intrarenal AGT protein expression in proximal tubular cells in the KKAy mice. On the other hand, hyperglycemia-induced mitochondrial superoxide production was not attenuated by NO-NIF in cultured endothelial cells. These findings suggest that NO-NIF prevents the progression of type 2 DN associated with endothelial dysfunction through selective antioxidative effects."},"publication_date":"2014-01-28","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.9","number":"No.1","starting_page":"e86335","ending_page":"e86335","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0086335"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:97, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23672178","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=262662","label":"url"}],"paper_title":{"en":"A novel prodrug strategy for extremely hydrophobic agents; - Conjugation to symmetrically branched glycerol trimer improves pharmacological and pharmacokinetic properties of fenofibrate","ja":"A novel prodrug strategy for extremely hydrophobic agents; - Conjugation to symmetrically branched glycerol trimer improves pharmacological and pharmacokinetic properties of fenofibrate"},"authors":{"en":[{"name":"Miyamoto Licht"},{"name":"Watanabe Masashi"},{"name":"Taoka Chiaki"},{"name":"Kono Mai"},{"name":"Tomida Yosuke"},{"name":"Matsushita Tsuyoshi"},{"name":"Kamiya Masaki"},{"name":"Hattori Hatsuhiko"},{"name":"Ishizawa Keisuke"},{"name":"Abe Shinji"},{"name":"Nemoto Hisao"},{"name":"Tsuchiya Koichiro"}],"ja":[{"name":"Miyamoto Licht"},{"name":"Watanabe Masashi"},{"name":"Taoka Chiaki"},{"name":"Kono Mai"},{"name":"Tomida Yosuke"},{"name":"Matsushita Tsuyoshi"},{"name":"Kamiya Masaki"},{"name":"Hattori Hatsuhiko"},{"name":"石澤 啓介"},{"name":"阿部 真治"},{"name":"根本 尚夫"},{"name":"土屋 浩一郎"}]},"description":{"en":"Management of a lipophilic-hydrophilic balance is a key element in drug design to achieve desirable pharmacokinetic characters. Therefore we have created unique modular molecules, symmetrically branched oligoglycerols (BGL), as an alternative way to endow hydrophobic molecules with sufficient hydrophilicity. We have successfully demonstrated amelioration of the water solubility and thermal stability of several hydrophobic agents by covalent conjugation to BGL so far. However, it has not been clarified whether the molecular modification by BGL also improves the pharmacological and/or pharmacokinetic properties indeed. Recently, we synthesized a novel BGL-prodrug derivative of fenofibrate, which is an antihyperlipidemic agent and one of the most hydrophobic medicinal compounds currently used clinically, by conjugating fenofibric acid to symmetrically branched glycerol trimer (BGL003), the simplest BGL. We have previously demonstrated that the hydrophilicity and water solubility of fenofibrate are improved more than 2000 times just by conjugation to the BGL003. To verify our hypothesis that the prodrug strategy with BGL should improve pharmacological efficacy and pharmacokinetic properties of extremely hydrophobic agents such as fenofibrate by the rise in hydrophilicity, we evaluated the BGL003-prodrug derivative of fenofibrate (FF-BGL) using rodent models. Here we demonstrate that the lipid-lowering effects of fenofibrate are much potentiated by chemical conjugation to BGL003 without exhibiting significant toxicity. Plasma concentration of fenofibric acid, an active metabolite of fenofibrate, after single oral administration of FF-BGL was more than 3 times higher than that of fenofibrate, in accordance. In fasting rats, plasma concentration of fenofibric acid after fenofibrate administration was curtailed into less than half of that in ad libitum-fed rats, while FF-BGL showed about the same plasma level even in the starving rats. This is the first report showing that BGL-prodrug improves pharmacological and pharmacokinetic properties as well as hydrophilicity of highly hydrophobic compounds. Furthermore, prodrug strategy using BGL suggests the possibility of diminishing the food-drug interaction effects, which should be advantageous for promoting drug compliance. BGL will be a suitable prodrug strategy to ameliorate physical, pharmacological, and pharmacokinetic characteristics of extremely hydrophobic compounds.","ja":"Management of a lipophilic-hydrophilic balance is a key element in drug design to achieve desirable pharmacokinetic characters. Therefore we have created unique modular molecules, symmetrically branched oligoglycerols (BGL), as an alternative way to endow hydrophobic molecules with sufficient hydrophilicity. We have successfully demonstrated amelioration of the water solubility and thermal stability of several hydrophobic agents by covalent conjugation to BGL so far. However, it has not been clarified whether the molecular modification by BGL also improves the pharmacological and/or pharmacokinetic properties indeed. Recently, we synthesized a novel BGL-prodrug derivative of fenofibrate, which is an antihyperlipidemic agent and one of the most hydrophobic medicinal compounds currently used clinically, by conjugating fenofibric acid to symmetrically branched glycerol trimer (BGL003), the simplest BGL. We have previously demonstrated that the hydrophilicity and water solubility of fenofibrate are improved more than 2000 times just by conjugation to the BGL003. To verify our hypothesis that the prodrug strategy with BGL should improve pharmacological efficacy and pharmacokinetic properties of extremely hydrophobic agents such as fenofibrate by the rise in hydrophilicity, we evaluated the BGL003-prodrug derivative of fenofibrate (FF-BGL) using rodent models. Here we demonstrate that the lipid-lowering effects of fenofibrate are much potentiated by chemical conjugation to BGL003 without exhibiting significant toxicity. Plasma concentration of fenofibric acid, an active metabolite of fenofibrate, after single oral administration of FF-BGL was more than 3 times higher than that of fenofibrate, in accordance. In fasting rats, plasma concentration of fenofibric acid after fenofibrate administration was curtailed into less than half of that in ad libitum-fed rats, while FF-BGL showed about the same plasma level even in the starving rats. This is the first report showing that BGL-prodrug improves pharmacological and pharmacokinetic properties as well as hydrophilicity of highly hydrophobic compounds. Furthermore, prodrug strategy using BGL suggests the possibility of diminishing the food-drug interaction effects, which should be advantageous for promoting drug compliance. BGL will be a suitable prodrug strategy to ameliorate physical, pharmacological, and pharmacokinetic characteristics of extremely hydrophobic compounds."},"publication_date":"2013-05","publication_name":{"en":"Molecular Pharmaceutics","ja":"Molecular Pharmaceutics"},"volume":"Vol.10","number":"No.7","starting_page":"2723","ending_page":"2729","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1021/mp400133j"],"issn":["1543-8384"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:98, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612717"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23339930","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=259173","label":"url"}],"paper_title":{"en":"Altered gene expression profiles associated with enhanced skin inflammation induced by 12-O-tetradecanoylphorbol-13-acetate in streptozotocin-diabetic mice","ja":"Altered gene expression profiles associated with enhanced skin inflammation induced by 12-O-tetradecanoylphorbol-13-acetate in streptozotocin-diabetic mice"},"authors":{"en":[{"name":"Iba Yoshinori"},{"name":"Watanabe Koushi"},{"name":"Ozaki Kiyokazu"},{"name":"Aozasa Osamu"},{"name":"Ishizawa Keisuke"},{"name":"Matsuura Tetsuro"},{"name":"Oyama Hiroshi"},{"name":"Masukawa Tohru"}],"ja":[{"name":"Iba Yoshinori"},{"name":"Watanabe Koushi"},{"name":"Ozaki Kiyokazu"},{"name":"Aozasa Osamu"},{"name":"石澤 啓介"},{"name":"Matsuura Tetsuro"},{"name":"Oyama Hiroshi"},{"name":"Masukawa Tohru"}]},"description":{"en":"To examine the mechanisms of diabetes-enhanced inflammation, ear inflammation was induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in streptozotocin (STZ)-injected diabetic and control mice. The inflammatory response was determined from ear thickness and histology. The mRNA expression of several inflammation-related genes 8, 24 and 32h after TPA treatment was determined by quantitative real-time RT-PCR. Ear thickness did not differ between the two groups at 8h, but was greater in the diabetic mice than control mice at 24 and 32h (late phase). STZ-diabetic conditions variously affected TPA-induced gene expression. The changes 8h after TPA treatment probably reflected transcriptional regulation, and the genes were divided into three groups, up-regulated (IL-6, MCP-1, HO-1 and SOCS3), unregulated (IL-1beta, TNF-alpha and IL-10) and down-regulated (RANTES) genes. TPA-induced gene expression of cytokines, except for RANTES, peaked at 8h and significantly declined in the late phase in control mice, while the expression of IL-1beta and TNF-alpha did not decline in the late phase in the diabetic mice. This result indicated the destabilization process for these mRNA, a type of post-transcriptional regulation, to be impaired under STZ-induced diabetic conditions; however, TPA-induced gene and protein expression of TTP, an RNA-binding protein involved in mRNA decay, were adversely enhanced in the diabetic mice. These findings suggested that STZ-induced diabetes affected the transcriptional and post-transcriptional control of TPA-induced inflammation, and greater mRNA levels of IL-1beta and TNF-alpha in the late phase were probably responsible for the diabetes-enhanced inflammation.","ja":"To examine the mechanisms of diabetes-enhanced inflammation, ear inflammation was induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in streptozotocin (STZ)-injected diabetic and control mice. The inflammatory response was determined from ear thickness and histology. The mRNA expression of several inflammation-related genes 8, 24 and 32h after TPA treatment was determined by quantitative real-time RT-PCR. Ear thickness did not differ between the two groups at 8h, but was greater in the diabetic mice than control mice at 24 and 32h (late phase). STZ-diabetic conditions variously affected TPA-induced gene expression. The changes 8h after TPA treatment probably reflected transcriptional regulation, and the genes were divided into three groups, up-regulated (IL-6, MCP-1, HO-1 and SOCS3), unregulated (IL-1beta, TNF-alpha and IL-10) and down-regulated (RANTES) genes. TPA-induced gene expression of cytokines, except for RANTES, peaked at 8h and significantly declined in the late phase in control mice, while the expression of IL-1beta and TNF-alpha did not decline in the late phase in the diabetic mice. This result indicated the destabilization process for these mRNA, a type of post-transcriptional regulation, to be impaired under STZ-induced diabetic conditions; however, TPA-induced gene and protein expression of TTP, an RNA-binding protein involved in mRNA decay, were adversely enhanced in the diabetic mice. These findings suggested that STZ-induced diabetes affected the transcriptional and post-transcriptional control of TPA-induced inflammation, and greater mRNA levels of IL-1beta and TNF-alpha in the late phase were probably responsible for the diabetes-enhanced inflammation."},"publication_date":"2013-03","publication_name":{"en":"International Immunopharmacology","ja":"International Immunopharmacology"},"volume":"Vol.15","number":"No.3","starting_page":"614","ending_page":"619","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.intimp.2013.01.007"],"issn":["1878-1705"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:99, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23389454","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=261038","label":"url"}],"paper_title":{"en":"Dietary iron restriction inhibits progression of diabetic nephropathy in db/db mice.","ja":"Dietary iron restriction inhibits progression of diabetic nephropathy in db/db mice."},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Enomoto Hideaki"},{"name":"Tajima Soichiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"榎本 英明"},{"name":"Tajima Soichiro"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Excess iron causes oxidative stress through hydroxyl-radical production via Fenton/Haber-Weiss reactions. Recently, body iron reduction has been found to ameliorate diabetes. In the present study, we examined the protective effect of dietary iron restriction against diabetic nephropathy in the db/db mouse model of diabetic nephropathy using db/m mice as controls. The db/db mice were divided into 2 groups and fed a normal diet (ND) or a low iron diet (LID). Increasing urinary albumin excretion was observed in the ND db/db mice, but this was suppressed in db/db mice with LID. Histologically, the db/db mice in the ND group had increased glomerular volume and mesangial area compared to the LID group. Augmented deposition of extracellular matrices was decreased in db/db mice with LID. In terms of oxidative stress, increased superoxide production observed in the kidneys of the ND db/db mice was diminished in the LID group. NADPH oxidase activity and renal expression of NADPH oxidase components p22(phox) and NOX4 were augmented in the ND group, and this was abolished by LID. There were no differences in expression of renal iron importers, transferrin receptor, or divalent metal transporter-1 between db/m mice and db/db mice. The level of ferroportin, an iron exporter, increased in the kidneys of the db/db mice. Urinary iron excretion was significantly higher in ND db/db mice and was reduced in the LID group. These findings suggest that dietary iron restriction exerts a preventive effect on the progression of diabetic nephropathy partly due to the reduction of oxidative stress.","ja":"Excess iron causes oxidative stress through hydroxyl-radical production via Fenton/Haber-Weiss reactions. Recently, body iron reduction has been found to ameliorate diabetes. In the present study, we examined the protective effect of dietary iron restriction against diabetic nephropathy in the db/db mouse model of diabetic nephropathy using db/m mice as controls. The db/db mice were divided into 2 groups and fed a normal diet (ND) or a low iron diet (LID). Increasing urinary albumin excretion was observed in the ND db/db mice, but this was suppressed in db/db mice with LID. Histologically, the db/db mice in the ND group had increased glomerular volume and mesangial area compared to the LID group. Augmented deposition of extracellular matrices was decreased in db/db mice with LID. In terms of oxidative stress, increased superoxide production observed in the kidneys of the ND db/db mice was diminished in the LID group. NADPH oxidase activity and renal expression of NADPH oxidase components p22(phox) and NOX4 were augmented in the ND group, and this was abolished by LID. There were no differences in expression of renal iron importers, transferrin receptor, or divalent metal transporter-1 between db/m mice and db/db mice. The level of ferroportin, an iron exporter, increased in the kidneys of the db/db mice. Urinary iron excretion was significantly higher in ND db/db mice and was reduced in the LID group. These findings suggest that dietary iron restriction exerts a preventive effect on the progression of diabetic nephropathy partly due to the reduction of oxidative stress."},"publication_date":"2013-02-06","publication_name":{"en":"American Journal of Physiology, Renal Physiology","ja":"American Journal of Physiology, Renal Physiology"},"volume":"Vol.304","number":"No.7","starting_page":"F1028","ending_page":"F1036","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1152/ajprenal.00473.2012"],"issn":["1522-1466"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:100, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113754","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23364610","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=259318","label":"url"}],"paper_title":{"en":"Bovine milk-derived lactoferrin exerts proangiogenic effects in an Src-Akt-eNOS-dependent manner in response to ischemia","ja":"Bovine milk-derived lactoferrin exerts proangiogenic effects in an Src-Akt-eNOS-dependent manner in response to ischemia"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Tajima Soichiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Yoshida Sumiko"},{"name":"Aihara Ken-ichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"Tajima Soichiro"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"吉田 守美子"},{"name":"粟飯原 賢一"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Lactoferrin (LF) exerts a variety of biological effects, including the promotion of angiogenesis by increasing the expression of angiogenesis-related genes and reducing blood pressure via a nitric oxide-dependent mechanism. In this study, we investigated the effects of LF on angiogenesis using C57BL/6J mice that received daily unilateral treatment with or without bovine milk-derived LF (bLF) after unilateral hindlimb surgery. The analysis of laser speckle blood flow showed that bLF treatment promoted blood flow recovery in response to ischemic hindlimb. The capillary density of ischemic adductor muscles and the phosphorylation of Src, Akt, and endothelial nitric oxide synthase (eNOS) were also significantly higher in bLF-treated mice than in vehicle-treated mice. Furthermore, bLF increased the phosphorylation levels of Src, Akt, and eNOS in in vitro experiments using human aortic endothelial cells. The action of bLF on eNOS phosphorylation was abolished by both LY294002, a phosphatidylinositol 3-kinase inhibitor, and 4-amino-5-(4-chlorophenyl)-7-(dimethylethyl)pyrazolo [3,4-d]pyrimidine (PP2), an Src inhibitor. Similarly, bLF-induced acceleration of tube formation, cell proliferation, and cell migration in human aortic endothelial cells were inhibited by LY294002 or PP2. Thus, bLF promotes vascular endothelial cell function via an Src Akt eNOS-dependent pathway, thereby contributing to revascularization in response to ischemia.","ja":"Lactoferrin (LF) exerts a variety of biological effects, including the promotion of angiogenesis by increasing the expression of angiogenesis-related genes and reducing blood pressure via a nitric oxide-dependent mechanism. In this study, we investigated the effects of LF on angiogenesis using C57BL/6J mice that received daily unilateral treatment with or without bovine milk-derived LF (bLF) after unilateral hindlimb surgery. The analysis of laser speckle blood flow showed that bLF treatment promoted blood flow recovery in response to ischemic hindlimb. The capillary density of ischemic adductor muscles and the phosphorylation of Src, Akt, and endothelial nitric oxide synthase (eNOS) were also significantly higher in bLF-treated mice than in vehicle-treated mice. Furthermore, bLF increased the phosphorylation levels of Src, Akt, and eNOS in in vitro experiments using human aortic endothelial cells. The action of bLF on eNOS phosphorylation was abolished by both LY294002, a phosphatidylinositol 3-kinase inhibitor, and 4-amino-5-(4-chlorophenyl)-7-(dimethylethyl)pyrazolo [3,4-d]pyrimidine (PP2), an Src inhibitor. Similarly, bLF-induced acceleration of tube formation, cell proliferation, and cell migration in human aortic endothelial cells were inhibited by LY294002 or PP2. Thus, bLF promotes vascular endothelial cell function via an Src Akt eNOS-dependent pathway, thereby contributing to revascularization in response to ischemia."},"publication_date":"2013-01","publication_name":{"en":"Journal of Cardiovascular Pharmacology","ja":"Journal of Cardiovascular Pharmacology"},"volume":"Vol.61","number":"No.5","starting_page":"423","ending_page":"429","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1097/FJC.0b013e318287d526"],"issn":["1533-4023"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:101, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23149861","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84872316103&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=257964","label":"url"}],"paper_title":{"en":"Nitrosonifedipine ameliorates angiotensin II-induced vascular remodeling via antioxidative effects","ja":"Nitrosonifedipine ameliorates angiotensin II-induced vascular remodeling via antioxidative effects"},"authors":{"en":[{"name":"Sakurada Takumi"},{"name":"Ishizawa Keisuke"},{"name":"Imanishi Masaki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Fujii Shoko"},{"name":"Tominaga Erika"},{"name":"Tsuneishi Teppei"},{"name":"Horinouchi Yuya"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Tomita Shuhei"},{"name":"Aihara Ken-ichi"},{"name":"Minakuchi Kazuo"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Sakurada Takumi"},{"name":"石澤 啓介"},{"name":"今西 正樹"},{"name":"石澤 有紀"},{"name":"Fujii Shoko"},{"name":"Tominaga Erika"},{"name":"Tsuneishi Teppei"},{"name":"堀ノ内 裕也"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"冨田 修平"},{"name":"粟飯原 賢一"},{"name":"水口 和生"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Nifedipine is unstable under light and decomposes to a stable nitroso analog, nitrosonifedipine (NO-NIF). The ability of NO-NIF to block calcium channels is quite weak compared with that of nifedipine. Recently, we have demonstrated that NO-NIF reacts with unsaturated fatty acid leading to generate NO-NIF radical, which acquires radical scavenging activity. However, the effects of NO-NIF on the pathogenesis related with oxidative stress, such as atherosclerosis and hypertension, are unclear. In this study, we investigated the effects of NO-NIF on angiotensin II (Ang II)-induced vascular remodeling. Ang II-induced thickening and fibrosis of aorta were inhibited by NO-NIF in mice. NO-NIF decreased reactive oxygen species (ROS) in the aorta and urinary 8-hydroxy-20-deoxyguanosine. Ang II-stimulated mRNA expressions of p22(phox), CD68, F4/80, monocyte chemoattractant protein-1, and collagen I in the aorta were inhibited by NO-NIF. Moreover, NO-NIF inhibited Ang II-induced cell migration and proliferation of vascular smooth muscle cells (VSMCs). NO-NIF reduced Ang II-induced ROS to the control level detected by dihydroethidium staining and lucigenin chemiluminescence assay in VSMCs. NO-NIF suppressed phosphorylations of Akt and epidermal growth factor receptor induced by Ang II. However, NO-NIF had no effects on intracellular Ca(2+) increase and protein kinase C-δ phosphorylation induced by Ang II in VSMCs. The electron paramagnetic resonance spectra indicated the continuous generation of NO-NIF radical of reaction with cultured VSMCs. These findings suggest that NO-NIF improves Ang II-induced vascular remodeling via the attenuation of oxidative stress.","ja":"Nifedipine is unstable under light and decomposes to a stable nitroso analog, nitrosonifedipine (NO-NIF). The ability of NO-NIF to block calcium channels is quite weak compared with that of nifedipine. Recently, we have demonstrated that NO-NIF reacts with unsaturated fatty acid leading to generate NO-NIF radical, which acquires radical scavenging activity. However, the effects of NO-NIF on the pathogenesis related with oxidative stress, such as atherosclerosis and hypertension, are unclear. In this study, we investigated the effects of NO-NIF on angiotensin II (Ang II)-induced vascular remodeling. Ang II-induced thickening and fibrosis of aorta were inhibited by NO-NIF in mice. NO-NIF decreased reactive oxygen species (ROS) in the aorta and urinary 8-hydroxy-20-deoxyguanosine. Ang II-stimulated mRNA expressions of p22(phox), CD68, F4/80, monocyte chemoattractant protein-1, and collagen I in the aorta were inhibited by NO-NIF. Moreover, NO-NIF inhibited Ang II-induced cell migration and proliferation of vascular smooth muscle cells (VSMCs). NO-NIF reduced Ang II-induced ROS to the control level detected by dihydroethidium staining and lucigenin chemiluminescence assay in VSMCs. NO-NIF suppressed phosphorylations of Akt and epidermal growth factor receptor induced by Ang II. However, NO-NIF had no effects on intracellular Ca(2+) increase and protein kinase C-δ phosphorylation induced by Ang II in VSMCs. The electron paramagnetic resonance spectra indicated the continuous generation of NO-NIF radical of reaction with cultured VSMCs. These findings suggest that NO-NIF improves Ang II-induced vascular remodeling via the attenuation of oxidative stress."},"publication_date":"2013-01","publication_name":{"en":"Naunyn-Schmiedeberg's Archives of Pharmacology","ja":"Naunyn-Schmiedeberg's Archives of Pharmacology"},"volume":"Vol.386","number":"No.1","starting_page":"29","ending_page":"39","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00210-012-0810-7"],"issn":["1432-1912"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:102, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://id.ndl.go.jp/bib/024151685","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23208440","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282679880737408/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=257258","label":"url"}],"paper_title":{"en":"Acute oral toxicity evaluation of symmetrically branched glycerol trimer in ddY mice","ja":"Acute oral toxicity evaluation of symmetrically branched glycerol trimer in ddY mice"},"authors":{"en":[{"name":"Miyamoto Licht"},{"name":"Watanabe Masashi"},{"name":"Tomida Yosuke"},{"name":"Kono Mai"},{"name":"Fujii Shoko"},{"name":"Matsushita Tsuyoshi"},{"name":"Hattori Hatsuhiko"},{"name":"Ishizawa Keisuke"},{"name":"Nemoto Hisao"},{"name":"Tsuchiya Koichiro"}],"ja":[{"name":"Miyamoto Licht"},{"name":"Watanabe Masashi"},{"name":"Tomida Yosuke"},{"name":"Kono Mai"},{"name":"Fujii Shoko"},{"name":"Matsushita Tsuyoshi"},{"name":"Hattori Hatsuhiko"},{"name":"石澤 啓介"},{"name":"根本 尚夫"},{"name":"土屋 浩一郎"}]},"description":{"en":"Lipophilic-hydrophilic balance is a quite important determinant of pharmacokinetic properties of pharmaceuticals. Thus it is a key step to successfully manage lipophilic-hydrophilic balance in drug design. We have designed unique modular molecules, symmetrically branched oligoglycerols (BGL) as an alternative means to endow hydrophobic molecules with much hydrophilicity. We have succeeded in improving the water-solubility of several hydrophobic medicinal small molecules and thermal stability of artificial protein by covalent conjugation to BGL. We have also demonstrated that a representative BGL, symmetrically branched glycerol trimer (BGL003) does not exhibit significant cytotoxicity against human hepatocarcinoma HepG2 cells. However, there have been no reports suggesting whether BGL could be used in safety in vivo. Therefore, evaluation of acute oral toxicity of BGL003 in healthy mice was conducted. Here we demonstrate that an oral administration of BGL003 did not exhibit acute lethal toxicity up to 3,000 mg/kg. Body weight, food intake, blood glucose levels and weights of tissues were not affected by a short-term repetitive administration of increasing doses of BGL003. Biochemical indications related to hepatic disorders and tissue damage were unchanged, either. A single administration study revealed that 50% lethal dose of BGL003 should be more than 2,000 mg/kg. BGL003 will be safe and suitable approach to improve hydrophilicity of hydrophobic compounds.","ja":"Lipophilic-hydrophilic balance is a quite important determinant of pharmacokinetic properties of pharmaceuticals. Thus it is a key step to successfully manage lipophilic-hydrophilic balance in drug design. We have designed unique modular molecules, symmetrically branched oligoglycerols (BGL) as an alternative means to endow hydrophobic molecules with much hydrophilicity. We have succeeded in improving the water-solubility of several hydrophobic medicinal small molecules and thermal stability of artificial protein by covalent conjugation to BGL. We have also demonstrated that a representative BGL, symmetrically branched glycerol trimer (BGL003) does not exhibit significant cytotoxicity against human hepatocarcinoma HepG2 cells. However, there have been no reports suggesting whether BGL could be used in safety in vivo. Therefore, evaluation of acute oral toxicity of BGL003 in healthy mice was conducted. Here we demonstrate that an oral administration of BGL003 did not exhibit acute lethal toxicity up to 3,000 mg/kg. Body weight, food intake, blood glucose levels and weights of tissues were not affected by a short-term repetitive administration of increasing doses of BGL003. Biochemical indications related to hepatic disorders and tissue damage were unchanged, either. A single administration study revealed that 50% lethal dose of BGL003 should be more than 2,000 mg/kg. BGL003 will be safe and suitable approach to improve hydrophilicity of hydrophobic compounds."