Tokushima University / Educator and Researcher Directory --- Izawa-Ishizawa, Yuki

Personal Web Page

https://researchmap.jp/yukiishizawa (researchmap)

Field of Study

○	Life sciences [Pharmacology]
○	Life sciences [Clinical pharmacy]
○	Life sciences [Cardiology]
○	Life sciences [Environmental and pharmaceutical development resources]
○	Other [Other]

Subject of Study

Book / Paper

Book:

1.	Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : ドラッグリポジショニング研究ー医療ビッグデータから医薬品の新たな効能を探るー, Tokyo Kagaku Dozin C., Ltd., Jun. 2021.
2.	Yasumasa Ikeda, 田島壮一郎, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 腎とフリーラジカル第11集, TOKYO IGAKUSHA, Tokyo, Jan. 2013.
3.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Shoko Fujii, Jumpei Taniguchi, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : 腎とフリーラジカル第11集, TOKYO IGAKUSHA, Tokyo, Jan. 2013.
4.	Keisuke Ishizawa, 三木恵里加, Yuki Izawa-Ishizawa, 大西秀樹, Narantungalag Dorjsuren, 元林有紀, Kunihisa Yamaguchi, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 腎とフリーラジカル第9集, TOKYO IGAKUSHA, Tokyo, Sep. 2008.

Academic Paper (Judged Full Paper):

1.	Takashi Bando, Masayuki Chuma, Hirofumi Hamano, Takahiro Niimura, Naoto Okada, Masateru Kondo, Yuki Izumi, Shunsuke Ishida, Toshihiko Yoshioka, Mizuho Asada, Yoshito Zamami, Kenshi Takechi, Mitsuhiro Goda, Koji Miyata, Kenta Yagi, Yuki Izawa-Ishizawa, Momoyo Azuma, Hiroaki Yanagawa, Yoshikazu Tasaki and Keisuke Ishizawa : Concomitant Use of Multiple Nephrotoxins including Renal Hypoperfusion Medications Causes Vancomycin-Associated Nephrotoxicity: Combined Retrospective Analyses of Two Real-World Databases., Acta Medica Okayama, Vol.77, No.6, 595-605, 2023. (Summary) 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. (Keyword) Humans / Vancomycin / Anti-Bacterial Agents / Retrospective Studies / Causality / Acute Kidney Injury (Link to Publication Site) ● Publication site (DOI): 10.18926/AMO/66151 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38145933 ● Search Scopus @ Elsevier (PMID): 38145933 ● Search Scopus @ Elsevier (DOI): 10.18926/AMO/66151 (DOI: 10.18926/AMO/66151, PubMed: 38145933)
2.	Toshihiko Yoshioka, Mitsuhiro Goda, Masaya Kanda, Sayuri Itobayashi, Yugo Sugimoto, Yuki Izawa-Ishizawa, Kenta Yagi, Fuka Aizawa, Koji Miyata, Takahiro Niimura, Hirofumi Hamano, Takumi Sakurada, Yoshito Zamami and Keisuke Ishizawa : Valproic acid treatment attenuates cisplatin-induced kidney injury by suppressing proximal tubular cell damage., Clinical and Translational Science, Vol.16, No.11, 2369-2381, 2023. (Summary) 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. (Keyword) Mice / Animals / Humans / Cisplatin / Valproic Acid / Prospective Studies / Acute Kidney Injury / Kidney / Apoptosis / Mice, Inbred C57BL (Link to Publication Site) ● Publication site (DOI): 10.1111/cts.13638 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37700528 ● Search Scopus @ Elsevier (PMID): 37700528 ● Search Scopus @ Elsevier (DOI): 10.1111/cts.13638 (DOI: 10.1111/cts.13638, PubMed: 37700528)
3.	Kaito Tsujinaka, Yuki Izawa-Ishizawa, Koji Miyata, Toshihiko Yoshioka, Kohei Oomine, Honoka Nishi, Masateru Kondo, Syuto Itokazu, Tatsumi Miyata, Takahiro Niimura, Maki Sato, Fuka Aizawa, Kenta Yagi, Masayuki Chuma, Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa : Angiogenesis inhibitor-specific hypertension increases the risk of developing aortic dissection., Biomedicine & Pharmacotherapy, Vol.167, 2023. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2023.115504 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37722188 ● Search Scopus @ Elsevier (PMID): 37722188 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2023.115504 (DOI: 10.1016/j.biopha.2023.115504, PubMed: 37722188)
4.	Takahiro Niimura, Koji Miyata, Hirofumi Hamano, Yuuki Nounin, Hiroto Unten, Masaki Yoshino, Satoru Mitsuboshi, Fuka Aizawa, Kenta Yagi, Toshihiro Koyama, Mitsuhiro Goda, Yasunari Kanda, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : Cardiovascular Toxicities Associated with Anaplastic Lymphoma Kinase Inhibitors: A Disproportionality Analysis of the WHO Pharmacovigilance Database (VigiBase)., Drug Safety, 2023. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.1007/s40264-023-01300-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37106270 ● Search Scopus @ Elsevier (PMID): 37106270 ● Search Scopus @ Elsevier (DOI): 10.1007/s40264-023-01300-9 (DOI: 10.1007/s40264-023-01300-9, PubMed: 37106270)
5.	Kenta Yagi, Akinori Maruo, Shunsuke Ishida, Fuka Aizawa, Soichiro Ushio, Satoshi Sakaguchi, Makoto Kajizono, Takahiro Niimura, Mitsuhiro Goda, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : Effects of vonoprazan and proton pump inhibitors on the efficacy of bevacizumab: a multicentre retrospective study., Clinical and Experimental Medicine, 2023. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10238-023-01008-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36738305 ● Search Scopus @ Elsevier (PMID): 36738305 ● Search Scopus @ Elsevier (DOI): 10.1007/s10238-023-01008-1 (DOI: 10.1007/s10238-023-01008-1, PubMed: 36738305)
6.	Takahiro Niimura, Yoshito Zamami, Koji Miyata, Takahisa Mikami, Mizuho Asada, Keijo Fukushima, Masaki Yoshino, Satoru Mitsuboshi, Naoto Okada