},"publication_date":"2012-12","publication_name":{"en":"The Journal of Toxicological Sciences","ja":"The Journal of Toxicological Sciences"},"volume":"Vol.37","number":"No.6","starting_page":"1253","ending_page":"1259","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2131/jts.37.1253"],"issn":["0388-1350"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:103, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23052181","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84867214872&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=256474","label":"url"}],"paper_title":{"en":"Angiotensin II receptor blocker improves tumor necrosis factor-α-induced cytotoxicity via antioxidative effect in human glomerular endothelial cells","ja":"Angiotensin II receptor blocker improves tumor necrosis factor-α-induced cytotoxicity via antioxidative effect in human glomerular endothelial cells"},"authors":{"en":[{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Sakurada Takumi"},{"name":"Imanishi Masaki"},{"name":"Miyamoto Licht"},{"name":"Fujii Shoko"},{"name":"Taira Hironori"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Hamano Shuichi"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 有紀"},{"name":"石澤 啓介"},{"name":"Sakurada Takumi"},{"name":"今西 正樹"},{"name":"宮本 理人"},{"name":"Fujii Shoko"},{"name":"Taira Hironori"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"濱野 修一"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Tumor necrosis factor-α (TNF-α) is known to involve the progression of renal dysfunction through its cytotoxicity and proinflammatory effects such as the induction of intercellular adhesion molecule (ICAM)-1 expression in vascular endothelial cells (ECs). Olmesartan, one of the angiotensin II type 1 receptor blockers (ARBs), has been reported to show protective effects on injured ECs by some causal factors of renal disorder other than angiotensin II. However, the effects of olmesartan on TNF-α-induced glomerular EC damage have not been investigated. In the present study, we investigated the effects of RNH-6270, an active metabolite of olmesartan, on TNF-α-induced human glomerular EC (HGEC) damage to clarify the renoprotective mechanisms of ARBs. Cultured HGECs were stimulated by TNF-α, and then cell viability and cytotoxicity were measured by MTT assay and lactate dehydrogenase release assay, respectively. TNF-α-induced oxidative stress was estimated by dihydroethidium assay and lucigenin chemiluminescence assay. ICAM-1 expression and the phosphorylations of mitogen-activated protein kinases were measured using Western blotting assay. RNH-6270 suppressed cell death and the increase in ICAM-1 expression induced by TNF-α via the inhibition of reactive oxygen species in HGECs. Our findings suggested that olmesartan might have protective effects against TNF-α-induced glomerular EC dysfunction.","ja":"Tumor necrosis factor-α (TNF-α) is known to involve the progression of renal dysfunction through its cytotoxicity and proinflammatory effects such as the induction of intercellular adhesion molecule (ICAM)-1 expression in vascular endothelial cells (ECs). Olmesartan, one of the angiotensin II type 1 receptor blockers (ARBs), has been reported to show protective effects on injured ECs by some causal factors of renal disorder other than angiotensin II. However, the effects of olmesartan on TNF-α-induced glomerular EC damage have not been investigated. In the present study, we investigated the effects of RNH-6270, an active metabolite of olmesartan, on TNF-α-induced human glomerular EC (HGEC) damage to clarify the renoprotective mechanisms of ARBs. Cultured HGECs were stimulated by TNF-α, and then cell viability and cytotoxicity were measured by MTT assay and lactate dehydrogenase release assay, respectively. TNF-α-induced oxidative stress was estimated by dihydroethidium assay and lucigenin chemiluminescence assay. ICAM-1 expression and the phosphorylations of mitogen-activated protein kinases were measured using Western blotting assay. RNH-6270 suppressed cell death and the increase in ICAM-1 expression induced by TNF-α via the inhibition of reactive oxygen species in HGECs. Our findings suggested that olmesartan might have protective effects against TNF-α-induced glomerular EC dysfunction."},"publication_date":"2012-12","publication_name":{"en":"Pharmacology","ja":"Pharmacology"},"volume":"Vol.90","number":"No.5-6","starting_page":"324","ending_page":"331","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1159/000343244"],"issn":["1423-0313"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:104, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/10030876787/","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23038013","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282679882410752/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=257255","label":"url"}],"paper_title":{"en":"Cytotoxicity evaluation of symmetrically branched glycerol trimer in human hepatocellular carcinoma HepG2 cells","ja":"Cytotoxicity evaluation of symmetrically branched glycerol trimer in human hepatocellular carcinoma HepG2 cells"},"authors":{"en":[{"name":"Miyamoto Licht"},{"name":"Watanabe Masashi"},{"name":"Kono Mai"},{"name":"Matsushita Tsuyoshi"},{"name":"Hattori Hatsuhiko"},{"name":"Ishizawa Keisuke"},{"name":"Nemoto Hisao"},{"name":"Tsuchiya Koichiro"}],"ja":[{"name":"Miyamoto Licht"},{"name":"Watanabe Masashi"},{"name":"Kono Mai"},{"name":"Matsushita Tsuyoshi"},{"name":"Hattori Hatsuhiko"},{"name":"石澤 啓介"},{"name":"根本 尚夫"},{"name":"土屋 浩一郎"}]},"publication_date":"2012-10-01","publication_name":{"en":"The Journal of Toxicological Sciences","ja":"The Journal of Toxicological Sciences"},"volume":"Vol.37","number":"No.5","starting_page":"1059","ending_page":"1063","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2131/jts.37.1059"],"issn":["0388-1350"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:105, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22904320","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=253941","label":"url"}],"paper_title":{"en":"Heparin cofactor II, a serine protease inhibitor, promotes angiogenesis via activation of the AMP-activated protein kinase-endothelial nitric-oxide synthase signaling pathway","ja":"Heparin cofactor II, a serine protease inhibitor, promotes angiogenesis via activation of the AMP-activated protein kinase-endothelial nitric-oxide synthase signaling pathway"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Aihara Ken-ichi"},{"name":"Yoshida Sumiko"},{"name":"Iwase Takashi"},{"name":"Tajima Soichiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Sata Masataka"},{"name":"Akaike Masashi"},{"name":"Kato Shigeaki"},{"name":"Matsumoto Toshio"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"粟飯原 賢一"},{"name":"吉田 守美子"},{"name":"岩瀬 俊"},{"name":"Tajima Soichiro"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"佐田 政隆"},{"name":"赤池 雅史"},{"name":"Kato Shigeaki"},{"name":"松本 俊夫"},{"name":"玉置 俊晃"}]},"description":{"en":"We previously clarified that heparin cofactor II (HCII), a serine proteinase inhibitor, exerts various protective actions on cardiovascular diseases in both experimental and clinical studies. In the present study, we aimed to clarify whether HCII participates in the regulation of angiogenesis. Male heterozygous HCII-deficient (HCII(+/-)) mice and male littermate wild-type (HCII(+/+)) mice at the age of 12-16 weeks were subjected to unilateral hindlimb ligation surgery. Laser speckle blood flow analysis showed that blood flow recovery in response to hindlimb ischemia was delayed in HCII(+/-) mice compared with that in HCII(+/+) mice. Capillary number, arteriole number, and endothelial nitric-oxide synthase (eNOS), AMP-activated protein kinase (AMPK), and liver kinase B1 (LKB1) phosphorylation in ischemic muscles were decreased in HCII(+/-) mice. Human purified HCII (h-HCII) administration almost restored blood flow recovery, capillary density, and arteriole number as well as phosphorylation levels of eNOS, AMPK, and LKB1 in ischemic muscles of HCII(+/-) mice. Although treatment with h-HCII increased phosphorylation levels of eNOS, AMPK, and LKB1 in human aortic endothelial cells (HAECs), the h-HCII-induced eNOS phosphorylation was abolished by compound C, an AMPK inhibitor, and by AMPK siRNA. In a similar fashion, tube formation, proliferation, and migration of HAECs were also promoted by h-HCII treatment and were abrogated by pretreatment with compound C. HCII potentiates the activation of vascular endothelial cells and the promotion of angiogenesis in response to hindlimb ischemia via an AMPK-eNOS signaling pathway. These findings suggest that HCII is a novel therapeutic target for treatment of patients with peripheral circulation insufficiency.","ja":"We previously clarified that heparin cofactor II (HCII), a serine proteinase inhibitor, exerts various protective actions on cardiovascular diseases in both experimental and clinical studies. In the present study, we aimed to clarify whether HCII participates in the regulation of angiogenesis. Male heterozygous HCII-deficient (HCII(+/-)) mice and male littermate wild-type (HCII(+/+)) mice at the age of 12-16 weeks were subjected to unilateral hindlimb ligation surgery. Laser speckle blood flow analysis showed that blood flow recovery in response to hindlimb ischemia was delayed in HCII(+/-) mice compared with that in HCII(+/+) mice. Capillary number, arteriole number, and endothelial nitric-oxide synthase (eNOS), AMP-activated protein kinase (AMPK), and liver kinase B1 (LKB1) phosphorylation in ischemic muscles were decreased in HCII(+/-) mice. Human purified HCII (h-HCII) administration almost restored blood flow recovery, capillary density, and arteriole number as well as phosphorylation levels of eNOS, AMPK, and LKB1 in ischemic muscles of HCII(+/-) mice. Although treatment with h-HCII increased phosphorylation levels of eNOS, AMPK, and LKB1 in human aortic endothelial cells (HAECs), the h-HCII-induced eNOS phosphorylation was abolished by compound C, an AMPK inhibitor, and by AMPK siRNA. In a similar fashion, tube formation, proliferation, and migration of HAECs were also promoted by h-HCII treatment and were abrogated by pretreatment with compound C. HCII potentiates the activation of vascular endothelial cells and the promotion of angiogenesis in response to hindlimb ischemia via an AMPK-eNOS signaling pathway. These findings suggest that HCII is a novel therapeutic target for treatment of patients with peripheral circulation insufficiency."},"publication_date":"2012-10","publication_name":{"en":"The Journal of Biological Chemistry","ja":"The Journal of Biological Chemistry"},"volume":"Vol.287","number":"No.41","starting_page":"34256","ending_page":"34263","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1074/jbc.M112.353532"],"issn":["1083-351X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:106, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612718"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22975299","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=257257","label":"url"}],"paper_title":{"en":"Synthesis of highly water-soluble fibrate derivatives via BGLation","ja":"Synthesis of highly water-soluble fibrate derivatives via BGLation"},"authors":{"en":[{"name":"Nemoto Hisao"},{"name":"Kamiya Masaki"},{"name":"Nakamoto Aki"},{"name":"Matsushita Tsuyoshi"},{"name":"Matsumura Kosuke"},{"name":"Hattori Hatsuhiko"},{"name":"Kawamura Tomoyuki"},{"name":"Taoka Chiaki"},{"name":"Abe Shinji"},{"name":"Ishizawa Keisuke"},{"name":"Miyamoto Licht"},{"name":"Tsuchiya Koichiro"}],"ja":[{"name":"根本 尚夫"},{"name":"Kamiya Masaki"},{"name":"Nakamoto Aki"},{"name":"Matsushita Tsuyoshi"},{"name":"Matsumura Kosuke"},{"name":"Hattori Hatsuhiko"},{"name":"Kawamura Tomoyuki"},{"name":"Taoka Chiaki"},{"name":"阿部 真治"},{"name":"石澤 啓介"},{"name":"Miyamoto Licht"},{"name":"土屋 浩一郎"}]},"description":{"en":"Three water-soluble fibrates (fenofibrate, bezafibrate and chlofibrate) conjugated with a symmetrically branched glyceryl trimer (BGL003) were synthesized, and an evaluation of the fenofibrate-BGL003 conjugate as a candidate for anti-hyperlipemia drug was carried out using rats. The water-solubility of the fenofibrate-BGL003 conjugate was several thousand times greater than that of the original fenofibrate. The lipid-lowering effects of the fenofibrate-BGL003 conjugate were as strong as those of the same grams of fenofibrate. The actual active species of fenofibrate, fenofibric acid, was detected in rats' blood, but neither the fenofibrate-BGL003 conjugate nor fenofibrate was detected, probably due to enzymatic hydrolysis of the ester bond. The plasma concentration of fenofibric acid derived from the fenofibrate-BGL003 conjugate was five times higher than that derived from fenofibrate 4h after administration.","ja":"Three water-soluble fibrates (fenofibrate, bezafibrate and chlofibrate) conjugated with a symmetrically branched glyceryl trimer (BGL003) were synthesized, and an evaluation of the fenofibrate-BGL003 conjugate as a candidate for anti-hyperlipemia drug was carried out using rats. The water-solubility of the fenofibrate-BGL003 conjugate was several thousand times greater than that of the original fenofibrate. The lipid-lowering effects of the fenofibrate-BGL003 conjugate were as strong as those of the same grams of fenofibrate. The actual active species of fenofibrate, fenofibric acid, was detected in rats' blood, but neither the fenofibrate-BGL003 conjugate nor fenofibrate was detected, probably due to enzymatic hydrolysis of the ester bond. The plasma concentration of fenofibric acid derived from the fenofibrate-BGL003 conjugate was five times higher than that derived from fenofibrate 4h after administration."},"publication_date":"2012-08-23","publication_name":{"en":"Bioorganic & Medicinal Chemistry Letters","ja":"Bioorganic & Medicinal Chemistry Letters"},"volume":"Vol.22","number":"No.20","starting_page":"6425","ending_page":"6428","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.bmcl.2012.08.057"],"issn":["1464-3405"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:107, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612719"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22892212","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=257256","label":"url"}],"paper_title":{"en":"Synthesis of paclitaxel-BGL conjugates","ja":"Synthesis of paclitaxel-BGL conjugates"},"authors":{"en":[{"name":"Nemoto Hisao"},{"name":"Katagiri Ayato"},{"name":"Kamiya Masaki"},{"name":"Kawamura Tomoyuki"},{"name":"Matsushita Tsuyoshi"},{"name":"Matsumura Kosuke"},{"name":"Itou Tomohiro"},{"name":"Hattori Hatsuhiko"},{"name":"Tamaki Miho"},{"name":"Ishizawa Keisuke"},{"name":"Miyamoto Licht"},{"name":"Abe Shinji"},{"name":"Tsuchiya Koichiro"}],"ja":[{"name":"根本 尚夫"},{"name":"Katagiri Ayato"},{"name":"Kamiya Masaki"},{"name":"Kawamura Tomoyuki"},{"name":"Matsushita Tsuyoshi"},{"name":"Matsumura Kosuke"},{"name":"Itou Tomohiro"},{"name":"Hattori Hatsuhiko"},{"name":"Tamaki Miho"},{"name":"石澤 啓介"},{"name":"Miyamoto Licht"},{"name":"阿部 真治"},{"name":"土屋 浩一郎"}]},"description":{"en":"Four kinds of symmetrically branched oligoglyceryl trimeric (BGL003)-paclitaxel conjugates and a corresponding heptameric (BGL007) conjugate were synthesized. Molecular weights of all the compounds were less than two times that of paclitaxel. The anti-tumor activity of the most water-soluble BGL003 conjugate was examined and found to be preserved in spite of the chemical modification that is displacement of the N3'-debenzoyl residue with the BGL003 succinyl residue.","ja":"Four kinds of symmetrically branched oligoglyceryl trimeric (BGL003)-paclitaxel conjugates and a corresponding heptameric (BGL007) conjugate were synthesized. Molecular weights of all the compounds were less than two times that of paclitaxel. The anti-tumor activity of the most water-soluble BGL003 conjugate was examined and found to be preserved in spite of the chemical modification that is displacement of the N3'-debenzoyl residue with the BGL003 succinyl residue."},"publication_date":"2012-07-25","publication_name":{"en":"Bioorganic & Medicinal Chemistry","ja":"Bioorganic & Medicinal Chemistry"},"volume":"Vol.20","number":"No.18","starting_page":"5559","ending_page":"5567","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.bmc.2012.07.031"],"issn":["1464-3391"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:108, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/40019353020/","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22792339","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84863827034&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=248250","label":"url"}],"paper_title":{"en":"Estrogen regulates hepcidin expression via GPR30-BMP6-dependent signaling in hepatocytes","ja":"Estrogen regulates hepcidin expression via GPR30-BMP6-dependent signaling in hepatocytes"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Tajima Soichiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"Tajima Soichiro"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Hepcidin, a liver-derived iron regulatory protein, plays a crucial role in iron metabolism. It is known that gender differences exist with respect to iron storage in the body; however, the effects of sex steroid hormones on iron metabolism are not completely understood. We focused on the effects of the female sex hormone estrogen on hepcidin expression. First, ovariectomized (OVX) and sham-operated mice were employed to investigate the effects of estrogen on hepcidin expression in an in vivo study. Hepcidin expression was decreased in the livers of OVX mice compared to the sham-operated mice. In OVX mice, bone morphologic protein-6 (BMP6), a regulator of hepcidin, was also found to be downregulated in the liver, whereas ferroportin (FPN), an iron export protein, was upregulated in the duodenum. Both serum and liver iron concentrations were elevated in OVX mice relative to their concentrations in sham-operated mice. In in vitro studies, 17β-estradiol (E(2)) increased the mRNA expression of hepcidin in HepG2 cells in a concentration-dependent manner. E(2)-induced hepatic hepcidin upregulation was not inhibited by ICI 182720, an inhibitor of the estrogen receptor; instead, hepcidin expression was increased by ICI 182720. E(2) and ICI 182720 exhibit agonist actions with G-protein coupled receptor 30 (GPR30), the 7-transmembrane estrogen receptor. G1, a GPR30 agonist, upregulated hepcidin expression, and GPR30 siRNA treatment abolished E(2)-induced hepcidin expression. BMP6 expression induced by E(2) was abolished by GPR30 silencing. Finally, both E(2) and G1 supplementation restored reduced hepatic hepcidin and BMP6 expression and reversed the augmentation of duodenal FPN expression in the OVX mice. In contrast, serum hepcidin was elevated in OVX mice, which was reversed in these mice with E(2) and G1. Thus, estrogen is involved in hepcidin expression via a GPR30-BMP6-dependent mechanism, providing new insight into the role of estrogen in iron metabolism.","ja":"Hepcidin, a liver-derived iron regulatory protein, plays a crucial role in iron metabolism. It is known that gender differences exist with respect to iron storage in the body; however, the effects of sex steroid hormones on iron metabolism are not completely understood. We focused on the effects of the female sex hormone estrogen on hepcidin expression. First, ovariectomized (OVX) and sham-operated mice were employed to investigate the effects of estrogen on hepcidin expression in an in vivo study. Hepcidin expression was decreased in the livers of OVX mice compared to the sham-operated mice. In OVX mice, bone morphologic protein-6 (BMP6), a regulator of hepcidin, was also found to be downregulated in the liver, whereas ferroportin (FPN), an iron export protein, was upregulated in the duodenum. Both serum and liver iron concentrations were elevated in OVX mice relative to their concentrations in sham-operated mice. In in vitro studies, 17β-estradiol (E(2)) increased the mRNA expression of hepcidin in HepG2 cells in a concentration-dependent manner. E(2)-induced hepatic hepcidin upregulation was not inhibited by ICI 182720, an inhibitor of the estrogen receptor; instead, hepcidin expression was increased by ICI 182720. E(2) and ICI 182720 exhibit agonist actions with G-protein coupled receptor 30 (GPR30), the 7-transmembrane estrogen receptor. G1, a GPR30 agonist, upregulated hepcidin expression, and GPR30 siRNA treatment abolished E(2)-induced hepcidin expression. BMP6 expression induced by E(2) was abolished by GPR30 silencing. Finally, both E(2) and G1 supplementation restored reduced hepatic hepcidin and BMP6 expression and reversed the augmentation of duodenal FPN expression in the OVX mice. In contrast, serum hepcidin was elevated in OVX mice, which was reversed in these mice with E(2) and G1. Thus, estrogen is involved in hepcidin expression via a GPR30-BMP6-dependent mechanism, providing new insight into the role of estrogen in iron metabolism."},"publication_date":"2012-07-11","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.7","number":"No.7","starting_page":"e40465","ending_page":"e40465","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0040465"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:109, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612720"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/111913","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22505188","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=246982","label":"url"}],"paper_title":{"en":"Development of a reduction-responsive amino acid that induces peptide bond cleavage in hypoxic cells","ja":"Development of a reduction-responsive amino acid that induces peptide bond cleavage in hypoxic cells"},"authors":{"en":[{"name":"Shigenaga Akira"},{"name":"Ogura Keiji"},{"name":"Hirakawa Hiroko"},{"name":"Yamamoto Jun"},{"name":"Ebisuno Koji"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Otaka Akira"}],"ja":[{"name":"重永 章"},{"name":"小倉 圭司"},{"name":"平川 寛子"},{"name":"山本 純"},{"name":"戎野 紘司"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"大髙 章"}]},"description":{"en":"Hypoxia-responsive amino acids are indispensable in the preparation of hypoxic tumor-specific peptidyl prodrugs. In this paper, the design and synthesis of a reduction-responsive amino acid that induces peptide bond cleavage after reduction of the nitro group are described. Application to hypoxia-responsive peptide bond cleavage system is also reported.","ja":"Hypoxia-responsive amino acids are indispensable in the preparation of hypoxic tumor-specific peptidyl prodrugs. In this paper, the design and synthesis of a reduction-responsive amino acid that induces peptide bond cleavage after reduction of the nitro group are described. Application to hypoxia-responsive peptide bond cleavage system is also reported."},"publication_date":"2012-04-13","publication_name":{"en":"ChemBioChem","ja":"ChemBioChem"},"volume":"Vol.13","starting_page":"968","ending_page":"971","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/cbic.201200141"],"issn":["1439-7633"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:110, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21917632","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=243340","label":"url"}],"paper_title":{"en":"Iron reduction by deferoxamine leads to amelioration of adiposity via the regulation of oxidative stress and inflammation in obese and type 2 diabetes KKAy mice.","ja":"Iron reduction by deferoxamine leads to amelioration of adiposity via the regulation of oxidative stress and inflammation in obese and type 2 diabetes KKAy mice."},"authors":{"en":[{"name":"Tajima Soichiro"},{"name":"Ikeda Yasumasa"},{"name":"Sawada Kaori"},{"name":"Yamano Noriko"},{"name":"Horinouchi Yuya"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tomita Shuhei"},{"name":"Minakuchi Kazuo"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Tajima Soichiro"},{"name":"池田 康将"},{"name":"澤田 香織"},{"name":"山野 範子"},{"name":"堀ノ内 裕也"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"石澤 有紀"},{"name":"川添 和義"},{"name":"冨田 修平"},{"name":"水口 和生"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Iron is an essential trace metal for most organisms. However, excess iron causes oxidative stress through production of highly toxic hydroxyl radicals via the Fenton/Haber-Weiss reaction. Iron storage in the body is reported to be associated with fat accumulation and type 2 diabetes mellitus. We investigated the role of iron in adiposity by using KKAy mice and obese and diabetic model mice. Eight-week-old KKAy mice were divided into two groups and treated with deferoxamine (DFO), an iron chelator agent, or a vehicle for 2 wk. DFO treatment diminished fat iron concentration and serum ferritin levels in KKAy mice. Fat weight and adipocyte size were reduced significantly in DFO-treated mice compared with vehicle-treated mice. Macrophage infiltration into fat was also decreased in DFO-treated mice compared with vehicle-treated mice. Superoxide production and NADPH oxidase activity in fat, as well as urinary 8-hydroxy-2'-deoxyguanosine excretion, were decreased in KKAy mice after DFO treatment while p22(phox) expression in adipose tissue was diminished in such mice. Ferritin expression in the fat of DFO-treated KKAy mice was decreased. In addition, F4/80-positive cells also presented through both p22(phox) and ferritin expression. The mRNA expression levels of inflammatory cytokines were also reduced in fat tissue of DFO-treated mice. These findings suggest that reduction of iron levels ameliorates adipocyte hypertrophy via suppression of oxidative stress, inflammatory cytokines, and macrophage infiltration, thereby breaking a vicious cycle in obesity.","ja":"Iron is an essential trace metal for most organisms. However, excess iron causes oxidative stress through production of highly toxic hydroxyl radicals via the Fenton/Haber-Weiss reaction. Iron storage in the body is reported to be associated with fat accumulation and type 2 diabetes mellitus. We investigated the role of iron in adiposity by using KKAy mice and obese and diabetic model mice. Eight-week-old KKAy mice were divided into two groups and treated with deferoxamine (DFO), an iron chelator agent, or a vehicle for 2 wk. DFO treatment diminished fat iron concentration and serum ferritin levels in KKAy mice. Fat weight and adipocyte size were reduced significantly in DFO-treated mice compared with vehicle-treated mice. Macrophage infiltration into fat was also decreased in DFO-treated mice compared with vehicle-treated mice. Superoxide production and NADPH oxidase activity in fat, as well as urinary 8-hydroxy-2'-deoxyguanosine excretion, were decreased in KKAy mice after DFO treatment while p22(phox) expression in adipose tissue was diminished in such mice. Ferritin expression in the fat of DFO-treated KKAy mice was decreased. In addition, F4/80-positive cells also presented through both p22(phox) and ferritin expression. The mRNA expression levels of inflammatory cytokines were also reduced in fat tissue of DFO-treated mice. These findings suggest that reduction of iron levels ameliorates adipocyte hypertrophy via suppression of oxidative stress, inflammatory cytokines, and macrophage infiltration, thereby breaking a vicious cycle in obesity."},"publication_date":"2012-01","publication_name":{"en":"American Journal of Physiology, Endocrinology and Metabolism","ja":"American Journal of Physiology, Endocrinology and Metabolism"},"volume":"Vol.302","number":"No.1","starting_page":"E77","ending_page":"86","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1152/ajpendo.00033.2011"],"issn":["1522-1555"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:111, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21810481","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=241773","label":"url"}],"paper_title":{"en":"Basic fibroblast growth factor regulates glucose metabolism through glucose transporter 1 induced by hypoxia-inducible factor-1α in adipocytes","ja":"Basic fibroblast growth factor regulates glucose metabolism through glucose transporter 1 induced by hypoxia-inducible factor-1α in adipocytes"},"authors":{"en":[{"name":"Kihira Yoshitaka"},{"name":"Yamano Noriko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"},{"name":"Tomita Shuhei"}],"ja":[{"name":"木平 孝高"},{"name":"山野 範子"},{"name":"石澤 有紀"},{"name":"石澤 啓介"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"},{"name":"冨田 修平"}]},"description":{"en":"Hypoxia-inducible factor-1 (HIF-1), which is a transcription factor that enhances glycolysis in cells in response to hypoxia, is induced in hypertrophied adipocytes in obesity. Recent studies have shown that growth factors are able to induce HIF-1 by mechanisms independent of hypoxia. Since basic fibroblast growth factor (bFGF), an angiogenic factor, is concentrated in expanding adipose tissue, the possible effects of bFGF on regulation of HIF-1 in adipocytes were investigated. Treatment of differentiated 3T3-L1 adipocytes with bFGF induced HIF-1. Concomitantly, glucose transporter 1 (GLUT1), which is a target gene of HIF-1, was induced at both mRNA and protein levels and was translocated to the plasma membrane. A chromatin immunoprecipitation assay and an RNA interference study indicated that bFGF-induced HIF-1 directly upregulates GLUT1. In addition, it was observed that bFGF increases lactate production of adipocytes. This result indicates that bFGF reprograms the metabolism toward glycolysis. Intraperitoneal injection of bFGF into mice upregulated HIF-1 and GLUT1 in adipose tissues, suggesting that bFGF regulates the metabolism of adipocytes via HIF-1-GLUT1 regulation in vivo. We also found that bFGF inhibits insulin-induced phosphorylation of insulin receptor substrate-1 and Akt, suggesting that bFGF attenuates the insulin signal in adipocytes. Taken together, the findings suggest that bFGF has a harmful effect on the development of type 2 diabetes through metabolism reprogramming and attenuation of the insulin signal.","ja":"Hypoxia-inducible factor-1 (HIF-1), which is a transcription factor that enhances glycolysis in cells in response to hypoxia, is induced in hypertrophied adipocytes in obesity. Recent studies have shown that growth factors are able to induce HIF-1 by mechanisms independent of hypoxia. Since basic fibroblast growth factor (bFGF), an angiogenic factor, is concentrated in expanding adipose tissue, the possible effects of bFGF on regulation of HIF-1 in adipocytes were investigated. Treatment of differentiated 3T3-L1 adipocytes with bFGF induced HIF-1. Concomitantly, glucose transporter 1 (GLUT1), which is a target gene of HIF-1, was induced at both mRNA and protein levels and was translocated to the plasma membrane. A chromatin immunoprecipitation assay and an RNA interference study indicated that bFGF-induced HIF-1 directly upregulates GLUT1. In addition, it was observed that bFGF increases lactate production of adipocytes. This result indicates that bFGF reprograms the metabolism toward glycolysis. Intraperitoneal injection of bFGF into mice upregulated HIF-1 and GLUT1 in adipose tissues, suggesting that bFGF regulates the metabolism of adipocytes via HIF-1-GLUT1 regulation in vivo. We also found that bFGF inhibits insulin-induced phosphorylation of insulin receptor substrate-1 and Akt, suggesting that bFGF attenuates the insulin signal in adipocytes. Taken together, the findings suggest that bFGF has a harmful effect on the development of type 2 diabetes through metabolism reprogramming and attenuation of the insulin signal."},"publication_date":"2011-11","publication_name":{"en":"The International Journal of Biochemistry & Cell Biology","ja":"The International Journal of Biochemistry & Cell Biology"},"volume":"Vol.43","number":"No.11","starting_page":"1602","ending_page":"1611","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.biocel.2011.07.009"],"issn":["1878-5875"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:112, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612721"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21422726","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-79955046642&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=227811","label":"url"}],"paper_title":{"en":"Pathophysiological Response to Hypoxia From the Molecular Mechanisms of Malady to Drug Discovery: Inflammatory Responses of Hypoxia-Inducible Factor 1 (HIF-1) in T Cells Observed in Development of Vascular Remodeling","ja":"Pathophysiological Response to Hypoxia From the Molecular Mechanisms of Malady to Drug Discovery: Inflammatory Responses of Hypoxia-Inducible Factor 1 (HIF-1) in T Cells Observed in Development of Vascular Remodeling"},"authors":{"en":[{"name":"Tomita Shuhei"},{"name":"Kihira Yoshitaka"},{"name":"Imanishi Masaki"},{"name":"Fukuhara Yayoi"},{"name":"Imamura Yuko"},{"name":"Ishizawa Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"冨田 修平"},{"name":"木平 孝高"},{"name":"今西 正樹"},{"name":"福原 弥生"},{"name":"今村 優子"},{"name":"石澤 啓介"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Recent studies have shown that the cellular immune response to the hypoxic microenvironment constructed by vascular remodeling development modulates the resulting pathologic alterations. A major mechanism mediating adaptive responses to reduced oxygen availability is the regulation of transcription by hypoxia-inducible factor 1 (HIF-1). Impairment of HIF-1-dependent inflammatory responses in T cells causes an augmented vascular remodeling induced by arterial injury, which is shown as prominent neointimal hyperplasia and increase in infiltration of inflammatory cells at the adventitia in mice lacking Hif-1α specifically in T cells. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice have shown enhanced production of cytokines in activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. This minireview shows that HIF-1α in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of the T cell-mediated immune response and suggests potential new therapeutic strategies that target HIF-1α.","ja":"Recent studies have shown that the cellular immune response to the hypoxic microenvironment constructed by vascular remodeling development modulates the resulting pathologic alterations. A major mechanism mediating adaptive responses to reduced oxygen availability is the regulation of transcription by hypoxia-inducible factor 1 (HIF-1). Impairment of HIF-1-dependent inflammatory responses in T cells causes an augmented vascular remodeling induced by arterial injury, which is shown as prominent neointimal hyperplasia and increase in infiltration of inflammatory cells at the adventitia in mice lacking Hif-1α specifically in T cells. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice have shown enhanced production of cytokines in activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. This minireview shows that HIF-1α in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of the T cell-mediated immune response and suggests potential new therapeutic strategies that target HIF-1α."},"publication_date":"2011-04","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.115","number":"No.4","starting_page":"433","ending_page":"439","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.10R22FM"],"issn":["1347-8648"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:113, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612722"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21436601","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=220416","label":"url"}],"paper_title":{"en":"Pharmacology in health food: Metabolism of quercetin in vivo and its protective effect against arteriosclerosis","ja":"Pharmacology in health food: Metabolism of quercetin in vivo and its protective effect against arteriosclerosis"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Yoshizumi Masanori"},{"name":"Kawai Yoshichika"},{"name":"Terao Junji"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Tomita Shuhei"},{"name":"Minakuchi Kazuo"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"吉栖 正典"},{"name":"河合 慶親"},{"name":"寺尾 純二"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"冨田 修平"},{"name":"水口 和生"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Quercetin, a member of the bioflavonoids family, has been proposed to have anti-atherogenic, anti-inflammatory, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. It was recently demonstrated that quercetin 3-O-β-D-glucuronide (Q3GA) is one of the major quercetin conjugates in human plasma, in which the aglycone could not be detected. Although most of the in vitro pharmacological studies have been carried out using only the quercetin aglycone form, experiments using Q3GA would be important to discover the preventive mechanisms of cardiovascular diseases by quercetin in vivo. Therefore we examined the effects of the chemically synthesized Q3GA, as an in vivo form, on vascular smooth muscle cell (VSMC) disorders related to the progression of arteriosclerosis. Platelet-derived growth factor-induced cell migration and proliferation were inhibited by Q3GA in VSMCs. Q3GA attenuated angiotensin II-induced VSMC hypertrophy via its inhibitory effect on JNK and the AP-1 signaling pathway. Q3GA scavenged 1,1-diphenyl-2-picrylhydrazyl radical measured by the electron paramagnetic resonance method. In addition, immunohistochemical studies with monoclonal antibody 14A2 targeting the Q3GA demonstrated that the positive staining specifically accumulates in human atherosclerotic lesions, but not in the normal aorta. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may have preventative effects on arteriosclerosis relevant to VSMC disorders.","ja":"Quercetin, a member of the bioflavonoids family, has been proposed to have anti-atherogenic, anti-inflammatory, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. It was recently demonstrated that quercetin 3-O-β-D-glucuronide (Q3GA) is one of the major quercetin conjugates in human plasma, in which the aglycone could not be detected. Although most of the in vitro pharmacological studies have been carried out using only the quercetin aglycone form, experiments using Q3GA would be important to discover the preventive mechanisms of cardiovascular diseases by quercetin in vivo. Therefore we examined the effects of the chemically synthesized Q3GA, as an in vivo form, on vascular smooth muscle cell (VSMC) disorders related to the progression of arteriosclerosis. Platelet-derived growth factor-induced cell migration and proliferation were inhibited by Q3GA in VSMCs. Q3GA attenuated angiotensin II-induced VSMC hypertrophy via its inhibitory effect on JNK and the AP-1 signaling pathway. Q3GA scavenged 1,1-diphenyl-2-picrylhydrazyl radical measured by the electron paramagnetic resonance method. In addition, immunohistochemical studies with monoclonal antibody 14A2 targeting the Q3GA demonstrated that the positive staining specifically accumulates in human atherosclerotic lesions, but not in the normal aorta. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may have preventative effects on arteriosclerosis relevant to VSMC disorders."},"publication_date":"2011-04","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.115","number":"No.4","starting_page":"466","ending_page":"470","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.10R38FM"],"issn":["1347-8648"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:114, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612723"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21297301","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-79551489998&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=314653","label":"url"}],"paper_title":{"en":"Antioxidant effects of photodegradation product of nifedipine","ja":"Antioxidant effects of photodegradation product of nifedipine"},"authors":{"en":[{"name":"Horinouchi Yuya"},{"name":"Tsuchiya Koichiro"},{"name":"Taoka Chiaki"},{"name":"Tajima Soichiro"},{"name":"Kihira Yoshitaka"},{"name":"Matsuda Yuko"},{"name":"Shishido Kozo"},{"name":"Yoshida Masahiro"},{"name":"Hamano Shuichi"},{"name":"Kawazoe Kazuyoshi"},{"name":"Ikeda Yasumasa"},{"name":"Ishizawa Keisuke"},{"name":"Tomita Shuhei"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"堀ノ内 裕也"},{"name":"土屋 浩一郎"},{"name":"Taoka Chiaki"},{"name":"Tajima Soichiro"},{"name":"木平 孝高"},{"name":"Matsuda Yuko"},{"name":"宍戸 宏造"},{"name":"吉田 昌裕"},{"name":"濱野 修一"},{"name":"川添 和義"},{"name":"池田 康将"},{"name":"石澤 啓介"},{"name":"冨田 修平"},{"name":"玉置 俊晃"}]},"description":{"en":"Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nifedipine is unstable under light and reportedly decomposes to a stable nitrosonifedipine (NO-NIF). NO-NIF has no antihypertensive effect, and it has been recognized as a contaminant of nifedipine. The present study for the first time demonstrated that NO-NIF changed to a NO-NIF radical in a time-dependent manner when it interacted with human umbilical vein endothelial cells (HUVECs). The electron paramagnetic resonance (EPR) signal of NO-NIF radicals in HUVECs showed an asymmetric pattern suggesting that the radicals were located in the membrane. The NO-NIF radicals had radical scavenging activity for 1,1-diphenyl-2-picrylhydrazyl, whereas neither NO-NIF nor nifedipine did. In addition, the NO-NIF radical more effectively quenched lipid peroxides than NO-NIF or nifedipine. Furthermore, NO-NIF attenuated the superoxide-derived free radicals in HUVECs stimulated with LY83583, and suppressed iron-nitrilotriacetic acid (Fe-NTA)-induced cytotoxicity in rat pheochromocytoma (PC12) cells. Our findings suggest that NO-NIF is a candidate for a new class of antioxidative drugs that protect cells against oxidative stress.","ja":"Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nifedipine is unstable under light and reportedly decomposes to a stable nitrosonifedipine (NO-NIF). NO-NIF has no antihypertensive effect, and it has been recognized as a contaminant of nifedipine. The present study for the first time demonstrated that NO-NIF changed to a NO-NIF radical in a time-dependent manner when it interacted with human umbilical vein endothelial cells (HUVECs). The electron paramagnetic resonance (EPR) signal of NO-NIF radicals in HUVECs showed an asymmetric pattern suggesting that the radicals were located in the membrane. The NO-NIF radicals had radical scavenging activity for 1,1-diphenyl-2-picrylhydrazyl, whereas neither NO-NIF nor nifedipine did. In addition, the NO-NIF radical more effectively quenched lipid peroxides than NO-NIF or nifedipine. Furthermore, NO-NIF attenuated the superoxide-derived free radicals in HUVECs stimulated with LY83583, and suppressed iron-nitrilotriacetic acid (Fe-NTA)-induced cytotoxicity in rat pheochromocytoma (PC12) cells. Our findings suggest that NO-NIF is a candidate for a new class of antioxidative drugs that protect cells against oxidative stress."},"publication_date":"2011-02","publication_name":{"en":"Chemical & Pharmaceutical Bulletin","ja":"Chemical & Pharmaceutical Bulletin"},"volume":"Vol.59","number":"No.2","starting_page":"208","ending_page":"214","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1248/cpb.59.208"],"issn":["1347-5223"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:115, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612724"},"force":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/130004465233/","label":"url"},{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/72667","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21372496","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390001204242892288/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=223410","label":"url"}],"paper_title":{"en":"Protective effect of photodegradation product of nifedipine against tumor necrosis factor alpha-induced oxidative stress in human glomerular endothelial cells","ja":"Protective effect of photodegradation product of nifedipine against tumor necrosis factor alpha-induced oxidative stress in human glomerular endothelial cells"},"authors":{"en":[{"name":"Fukuhara Yayoi"},{"name":"Tsuchiya Koichiro"},{"name":"Horinouchi Yuya"},{"name":"Tajima Soichiro"},{"name":"Kihira Yoshitaka"},{"name":"Hamano Shuichi"},{"name":"Kawazoe Kazuyoshi"},{"name":"Ikeda Yasumasa"},{"name":"Ishizawa Keisuke"},{"name":"Tomita Shuhei"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"福原 弥生"},{"name":"土屋 浩一郎"},{"name":"堀ノ内 裕也"},{"name":"Tajima Soichiro"},{"name":"木平 孝高"},{"name":"濱野 修一"},{"name":"川添 和義"},{"name":"池田 康将"},{"name":"石澤 啓介"},{"name":"冨田 修平"},{"name":"玉置 俊晃"}]},"description":{"en":"Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nitrosonifedipine (NO-NIF) is metabolically and photochemically produced from nifedipine, and NO-NIF has been recognized as a contaminant of nifedipine because it has no antihypertensive effect. Treatment of tumor necrosis factor-α (TNF-α) suppressed the cell viability and facilitated the expression of Inter-Cellular Adhesion Molecule 1(ICAM-1) in human glomerular endothelial cells (HGECs) though, pretreatment of NO-NIF significantly recovered the TNF-α-induced cell damage to the same extent as Trolox-C did, and suppressed the ICAM-1 expression in a concentration dependent manner. In addition, NO-NIF inhibited the cell toxicity induced by cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, as effective as Trolox-c. These data suggest that NO-NIF is a candidate for a new class of antioxidative drug that protect cells against oxidative stress in glomerular endothelial cells.","ja":"Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nitrosonifedipine (NO-NIF) is metabolically and photochemically produced from nifedipine, and NO-NIF has been recognized as a contaminant of nifedipine because it has no antihypertensive effect. Treatment of tumor necrosis factor-α (TNF-α) suppressed the cell viability and facilitated the expression of Inter-Cellular Adhesion Molecule 1(ICAM-1) in human glomerular endothelial cells (HGECs) though, pretreatment of NO-NIF significantly recovered the TNF-α-induced cell damage to the same extent as Trolox-C did, and suppressed the ICAM-1 expression in a concentration dependent manner. In addition, NO-NIF inhibited the cell toxicity induced by cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, as effective as Trolox-c. These data suggest that NO-NIF is a candidate for a new class of antioxidative drug that protect cells against oxidative stress in glomerular endothelial cells."},"publication_date":"2011-02","publication_name":{"en":"The Journal of Medical Investigation : JMI","ja":"The Journal of Medical Investigation : JMI"},"volume":"Vol.58","number":"No.1, 2","starting_page":"118","ending_page":"126","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2152/jmi.58.118"],"issn":["1349-6867"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:116, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21315355","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=222278","label":"url"}],"paper_title":{"en":"Deferoxamine promotes angiogenesis via the activation of vascular endothelial cell function.","ja":"Deferoxamine promotes angiogenesis via the activation of vascular endothelial cell function."},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Tajima Soichiro"},{"name":"Yoshida Sumiko"},{"name":"Yamano Noriko"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Aihara Ken-ichi"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"Tajima Soichiro"},{"name":"吉田 守美子"},{"name":"山野 範子"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"粟飯原 賢一"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"BACKGROUND: Deferoxamine (DFO), an iron chelator for disorders of excess iron, upregulates the expression of angiogenic factors, such as vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2), indicating that it affects angiogenesis. Herein, we clarify the effect and mechanism of action of DFO on angiogenesis. METHODS AND RESULTS: In an in vitro study, DFO increased endothelial nitric oxide synthesis (eNOS) phosphorylation in human aortic endothelial cells (HAECs), which were inhibited by the phosphatidylinositol 3-kinase inhibitor LY294002. Tube formation, cell proliferation, and cell migration in HAECs were promoted by DFO, which were significantly reduced by LY294002. In an in vivo study, DFO promoted blood flow recovery in response to the hindlimb ischemia in mice with unilateral hindlimb surgery. The density of capillaries and arterioles in ischemic muscle was higher in DFO-treated mice compared to vehicle-treated mice. Endothelial cell proliferation increased and oxidative stress and apoptosis decreased in ischemic muscles of DFO-treated mice. The phosphorylation of Akt and eNOS on the ischemic side was elevated and urinary nitric oxide/nitric dioxide (NOx) excretion was higher in DFO-treated mice compared to vehicle-treated mice. The effect of DFO on angiogenesis was abolished in eNOS-deficient mice with hindlimb ischemia. CONCLUSION: These findings indicate that DFO promotes revascularization via the activation of vascular endothelial cell function by an Akt-eNOS-dependent mechanism.","ja":"BACKGROUND: Deferoxamine (DFO), an iron chelator for disorders of excess iron, upregulates the expression of angiogenic factors, such as vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2), indicating that it affects angiogenesis. Herein, we clarify the effect and mechanism of action of DFO on angiogenesis. METHODS AND RESULTS: In an in vitro study, DFO increased endothelial nitric oxide synthesis (eNOS) phosphorylation in human aortic endothelial cells (HAECs), which were inhibited by the phosphatidylinositol 3-kinase inhibitor LY294002. Tube formation, cell proliferation, and cell migration in HAECs were promoted by DFO, which were significantly reduced by LY294002. In an in vivo study, DFO promoted blood flow recovery in response to the hindlimb ischemia in mice with unilateral hindlimb surgery. The density of capillaries and arterioles in ischemic muscle was higher in DFO-treated mice compared to vehicle-treated mice. Endothelial cell proliferation increased and oxidative stress and apoptosis decreased in ischemic muscles of DFO-treated mice. The phosphorylation of Akt and eNOS on the ischemic side was elevated and urinary nitric oxide/nitric dioxide (NOx) excretion was higher in DFO-treated mice compared to vehicle-treated mice. The effect of DFO on angiogenesis was abolished in eNOS-deficient mice with hindlimb ischemia. CONCLUSION: These findings indicate that DFO promotes revascularization via the activation of vascular endothelial cell function by an Akt-eNOS-dependent mechanism."},"publication_date":"2011-01-21","publication_name":{"en":"Atherosclerosis","ja":"Atherosclerosis"},"volume":"Vol.215","number":"No.2","starting_page":"339","ending_page":"347","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.atherosclerosis.2011.01.009"],"issn":["1879-1484"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:117, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612725"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/20431588","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-77954369377&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=207897","label":"url"}],"paper_title":{"en":"Effect of angiotensin II on iron-transporting protein expression and subsequent intracellular labile iron concentration in human glomerular endothelial cells","ja":"Effect of angiotensin II on iron-transporting protein expression and subsequent intracellular labile iron concentration in human glomerular endothelial cells"},"authors":{"en":[{"name":"Tajima Soichiro"},{"name":"Tsuchiya Koichiro"},{"name":"Horinouchi Yuya"},{"name":"Ishizawa Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Kihira Yoshitaka"},{"name":"Shono Masayuki"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tomita Shuhei"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Tajima Soichiro"},{"name":"土屋 浩一郎"},{"name":"堀ノ内 裕也"},{"name":"石澤 啓介"},{"name":"池田 康将"},{"name":"木平 孝高"},{"name":"庄野 正行"},{"name":"川添 和義"},{"name":"冨田 修平"},{"name":"玉置 俊晃"}]},"description":{"en":"Angiotensin II (Ang II)-induced endothelial injury, which is associated with atherosclerosis, is believed to be mediated by intracellular reactive oxygen species (ROS) through stimulation of nicotinamide adenine dinucleotide phosphate oxidase (NOX). Iron is essential for the amplification of oxidative stress. In this study, we investigated whether Ang II altered iron metabolism and whether the Ang II-induced endothelial injury is attributable to changes in iron metabolism of human glomerular endothelial cells (HGECs). When 90% iron-saturated human transferrin (90% Tf) was applied to HGECs without Ang II, the labile ferrous iron level was same as the effect of control in spite of a significant increase in the total cellular iron concentration. Treatment with Ang II and 30% Tf or 90% Tf significantly (P<0.01) increased the intracellular iron concentration, as well as labile ferrous iron and protein oxidation levels, compared with the effect of separate administration of each compound. Ang II treatment facilitated the protein expression of the Tf receptor, divalent metal transporter 1, and ferroportin 1 in a dose- and time-dependent manner. It was also found that simultaneous exposure of HGECs to Ang II and 90% Tf accelerated hydroxyl radical production, as shown by using an electron paramagnetic resonance spectrometer. These results suggest that Ang II not only induces production of ROS by NOX activation but also iron incorporation followed by an increase in labile iron in HGECs. Both of these events may participate in the progression of oxidative stress because of endothelial cell dysfunction through ferrous iron-mediated ROS generation.","ja":"Angiotensin II (Ang II)-induced endothelial injury, which is associated with atherosclerosis, is believed to be mediated by intracellular reactive oxygen species (ROS) through stimulation of nicotinamide adenine dinucleotide phosphate oxidase (NOX). Iron is essential for the amplification of oxidative stress. In this study, we investigated whether Ang II altered iron metabolism and whether the Ang II-induced endothelial injury is attributable to changes in iron metabolism of human glomerular endothelial cells (HGECs). When 90% iron-saturated human transferrin (90% Tf) was applied to HGECs without Ang II, the labile ferrous iron level was same as the effect of control in spite of a significant increase in the total cellular iron concentration. Treatment with Ang II and 30% Tf or 90% Tf significantly (P<0.01) increased the intracellular iron concentration, as well as labile ferrous iron and protein oxidation levels, compared with the effect of separate administration of each compound. Ang II treatment facilitated the protein expression of the Tf receptor, divalent metal transporter 1, and ferroportin 1 in a dose- and time-dependent manner. It was also found that simultaneous exposure of HGECs to Ang II and 90% Tf accelerated hydroxyl radical production, as shown by using an electron paramagnetic resonance spectrometer. These results suggest that Ang II not only induces production of ROS by NOX activation but also iron incorporation followed by an increase in labile iron in HGECs. Both of these events may participate in the progression of oxidative stress because of endothelial cell dysfunction through ferrous iron-mediated ROS generation."},"publication_date":"2010-04-30","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.33","number":"No.7","starting_page":"713","ending_page":"721","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/hr.2010.63"],"issn":["1348-4214"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:118, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19812233","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=194522","label":"url"}],"paper_title":{"en":"Angiotensin II receptor blocker attenuates PDGF-induced mesangial cell migration in a receptor-independent manner","ja":"Angiotensin II receptor blocker attenuates PDGF-induced mesangial cell migration in a receptor-independent manner"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Dorjsuren Narantungalag"},{"name":"Miki Erika"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Hamano Shuichi"},{"name":"Kawazoe Kazuyoshi"},{"name":"Minakuchi Kazuo"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"石澤 有紀"},{"name":"Dorjsuren Narantungalag"},{"name":"Miki Erika"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"濱野 修一"},{"name":"川添 和義"},{"name":"水口 和生"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Clinical studies have shown that angiotensin II (Ang II) type 1 (AT1) receptor blockers (ARBs) are able to provide renoprotection independent of their blood pressure lowering effects. ARBs also are reported to suppress oxidative stress, inflammation and certain other cellular responses in a receptor-independent manner. We investigated the effects of an ARB, olmesartan, on the cell migration induced by platelet-derived growth factor (PDGF), a major mitogen involved in the pathogenesis of glomerulonephritis in rat mesangial cells (RMCs). Cell migration was determined by a modified Boyden chamber assay. The intracellular signalling pathway was examined by western blotting. AT1 receptor expression was knocked down by small interfering RNAs. The intracellular reactive oxygen species (ROS) was measured by using a fluorescent probe. The O(2)(.-) scavenging activities were studied by the electron paramagnetic resonance-spin trapping method. PDGF-induced cell migration was inhibited by olmesartan in AT1 receptor knockdown RMCs. Olmesartan attenuated big mitogen-activated protein (MAP) kinase 1 (BMK1) and Src activation by PDGF in AT1 receptor knockdown RMCs. PDGF-induced BMK1 activation was suppressed by the Src family tyrosine kinase inhibitors, indicating that Src exists upstream of BMK1. The NADPH oxidase inhibitors inhibited not only PDGF-induced BMK1 and Src activation but also RMC migration. The elevation in ROS generation induced by PDGF was decreased by olmesartan. Olmesartan displayed neither directly ROS scavenging activity nor the inhibition of ROS-mediated intracellular signalling in RMCs. Olmesartan attenuates ROS generation by PDGF, leading to the subsequent inhibition of Src/ BMK1/migration in an AT1 receptor-independent manner in RMCs.","ja":"Clinical studies have shown that angiotensin II (Ang II) type 1 (AT1) receptor blockers (ARBs) are able to provide renoprotection independent of their blood pressure lowering effects. ARBs also are reported to suppress oxidative stress, inflammation and certain other cellular responses in a receptor-independent manner. We investigated the effects of an ARB, olmesartan, on the cell migration induced by platelet-derived growth factor (PDGF), a major mitogen involved in the pathogenesis of glomerulonephritis in rat mesangial cells (RMCs). Cell migration was determined by a modified Boyden chamber assay. The intracellular signalling pathway was examined by western blotting. AT1 receptor expression was knocked down by small interfering RNAs. The intracellular reactive oxygen species (ROS) was measured by using a fluorescent probe. The O(2)(.-) scavenging activities were studied by the electron paramagnetic resonance-spin trapping method. PDGF-induced cell migration was inhibited by olmesartan in AT1 receptor knockdown RMCs. Olmesartan attenuated big mitogen-activated protein (MAP) kinase 1 (BMK1) and Src activation by PDGF in AT1 receptor knockdown RMCs. PDGF-induced BMK1 activation was suppressed by the Src family tyrosine kinase inhibitors, indicating that Src exists upstream of BMK1. The NADPH oxidase inhibitors inhibited not only PDGF-induced BMK1 and Src activation but also RMC migration. The elevation in ROS generation induced by PDGF was decreased by olmesartan. Olmesartan displayed neither directly ROS scavenging activity nor the inhibition of ROS-mediated intracellular signalling in RMCs. Olmesartan attenuates ROS generation by PDGF, leading to the subsequent inhibition of Src/ BMK1/migration in an AT1 receptor-independent manner in RMCs."},"publication_date":"2010-02","publication_name":{"en":"Nephrology, Dialysis, Transplantation","ja":"Nephrology, Dialysis, Transplantation"},"volume":"Vol.25","number":"No.2","starting_page":"364","ending_page":"372","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/ndt/gfp520"],"issn":["1460-2385"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:119, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612726"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/20005970","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=204466","label":"url"}],"paper_title":{"en":"Dietary nitrite ameliorates renal injury in l-NAME-induced hypertensive rats","ja":"Dietary nitrite ameliorates renal injury in l-NAME-induced hypertensive rats"},"authors":{"en":[{"name":"Tsuchiya Koichiro"},{"name":"Tomita Shuhei"},{"name":"Ishizawa Keisuke"},{"name":"Abe Shinji"},{"name":"Ikeda Yasumasa"},{"name":"Kihira Yoshitaka"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"土屋 浩一郎"},{"name":"冨田 修平"},{"name":"石澤 啓介"},{"name":"阿部 真治"},{"name":"池田 康将"},{"name":"木平 孝高"},{"name":"玉置 俊晃"}]},"description":{"en":"Nitric oxide (NO) has numerous important functions in the kidney, and long-term blockage of nitric oxide synthases in rats by L-NAME results in severe hypertension and progressive kidney damage. On the other hand, NO production seems to be low in patients with chronic kidney disease (CKD), and NO deficiency may play a role in CKD progression. In this review, we summarized the mechanisms of amelioration of renal injury induced by L-NAME treated rats by treatment of nitrite. First, we demonstrate whether orally-administrated nitrite-derived NO can shift to the circulation. When 3mg/kg body weight Na(15)NO(2) was orally administered to rats, an apparent EPR signal derived from Hb(15)NO (A(z)=23.4 gauss) appeared in the blood, indicating that orally ingested nitrite can be a source of NO in vivo. Next, in order to clarify the capacity of nitrite to prevent renal disease, we administered low-dose nitrite (LDN: 0.1mg of sodium nitrite in 1L of drinking water), medium-dose nitrite (MDN: 1mg sodium nitrite/L, which corresponds to the amount of nitrite ingested by vegetarians), or high-dose nitrite (HDN: 10mg sodium nitrite/L) to rats simultaneously with L-NAME (1 g l-NAME/L) for 8 weeks, then examined the blood NO level as a hemoglobin-NO adduct (iron-nitrosyl-hemoglobin) using electron paramagnetic resonance spectroscopy, urinary protein excretion, and renal histological changes at the end of the experiment. It was found that oral administration of MDN and HDN but not LDN increased the blood iron-nitrosyl-hemoglobin concentration to the normal level, ameliorated the L-NAME-induced proteinuria, and reduced renal histological damage. The findings demonstrate that chronic administration of a mid-level dietary dose of nitrite restores the circulating iron-nitrosyl-hemoglobin levels reduced by L-NAME and that maintenance of the circulating iron-nitrosyl-hemoglobin level in a controlled range protects against L-NAME-induced renal injury. Taking these findings together, we propose that dietary supplementation of nitrite is a potentially useful nonpharmacological strategy for maintaining circulating NO level in order to prevent or slow the progression of renal disease. It had been believed that nitrite could result in intragastric formation of nitrosamines, which had been linked to esophageal and other gastrointestinal cancers. However, there is no positive association between the intake of nitrate or nitrite and gastric and pancreatic cancer by recent researches. Furthermore, nitrate-derived NO formation pathway is a possible mechanism for the hypotensive effect of vegetable- and fruit-rich diets, which may explain, at least in part, the mechanism of the Dietary Approach to Stop Hypertension (DASH) diet-induced hypotensive and organ-protective effects. Further research is needed to investigate the interaction between nitrite-nitrate intakes and human health.","ja":"Nitric oxide (NO) has numerous important functions in the kidney, and long-term blockage of nitric oxide synthases in rats by L-NAME results in severe hypertension and progressive kidney damage. On the other hand, NO production seems to be low in patients with chronic kidney disease (CKD), and NO deficiency may play a role in CKD progression. In this review, we summarized the mechanisms of amelioration of renal injury induced by L-NAME treated rats by treatment of nitrite. First, we demonstrate whether orally-administrated nitrite-derived NO can shift to the circulation. When 3mg/kg body weight Na(15)NO(2) was orally administered to rats, an apparent EPR signal derived from Hb(15)NO (A(z)=23.4 gauss) appeared in the blood, indicating that orally ingested nitrite can be a source of NO in vivo. Next, in order to clarify the capacity of nitrite to prevent renal disease, we administered low-dose nitrite (LDN: 0.1mg of sodium nitrite in 1L of drinking water), medium-dose nitrite (MDN: 1mg sodium nitrite/L, which corresponds to the amount of nitrite ingested by vegetarians), or high-dose nitrite (HDN: 10mg sodium nitrite/L) to rats simultaneously with L-NAME (1 g l-NAME/L) for 8 weeks, then examined the blood NO level as a hemoglobin-NO adduct (iron-nitrosyl-hemoglobin) using electron paramagnetic resonance spectroscopy, urinary protein excretion, and renal histological changes at the end of the experiment. It was found that oral administration of MDN and HDN but not LDN increased the blood iron-nitrosyl-hemoglobin concentration to the normal level, ameliorated the L-NAME-induced proteinuria, and reduced renal histological damage. The findings demonstrate that chronic administration of a mid-level dietary dose of nitrite restores the circulating iron-nitrosyl-hemoglobin levels reduced by L-NAME and that maintenance of the circulating iron-nitrosyl-hemoglobin level in a controlled range protects against L-NAME-induced renal injury. Taking these findings together, we propose that dietary supplementation of nitrite is a potentially useful nonpharmacological strategy for maintaining circulating NO level in order to prevent or slow the progression of renal disease. It had been believed that nitrite could result in intragastric formation of nitrosamines, which had been linked to esophageal and other gastrointestinal cancers. However, there is no positive association between the intake of nitrate or nitrite and gastric and pancreatic cancer by recent researches. Furthermore, nitrate-derived NO formation pathway is a possible mechanism for the hypotensive effect of vegetable- and fruit-rich diets, which may explain, at least in part, the mechanism of the Dietary Approach to Stop Hypertension (DASH) diet-induced hypotensive and organ-protective effects. Further research is needed to investigate the interaction between nitrite-nitrate intakes and human health."},"publication_date":"2010-02","publication_name":{"en":"Nitric Oxide: Biology and Chemistry","ja":"Nitric Oxide: Biology and Chemistry"},"volume":"Vol.22","number":"No.2","starting_page":"98","ending_page":"103","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.niox.2009.12.002"],"issn":["1089-8611"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:120, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/20007912","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=202019","label":"url"}],"paper_title":{"en":"Role of Hypoxia-Inducible Factor 1α in T Cells as a Negative Regulator in Development of Vascular Remodeling","ja":"Role of Hypoxia-Inducible Factor 1α in T Cells as a Negative Regulator in Development of Vascular Remodeling"},"authors":{"en":[{"name":"Kurobe Hirotsugu"},{"name":"Urata Masahisa"},{"name":"Ueno Masaki"},{"name":"Ueki Masaaki"},{"name":"Ono Shiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Fukuhara Yayoi"},{"name":"Lei Yu"},{"name":"Ripen Mat Adiratna"},{"name":"Kanbara Tamotsu"},{"name":"Aihara Ken-ichi"},{"name":"Ishizawa Keisuke"},{"name":"Akaike Masashi"},{"name":"Gonzalez J. Frank"},{"name":"Tamaki Toshiaki"},{"name":"Takahama Yousuke"},{"name":"Yoshizumi Masanori"},{"name":"Kitagawa Tetsuya"},{"name":"Tomita Shuhei"}],"ja":[{"name":"黒部 裕嗣"},{"name":"Urata Masahisa"},{"name":"Ueno Masaki"},{"name":"Ueki Masaaki"},{"name":"Ono Shiro"},{"name":"石澤 有紀"},{"name":"Fukuhara Yayoi"},{"name":"Lei Yu"},{"name":"Ripen Mat Adiratna"},{"name":"神原 保"},{"name":"粟飯原 賢一"},{"name":"石澤 啓介"},{"name":"赤池 雅史"},{"name":"Gonzalez J. Frank"},{"name":"玉置 俊晃"},{"name":"高浜 洋介"},{"name":"吉栖 正典"},{"name":"北川 哲也"},{"name":"冨田 修平"}]},"description":{"en":"Recent studies have shown that the cellular immune response in the development of vascular remodeling modulates the resulting pathological alterations. We show that hypoxia-inducible factor 1 (Hif-1) (specifically expressed in T cells) is involved in the immune response to vascular remodeling that accompanies arteriosclerosis. To study the role of T cells in the development of vascular remodeling, femoral arterial injury induced by an external vascular polyethylene cuff was examined in mice lacking Hif-1 (specifically in T cells). We found that cuff placement caused prominent neointimal hyperplasia of the femoral artery in Hif-1- (T-cell)-deficient mice compared with that in control mice and that infiltration of inflammatory cells at the adventitia was markedly increased in the mutant mice. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice showed enhanced production of cytokines by activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. The results of this study revealed that Hif-1alpha in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of T cell-mediated immune response. Potential new therapeutic strategies that target Hif-1alpha are described.","ja":"Recent studies have shown that the cellular immune response in the development of vascular remodeling modulates the resulting pathological alterations. We show that hypoxia-inducible factor 1 (Hif-1) (specifically expressed in T cells) is involved in the immune response to vascular remodeling that accompanies arteriosclerosis. To study the role of T cells in the development of vascular remodeling, femoral arterial injury induced by an external vascular polyethylene cuff was examined in mice lacking Hif-1 (specifically in T cells). We found that cuff placement caused prominent neointimal hyperplasia of the femoral artery in Hif-1- (T-cell)-deficient mice compared with that in control mice and that infiltration of inflammatory cells at the adventitia was markedly increased in the mutant mice. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice showed enhanced production of cytokines by activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. The results of this study revealed that Hif-1alpha in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of T cell-mediated immune response. Potential new therapeutic strategies that target Hif-1alpha are described."},"publication_date":"2010-02","publication_name":{"en":"Arteriosclerosis, Thrombosis, and Vascular Biology","ja":"Arteriosclerosis, Thrombosis, and Vascular Biology"},"volume":"Vol.30","number":"No.2","starting_page":"210","ending_page":"217","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1161/ATVBAHA.109.192666"],"issn":["1524-4636"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:121, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19460854","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193058","label":"url"}],"paper_title":{"en":"Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration","ja":"Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Dorjsuren Narantungalag"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Sugimoto Rika"},{"name":"Ikeda Yasumasa"},{"name":"Kihira Yoshitaka"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Minakuchi Kazuo"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"Dorjsuren Narantungalag"},{"name":"石澤 有紀"},{"name":"Sugimoto Rika"},{"name":"池田 康将"},{"name":"木平 孝高"},{"name":"川添 和義"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"水口 和生"},{"name":"玉置 俊晃"}]},"description":{"en":"Adiponectin, an adipocyte-derived hormone, has been involved in metabolic syndrome, a known risk factor for the development of chronic kidney disease (CKD). Recent studies have demonstrated that plasma adiponectin levels are elevated when kidney function declines in patients with CKD. Excessive mesangial cell (MC) turnover is one of the important features of CKD. The aim of the present study is to elucidate the effects of adiponectin on platelet-derived growth factor (PDGF)-induced cell migration and intracellular signaling pathways, in cultured rat MCs (RMCs). PDGF-induced RMC migration was significantly inhibited by the pretreatment of adiponectin. Adiponectin alone had no effect on RMC migration. Big mitogen-activated protein (MAP) kinase 1 (BMK1), p38 MAP kinase, and Akt were activated by PDGF stimulation in a time- and concentration-dependent manner in RMC. Adiponectin alone did not affect BMK1, p38 MAP kinase, and Akt phosphorylations in RMC. PDGF-induced BMK1 and p38 MAP kinase phosphorylations were significantly attenuated by the pretreatment of adiponectin in RMCs. On the other hand, the phosphorylation of Akt by PDGF was not diminished by the pretreatment of adiponectin. Adiponectin had no effects on PDGF-receptor autophosphorylation by PDGF. We also confirmed that PDGF-induced RMC migration was significantly suppressed by siBMK1 transfection or SB203580, a p38 MAP kinase inhibitor. From these findings, it is implied that the elevated plasma adiponectin levels in patients with CKD might play a compensatory role aimed at counteracting renal dysfunction related to MC disorders.","ja":"Adiponectin, an adipocyte-derived hormone, has been involved in metabolic syndrome, a known risk factor for the development of chronic kidney disease (CKD). Recent studies have demonstrated that plasma adiponectin levels are elevated when kidney function declines in patients with CKD. Excessive mesangial cell (MC) turnover is one of the important features of CKD. The aim of the present study is to elucidate the effects of adiponectin on platelet-derived growth factor (PDGF)-induced cell migration and intracellular signaling pathways, in cultured rat MCs (RMCs). PDGF-induced RMC migration was significantly inhibited by the pretreatment of adiponectin. Adiponectin alone had no effect on RMC migration. Big mitogen-activated protein (MAP) kinase 1 (BMK1), p38 MAP kinase, and Akt were activated by PDGF stimulation in a time- and concentration-dependent manner in RMC. Adiponectin alone did not affect BMK1, p38 MAP kinase, and Akt phosphorylations in RMC. PDGF-induced BMK1 and p38 MAP kinase phosphorylations were significantly attenuated by the pretreatment of adiponectin in RMCs. On the other hand, the phosphorylation of Akt by PDGF was not diminished by the pretreatment of adiponectin. Adiponectin had no effects on PDGF-receptor autophosphorylation by PDGF. We also confirmed that PDGF-induced RMC migration was significantly suppressed by siBMK1 transfection or SB203580, a p38 MAP kinase inhibitor. From these findings, it is implied that the elevated plasma adiponectin levels in patients with CKD might play a compensatory role aimed at counteracting renal dysfunction related to MC disorders."},"publication_date":"2009-08","publication_name":{"en":"The Journal of Endocrinology","ja":"The Journal of Endocrinology"},"volume":"Vol.202","number":"No.2","starting_page":"309","ending_page":"316","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1677/JOE-08-0469"],"issn":["1479-6805"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:122, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19262481","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193054","label":"url"}],"paper_title":{"en":"Adiponectin inhibits insulin-like growth factor-1-induced cell migration by the suppression of extracellular signal-regulated kinase 1/2 activation, but not Akt in vascular smooth muscle cells","ja":"Adiponectin inhibits insulin-like growth factor-1-induced cell migration by the suppression of extracellular signal-regulated kinase 1/2 activation, but not Akt in vascular smooth muscle cells"},"authors":{"en":[{"name":"Motobayashi Yuki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Orino Sakiko"},{"name":"Yamaguchi Kunihisa"},{"name":"Kawazoe Kazuyoshi"},{"name":"Hamano Shuichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tomita Shuhei"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Motobayashi Yuki"},{"name":"石澤 有紀"},{"name":"石澤 啓介"},{"name":"Orino Sakiko"},{"name":"山口 邦久"},{"name":"川添 和義"},{"name":"濱野 修一"},{"name":"土屋 浩一郎"},{"name":"冨田 修平"},{"name":"玉置 俊晃"}]},"description":{"en":"Adiponectin, an adipocyte-derived hormone, has been proposed to show antiatherogenic properties through the inhibitory effects against various growth factors. Insulin-like growth factor-1 (IGF-1) is one of the potent mitogens, which has been considered to play important roles in both atherogenesis and plaque stabilization in accordance to the phase of atherosclerosis. The aim of this study is to elucidate the adiponectin effects on IGF-1-induced cell migration and its intracellular signaling pathways in vascular smooth muscle cells (VSMCs). In this study, we assessed cell migration and several kinase activities in cultured rat aortic smooth muscle cells (RASMCs). Adiponectin pretreatment suppressed IGF-1-induced cell migration and extracellular signal-regulated kinase (ERK)1/2 activation, which is one of the major mediators for IGF-1-induced cell migration. In RASMCs, adiponectin and 5-aminoimidazole-4-carboxamide riboside (AICAR), a 5'-AMP-activated protein kinase (AMPK) activator, stimulated AMPK activation. AMPK activation by AICAR inhibited IGF-1-induced ERK1/2 activation and cell migration in RASMCs. On the other hand, phosphorylation of Akt and Bad, proapoptotic molecules of the Bcl-2 family, which were increased by IGF-1 stimulation, was not diminished by the pretreatment with adiponectin. It was shown that adiponectin inhibited IGF-1-induced VSMC migration through suppression of ERK1/2 activation, which might be implicated in AMPK activation. Furthermore, adiponectin selectively inhibited ERK1/2 pathway, not Akt-Bad pathway, stimulated by IGF-1. From these findings, it was implied that adiponectin suppressed IGF-1-induced VSMC migration and its signaling selectivity.","ja":"Adiponectin, an adipocyte-derived hormone, has been proposed to show antiatherogenic properties through the inhibitory effects against various growth factors. Insulin-like growth factor-1 (IGF-1) is one of the potent mitogens, which has been considered to play important roles in both atherogenesis and plaque stabilization in accordance to the phase of atherosclerosis. The aim of this study is to elucidate the adiponectin effects on IGF-1-induced cell migration and its intracellular signaling pathways in vascular smooth muscle cells (VSMCs). In this study, we assessed cell migration and several kinase activities in cultured rat aortic smooth muscle cells (RASMCs). Adiponectin pretreatment suppressed IGF-1-induced cell migration and extracellular signal-regulated kinase (ERK)1/2 activation, which is one of the major mediators for IGF-1-induced cell migration. In RASMCs, adiponectin and 5-aminoimidazole-4-carboxamide riboside (AICAR), a 5'-AMP-activated protein kinase (AMPK) activator, stimulated AMPK activation. AMPK activation by AICAR inhibited IGF-1-induced ERK1/2 activation and cell migration in RASMCs. On the other hand, phosphorylation of Akt and Bad, proapoptotic molecules of the Bcl-2 family, which were increased by IGF-1 stimulation, was not diminished by the pretreatment with adiponectin. It was shown that adiponectin inhibited IGF-1-induced VSMC migration through suppression of ERK1/2 activation, which might be implicated in AMPK activation. Furthermore, adiponectin selectively inhibited ERK1/2 pathway, not Akt-Bad pathway, stimulated by IGF-1. From these findings, it was implied that adiponectin suppressed IGF-1-induced VSMC migration and its signaling selectivity."},"publication_date":"2009-03","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.32","number":"No.3","starting_page":"188","ending_page":"193","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/hr.2008.19"],"issn":["1348-4214"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:123, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19202317","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193051","label":"url"}],"paper_title":{"en":"Quercetin Glucuronide Inhibits Cell Migration and Proliferation by Platelet-Derived Growth Factor in Vascular Smooth Muscle Cells","ja":"Quercetin Glucuronide Inhibits Cell Migration and Proliferation by Platelet-Derived Growth Factor in Vascular Smooth Muscle Cells"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ohnishi Sachiyo"},{"name":"Motobayashi Yuki"},{"name":"Kawazoe Kazuyoshi"},{"name":"Hamano Shuichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tomita Shuhei"},{"name":"Minakuchi Kazuo"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"石澤 有紀"},{"name":"Ohnishi Sachiyo"},{"name":"Motobayashi Yuki"},{"name":"川添 和義"},{"name":"濱野 修一"},{"name":"土屋 浩一郎"},{"name":"冨田 修平"},{"name":"水口 和生"},{"name":"玉置 俊晃"}]},"description":{"en":"Many epidemiologic studies have reported that dietary flavonoids provide protection against cardiovascular disease. Quercetin, a member of the bioflavonoids family, has been proposed to have anti-inflammatory, anti-atherogenic, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. Recent studies demonstrated that orally administered quercetin appeared in plasma as glucuronide-conjugated forms in rats and humans. Therefore, we examined the effect of chemically synthesized quercetin glucuronide on platelet-derived growth factor (PDGF)-induced cell migration and kinase activation in cultured rat aortic smooth muscle cells (RASMCs). PDGF-induced RASMC migration was inhibited by quercetin 3-O-beta-D-glucuronide (Q3GA). Q3GA also attenuated PDGF-induced cell proliferation in RASMCs. PDGF activated extracellular-signal regulated kinase (ERK) 1/2, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and Akt in RASMCs. PDGF-induced JNK and Akt activations were suppressed by Q3GA, whereas ERK1/2 and p38 MAP kinase activations were not affected. We also confirmed that PDGF-induced JNK and Akt activations were inhibited by antioxidants, N-acetylcysteine and diphenyleneiodonium chloride, in RASMCs. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may possess preventing effects for cardiovascular diseases relevant to vascular smooth muscle cell disorders.","ja":"Many epidemiologic studies have reported that dietary flavonoids provide protection against cardiovascular disease. Quercetin, a member of the bioflavonoids family, has been proposed to have anti-inflammatory, anti-atherogenic, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. Recent studies demonstrated that orally administered quercetin appeared in plasma as glucuronide-conjugated forms in rats and humans. Therefore, we examined the effect of chemically synthesized quercetin glucuronide on platelet-derived growth factor (PDGF)-induced cell migration and kinase activation in cultured rat aortic smooth muscle cells (RASMCs). PDGF-induced RASMC migration was inhibited by quercetin 3-O-beta-D-glucuronide (Q3GA). Q3GA also attenuated PDGF-induced cell proliferation in RASMCs. PDGF activated extracellular-signal regulated kinase (ERK) 1/2, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and Akt in RASMCs. PDGF-induced JNK and Akt activations were suppressed by Q3GA, whereas ERK1/2 and p38 MAP kinase activations were not affected. We also confirmed that PDGF-induced JNK and Akt activations were inhibited by antioxidants, N-acetylcysteine and diphenyleneiodonium chloride, in RASMCs. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may possess preventing effects for cardiovascular diseases relevant to vascular smooth muscle cell disorders."},"publication_date":"2009-02-07","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.109","number":"No.2","starting_page":"257","ending_page":"264","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.08236FP"],"issn":["1347-8613"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:124, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19151535","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193050","label":"url"}],"paper_title":{"en":"Toward drug discovery for overcoming CKD: Development of drugs on endothelial cell protection for overcoming CKD","ja":"Toward drug discovery for overcoming CKD: Development of drugs on endothelial cell protection for overcoming CKD"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Yamaguchi Kunihisa"},{"name":"Horinouchi Yuya"},{"name":"Fukuhara Yayoi"},{"name":"Tajima Soichiro"},{"name":"Hamano Shuichi"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"山口 邦久"},{"name":"堀ノ内 裕也"},{"name":"Fukuhara Yayoi"},{"name":"Tajima Soichiro"},{"name":"濱野 修一"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Chronic kidney disease (CKD) is becoming a major public health problem worldwide. It is important to protect endothelial function in CKD treatment because injury of the endothelium is a critical event for the generation and progression of CKD. Recently, clinical studies showed that nifedipine, an antihypertensive drug, acts as a protective agent of endothelial cells (ECs). Nifedipine is reported to partially decompose to a nitrosonifedipine that has high reactivity against lipid-derived radicals in vitro. However, it is still unclear whether nitrosonifedipine is a biologically active agent against endothelial injury. We observed that nitrosonifedipine was converted to radical form by reaction with cultured ECs. The cumene hydroperoxide mediated cytotoxity was reduced by nitrosonifedipine in cultured human glomerular ECs (HGECs). Also nitrosonifedipine suppressed the expression of TNF-alpha-induced intercellular cell adhesion molecule-1 in HGECs. Chronic administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) caused systemic arterial hypertension, endothelial injury, and renal dysfunction. In L-NAME-induced hypertensive rats, nitrosonifedipine treatment improved not only the acetylcholine-induced vasodilation of the aortic rings, but also renal dysfunction such as increasing the levels of serum creatinine and urinary protein excretion. Our preliminary data suggest that nitrosonifedipine is a new and useful drug for the treatment of CKD involving ameliorating effects on EC disorder.","ja":"Chronic kidney disease (CKD) is becoming a major public health problem worldwide. It is important to protect endothelial function in CKD treatment because injury of the endothelium is a critical event for the generation and progression of CKD. Recently, clinical studies showed that nifedipine, an antihypertensive drug, acts as a protective agent of endothelial cells (ECs). Nifedipine is reported to partially decompose to a nitrosonifedipine that has high reactivity against lipid-derived radicals in vitro. However, it is still unclear whether nitrosonifedipine is a biologically active agent against endothelial injury. We observed that nitrosonifedipine was converted to radical form by reaction with cultured ECs. The cumene hydroperoxide mediated cytotoxity was reduced by nitrosonifedipine in cultured human glomerular ECs (HGECs). Also nitrosonifedipine suppressed the expression of TNF-alpha-induced intercellular cell adhesion molecule-1 in HGECs. Chronic administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) caused systemic arterial hypertension, endothelial injury, and renal dysfunction. In L-NAME-induced hypertensive rats, nitrosonifedipine treatment improved not only the acetylcholine-induced vasodilation of the aortic rings, but also renal dysfunction such as increasing the levels of serum creatinine and urinary protein excretion. Our preliminary data suggest that nitrosonifedipine is a new and useful drug for the treatment of CKD involving ameliorating effects on EC disorder."},"publication_date":"2009-01","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.109","number":"No.1","starting_page":"14","ending_page":"19","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.08R08FM"],"issn":["1347-8613"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:125, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612727"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/18831560","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=191889","label":"url"}],"paper_title":{"en":"Effect of iron-quercetin complex on reduction of nitrite in in vitro and in vivo systems","ja":"Effect of iron-quercetin complex on reduction of nitrite in in vitro and in vivo systems"},"authors":{"en":[{"name":"Ohnishi Hideki"},{"name":"Iwanaga Satoshi"},{"name":"Kawazoe Kazuyoshi"},{"name":"Ishizawa Keisuke"},{"name":"Orino Sakiko"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Kanematsu Yasuhisa"},{"name":"Harada Nagakatsu"},{"name":"Mori Kazuhiro"},{"name":"Tsuchihashi Tomoko"},{"name":"Ishikawa Yasuko"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Ohnishi Hideki"},{"name":"Iwanaga Satoshi"},{"name":"川添 和義"},{"name":"石澤 啓介"},{"name":"Orino Sakiko"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"兼松 康久"},{"name":"原田 永勝"},{"name":"森 一博"},{"name":"Tsuchihashi Tomoko"},{"name":"石川 康子"},{"name":"玉置 俊晃"}]},"description":{"en":"This study investigated whether reducing agents such as quercetin and iron(II) facilitate formation of nitric oxide (NO) gas from orally ingested nitrite in an vivo study. When 3 mg/kg Na (15)NO2 was orally administered to rats with or without iron(II) or quercetin, Hb (15)NO, which is indicative of systemic (15)NO, was detected in the blood, with the maximum blood concentration of Hb (15)NO at 15 min after nitrite or nitrite plus quercetin treatment, whereas after administration of nitrite plus iron(II) or nitrite plus iron(II) and quercetin, the time was shortened to 10 min. Interestingly, iron(II), quercetin, or iron(II) plus quercetin did not affect the total amount of Hb (15)NO generated from orally administered Na (15)NO2. However, the systemic nitrite concentration was significantly decreased in the presence of iron(II) or iron(II) plus quercetin. These results may indicate that iron(II) is critical to the generation of NO gas from nitrite, whereas quercetin contributed little under the in vivo experimental conditions.","ja":"This study investigated whether reducing agents such as quercetin and iron(II) facilitate formation of nitric oxide (NO) gas from orally ingested nitrite in an vivo study. When 3 mg/kg Na (15)NO2 was orally administered to rats with or without iron(II) or quercetin, Hb (15)NO, which is indicative of systemic (15)NO, was detected in the blood, with the maximum blood concentration of Hb (15)NO at 15 min after nitrite or nitrite plus quercetin treatment, whereas after administration of nitrite plus iron(II) or nitrite plus iron(II) and quercetin, the time was shortened to 10 min. Interestingly, iron(II), quercetin, or iron(II) plus quercetin did not affect the total amount of Hb (15)NO generated from orally administered Na (15)NO2. However, the systemic nitrite concentration was significantly decreased in the presence of iron(II) or iron(II) plus quercetin. These results may indicate that iron(II) is critical to the generation of NO gas from nitrite, whereas quercetin contributed little under the in vivo experimental conditions."},"publication_date":"2008-11","publication_name":{"en":"Journal of Agricultural and Food Chemistry","ja":"Journal of Agricultural and Food Chemistry"},"volume":"Vol.56","number":"No.21","starting_page":"10092","ending_page":"10098","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1021/jf801010j"],"issn":["1520-5118"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:126, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/18753302","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=189061","label":"url"}],"paper_title":{"en":"Dietary doses of nitrite restore circulating nitric oxide level and improve renal injury in L-NAME-induced hypertensive rats","ja":"Dietary doses of nitrite restore circulating nitric oxide level and improve renal injury in L-NAME-induced hypertensive rats"},"authors":{"en":[{"name":"Kanematsu Yasuhisa"},{"name":"Yamaguchi Kunihisa"},{"name":"Ohnishi Hideki"},{"name":"Motobayashi Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Izawa Yuki"},{"name":"Kawazoe Kazuyoshi"},{"name":"Kondo Shuji"},{"name":"Kagami Shoji"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"兼松 康久"},{"name":"山口 邦久"},{"name":"大西 秀樹"},{"name":"元林 有紀"},{"name":"石澤 啓介"},{"name":"井澤 有紀"},{"name":"川添 和義"},{"name":"近藤 秀治"},{"name":"香美 祥二"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"We have reported that pharmacological doses of oral nitrite increase circulating nitric oxide (NO) and exert hypotensive effects in Nomega-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. In this study, we examined the effect of a chronic dietary dose of nitrite on the hypertension and renal damage induced by chronic L-NAME administration in rats. The animals were administered tap water containing L-NAME (1 g/l) or L-NAME + nitrite (low dose: 0.1 mg/l, medium dose: 1 mg/l, high dose: 10 mg/l) for 8 wk. We evaluated blood NO levels as hemoglobin-NO adducts (iron-nitrosyl-hemoglobin), using an electron paramagnetic resonance method. Chronic administration of L-NAME for 8 wk induced hypertension and renal injury and reduced the blood iron-nitrosyl-hemoglobin level (control 38.8 +/- 8.9 vs. L-NAME 6.0 +/- 3.1 arbitrary units). Coadministration of a low dose of nitrite with L-NAME did not change the reduced iron-nitrosyl-hemoglobin signal and did not improve the L-NAME-induced renal injury. The blood iron-nitrosyl-hemoglobin signals of the medium dose and high dose of nitrite were significantly higher than that of L-NAME alone. Chronic administration of a medium dose of nitrite attenuated L-NAME-induced renal histological changes and proteinuria. A high dose of nitrite also attenuated L-NAME-induced renal injury. These findings suggest that dietary doses of nitrite that protect the kidney are associated with significant increase in iron-nitrosyl-hemoglobin levels. We conclude that dietary nitrite-derived NO generation may serve as a backup system when the nitric oxide synthase/L-arginine-dependent NO generation system is compromised.","ja":"We have reported that pharmacological doses of oral nitrite increase circulating nitric oxide (NO) and exert hypotensive effects in Nomega-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. In this study, we examined the effect of a chronic dietary dose of nitrite on the hypertension and renal damage induced by chronic L-NAME administration in rats. The animals were administered tap water containing L-NAME (1 g/l) or L-NAME + nitrite (low dose: 0.1 mg/l, medium dose: 1 mg/l, high dose: 10 mg/l) for 8 wk. We evaluated blood NO levels as hemoglobin-NO adducts (iron-nitrosyl-hemoglobin), using an electron paramagnetic resonance method. Chronic administration of L-NAME for 8 wk induced hypertension and renal injury and reduced the blood iron-nitrosyl-hemoglobin level (control 38.8 +/- 8.9 vs. L-NAME 6.0 +/- 3.1 arbitrary units). Coadministration of a low dose of nitrite with L-NAME did not change the reduced iron-nitrosyl-hemoglobin signal and did not improve the L-NAME-induced renal injury. The blood iron-nitrosyl-hemoglobin signals of the medium dose and high dose of nitrite were significantly higher than that of L-NAME alone. Chronic administration of a medium dose of nitrite attenuated L-NAME-induced renal histological changes and proteinuria. A high dose of nitrite also attenuated L-NAME-induced renal injury. These findings suggest that dietary doses of nitrite that protect the kidney are associated with significant increase in iron-nitrosyl-hemoglobin levels. We conclude that dietary nitrite-derived NO generation may serve as a backup system when the nitric oxide synthase/L-arginine-dependent NO generation system is compromised."},"publication_date":"2008-08-27","publication_name":{"en":"American Journal of Physiology, Renal Physiology","ja":"American Journal of Physiology, Renal Physiology"},"volume":"Vol.295","number":"No.5","starting_page":"F1457","ending_page":"F1462","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1152/ajprenal.00621.2007"],"issn":["1931-857X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:127, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/18250560","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=176515","label":"url"}],"paper_title":{"en":"Big mitogen-activated protein kinase 1 (BMK1)/extracellular signal regulated kinase 5 (ERK5) is involved in platelet-derived growth factor (PDGF)-induced vascular smooth muscle cell migration","ja":"Big mitogen-activated protein kinase 1 (BMK1)/extracellular signal regulated kinase 5 (ERK5) is involved in platelet-derived growth factor (PDGF)-induced vascular smooth muscle cell migration"},"authors":{"en":[{"name":"Izawa Yuki"},{"name":"Yoshizumi Masanori"},{"name":"Ishizawa Keisuke"},{"name":"Fujita Yoshiko"},{"name":"Kondo Shuji"},{"name":"Kagami Shoji"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tsuchiya Koichiro"},{"name":"Tomita Shuhei"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"井澤 有紀"},{"name":"吉栖 正典"},{"name":"石澤 啓介"},{"name":"Fujita Yoshiko"},{"name":"近藤 秀治"},{"name":"香美 祥二"},{"name":"川添 和義"},{"name":"土屋 浩一郎"},{"name":"冨田 修平"},{"name":"玉置 俊晃"}]},"description":{"en":"Big mitogen-activated protein kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a newly identified member of the mitogen-activated protein (MAP) kinase family. Recently, several studies have suggested that BMK1 plays an important role in the pathogenesis of cardiovascular disease. To clarify the pathophysiological significance of BMK1 in the process of vascular remodeling, we explored the molecular mechanisms of BMK1 activation in vascular smooth muscle cells (VSMCs). From the results of co-immunoprecipitation and immunoblotting analyses, it was found that platelet-derived growth factor (PDGF), a known potent mitogen, activated BMK1 and triggered the Gab1-SHP-2 interaction in rat aortic smooth muscle cells (RASMCs). The abrogation of SHP-2 phosphatase activity by transfection of the SHP-2-C/S mutant suppressed PDGF-stimulated BMK1 activation. Infection with an adenoviral vector expressing dominant-negative MEK5alpha, which can suppress PDGF-stimulated BMK1 activation to the control level, inhibited PDGF-induced RASMC migration. Moreover, we observed an increase of BMK1 activation in injured mouse femoral arteries. From these findings, it is suggested that BMK1 activation leads to VSMC migration induced by PDGF via Gab1-SHP-2 interaction, and that BMK1-mediated VSMC migration may play a role in the pathogenesis of vascular remodeling.","ja":"Big mitogen-activated protein kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a newly identified member of the mitogen-activated protein (MAP) kinase family. Recently, several studies have suggested that BMK1 plays an important role in the pathogenesis of cardiovascular disease. To clarify the pathophysiological significance of BMK1 in the process of vascular remodeling, we explored the molecular mechanisms of BMK1 activation in vascular smooth muscle cells (VSMCs). From the results of co-immunoprecipitation and immunoblotting analyses, it was found that platelet-derived growth factor (PDGF), a known potent mitogen, activated BMK1 and triggered the Gab1-SHP-2 interaction in rat aortic smooth muscle cells (RASMCs). The abrogation of SHP-2 phosphatase activity by transfection of the SHP-2-C/S mutant suppressed PDGF-stimulated BMK1 activation. Infection with an adenoviral vector expressing dominant-negative MEK5alpha, which can suppress PDGF-stimulated BMK1 activation to the control level, inhibited PDGF-induced RASMC migration. Moreover, we observed an increase of BMK1 activation in injured mouse femoral arteries. From these findings, it is suggested that BMK1 activation leads to VSMC migration induced by PDGF via Gab1-SHP-2 interaction, and that BMK1-mediated VSMC migration may play a role in the pathogenesis of vascular remodeling."},"publication_date":"2007-11","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.30","number":"No.11","starting_page":"1107","ending_page":"1117","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1291/hypres.30.1107"],"issn":["0916-9636"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:128, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16974068","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=160314","label":"url"}],"paper_title":{"en":"The novel Src kinase inhibitor M475271 inhibits VEGF-induced vascular endothelial-cadherin and β-catenin phosphorylation but increases their association","ja":"The novel Src kinase inhibitor M475271 inhibits VEGF-induced vascular endothelial-cadherin and β-catenin phosphorylation but increases their association"},"authors":{"en":[{"name":"Nermin Ali"},{"name":"Yoshizumi Masanori"},{"name":"Yano Seiji"},{"name":"Sone Saburo"},{"name":"Ohnishi Hideki"},{"name":"Ishizawa Keisuke"},{"name":"Kanematsu Yasuhisa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Nermin Ali"},{"name":"吉栖 正典"},{"name":"矢野 聖二"},{"name":"曽根 三郎"},{"name":"大西 秀樹"},{"name":"石澤 啓介"},{"name":"兼松 康久"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"M475271, 4-quinazolinamine, N-(2-chloro-5-methoxyphenyl)-6-methoxy-7-[(1-methyl-4-piperidinyl) methoxy]-(9Cl), is a new anilinoquinazoline derivative that displays selective inhibition of Src kinase activity and tumor growth in vivo. Vascular endothelial growth factor (VEGF)-induced angiogenesis plays a pivotal role in tumor growth and metastasis. Vascular endothelial (VE)-cadherin is an endothelial cell-specific adhesion molecule that can interact with the cytoskeleton via several anchoring molecules such as beta-catenin. Here, we examined the effect of M475271 on VE-cadherin and beta-catenin phosphorylation and association. We also examined its effect on VEGF-induced human umbilical vein endothelial cell (HUVEC) proliferation, migration, and tube formation. The findings reveal pretreatment with M475271 significantly inhibits VEGF-induced VE-cadherin and beta-catenin phosphorylation. However, M475271 significantly increases VE-cadherin and beta-catenin association compared to the VEGF-treated group. Confocal laser microscopic examination confirmed the augmentation effect of M475271 on VE-cadherin and beta-catenin association. Finally, M475271 was shown to have inhibitory effects comparable to those of PP2 and Herbimycin A on VEGF-induced HUVEC proliferation, migration, and tube formation. These findings suggest that M475271 attenuates VEGF-induced angiogenesis by maintaining cell-cell junction stability. Although the involvement of other signaling molecules cannot be ruled out, M475271 has potential as a drug for the inhibition of the angiogenesis needed for tumor growth and metastasis.","ja":"M475271, 4-quinazolinamine, N-(2-chloro-5-methoxyphenyl)-6-methoxy-7-[(1-methyl-4-piperidinyl) methoxy]-(9Cl), is a new anilinoquinazoline derivative that displays selective inhibition of Src kinase activity and tumor growth in vivo. Vascular endothelial growth factor (VEGF)-induced angiogenesis plays a pivotal role in tumor growth and metastasis. Vascular endothelial (VE)-cadherin is an endothelial cell-specific adhesion molecule that can interact with the cytoskeleton via several anchoring molecules such as beta-catenin. Here, we examined the effect of M475271 on VE-cadherin and beta-catenin phosphorylation and association. We also examined its effect on VEGF-induced human umbilical vein endothelial cell (HUVEC) proliferation, migration, and tube formation. The findings reveal pretreatment with M475271 significantly inhibits VEGF-induced VE-cadherin and beta-catenin phosphorylation. However, M475271 significantly increases VE-cadherin and beta-catenin association compared to the VEGF-treated group. Confocal laser microscopic examination confirmed the augmentation effect of M475271 on VE-cadherin and beta-catenin association. Finally, M475271 was shown to have inhibitory effects comparable to those of PP2 and Herbimycin A on VEGF-induced HUVEC proliferation, migration, and tube formation. These findings suggest that M475271 attenuates VEGF-induced angiogenesis by maintaining cell-cell junction stability. Although the involvement of other signaling molecules cannot be ruled out, M475271 has potential as a drug for the inhibition of the angiogenesis needed for tumor growth and metastasis."},"publication_date":"2006-09-15","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.102","number":"No.1","starting_page":"112","ending_page":"120","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.FP0060357"],"issn":["1347-8613"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:129, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16990703","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=160315","label":"url"}],"paper_title":{"en":"Calcium and reactive oxygen species mediated Zn2+-induced apoptosis in PC12 cells","ja":"Calcium and reactive oxygen species mediated Zn2+-induced apoptosis in PC12 cells"},"authors":{"en":[{"name":"Abe Shinji"},{"name":"Ohnishi Hideki"},{"name":"Tsuchiya Koichiro"},{"name":"Ishizawa Keisuke"},{"name":"Torii Mayumi"},{"name":"Kanematsu Yasuhisa"},{"name":"Kawazoe Kazuyoshi"},{"name":"Minakuchi Kazuo"},{"name":"Yoshizumi Masanori"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"阿部 真治"},{"name":"大西 秀樹"},{"name":"土屋 浩一郎"},{"name":"石澤 啓介"},{"name":"鳥井 真由美"},{"name":"兼松 康久"},{"name":"川添 和義"},{"name":"水口 和生"},{"name":"吉栖 正典"},{"name":"玉置 俊晃"}]},"description":{"en":"The release of excessive Zn(2+) from presynaptic boutons into extracellular regions contributes to neuronal apoptotic events, which result in neuronal cell death. However, the mechanisms of Zn(2+)-induced neuronal cell death are still unclear. Therefore, we investigated the dynamics of intracellular Zn(2+), calcium, and reactive oxygen species in PC12 cells. The addition of Zn(2+) produced cell death in a concentration- and time-dependent manner. (45)Ca(2+) influx occurred just after the treatment with Zn(2+), although subsequent hydroxyl radical ((*)OH) production did not begin until 3 h after Zn(2+) exposure. (*)OH production was significantly attenuated in Ca(2+)-free medium or by L-type Ca(2+) channel antagonist treatment, but it was independent of the intracellular Zn(2+) content. Dantrolene treatment had no protective effects against Zn(2+)-induced cell death. Treatment with N-acetyl-L-cysteine blocked (*)OH generation and subsequent cell death. These data indicate that Ca(2+) influx and subsequent (*)OH production are critical events in Zn(2+)-induced toxicity in PC12 cells.","ja":"The release of excessive Zn(2+) from presynaptic boutons into extracellular regions contributes to neuronal apoptotic events, which result in neuronal cell death. However, the mechanisms of Zn(2+)-induced neuronal cell death are still unclear. Therefore, we investigated the dynamics of intracellular Zn(2+), calcium, and reactive oxygen species in PC12 cells. The addition of Zn(2+) produced cell death in a concentration- and time-dependent manner. (45)Ca(2+) influx occurred just after the treatment with Zn(2+), although subsequent hydroxyl radical ((*)OH) production did not begin until 3 h after Zn(2+) exposure. (*)OH production was significantly attenuated in Ca(2+)-free medium or by L-type Ca(2+) channel antagonist treatment, but it was independent of the intracellular Zn(2+) content. Dantrolene treatment had no protective effects against Zn(2+)-induced cell death. Treatment with N-acetyl-L-cysteine blocked (*)OH generation and subsequent cell death. These data indicate that Ca(2+) influx and subsequent (*)OH production are critical events in Zn(2+)-induced toxicity in PC12 cells."},"publication_date":"2006-09","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.102","number":"No.1","starting_page":"103","ending_page":"111","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.FP0060342"],"issn":["1347-8613"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:130, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16832158","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=160310","label":"url"}],"paper_title":{"en":"Effects of angiotensin II type 1 receptor blockade on the systemic blood nitric oxide dynamics in Nω-nitro-L-arginine methyl ester-treated rats","ja":"Effects of angiotensin II type 1 receptor blockade on the systemic blood nitric oxide dynamics in Nω-nitro-L-arginine methyl ester-treated rats"},"authors":{"en":[{"name":"Kanematsu Yasuhisa"},{"name":"Tsuchiya Koichiro"},{"name":"Onishi Hideki"},{"name":"Motobayashi Yuki"},{"name":"Izawa Yuki"},{"name":"Ishihara Manabu"},{"name":"Ishizawa Keisuke"},{"name":"Abe Shinji"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"兼松 康久"},{"name":"土屋 浩一郎"},{"name":"大西 秀樹"},{"name":"元林 有紀"},{"name":"井澤 有紀"},{"name":"石原 学"},{"name":"石澤 啓介"},{"name":"阿部 真治"},{"name":"川添 和義"},{"name":"玉置 俊晃"}]},"description":{"en":"We previously succeeded in measuring the nitrosylhemoglobin (HbNO) level as an index of blood nitric oxide (NO) by the electron paramagnetic resonance (EPR) HbNO signal subtraction method. In this study, we examined the effects of olmesartan, an angiotensin II type 1 receptor blocker (ARB), on NO dynamics in N(omega)-nitro-L-arginine methyl ester (L-NAME)-treated rats by the EPR-subtraction method. Oral administration of L-NAME for 2 weeks induced serious hypertension, and the HbNO concentration was reduced to 37.6% of the level in controls. Coadministration of olmesartan improved hypertension and increased the blood HbNO concentration of L-NAME-treated rats. In contrast, coadministration of hydralazine improved hypertension but did not affect the blood HbNO concentration. In conclusion, our findings suggested that chronic administration of olmesartan ameliorated the endothelial dysfunction in L-NAME-treated rats.","ja":"We previously succeeded in measuring the nitrosylhemoglobin (HbNO) level as an index of blood nitric oxide (NO) by the electron paramagnetic resonance (EPR) HbNO signal subtraction method. In this study, we examined the effects of olmesartan, an angiotensin II type 1 receptor blocker (ARB), on NO dynamics in N(omega)-nitro-L-arginine methyl ester (L-NAME)-treated rats by the EPR-subtraction method. Oral administration of L-NAME for 2 weeks induced serious hypertension, and the HbNO concentration was reduced to 37.6% of the level in controls. Coadministration of olmesartan improved hypertension and increased the blood HbNO concentration of L-NAME-treated rats. In contrast, coadministration of hydralazine improved hypertension but did not affect the blood HbNO concentration. In conclusion, our findings suggested that chronic administration of olmesartan ameliorated the endothelial dysfunction in L-NAME-treated rats."},"publication_date":"2006-05","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.29","number":"No.5","starting_page":"369","ending_page":"374","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1291/hypres.29.369"],"issn":["0916-9636"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:131, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16322069","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-32644452665&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=139866","label":"url"}],"paper_title":{"en":"Transactivation of fetal liver kinase-1/kinase-insert domain-containing receptor by lysophosphatidylcholine induces vascular endothelial cell proliferation.","ja":"Transactivation of fetal liver kinase-1/kinase-insert domain-containing receptor by lysophosphatidylcholine induces vascular endothelial cell proliferation."},"authors":{"en":[{"name":"Fujita Yoshiko"},{"name":"Yoshizumi Masanori"},{"name":"Izawa Yuki"},{"name":"Ali Nermin"},{"name":"Kanematsu Yasuhisa"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"藤田 佳子"},{"name":"吉栖 正典"},{"name":"井澤 有紀"},{"name":"アリ ネルミン"},{"name":"兼松 康久"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Lysophosphatidylcholine (LPC), a major lipid component of oxidized low-density lipoprotein, is a bioactive lipid molecule involved in numerous biological processes including the progression of atherosclerosis. Recently orphan G protein-coupled receptors were identified as high-affinity receptors for LPC. Although several G protein-coupled receptor ligands transactivate receptor tyrosine kinases, LPC-stimulated transactivation of receptor tyrosine kinase has not yet been reported. Here we observed for the first time that LPC treatment of human umbilical vein endothelial cells (HUVECs) induces tyrosyl phosphorylation of vascular endothelial growth factor receptor 2 [fetal liver kinase-1/kinase-insert domain-containing receptor, Flk-1/KDR)]. Flk-1/KDR transactivation by LPC was inhibited by vascular endothelial growth factor receptor tyrosine kinase inhibitors, SU1498 and 4-[(4'-chloro-2'-fluoro) phenylamino]6,7-dimethoxyquinazoline (VTKi) in immunoprecipitation. Furthermore, we examined the effects of the Src family kinases inhibitors, herbimycin A and 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d] pyrimidine (PP2), on LPC-induced Flk-1/KDR transactivation. Results from Western blots, c-Src is involved in LPC-induced Flk-1/KDR transactivation because herbimycin A and PP2 inhibited this transactivation. Kinase-inactive (KI) Src transfection also inhibited LPC-induced Flk-1/KDR transactivation. In addition, results from Western blots, ERK1/2 and Akt, which are downstream effectors of Flk-1/KDR, were also activated by LPC, and this was inhibited by SU1498, VTKi, herbimycin A, PP2, and KI Src transfection in HUVECs. LPC-induced stimulation of HUVEC proliferation was shown to be secondary to transactivation because it was suppressed by SU1498, VTKi, herbimycin A, PP2, and KI Src transfection in dimethylthiazoldiphenyltetra-zoliumbromide assay. These findings suggest that LPC-induced Flk-1/KDR transactivation via c-Src may have important implications for the progression of atherosclerosis.","ja":"Lysophosphatidylcholine (LPC), a major lipid component of oxidized low-density lipoprotein, is a bioactive lipid molecule involved in numerous biological processes including the progression of atherosclerosis. Recently orphan G protein-coupled receptors were identified as high-affinity receptors for LPC. Although several G protein-coupled receptor ligands transactivate receptor tyrosine kinases, LPC-stimulated transactivation of receptor tyrosine kinase has not yet been reported. Here we observed for the first time that LPC treatment of human umbilical vein endothelial cells (HUVECs) induces tyrosyl phosphorylation of vascular endothelial growth factor receptor 2 [fetal liver kinase-1/kinase-insert domain-containing receptor, Flk-1/KDR)]. Flk-1/KDR transactivation by LPC was inhibited by vascular endothelial growth factor receptor tyrosine kinase inhibitors, SU1498 and 4-[(4'-chloro-2'-fluoro) phenylamino]6,7-dimethoxyquinazoline (VTKi) in immunoprecipitation. Furthermore, we examined the effects of the Src family kinases inhibitors, herbimycin A and 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d] pyrimidine (PP2), on LPC-induced Flk-1/KDR transactivation. Results from Western blots, c-Src is involved in LPC-induced Flk-1/KDR transactivation because herbimycin A and PP2 inhibited this transactivation. Kinase-inactive (KI) Src transfection also inhibited LPC-induced Flk-1/KDR transactivation. In addition, results from Western blots, ERK1/2 and Akt, which are downstream effectors of Flk-1/KDR, were also activated by LPC, and this was inhibited by SU1498, VTKi, herbimycin A, PP2, and KI Src transfection in HUVECs. LPC-induced stimulation of HUVEC proliferation was shown to be secondary to transactivation because it was suppressed by SU1498, VTKi, herbimycin A, PP2, and KI Src transfection in dimethylthiazoldiphenyltetra-zoliumbromide assay. These findings suggest that LPC-induced Flk-1/KDR transactivation via c-Src may have important implications for the progression of atherosclerosis."},"publication_date":"2006-03","publication_name":{"en":"Endocrinology","ja":"Endocrinology"},"volume":"Vol.147","number":"No.3","starting_page":"1377","ending_page":"1385","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1210/en.2005-0644"],"issn":["0013-7227"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:132, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15921682","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=131104","label":"url"}],"paper_title":{"en":"ERK1/2 activation by angiotensin II inhibits insulin-induced glucose uptake in vascular smooth muscle cells","ja":"ERK1/2 activation by angiotensin II inhibits insulin-induced glucose uptake in vascular smooth muscle cells"},"authors":{"en":[{"name":"Izawa Yuki"},{"name":"Yoshizumi Masanori"},{"name":"Ishizawa Keisuke"},{"name":"Fujita Yoshiko"},{"name":"Kondo Shuji"},{"name":"Kagami Shoji"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tsuchiya Koichiro"},{"name":"Tomita Shuhei"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"井澤 有紀"},{"name":"吉栖 正典"},{"name":"石澤 啓介"},{"name":"藤田 佳子"},{"name":"近藤 秀治"},{"name":"香美 祥二"},{"name":"川添 和義"},{"name":"土屋 浩一郎"},{"name":"冨田 修平"},{"name":"玉置 俊晃"}]},"description":{"en":"Clinical evidence suggests a relationship between hypertension and insulin resistance, and cross-talk between angiotensin II (Ang II) and insulin signaling pathways may take place. We now report the effect of Ang II on insulin-induced glucose uptake and its intracellular mechanisms in vascular smooth muscle cells (VSMC). We examined the translocation of glucose transporter-4 (GLUT-4) and glucose uptake in rat aortic smooth muscle cells (RASMC). Mitogen-activated protein (MAP) kinases and Akt activities, and phosphorylation of insulin receptor substrate-1 (IRS-1) at the serine and tyrosine residues were measured by immunoprecipitation and immunoblotting. As a result, Ang II inhibited insulin-induced GLUT-4 translocation from cytoplasm to the plasma membrane in RASMC. Ang II induced extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) activation and IRS-1 phosphorylation at Ser307 and Ser616. Ang II-induced Ser307 and Ser616 phophorylation of IRS-1 was inhibited by a MEK inhibitor, PD98059, and a JNK inhibitor, SP600125. Ang II inhibition of insulin-stimulated IRS-1 tyrosyl phophorylation and Akt activation were reversed by PD98059 but not by SP600125. Ang II inhibited insulin-induced glucose uptake, which was also reversed by PD98059 but not by SP600125. It is shown that Ang II-induced ERK1/2 activation inhibits insulin-dependent glucose uptake through serine phophorylation of IRS-1 in RASMC.","ja":"Clinical evidence suggests a relationship between hypertension and insulin resistance, and cross-talk between angiotensin II (Ang II) and insulin signaling pathways may take place. We now report the effect of Ang II on insulin-induced glucose uptake and its intracellular mechanisms in vascular smooth muscle cells (VSMC). We examined the translocation of glucose transporter-4 (GLUT-4) and glucose uptake in rat aortic smooth muscle cells (RASMC). Mitogen-activated protein (MAP) kinases and Akt activities, and phosphorylation of insulin receptor substrate-1 (IRS-1) at the serine and tyrosine residues were measured by immunoprecipitation and immunoblotting. As a result, Ang II inhibited insulin-induced GLUT-4 translocation from cytoplasm to the plasma membrane in RASMC. Ang II induced extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) activation and IRS-1 phosphorylation at Ser307 and Ser616. Ang II-induced Ser307 and Ser616 phophorylation of IRS-1 was inhibited by a MEK inhibitor, PD98059, and a JNK inhibitor, SP600125. Ang II inhibition of insulin-stimulated IRS-1 tyrosyl phophorylation and Akt activation were reversed by PD98059 but not by SP600125. Ang II inhibited insulin-induced glucose uptake, which was also reversed by PD98059 but not by SP600125. It is shown that Ang II-induced ERK1/2 activation inhibits insulin-dependent glucose uptake through serine phophorylation of IRS-1 in RASMC."},"publication_date":"2005-08-15","publication_name":{"en":"Experimental Cell Research","ja":"Experimental Cell Research"},"volume":"Vol.308","number":"No.2","starting_page":"291","ending_page":"299","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.yexcr.2005.04.028"],"issn":["0014-4827"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:133, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16087789","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=139855","label":"url"}],"paper_title":{"en":"Aldosterone stimulates vascular smooth muscle cell proliferation via big mitoten-activated protein kinase 1 activation","ja":"Aldosterone stimulates vascular smooth muscle cell proliferation via big mitoten-activated protein kinase 1 activation"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Izawa Yuki"},{"name":"Ito Hiroyuki"},{"name":"Miki Chieko"},{"name":"Miyama Kayoko"},{"name":"Fujita Yoshiko"},{"name":"Kanematsu Yasuhisa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"},{"name":"Nishiyama Akira"},{"name":"Yoshizumi Masanori"}],"ja":[{"name":"石澤 啓介"},{"name":"井澤 有紀"},{"name":"伊藤 浩敬"},{"name":"Miki Chieko"},{"name":"Miyama Kayoko"},{"name":"藤田 佳子"},{"name":"兼松 康久"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"},{"name":"西山 成"},{"name":"吉栖 正典"}]},"description":{"en":"The nongenomic effects of aldosterone have been implicated in the pathogenesis of various cardiovascular diseases. Aldosterone-induced nongenomic effects are attributable in part to the activation of extracellular signal-regulated kinase 1/2 (ERK1/2), a classical mitogen-activated protein (MAP) kinase. Big MAP kinase 1 (BMK1), a newly identified MAP kinase, has been shown to be involved in cell proliferation, differentiation, and survival. We examined whether aldosterone stimulates BMK1-mediated proliferation of cultured rat aortic smooth muscle cells (RASMCs). Mineralocorticoid receptor (MR) expression and localization were evaluated by Western blotting analysis and fluorolabeling methods. ERK1/2 and BMK1 activities were measured by Western blotting analysis with the respective phosphospecific antibodies. Cell proliferation was determined by Alamar Blue colorimetric assay. Aldosterone (0.1 to 100 nmol/L) dose-dependently activated BMK1 in RASMCs, with a peak at 30 minutes. To clarify whether aldosterone-induced BMK1 activation is an MR-mediated phenomenon, we examined the effect of eplerenone, a selective MR antagonist, on aldosterone-induced BMK1 activation. Eplerenone (0.1 to 10 micromol/L) dose-dependently inhibited aldosterone-induced BMK1 activation in RASMCs. Aldosterone also stimulated RASMC proliferation, which was inhibited by eplerenone. Aldosterone-mediated phenomena were concluded to be attributable to a nongenomic effect because cycloheximide failed to inhibit aldosterone-induced BMK1 activation. Transfection of dominant-negative MAP kinase/ERK kinase 5 (MEK5), which is an upstream regulator of BMK1, partially inhibited aldosterone-induced RASMC proliferation, which was almost completely inhibited by MEK inhibitor PD98059. In addition to the classical steroid activity, rapid nongenomic effects induced by aldosterone may represent an alternative etiology for vascular diseases such as hypertension.","ja":"The nongenomic effects of aldosterone have been implicated in the pathogenesis of various cardiovascular diseases. Aldosterone-induced nongenomic effects are attributable in part to the activation of extracellular signal-regulated kinase 1/2 (ERK1/2), a classical mitogen-activated protein (MAP) kinase. Big MAP kinase 1 (BMK1), a newly identified MAP kinase, has been shown to be involved in cell proliferation, differentiation, and survival. We examined whether aldosterone stimulates BMK1-mediated proliferation of cultured rat aortic smooth muscle cells (RASMCs). Mineralocorticoid receptor (MR) expression and localization were evaluated by Western blotting analysis and fluorolabeling methods. ERK1/2 and BMK1 activities were measured by Western blotting analysis with the respective phosphospecific antibodies. Cell proliferation was determined by Alamar Blue colorimetric assay. Aldosterone (0.1 to 100 nmol/L) dose-dependently activated BMK1 in RASMCs, with a peak at 30 minutes. To clarify whether aldosterone-induced BMK1 activation is an MR-mediated phenomenon, we examined the effect of eplerenone, a selective MR antagonist, on aldosterone-induced BMK1 activation. Eplerenone (0.1 to 10 micromol/L) dose-dependently inhibited aldosterone-induced BMK1 activation in RASMCs. Aldosterone also stimulated RASMC proliferation, which was inhibited by eplerenone. Aldosterone-mediated phenomena were concluded to be attributable to a nongenomic effect because cycloheximide failed to inhibit aldosterone-induced BMK1 activation. Transfection of dominant-negative MAP kinase/ERK kinase 5 (MEK5), which is an upstream regulator of BMK1, partially inhibited aldosterone-induced RASMC proliferation, which was almost completely inhibited by MEK inhibitor PD98059. In addition to the classical steroid activity, rapid nongenomic effects induced by aldosterone may represent an alternative etiology for vascular diseases such as hypertension."},"publication_date":"2005-08-08","publication_name":{"en":"Hypertension","ja":"Hypertension"},"volume":"Vol.46","number":"No.4","starting_page":"1046","ending_page":"1052","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1161/01.HYP.0000172622.51973.f5"],"issn":["1524-4563"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:134, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://www.jstage.jst.go.jp/article/jphs/98/2/98_130/_article/-char/ja/","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15937404","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=131109","label":"url"}],"paper_title":{"en":"A Novel Src Kinase Inhibitor, M475271, Inhibits VEGF-Induced Human Umbilical Vein Endothelial Cell Proliferation and Migration","ja":"A Novel Src Kinase Inhibitor, M475271, Inhibits VEGF-Induced Human Umbilical Vein Endothelial Cell Proliferation and Migration"},"authors":{"en":[{"name":"Nermin Ali"},{"name":"Yoshizumi Masanori"},{"name":"Fujita Yoshiko"},{"name":"Izawa Yuki"},{"name":"Kanematsu Yasuhisa"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Yano Seiji"},{"name":"Sone Saburo"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Nermin Ali"},{"name":"吉栖 正典"},{"name":"Fujita Yoshiko"},{"name":"井澤 有紀"},{"name":"兼松 康久"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"矢野 聖二"},{"name":"曽根 三郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Vascular endothelial growth factor (VEGF) was reported to be a potent proangiogenic factor that plays a pivotal role in both physiological and pathological angiogenesis. M475271, 4-quinazolinamine, N-(2-chloro-5-methoxyphenyl)-6-methoxy-7-[(1-methyl-4-piperidinyl) methoxy]-(9Cl), is a new anilinoquinazoline derivative that showed selective inhibition of Src kinase activity and tumor growth in vivo. Here, we examined the effect of M475271 on VEGF-induced human umbilical vein endothelial cell (HUVEC) proliferation and migration and their intracellular mechanisms. Our findings showed that M475271 pretreatment resulted in a significant inhibition of VEGF-induced HUVEC proliferation, [(3)H]thymidine incorporation, and migration. M475271 inhibited VEGF-induced Flk-1 and Src phosphorylation and their association. Confocal laser microscopic examination confirmed the inhibitory effect of M475271 on VEGF-induced Flk-1/Src association. M475271 inhibited VEGF-induced extracellular signal-regulated kinase1/2 (ERK1/2) and p38 but not Akt activation in a concentration-dependent manner. M475271, PI3-K inhibitor, and p38 inhibitor inhibited VEGF-induced HUVEC proliferation and migration. However, a MEK1/2 inhibitor inhibited VEGF-induced proliferation but not migration. These findings suggest that M475271 attenuates VEGF-induced HUVEC proliferation and migration through the inhibition of signaling pathways involving Src, ERK1/2, and/or p38. Taken together, these data indicate that M475271 may be a useful candidate for inhibition of endothelial cell proliferation and migration relevant to angiogenesis.","ja":"Vascular endothelial growth factor (VEGF) was reported to be a potent proangiogenic factor that plays a pivotal role in both physiological and pathological angiogenesis. M475271, 4-quinazolinamine, N-(2-chloro-5-methoxyphenyl)-6-methoxy-7-[(1-methyl-4-piperidinyl) methoxy]-(9Cl), is a new anilinoquinazoline derivative that showed selective inhibition of Src kinase activity and tumor growth in vivo. Here, we examined the effect of M475271 on VEGF-induced human umbilical vein endothelial cell (HUVEC) proliferation and migration and their intracellular mechanisms. Our findings showed that M475271 pretreatment resulted in a significant inhibition of VEGF-induced HUVEC proliferation, [(3)H]thymidine incorporation, and migration. M475271 inhibited VEGF-induced Flk-1 and Src phosphorylation and their association. Confocal laser microscopic examination confirmed the inhibitory effect of M475271 on VEGF-induced Flk-1/Src association. M475271 inhibited VEGF-induced extracellular signal-regulated kinase1/2 (ERK1/2) and p38 but not Akt activation in a concentration-dependent manner. M475271, PI3-K inhibitor, and p38 inhibitor inhibited VEGF-induced HUVEC proliferation and migration. However, a MEK1/2 inhibitor inhibited VEGF-induced proliferation but not migration. These findings suggest that M475271 attenuates VEGF-induced HUVEC proliferation and migration through the inhibition of signaling pathways involving Src, ERK1/2, and/or p38. Taken together, these data indicate that M475271 may be a useful candidate for inhibition of endothelial cell proliferation and migration relevant to angiogenesis."},"publication_date":"2005-06-04","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.98","number":"No.2","starting_page":"130","ending_page":"141","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.FP0040850"],"issn":["1347-8613"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:135, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/110001240344/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282679753550336/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=160301","label":"url"}],"paper_title":{"en":"徳島大学病院におけるTPN処方設計支援ソフトの使用評価と改良","ja":"徳島大学病院におけるTPN処方設計支援ソフトの使用評価と改良"},"authors":{"en":[{"name":"生田 雅子"},{"name":"会田 真規"},{"name":"Ishizawa Keisuke"},{"name":"Minakuchi Kazuo"},{"name":"Tsuchiya Koichiro"},{"name":"Kihara Masaru"},{"name":"Yamauchi Aiko"}],"ja":[{"name":"生田 雅子"},{"name":"会田 真規"},{"name":"石澤 啓介"},{"name":"水口 和生"},{"name":"土屋 浩一郎"},{"name":"木原 勝"},{"name":"山内 あい子"}]},"description":{"en":"Fluid therapy is a fundamental treatment for almost all inpatients, and nutritional therapy is the most important type of such therapy. Currently, total parenteral nutrition (TPN) is widely used to provide complete nutritional support but 30-40% of TPN recipients are considered to in a malnourished state due to inappropriate TPN prescriptions. Computer-assisted TPN prescription systems are thought to be useful to clinical professionals in solving this problem because they can perform complicated calculations that make it easy to draw up correct TPN prescriptions. So, we made a prototype system for aiding the preparation of TPN prescriptions based on Microsoft^[ !R] EXCEL and it was tested by physicians, pharmacists, dietitians and nurses engaged in TPN therapy at Tokushima University Hospital. We also had them fill out a questionnaire on the system in which they rated it for ease of operation and usefulness according to a scoring system in which 5 indicated full marks. Our Computer-Assisted TPN Prescription System was improved on the basis of the questionnaire results and is now being effectively used by the nutrition support team (NST) in Tokushima University Hospital.","ja":"Fluid therapy is a fundamental treatment for almost all inpatients, and nutritional therapy is the most important type of such therapy. Currently, total parenteral nutrition (TPN) is widely used to provide complete nutritional support but 30-40% of TPN recipients are considered to in a malnourished state due to inappropriate TPN prescriptions. Computer-assisted TPN prescription systems are thought to be useful to clinical professionals in solving this problem because they can perform complicated calculations that make it easy to draw up correct TPN prescriptions. So, we made a prototype system for aiding the preparation of TPN prescriptions based on Microsoft^[ !R] EXCEL and it was tested by physicians, pharmacists, dietitians and nurses engaged in TPN therapy at Tokushima University Hospital. We also had them fill out a questionnaire on the system in which they rated it for ease of operation and usefulness according to a scoring system in which 5 indicated full marks. Our Computer-Assisted TPN Prescription System was improved on the basis of the questionnaire results and is now being effectively used by the nutrition support team (NST) in Tokushima University Hospital."},"publication_date":"2005-04-10","publication_name":{"en":"Japanese Journal of Pharmaceutical Health Care and Sciences","ja":"医療薬学"},"volume":"Vol.31","number":"No.4","starting_page":"279","ending_page":"286","languages":["jpn"],"referee":true,"identifiers":{"doi":["10.5649/jjphcs.31.279"],"issn":["1346-342X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:136, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15297771","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=113755","label":"url"}],"paper_title":{"en":"Antioxidant effects of stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on angiotensin II-stimulated MAP kinase activation and vascular smooth muscle cell proliferation","ja":"Antioxidant effects of stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on angiotensin II-stimulated MAP kinase activation and vascular smooth muscle cell proliferation"},"authors":{"en":[{"name":"Kyaw Moe"},{"name":"Yoshizumi Masanori"},{"name":"Tsuchiya Koichiro"},{"name":"Izawa Yuki"},{"name":"Kanematsu Yasuhisa"},{"name":"Fujita Yoshiko"},{"name":"Ali Nermin"},{"name":"Ishizawa Keisuke"},{"name":"Yamauchi Aiko"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Kyaw Moe"},{"name":"吉栖 正典"},{"name":"土屋 浩一郎"},{"name":"井澤 有紀"},{"name":"兼松 康久"},{"name":"藤田 佳子"},{"name":"Ali Nermin"},{"name":"石澤 啓介"},{"name":"山内 あい子"},{"name":"玉置 俊晃"}]},"description":{"en":"We examined the effects of the stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on cellular glutathione (GSH) concentration and whether NAC-regulated cellular GSH levels are directly associated with angiotensin II (Ang II)-induced intracellular signaling events in vascular smooth muscle cells (VSMC). Both L-NAC and D-NAC similarly increased intracellular GSH concentration. We found that L-NAC and D-NAC both inhibited Ang II-induced c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and [(3)H]-thymidine incorporation in VSMC. Our present study indicates the comparable effects of NAC stereoisomers in regulating intracellular GSH and the redox-dependent intracellular signaling mechanisms in VSMC.","ja":"We examined the effects of the stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on cellular glutathione (GSH) concentration and whether NAC-regulated cellular GSH levels are directly associated with angiotensin II (Ang II)-induced intracellular signaling events in vascular smooth muscle cells (VSMC). Both L-NAC and D-NAC similarly increased intracellular GSH concentration. We found that L-NAC and D-NAC both inhibited Ang II-induced c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and [(3)H]-thymidine incorporation in VSMC. Our present study indicates the comparable effects of NAC stereoisomers in regulating intracellular GSH and the redox-dependent intracellular signaling mechanisms in VSMC."},"publication_date":"2004-08-05","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.95","number":"No.4","starting_page":"483","ending_page":"486","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.SC0040061"],"issn":["1347-8613"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:137, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15253109","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=113754","label":"url"}],"paper_title":{"en":"Dual effects of endothelin-1 (1-31): induction of mesangial cell migration and facilitation of monocyte recruitment through monocyte chemoattractant protein-1 production by mesangial cells","ja":"Dual effects of endothelin-1 (1-31): induction of mesangial cell migration and facilitation of monocyte recruitment through monocyte chemoattractant protein-1 production by mesangial cells"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Yoshizumi Masanori"},{"name":"Tsuchiya Koichiro"},{"name":"Houchi Hitoshi"},{"name":"Minakuchi Kazuo"},{"name":"Izawa Yuki"},{"name":"Kanematsu Yasuhisa"},{"name":"Kagami Shoji"},{"name":"Hirose Masao"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"吉栖 正典"},{"name":"土屋 浩一郎"},{"name":"芳地 一"},{"name":"水口 和生"},{"name":"井澤 有紀"},{"name":"兼松 康久"},{"name":"香美 祥二"},{"name":"Hirose Masao"},{"name":"玉置 俊晃"}]},"description":{"en":"We previously found that human chymase selectively cleaves big endothelin-1 (ET-1) at the Tyr31-Gly32 bond and produces 31-amino acid endothelins, ET-1 (1-31), without any further degradation products. In this study, we investigated the effect of ET-1 (1-31) on the migration of cultured rat mesangial cells (RMCs) and on cells of the human monocytic cell line, THP-1. In addition, we examined the interaction between RMCs and THP-1 cells using conditioned media from ET-1 (1-31)-stimulated RMCs. ET-1 (1-31) caused an increase in RMC migration in a concentration-dependent manner, and the degree of increase was similar to those by ET-1 and angiotensin II (All). The ET-1 (1-31)-induced increase in RMC migration was inhibited by BQ123, an endothelin ETA receptor antagonist, but not by BQ788, an endothelin ETB receptor antagonist. ET-1 (1-31) alone did not cause significant migration of THP-1 cells. However, significant recruitment of THP-1 cells was observed with conditioned media taken from ET-1 (1-31)-stimulated RMCs. The conditioned media-induced migration of THP-1 cells was inhibited by BQ123, but not by BQ788. Western blotting analysis of the lysate of RMCs revealed that the expression of monocyte chemoattractant protein-1 (MCP-1) protein in RMCs was increased by treatment with ET-1 (1-31). The addition of neutralizing antibody for MCP-1 to the medium inhibited the migration of THP-1 cells induced by conditioned media from ET-1 (1-31)-stimulated RMCs. These findings suggest that ET-1 (1-31) play a role in glomerulonephritis (GN) via dual effects that directly cause the migration of mesangial cells (MCs) and may be responsible for the recruitment of mononuclear cells mediated through the activation of MCs. Since human chymase has been reported to be involved in glomerular disease, ET-1 (1-31) may be among the mediators.","ja":"We previously found that human chymase selectively cleaves big endothelin-1 (ET-1) at the Tyr31-Gly32 bond and produces 31-amino acid endothelins, ET-1 (1-31), without any further degradation products. In this study, we investigated the effect of ET-1 (1-31) on the migration of cultured rat mesangial cells (RMCs) and on cells of the human monocytic cell line, THP-1. In addition, we examined the interaction between RMCs and THP-1 cells using conditioned media from ET-1 (1-31)-stimulated RMCs. ET-1 (1-31) caused an increase in RMC migration in a concentration-dependent manner, and the degree of increase was similar to those by ET-1 and angiotensin II (All). The ET-1 (1-31)-induced increase in RMC migration was inhibited by BQ123, an endothelin ETA receptor antagonist, but not by BQ788, an endothelin ETB receptor antagonist. ET-1 (1-31) alone did not cause significant migration of THP-1 cells. However, significant recruitment of THP-1 cells was observed with conditioned media taken from ET-1 (1-31)-stimulated RMCs. The conditioned media-induced migration of THP-1 cells was inhibited by BQ123, but not by BQ788. Western blotting analysis of the lysate of RMCs revealed that the expression of monocyte chemoattractant protein-1 (MCP-1) protein in RMCs was increased by treatment with ET-1 (1-31). The addition of neutralizing antibody for MCP-1 to the medium inhibited the migration of THP-1 cells induced by conditioned media from ET-1 (1-31)-stimulated RMCs. These findings suggest that ET-1 (1-31) play a role in glomerulonephritis (GN) via dual effects that directly cause the migration of mesangial cells (MCs) and may be responsible for the recruitment of mononuclear cells mediated through the activation of MCs. Since human chymase has been reported to be involved in glomerular disease, ET-1 (1-31) may be among the mediators."},"publication_date":"2004-06","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.27","number":"No.6","starting_page":"433","ending_page":"440","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1291/hypres.27.433"],"issn":["0916-9636"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:138, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/14871022","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=160302","label":"url"}],"paper_title":{"en":"Inhibitory action of novel arginine derivative on catecholamine secretion evoked by acetylcholine from cultured bovine adrenal chromaffin cells","ja":"Inhibitory action of novel arginine derivative on catecholamine secretion evoked by acetylcholine from cultured bovine adrenal chromaffin cells"},"authors":{"en":[{"name":"Azuma Mami"},{"name":"Houchi Hitoshi"},{"name":"Nishisako Hirotaka"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Teraoka Kazuhiko"},{"name":"Ikehara Toshitaka"},{"name":"Kusumi Takenori"},{"name":"Minakuchi Kazuo"}],"ja":[{"name":"東 満美"},{"name":"芳地 一"},{"name":"Nishisako Hirotaka"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"Teraoka Kazuhiko"},{"name":"池原 敏孝"},{"name":"楠見 武徳"},{"name":"水口 和生"}]},"description":{"en":"A novel product, 4-amino-5-guanidinopentanoic acid 15-[(4-aminobutyl)-3-aminopropylcarbamoyl] pentadecyl ester (Arg-HSA-Spm), was synthesized based on ptilomycalin A, which is one of the extracts from marine sponge. Arg-HSA-Spm contains arginine in its chemical structure. The pharmacological action of Arg-HSA-Spm on catecholamine secretion from cultured bovine adrenal chromaffin cells was examined. Arg-HSA-Spm inhibited catecholamine secretion stimulated by the physiological secretagog acetylcholine. This inhibitory action of Arg-HSA-Spm on catecholamine secretion induced by 10(-4) M acetylcholine was dose-dependent from 10(-8) M to 10(-5) M. In the presence of 3 x 10(-7) M Arg-HSA-Spm, the stimulation of catecholamine secretion observed by increasing acetylcholine up to 10(-3) M did not reach the maximal level observed without Arg-HSA-Spm. Arg-HSA-Spm at 10(-5) M suppressed both the increase in intracellular free Ca2+ level and the influx of 45Ca2+ induced by 10(-4) M acetylcholine. The Arg-HSA-Spm-induced suppression of intracellular free Ca2+ level, the influx of 45Ca2+ and catecholamine secretion were not observed in the presence of extracellular K+ at 56 mM. The results presented in this study suggested that Arg-HSA-Spm may inhibit the influx of extracellular Ca2+ into the cells, probably through its blocking action related to acetylcholine receptors, resulting in the inhibition of catecholamine secretion in adrenal chromaffin cells.","ja":"A novel product, 4-amino-5-guanidinopentanoic acid 15-[(4-aminobutyl)-3-aminopropylcarbamoyl] pentadecyl ester (Arg-HSA-Spm), was synthesized based on ptilomycalin A, which is one of the extracts from marine sponge. Arg-HSA-Spm contains arginine in its chemical structure. The pharmacological action of Arg-HSA-Spm on catecholamine secretion from cultured bovine adrenal chromaffin cells was examined. Arg-HSA-Spm inhibited catecholamine secretion stimulated by the physiological secretagog acetylcholine. This inhibitory action of Arg-HSA-Spm on catecholamine secretion induced by 10(-4) M acetylcholine was dose-dependent from 10(-8) M to 10(-5) M. In the presence of 3 x 10(-7) M Arg-HSA-Spm, the stimulation of catecholamine secretion observed by increasing acetylcholine up to 10(-3) M did not reach the maximal level observed without Arg-HSA-Spm. Arg-HSA-Spm at 10(-5) M suppressed both the increase in intracellular free Ca2+ level and the influx of 45Ca2+ induced by 10(-4) M acetylcholine. The Arg-HSA-Spm-induced suppression of intracellular free Ca2+ level, the influx of 45Ca2+ and catecholamine secretion were not observed in the presence of extracellular K+ at 56 mM. The results presented in this study suggested that Arg-HSA-Spm may inhibit the influx of extracellular Ca2+ into the cells, probably through its blocking action related to acetylcholine receptors, resulting in the inhibition of catecholamine secretion in adrenal chromaffin cells."},"publication_date":"2003-12","publication_name":{"en":"Journal of Cardiovascular Pharmacology","ja":"Journal of Cardiovascular Pharmacology"},"volume":"Vol.42","number":"No.Suppl. 1","starting_page":"S15","ending_page":"S18","languages":["eng"],"referee":true,"invited":true,"identifiers":{"doi":["10.1097/00005344-200312001-00005"],"issn":["0160-2446"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:139, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/12145102","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=113744","label":"url"}],"paper_title":{"en":"Ebselen attenuates oxidative styress-induced apoptosis via the inhibition of the c jun N-terminal kinase and activator protein-1 signaling pathway in PC12 cells.","ja":"Ebselen attenuates oxidative styress-induced apoptosis via the inhibition of the c jun N-terminal kinase and activator protein-1 signaling pathway in PC12 cells."},"authors":{"en":[{"name":"Yoshizumi Masanori"},{"name":"Kogame Toshiaki"},{"name":"Suzaki Yuki"},{"name":"Fujita Yoshiko"},{"name":"Kyaw Moe"},{"name":"Kirima Kazuyoshi"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Kagami Shoji"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"吉栖 正典"},{"name":"Kogame Toshiaki"},{"name":"須崎 友紀"},{"name":"藤田 佳子"},{"name":"Kyaw Moe"},{"name":"桐間 一嘉"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"香美 祥二"},{"name":"玉置 俊晃"}]},"description":{"en":"1: Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one) is a selenoorganic compound exhibiting both glutathione peroxidase activity and antioxidant activity. Although it has been reported that ebselen is effective for oxidative stress-induced neuronal damage both in vivo and clinically, the precise mechanisms of the efficacy have not yet been elucidated. Thus, we hypothesized that ebselen may affect reactive oxygen species-induced mitogen-activated protein (MAP) kinase activation in cultured PC12 cells. 2: Our findings showed that hydrogen peroxide (H(2)O(2)) stimulated rapid and significant activation of extracellular signal-regulated kinase (ERK)1/2, c-Jun N-terminal kinase (JNK) and p38 in PC12 cells, which is a model of catecholamine-containing neurons. 3: H(2)O(2)-induced JNK activation was inhibited by ebselen, whereas ERK1/2 and p38 activation by H(2)O(2) were not affected by ebselen. 4: Inhibition by ebselen of H(2)O(2)-induced hydroxyl radical generation in PC12 cells was observed using electron paramagnetic resonance measurements. Ebselen also inhibited H(2)O(2)-induced increases in DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK, composed of the c-Jun homo/heterodimer. 5: Finally, pretreatment of cells with ebselen resulted in a significant recovery from cell death including apoptosis by H(2)O(2) in PC12 cells. 6 These findings suggest that ebselen attenuates oxidative stress-induced neuronal cell death through the inhibition of the JNK and AP-1 signalling pathway. Thus, inhibition of JNK by ebselen may imply its usefulness for treatment of ischaemic cerebral diseases relevant to neuronal cell death.","ja":"1: Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one) is a selenoorganic compound exhibiting both glutathione peroxidase activity and antioxidant activity. Although it has been reported that ebselen is effective for oxidative stress-induced neuronal damage both in vivo and clinically, the precise mechanisms of the efficacy have not yet been elucidated. Thus, we hypothesized that ebselen may affect reactive oxygen species-induced mitogen-activated protein (MAP) kinase activation in cultured PC12 cells. 2: Our findings showed that hydrogen peroxide (H(2)O(2)) stimulated rapid and significant activation of extracellular signal-regulated kinase (ERK)1/2, c-Jun N-terminal kinase (JNK) and p38 in PC12 cells, which is a model of catecholamine-containing neurons. 3: H(2)O(2)-induced JNK activation was inhibited by ebselen, whereas ERK1/2 and p38 activation by H(2)O(2) were not affected by ebselen. 4: Inhibition by ebselen of H(2)O(2)-induced hydroxyl radical generation in PC12 cells was observed using electron paramagnetic resonance measurements. Ebselen also inhibited H(2)O(2)-induced increases in DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK, composed of the c-Jun homo/heterodimer. 5: Finally, pretreatment of cells with ebselen resulted in a significant recovery from cell death including apoptosis by H(2)O(2) in PC12 cells. 6 These findings suggest that ebselen attenuates oxidative stress-induced neuronal cell death through the inhibition of the JNK and AP-1 signalling pathway. Thus, inhibition of JNK by ebselen may imply its usefulness for treatment of ischaemic cerebral diseases relevant to neuronal cell death."},"publication_date":"2002-08","publication_name":{"en":"British Journal of Pharmacology","ja":"British Journal of Pharmacology"},"volume":"Vol.136","number":"No.7","starting_page":"1023","ending_page":"1032","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/sj.bjp.0704808"],"issn":["0007-1188"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:140, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/11711055","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-0035798388&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=63846","label":"url"}],"paper_title":{"en":"Effects of losartan in combination with or without exercise on insulin resistance in Otsuka Long-Evans Tokushima Fatty rats.","ja":"Effects of losartan in combination with or without exercise on insulin resistance in Otsuka Long-Evans Tokushima Fatty rats."},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Yoshizumi Masanori"},{"name":"Tsuchiya Koichiro"},{"name":"Takishita Eiko"},{"name":"Nakaya Yutaka"},{"name":"Kishi Kazuhiro"},{"name":"Ebina Yousuke"},{"name":"Houchi Hitoshi"},{"name":"Minakuchi Kazuo"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"吉栖 正典"},{"name":"土屋 浩一郎"},{"name":"瀧下 英子"},{"name":"中屋 豊"},{"name":"岸 和弘"},{"name":"蛯名 洋介"},{"name":"芳地 一"},{"name":"水口 和生"},{"name":"玉置 俊晃"}]},"description":{"en":"Hypertension often complicates type 2 diabetes mellitus, and angiotensin converting enzyme inhibitor treatment has been shown to improve insulin resistance in such cases. However, the effect of angiotensin II type-1 (AT(1)) receptor antagonists on insulin resistance is still controversial. To gain further information on this effect, we examined the effect of losartan on insulin resistance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus. Losartan administration alone lowered systolic blood pressure, but did not improve oral glucose tolerance test or insulin resistance in OLETF rats. However, the administration of losartan with exercise significantly improved both systolic blood pressure and insulin resistance relative to control OLETF rats. On the other hand, losartan treatment, regardless of exercise, increased glucose uptake in excised soleus muscle and fat cells. To explore the beneficial effect of losartan on skeletal muscle glucose uptake, we examined intracellular signaling of soleus muscle. Although Akt activity and glucose transporter type 4 (GLUT4) expressions were not affected by losartan with or without exercise, extracellular signal-regulated kinase (ERK1/2) and p38 mitogen-activated protein (MAP) kinase activities were increased by both interventions. These results indicate that angiotensin AT(1) receptor antagonist improved local insulin resistance, but not systemic insulin resistance. These findings may explain the controversy over the effect of angiotensin AT(1) receptor antagonists on insulin resistance in clinical use. The enhancing effect of angiotensin AT(1) receptor antagonist on skeletal muscle glucose uptake may be attributable to MAP kinase activation or other mechanisms rather than phosphatidylinositol 3-kinase activation.","ja":"Hypertension often complicates type 2 diabetes mellitus, and angiotensin converting enzyme inhibitor treatment has been shown to improve insulin resistance in such cases. However, the effect of angiotensin II type-1 (AT(1)) receptor antagonists on insulin resistance is still controversial. To gain further information on this effect, we examined the effect of losartan on insulin resistance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus. Losartan administration alone lowered systolic blood pressure, but did not improve oral glucose tolerance test or insulin resistance in OLETF rats. However, the administration of losartan with exercise significantly improved both systolic blood pressure and insulin resistance relative to control OLETF rats. On the other hand, losartan treatment, regardless of exercise, increased glucose uptake in excised soleus muscle and fat cells. To explore the beneficial effect of losartan on skeletal muscle glucose uptake, we examined intracellular signaling of soleus muscle. Although Akt activity and glucose transporter type 4 (GLUT4) expressions were not affected by losartan with or without exercise, extracellular signal-regulated kinase (ERK1/2) and p38 mitogen-activated protein (MAP) kinase activities were increased by both interventions. These results indicate that angiotensin AT(1) receptor antagonist improved local insulin resistance, but not systemic insulin resistance. These findings may explain the controversy over the effect of angiotensin AT(1) receptor antagonists on insulin resistance in clinical use. The enhancing effect of angiotensin AT(1) receptor antagonist on skeletal muscle glucose uptake may be attributable to MAP kinase activation or other mechanisms rather than phosphatidylinositol 3-kinase activation."},"publication_date":"2001-11-02","publication_name":{"en":"European Journal of Pharmacology","ja":"European Journal of Pharmacology"},"volume":"Vol.430","number":"No.2-3","starting_page":"359","ending_page":"367","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/S0014-2999(01)01405-4"],"issn":["0014-2999"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:141, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/10940782","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193068","label":"url"}],"paper_title":{"en":"Effect of mometasone furoate by topical application on allergic rhinitis model in rats","ja":"Effect of mometasone furoate by topical application on allergic rhinitis model in rats"},"authors":{"en":[{"name":"Sugimoto Yukio"},{"name":"Ishizawa Keisuke"},{"name":"Saitou Kouichi"},{"name":"Suzuki Genzo"},{"name":"Tarumi Tadatsugu"},{"name":"Nakahara Hiroto"},{"name":"Kirino Yasushi"},{"name":"Kamei Chiaki"}],"ja":[{"name":"Sugimoto Yukio"},{"name":"石澤 啓介"},{"name":"Saitou Kouichi"},{"name":"Suzuki Genzo"},{"name":"Tarumi Tadatsugu"},{"name":"Nakahara Hiroto"},{"name":"Kirino Yasushi"},{"name":"Kamei Chiaki"}]},"description":{"en":"The effects of mometasone furoate on experimental allergic rhinitis in rats were studied in comparison with that of fluticasone propionate. Topical application of both drugs inhibited dose-dependently the increase of nasal symptoms (sneezing and nasal rubbing) after antigen challenge to the nasal cavity of actively sensitized rats. Mometasone furoate and fluticasone propionate at concentrations of 0.01 or 0.1% significantly inhibited both nasal rubbing and sneezing 1 h after topical application of both drugs. The relative potencies of mometasone furoate in nasal rubbing and sneezing compared to fluticasone propionate were 5.01 and 6.87, respectively. Mometasone furoate (0.02%) and fluticasone propionate (0.1%) significantly inhibited the increase of antigen-induced nasal rubbing even 6 h after topical application, indicating that both drugs have a long-lasting effect.","ja":"The effects of mometasone furoate on experimental allergic rhinitis in rats were studied in comparison with that of fluticasone propionate. Topical application of both drugs inhibited dose-dependently the increase of nasal symptoms (sneezing and nasal rubbing) after antigen challenge to the nasal cavity of actively sensitized rats. Mometasone furoate and fluticasone propionate at concentrations of 0.01 or 0.1% significantly inhibited both nasal rubbing and sneezing 1 h after topical application of both drugs. The relative potencies of mometasone furoate in nasal rubbing and sneezing compared to fluticasone propionate were 5.01 and 6.87, respectively. Mometasone furoate (0.02%) and fluticasone propionate (0.1%) significantly inhibited the increase of antigen-induced nasal rubbing even 6 h after topical application, indicating that both drugs have a long-lasting effect."},"publication_date":"2000-08","publication_name":{"en":"Pharmacology","ja":"Pharmacology"},"volume":"Vol.61","number":"No.2","starting_page":"91","ending_page":"95","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1159/000028386"],"issn":["0031-7012"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:142, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=160365","label":"url"}],"paper_title":{"en":"Participation of GABAergic and histaminergic systems in inhibiting amygdaloid kindled seizures","ja":"Participation of GABAergic and histaminergic systems in inhibiting amygdaloid kindled seizures"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Chen Zhong"},{"name":"Okuma Chihiro"},{"name":"Sugimoto Yukio"},{"name":"Fujii Yoko"},{"name":"Kamei Chiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"Chen Zhong"},{"name":"Okuma Chihiro"},{"name":"Sugimoto Yukio"},{"name":"Fujii Yoko"},{"name":"Kamei Chiaki"}]},"publication_date":"2000","publication_name":{"en":"The Japanese Journal of Pharmacology","ja":"The Japanese Journal of Pharmacology"},"volume":"Vol.82","number":"No.1","starting_page":"48","ending_page":"53","languages":["eng"],"referee":true,"identifiers":{"issn":["0021-5198"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:143, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/10631382","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193069","label":"url"}],"paper_title":{"en":"Effects of levocabastine on lipid mediator release from guinea pig lung fragments","ja":"Effects of levocabastine on lipid mediator release from guinea pig lung fragments"},"authors":{"en":[{"name":"Sugimoto Yukio"},{"name":"Iba Yoshinori"},{"name":"Ishizawa Keisuke"},{"name":"Suzuki Genzo"},{"name":"Kamei Chiaki"}],"ja":[{"name":"Sugimoto Yukio"},{"name":"Iba Yoshinori"},{"name":"石澤 啓介"},{"name":"Suzuki Genzo"},{"name":"Kamei Chiaki"}]},"description":{"en":"The effects of levocabastine, a novel histamine H1-receptor antagonist, on lipid mediator release induced by antigen-antibody reaction from actively sensitized guinea pig lung fragments were studied. Levocabastine dose-dependently inhibited the release of leukotriene C4 from guinea pig lung fragments induced by antigen. A significant effect was observed with levocabastine at a concentration of 10(-4) M. On the other hand, levocabastine produced no effect on the release of leukotriene E4 or thromoboxane B2. From these findings, it was concluded that levocabastine may be useful for relieving the nasal obstruction in allergic rhinitis caused by inhibition of leukotriene C4 release.","ja":"The effects of levocabastine, a novel histamine H1-receptor antagonist, on lipid mediator release induced by antigen-antibody reaction from actively sensitized guinea pig lung fragments were studied. Levocabastine dose-dependently inhibited the release of leukotriene C4 from guinea pig lung fragments induced by antigen. A significant effect was observed with levocabastine at a concentration of 10(-4) M. On the other hand, levocabastine produced no effect on the release of leukotriene E4 or thromoboxane B2. From these findings, it was concluded that levocabastine may be useful for relieving the nasal obstruction in allergic rhinitis caused by inhibition of leukotriene C4 release."},"publication_date":"1999-12","publication_name":{"en":"Acta Medica Okayama","ja":"Acta Medica Okayama"},"volume":"Vol.53","number":"No.6","starting_page":"271","ending_page":"274","languages":["eng"],"referee":true,"identifiers":{"issn":["0386-300X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:144, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/9742288","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1571135651705617792/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193073","label":"url"}],"paper_title":{"en":"Anticonvulsant properties of 1,4-benzodiazepine derivatives in amygdaloid-kindled seizures and their chemical structure-related anticonvulsant action","ja":"Anticonvulsant properties of 1,4-benzodiazepine derivatives in amygdaloid-kindled seizures and their chemical structure-related anticonvulsant action"},"authors":{"en":[{"name":"Fukinaga Masafumi"},{"name":"Ishizawa Keisuke"},{"name":"Kamei Chiaki"}],"ja":[{"name":"Fukinaga Masafumi"},{"name":"石澤 啓介"},{"name":"Kamei Chiaki"}]},"description":{"en":"The effects of 14 different 1,4-benzodiazepines on amygdaloid-kindled seizures and their chemical structure-related anticonvulsive actions were studied. The prophylactic effects of 1, 4-benzodiazepines on amygdaloid-kindled seizures were also examined. Male Wistar strain rats were used in this study. Rats were anesthetized with pentobarbital sodium (35 mg/kg i.p.) and bipolar electrodes were implanted into the right amygdala. The stimulating parameters were 1 ms pulse duration, 60 Hz frequency and a 1 s duration at an intensity just sufficient to induce afterdischarge (AD). All the 1,4-benzodiazepines depressed both seizure stage and AD duration of amygdaloid-kindled seizures. Of the 1, 4-benzodiazepines, prazepam, flutoprazepam and flurazepam with a long alkyl chain at position 1 were less effective than the drugs having a hydrogen or methyl group at the same position. Nitrazepam, nimetazepam, flunitrazepam and clonazepam which have a nitro group at position 7 showed more potent antiepileptic activity than the drugs with a chloro group. Certain 1,4-benzodiazepines caused inhibition of the development of amygdaloid-kindled seizures. The existence of a hydrogen or methyl group at position 1 and a nitro group at position 7 is important for exhibiting potent anticonvulsant activity in amygdaloid-kindled seizures. Introduction of an oxygen group at position 2 is also necessary for high activity. 1,4-benzodiazepines had not only therapeutic but also prophylactic effects on amygdaloid-kindled seizures.","ja":"The effects of 14 different 1,4-benzodiazepines on amygdaloid-kindled seizures and their chemical structure-related anticonvulsive actions were studied. The prophylactic effects of 1, 4-benzodiazepines on amygdaloid-kindled seizures were also examined. Male Wistar strain rats were used in this study. Rats were anesthetized with pentobarbital sodium (35 mg/kg i.p.) and bipolar electrodes were implanted into the right amygdala. The stimulating parameters were 1 ms pulse duration, 60 Hz frequency and a 1 s duration at an intensity just sufficient to induce afterdischarge (AD). All the 1,4-benzodiazepines depressed both seizure stage and AD duration of amygdaloid-kindled seizures. Of the 1, 4-benzodiazepines, prazepam, flutoprazepam and flurazepam with a long alkyl chain at position 1 were less effective than the drugs having a hydrogen or methyl group at the same position. Nitrazepam, nimetazepam, flunitrazepam and clonazepam which have a nitro group at position 7 showed more potent antiepileptic activity than the drugs with a chloro group. Certain 1,4-benzodiazepines caused inhibition of the development of amygdaloid-kindled seizures. The existence of a hydrogen or methyl group at position 1 and a nitro group at position 7 is important for exhibiting potent anticonvulsant activity in amygdaloid-kindled seizures. Introduction of an oxygen group at position 2 is also necessary for high activity. 1,4-benzodiazepines had not only therapeutic but also prophylactic effects on amygdaloid-kindled seizures."},"publication_date":"1998-11","publication_name":{"en":"Pharmacology","ja":"Pharmacology"},"volume":"Vol.57","number":"No.5","starting_page":"233","ending_page":"241","languages":["eng"],"referee":true,"identifiers":{"issn":["0031-7012"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:145, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193072","label":"url"}],"paper_title":{"en":"The effects of histamine H3-receptor antagonists on amygdaloid kindled seizures in rats","ja":"The effects of histamine H3-receptor antagonists on amygdaloid kindled seizures in rats"},"authors":{"en":[{"name":"Kakinoki Hiroshi"},{"name":"Ishizawa Keisuke"},{"name":"Fukunaga Masatumi"},{"name":"Fujii Yoko"},{"name":"Kamei Chiaki"}],"ja":[{"name":"Kakinoki Hiroshi"},{"name":"石澤 啓介"},{"name":"Fukunaga Masatumi"},{"name":"Fujii Yoko"},{"name":"Kamei Chiaki"}]},"publication_date":"1998-07","publication_name":{"en":"Brain Research Bulletin","ja":"Brain Research Bulletin"},"volume":"Vol.46","number":"No.5","starting_page":"461","ending_page":"465","languages":["eng"],"referee":true,"identifiers":{"issn":["0361-9230"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:146, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193071","label":"url"}],"paper_title":{"en":"Histaminergic mechanisms in amygdaloid-kindled seizures in rats","ja":"Histaminergic mechanisms in amygdaloid-kindled seizures in rats"},"authors":{"en":[{"name":"Kamei Chiaki"},{"name":"Ishizawa Keisuke"},{"name":"Kakinoki Hiroshi"},{"name":"Fukunaga Masafumi"}],"ja":[{"name":"Kamei Chiaki"},{"name":"石澤 啓介"},{"name":"Kakinoki Hiroshi"},{"name":"Fukunaga Masafumi"}]},"publication_date":"1998-03","publication_name":{"en":"Epilepsy Research","ja":"Epilepsy Research"},"volume":"Vol.30","number":"No.3","starting_page":"187","ending_page":"194","languages":["eng"],"referee":true,"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:147, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=277793","label":"url"}],"paper_title":{"en":"Development of hydrogen peroxide-responsive amide bond cleavage device","ja":"Development of hydrogen peroxide-responsive amide bond cleavage device"},"authors":{"en":[{"name":"Kita Miku"},{"name":"Yamamoto Jun"},{"name":"Ebisuno Koji"},{"name":"Komiya Chiaki"},{"name":"Shigenaga Akira"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Otaka Akira"}],"ja":[{"name":"北 未来"},{"name":"山本 純"},{"name":"戎野 紘司"},{"name":"小宮 千明"},{"name":"重永 章"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"大髙 章"}]},"publication_date":"2014-05","publication_name":{"en":"Peptide Science 2013","ja":"Peptide Science 2013"},"starting_page":"203","ending_page":"204","languages":["eng"],"published_paper_type":"research_institution"},"priority":"input_data"}
line:148, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/10031161576/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1570854176180146304/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=261222","label":"url"}],"paper_title":{"en":"Design and synthesis of hypoxia-responsive amino acid which causes peptide bond cleavage in hypoxic cells","ja":"Design and synthesis of hypoxia-responsive amino acid which causes peptide bond cleavage in hypoxic cells"},"authors":{"en":[{"name":"Shigenaga Akira"},{"name":"Ogura Keiji"},{"name":"Hirakawa Hiroko"},{"name":"Yamamoto Jun"},{"name":"Ebisuno Koji"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Otaka Akira"}],"ja":[{"name":"重永 章"},{"name":"小倉 圭司"},{"name":"平川 寛子"},{"name":"山本 純"},{"name":"戎野 紘司"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"大髙 章"}]},"publication_date":"2013-03-01","publication_name":{"en":"Peptide Science 2012","ja":"Peptide Science 2012"},"starting_page":"135","ending_page":"136","languages":["eng"],"identifiers":{"issn":["1344-7661"]},"published_paper_type":"research_institution"},"priority":"input_data"}
line:149, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612728"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=274823","label":"url"}],"paper_title":{"en":"2型糖尿病治療に対する標的分子としてのHIF-1αの可能性","ja":"2型糖尿病治療に対する標的分子としてのHIF-1αの可能性"},"authors":{"en":[{"name":"Ishizawa Keisuke"}],"ja":[{"name":"石澤 啓介"}]},"publication_date":"2011-02","publication_name":{"en":"Farumashia","ja":"ファルマシア"},"volume":"Vol.47","number":"No.2","starting_page":"160","ending_page":"161","languages":["jpn"],"invited":true,"identifiers":{"issn":["0014-8601"]},"published_paper_type":"research_institution"},"priority":"input_data"}
line:150, {"insert":{"user_id":"6000008820","type":"published_papers","id":"30612729"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=145144","label":"url"}],"paper_title":{"en":"Effect of time-varying magnetic field on cell volume regulation of adrenal chromaffin cells","ja":"副賢クロマフィン細胞の細胞容積調節に及ぼす変動磁界の影響"},"authors":{"en":[{"name":"Minami Yuki"},{"name":"Ikehara Toshitaka"},{"name":"Hosokawa Keiko"},{"name":"Yamaguchi Hisao"},{"name":"Ishizawa Keisuke"},{"name":"Shono Masayuki"},{"name":"Kawazoe Kazuyoshi"},{"name":"Minakuchi Kazuo"},{"name":"Yoshizaki Kazuo"},{"name":"Kinouchi Yohsuke"},{"name":"Miyamoto Hiroshi"}],"ja":[{"name":"南 有紀"},{"name":"池原 敏孝"},{"name":"細川 敬子"},{"name":"山口 久雄"},{"name":"石澤 啓介"},{"name":"庄野 正行"},{"name":"川添 和義"},{"name":"水口 和生"},{"name":"吉﨑 和男"},{"name":"木内 陽介"},{"name":"宮本 博司"}]},"publication_date":"2006-06-01","publication_name":{"en":"The Journal of Japan Biomagnetism and Bioelectromagnetics Society","ja":"日本生体磁気学会誌"},"volume":"Vol.19","number":"No.1","starting_page":"156","ending_page":"157","languages":["jpn"],"published_paper_type":"research_institution"},"priority":"input_data"}
line:151, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35174631","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390809","label":"url"}],"paper_title":{"en":"Atenolol and mortality events in patients with chronic kidney disease: Analysis of data from the Japanese Adverse Drug Event Report database.","ja":"Atenolol and mortality events in patients with chronic kidney disease: Analysis of data from the Japanese Adverse Drug Event Report database."},"authors":{"en":[{"name":"Mitsuboshi Satoru"},{"name":"Niimura Takahiro"},{"name":"Aizawa Fuka"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Mitsuboshi Satoru"},{"name":"新村 貴博"},{"name":"相澤 風花"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"publication_date":"2022-02-23","publication_name":{"en":"Basic & Clinical Pharmacology & Toxicology","ja":"Basic & Clinical Pharmacology & Toxicology"},"volume":"Vol.130","number":"No.4","starting_page":"553","ending_page":"556","languages":["eng"],"identifiers":{"doi":["10.1111/bcpt.13717"],"issn":["1742-7843"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:152, {"insert":{"user_id":"6000008820","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/34482500","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390801","label":"url"}],"paper_title":{"en":"Fluoropyridmidine use and hypertriglyceridemia among Japanese patients: analysis of adverse event database.","ja":"Fluoropyridmidine use and hypertriglyceridemia among Japanese patients: analysis of adverse event database."},"authors":{"en":[{"name":"Mitsuboshi Satoru"},{"name":"Niimura Takahiro"},{"name":"Yoshino Masaki"},{"name":"Sakamoto Yoshika"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Mitsuboshi Satoru"},{"name":"新村 貴博"},{"name":"Yoshino Masaki"},{"name":"Sakamoto Yoshika"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Background The association between fluoropyrimidines except for capecitabine and the risk of hypertriglyceridemia is unclear. Objective To investigate hypertriglyceridemia in patients receiving fluoropyrimidines. Method This observational study used anonymized patient data recorded in the open-access Japanese Adverse Drug Event Report database. All fluoropyrimidine and taxane users were investigated. Results We identified 29,451 fluoropyrimidine users and 21,266 taxane users. Disproportionality for both hypertriglyceridemia and an increase in serum triglyceride levels was observed in fluoropyrimidine users compared with in taxane users (reporting odds ratio, 6.74; 95% confidence interval [CI] 2.05-22.17; P < .001). Multivariate logistic analysis showed that both hypertriglyceridemia and an increase in serum triglyceride levels among fluoropyrimidines users were significantly associated with doxifluridine use (odds ratio [OR] 42.50; 95% CI 5.34-338.00; P < .001), tegafur use (OR 9.56; 95% CI 2.08-43.90; P < .001), capecitabine use (OR 12.30; 95% CI 2.67-56.80; P < .001), and breast cancer (OR 5.61; 95% CI 1.07-29.50; P = .042). Conclusion This study suggests that the use of tegafur and doxifluridine is associated with an increased risk of hypertriglyceridemia similar to that with the use of capecitabine; in particular, fluoropyrimidine users with breast cancer may have a high risk of hypertriglyceridemia.","ja":"Background The association between fluoropyrimidines except for capecitabine and the risk of hypertriglyceridemia is unclear. Objective To investigate hypertriglyceridemia in patients receiving fluoropyrimidines. Method This observational study used anonymized patient data recorded in the open-access Japanese Adverse Drug Event Report database. All fluoropyrimidine and taxane users were investigated. Results We identified 29,451 fluoropyrimidine users and 21,266 taxane users. Disproportionality for both hypertriglyceridemia and an increase in serum triglyceride levels was observed in fluoropyrimidine users compared with in taxane users (reporting odds ratio, 6.74; 95% confidence interval [CI] 2.05-22.17; P < .001). Multivariate logistic analysis showed that both hypertriglyceridemia and an increase in serum triglyceride levels among fluoropyrimidines users were significantly associated with doxifluridine use (odds ratio [OR] 42.50; 95% CI 5.34-338.00; P < .001), tegafur use (OR 9.56; 95% CI 2.08-43.90; P < .001), capecitabine use (OR 12.30; 95% CI 2.67-56.80; P < .001), and breast cancer (OR 5.61; 95% CI 1.07-29.50; P = .042). Conclusion This study suggests that the use of tegafur and doxifluridine is associated with an increased risk of hypertriglyceridemia similar to that with the use of capecitabine; in particular, fluoropyrimidine users with breast cancer may have a high risk of hypertriglyceridemia."},"publication_date":"2021-09-05","publication_name":{"en":"International Journal of Clinical Pharmacy","ja":"International Journal of Clinical Pharmacy"},"volume":"Vol.44","number":"No.1","starting_page":"260","ending_page":"263","languages":["eng"],"identifiers":{"doi":["10.1007/s11096-021-01324-0"],"issn":["2210-7711"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
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==== begin registerFile(/WWW/pub2/data/ERD/person/141809/researchmap/misc.jsonl) ====
line:1, {"insert":{"user_id":"6000008820","type":"misc","id":"46098812"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/38432934","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=406561","label":"url"}],"paper_title":{"en":"[Development of Preventive Methods for Drug-induced Cardiotoxicity Using a Large-scale Medical Information Database].","ja":"[Development of Preventive Methods for Drug-induced Cardiotoxicity Using a Large-scale Medical Information Database]."},"authors":{"en":[{"name":"Hamano Hirofumi"},{"name":"Zamami Yoshito"},{"name":"Ushio Soichiro"},{"name":"Niimura Takahiro"},{"name":"Goda Mitsuhiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"濱野 裕章"},{"name":"座間味 義人"},{"name":"Ushio Soichiro"},{"name":"新村 貴博"},{"name":"合田 光寛"},{"name":"石澤 有紀"},{"name":"石澤 啓介"}]},"description":{"en":"Cancer therapies have evolved considerably thereby substantially improving the survival of patients with cancer. However, cardiotoxicity, such as myocarditis and heart failure, induced by anticancer drugs, including immune checkpoint inhibitor(ICI)s and doxorubicin, present serious challenges. Numerous observations have indicated increased risks of cardiotoxicity- and cancer-related mortality in patients with drug-induced cardiotoxicity. Therefore, the prevention and management of drug-induced cardiotoxicity should be prioritized to enable sustainable long-term treatment while preserving patients' quality of life. Recently, medical research has been primarily focused on elucidation of therapeutic benefits and adverse events using medical big data, including worldwide databases of adverse events. The aim of the present study was to establish prevention strategies for drug-induced cardiotoxicity and advance data analytics. A data-driven approach was adopted to comprehensively analyze patient data and drug-induced cardiotoxicity. These data analytics revealed numerous risk factors, leading to the development of drugs that mitigate these factors. Furthermore, many unknown adverse events with molecularly targeted drugs were brought to light. Consequently, the importance of managing adverse events, guided by insights from data science, is predicted to increase. In this symposium review, we introduce our research exemplifying pharmaceutical studies utilizing medical big data. In particular, we discuss in detail the risk factors associated with myocarditis induced by immune checkpoint inhibitors along with prophylactic agents to mitigate doxorubicin-induced cardiotoxicity.","ja":"Cancer therapies have evolved considerably thereby substantially improving the survival of patients with cancer. However, cardiotoxicity, such as myocarditis and heart failure, induced by anticancer drugs, including immune checkpoint inhibitor(ICI)s and doxorubicin, present serious challenges. Numerous observations have indicated increased risks of cardiotoxicity- and cancer-related mortality in patients with drug-induced cardiotoxicity. Therefore, the prevention and management of drug-induced cardiotoxicity should be prioritized to enable sustainable long-term treatment while preserving patients' quality of life. Recently, medical research has been primarily focused on elucidation of therapeutic benefits and adverse events using medical big data, including worldwide databases of adverse events. The aim of the present study was to establish prevention strategies for drug-induced cardiotoxicity and advance data analytics. A data-driven approach was adopted to comprehensively analyze patient data and drug-induced cardiotoxicity. These data analytics revealed numerous risk factors, leading to the development of drugs that mitigate these factors. Furthermore, many unknown adverse events with molecularly targeted drugs were brought to light. Consequently, the importance of managing adverse events, guided by insights from data science, is predicted to increase. In this symposium review, we introduce our research exemplifying pharmaceutical studies utilizing medical big data. In particular, we discuss in detail the risk factors associated with myocarditis induced by immune checkpoint inhibitors along with prophylactic agents to mitigate doxorubicin-induced cardiotoxicity."},"publication_date":"2024","publication_name":{"en":"Journal of the Pharmaceutical Society of Japan","ja":"薬学雑誌"},"volume":"Vol.144","number":"No.3","starting_page":"257","ending_page":"264","languages":["jpn"],"identifiers":{"doi":["10.1248/yakushi.23-00164-2"],"issn":["1347-5231"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:2, {"insert":{"user_id":"6000008820","type":"misc","id":"36014060"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116895","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=383376","label":"url"}],"paper_title":{"en":"Drug-Repositioning Approaches Based on Medical and Life Science Databases.","ja":"Drug-Repositioning Approaches Based on Medical and Life Science Databases."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Hamano Hirofumi"},{"name":"Niimura Takahiro"},{"name":"Aizawa Fuka"},{"name":"Yagi Kenta"},{"name":"Goda Mitsuhiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"濱野 裕章"},{"name":"新村 貴博"},{"name":"相澤 風花"},{"name":"八木 健太"},{"name":"合田 光寛"},{"name":"石澤 有紀"},{"name":"石澤 啓介"}]},"publication_date":"2021-11-01","publication_name":{"en":"Frontiers in Pharmacology","ja":"Frontiers in Pharmacology"},"volume":"Vol.12","number":"No.752174","languages":["eng"],"identifiers":{"doi":["10.3389/fphar.2021.752174"],"issn":["1663-9812"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:3, {"insert":{"user_id":"6000008820","type":"misc","id":"30612731"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/111115","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28954981","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=333968","label":"url"}],"paper_title":{"en":"Pharmacological approach for drug repositioning against cardiorenal diseases.","ja":"Pharmacological approach for drug repositioning against cardiorenal diseases."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Imanishi Masaki"},{"name":"Takechi Kenshi"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"今西 正樹"},{"name":"武智 研志"},{"name":"石澤 啓介"}]},"description":{"en":"New applications of approved clinically used drugs are being discovered. Drug repositioning is a proposed strategy for developing these drugs as therapeutic agents for different diseases. Currently, approximately 2000 drugs are used in Japan. However, the compound targets and pathways involved in the pharmacological actions of 70-80% of these drugs have not been adequately clarified. Pharmacological examination of approved drugs is an important task in drug repositioning and vital for improving drug development efficiency. This review reports that angiotensin II type 1 receptor blockers show receptor-independent effects against reactive oxygen species generation in renal cells. Additionally, nitrosonifedipine has an antioxidative effect and protects endothelial cells against oxidative stress, and pioglitazone has multiple effects that improve dysfunctions in vascular control regulated by adrenergic and calcitonin gene-related peptide-containing nerves in animal models of diabetes. These data suggest that some approved drugs could be useful for treating cardiorenal diseases. Since cardiorenal diseases are likely to have chronic pathological conditions and require chronic drug administration, highly safe drugs are needed. Compared to newly developed drugs, drug repositioning of approved drugs with safety information is considered a particularly useful technique for searching new treatments for cardiorenal diseases. J. Med. Invest. 64: 197-201, August, 2017.","ja":"New applications of approved clinically used drugs are being discovered. Drug repositioning is a proposed strategy for developing these drugs as therapeutic agents for different diseases. Currently, approximately 2000 drugs are used in Japan. However, the compound targets and pathways involved in the pharmacological actions of 70-80% of these drugs have not been adequately clarified. Pharmacological examination of approved drugs is an important task in drug repositioning and vital for improving drug development efficiency. This review reports that angiotensin II type 1 receptor blockers show receptor-independent effects against reactive oxygen species generation in renal cells. Additionally, nitrosonifedipine has an antioxidative effect and protects endothelial cells against oxidative stress, and pioglitazone has multiple effects that improve dysfunctions in vascular control regulated by adrenergic and calcitonin gene-related peptide-containing nerves in animal models of diabetes. These data suggest that some approved drugs could be useful for treating cardiorenal diseases. Since cardiorenal diseases are likely to have chronic pathological conditions and require chronic drug administration, highly safe drugs are needed. Compared to newly developed drugs, drug repositioning of approved drugs with safety information is considered a particularly useful technique for searching new treatments for cardiorenal diseases. J. Med. Invest. 64: 197-201, August, 2017."},"publication_date":"2017","publication_name":{"en":"The Journal of Medical Investigation : JMI","ja":"The Journal of Medical Investigation : JMI"},"volume":"Vol.64","number":"No.3.4","starting_page":"197","ending_page":"201","languages":["eng"],"identifiers":{"doi":["10.2152/jmi.64.197"],"issn":["1349-6867"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:4, {"insert":{"user_id":"6000008820","type":"misc","id":"30612732"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/29199254","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85037339843&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=329188","label":"url"}],"paper_title":{"en":"Drug repositioning research to improve the survival rate after cardiopulmonary arrest - utilizing large scale Medical Claims Database -","ja":"Drug repositioning research to improve the survival rate after cardiopulmonary arrest - utilizing large scale Medical Claims Database -"},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Takechi Kenshi"},{"name":"Imanishi Masaki"},{"name":"Koyama T"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"武智 研志"},{"name":"今西 正樹"},{"name":"Koyama T"},{"name":"石澤 啓介"}]},"description":{"en":"Approximately 100000 people suffer cardiopulmonary arrest in Japan every year, and the aging of society means that this number is expected to increase. Worldwide, approximately 100 million develop cardiac arrest annually, making it an international issue. Although survival has improved thanks to advances in cardiopulmonary resuscitation, there is a high rate of postresuscitation encephalopathy after the return of spontaneous circulation, and the proportion of patients who can return to normal life is extremely low. Treatment for postresuscitation encephalopathy is long term, and if sequelae persist then nursing care is required, causing immeasurable economic burdens as a result of ballooning medical costs. As at present there is no drug treatment to improve postresuscitation encephalopathy as a complication of cardiopulmonary arrest, the development of novel drug treatments is desirable. In recent years, new efficacy for existing drugs used in the clinical setting has been discovered, and drug repositioning has been proposed as a strategy for developing those drugs as therapeutic agents for different diseases. This review describes a large-scale database study carried out following a discovery strategy for drug repositioning with the objective of improving survival rates after cardiopulmonary arrest and discusses future repositioning prospects.","ja":"Approximately 100000 people suffer cardiopulmonary arrest in Japan every year, and the aging of society means that this number is expected to increase. Worldwide, approximately 100 million develop cardiac arrest annually, making it an international issue. Although survival has improved thanks to advances in cardiopulmonary resuscitation, there is a high rate of postresuscitation encephalopathy after the return of spontaneous circulation, and the proportion of patients who can return to normal life is extremely low. Treatment for postresuscitation encephalopathy is long term, and if sequelae persist then nursing care is required, causing immeasurable economic burdens as a result of ballooning medical costs. As at present there is no drug treatment to improve postresuscitation encephalopathy as a complication of cardiopulmonary arrest, the development of novel drug treatments is desirable. In recent years, new efficacy for existing drugs used in the clinical setting has been discovered, and drug repositioning has been proposed as a strategy for developing those drugs as therapeutic agents for different diseases. This review describes a large-scale database study carried out following a discovery strategy for drug repositioning with the objective of improving survival rates after cardiopulmonary arrest and discusses future repositioning prospects."},"publication_date":"2017","publication_name":{"en":"Journal of the Pharmaceutical Society of Japan","ja":"薬学雑誌"},"volume":"Vol.137","number":"No.12","starting_page":"1439","ending_page":"1442","languages":["jpn"],"identifiers":{"doi":["10.1248/yakushi.17-00139-3"],"issn":["1347-5231"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:5, {"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=306190","label":"url"}],"paper_title":{"en":"今求められているNSTと薬剤師の役割: 臨床・研究・教育を柱とするNST活動の実践","ja":"今求められているNSTと薬剤師の役割: 臨床・研究・教育を柱とするNST活動の実践"},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"石澤 啓介"}]},"publication_date":"2015-12","publication_name":{"en":"薬事新報","ja":"薬事新報"},"volume":"Vol.2921","starting_page":"1306","ending_page":"1310","languages":["jpn"],"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:6, {"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24882646","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=278303","label":"url"}],"paper_title":{"en":"Drug development for cardiorenal disease based on oxidative stress control","ja":"酸化ストレス制御を基盤とする新規心腎血管障害治療薬の開発"},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Ishizawa Keisuke"},{"name":"SAKURADA TAKUMI"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yamano Noriko"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"今西 正樹"},{"name":"石澤 啓介"},{"name":"櫻田 巧"},{"name":"石澤 有紀"},{"name":"山野 範子"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Oxidative stress is a key factor involved in the pathogenesis and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). Reactive oxygen species (ROS), produced as a result of redox reactions in various cells, have been recognized as key chemical mediators causing cellular damage and organ dysfunction in CVD and CKD. Nifedipine, a well-known calcium channel blocker, is extremely sensitive to light which gets converted to its nitroso analog, nitrosonifedipine (NO-NIF) in the presence of ultraviolet and visible light. The so formed NO-NIF blocks calcium channel quite weakly compared to that of nifedipine. However, we elucidated for the first time that NO-NIF is converted to NO-NIF radical which acquires extremely strong antioxidant property via reaction with unsaturated fatty acid or endothelial cells. We have already reported that NO-NIF reduces the cytotoxicity of cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, in endothelial cells. Additionally, we demonstrated that NO-NIF restored acetylcholine-responsive vascular relaxation and suppressed intercellular adhesion molecule-1 expression in the aorta of N(ω)-nitro-L-arginine methyl ester-treated rats, a model of vascular endothelial dysfunction. Recently, we reported that NO-NIF ameliorates angiotensin II-induced vascular remodeling via antioxidative effects in vivo and in vitro. These observations point towards the plausible, unique role of NO-NIF as a novel antioxidant which improves vascular dysfunction for overcoming CVD and CKD and the same has been highlighted in this review.","ja":"Oxidative stress is a key factor involved in the pathogenesis and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). Reactive oxygen species (ROS), produced as a result of redox reactions in various cells, have been recognized as key chemical mediators causing cellular damage and organ dysfunction in CVD and CKD. Nifedipine, a well-known calcium channel blocker, is extremely sensitive to light which gets converted to its nitroso analog, nitrosonifedipine (NO-NIF) in the presence of ultraviolet and visible light. The so formed NO-NIF blocks calcium channel quite weakly compared to that of nifedipine. However, we elucidated for the first time that NO-NIF is converted to NO-NIF radical which acquires extremely strong antioxidant property via reaction with unsaturated fatty acid or endothelial cells. We have already reported that NO-NIF reduces the cytotoxicity of cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, in endothelial cells. Additionally, we demonstrated that NO-NIF restored acetylcholine-responsive vascular relaxation and suppressed intercellular adhesion molecule-1 expression in the aorta of N(ω)-nitro-L-arginine methyl ester-treated rats, a model of vascular endothelial dysfunction. Recently, we reported that NO-NIF ameliorates angiotensin II-induced vascular remodeling via antioxidative effects in vivo and in vitro. These observations point towards the plausible, unique role of NO-NIF as a novel antioxidant which improves vascular dysfunction for overcoming CVD and CKD and the same has been highlighted in this review."},"publication_date":"2014-06","publication_name":{"en":"Journal of the Pharmaceutical Society of Japan","ja":"薬学雑誌"},"volume":"Vol.134","number":"No.6","starting_page":"715","ending_page":"719","languages":["jpn"],"identifiers":{"doi":["10.1248/yakushi.13-00255-4"],"issn":["1347-5231"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:7, {"insert":{"user_id":"6000008820","type":"misc","id":"30612733"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=313674","label":"url"}],"paper_title":{"en":"Nitrosonifedipineはangiotensin IIによるマウス血管リモデリングを抑制する","ja":"Nitrosonifedipineはangiotensin IIによるマウス血管リモデリングを抑制する"},"authors":{"en":[{"name":"櫻田 巧"},{"name":"Ishizawa Keisuke"},{"name":"Imanishi Masaki"},{"name":"藤井 聖子"},{"name":"谷口 順平"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyamoto Licht"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Tomita Shuhei"},{"name":"Minakuchi Kazuo"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"櫻田 巧"},{"name":"石澤 啓介"},{"name":"今西 正樹"},{"name":"藤井 聖子"},{"name":"谷口 順平"},{"name":"石澤 有紀"},{"name":"宮本 理人"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"冨田 修平"},{"name":"水口 和生"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"publication_date":"2013-01-10","publication_name":{"en":"腎とフリーラジカル","ja":"腎とフリーラジカル"},"volume":"Vol.11","starting_page":"78","ending_page":"81","languages":["jpn"],"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:8, {"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/130001871942/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282681104589184/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=230718","label":"url"}],"paper_title":{"en":"Drug Discovery for Improvement of Chronic Kidney Disease and Cardiovascular Disease","ja":"腎・心血管障害における細胞内分子機構の解明とその治療法の開発"},"authors":{"en":[{"name":"Ishizawa Keisuke"}],"ja":[{"name":"石澤 啓介"}]},"description":{"en":"Chronic kidney disease (CKD) has been increasingly recognized as a major public health problem in the world. Recent studies have showed that CKD is an independent risk factor for the occurrence of cardiovascular disease (CVD). Reactive oxygen species (ROS), generated by reduction-oxidation actions, have been generated by reduction-oxidation actions, recognized as the important chemical mediators that regulate signal transduction in various cells including vascular smooth muscle cells (VSMC) and mesangial cells (MC). It has been showed that increase in ROS generation may relate to a risk for CVD and CKD. In addition, ROS mediate activation of mitogen-activated protein (MAP) kinases, extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase, p38, and big MAP kinase 1, in various cells leading to change in gene expressions. Control of the oxidative stress and ROS-mediated alterations of signaling molecules including MAP kinases may provide new therapeutic strategy against CKD and CVD. In this review, we summarize mainly our data regarding the pharmacological effects of renin-angiotensin-aldosterone system blockers, bioflavonoids and adiponectin in VSMC and MC. Also we review the data on a possible new class drug against oxidative stress to improve CKD and CVD.","ja":"Chronic kidney disease (CKD) has been increasingly recognized as a major public health problem in the world. Recent studies have showed that CKD is an independent risk factor for the occurrence of cardiovascular disease (CVD). Reactive oxygen species (ROS), generated by reduction-oxidation actions, have been generated by reduction-oxidation actions, recognized as the important chemical mediators that regulate signal transduction in various cells including vascular smooth muscle cells (VSMC) and mesangial cells (MC). It has been showed that increase in ROS generation may relate to a risk for CVD and CKD. In addition, ROS mediate activation of mitogen-activated protein (MAP) kinases, extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase, p38, and big MAP kinase 1, in various cells leading to change in gene expressions. Control of the oxidative stress and ROS-mediated alterations of signaling molecules including MAP kinases may provide new therapeutic strategy against CKD and CVD. In this review, we summarize mainly our data regarding the pharmacological effects of renin-angiotensin-aldosterone system blockers, bioflavonoids and adiponectin in VSMC and MC. Also we review the data on a possible new class drug against oxidative stress to improve CKD and CVD."},"publication_date":"2011-09","publication_name":{"en":"Journal of the Pharmaceutical Society of Japan","ja":"薬学雑誌"},"volume":"Vol.131","number":"No.9","starting_page":"1347","ending_page":"1352","languages":["jpn"],"invited":true,"identifiers":{"doi":["10.1248/yakushi.131.1347"],"issn":["0031-6903"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
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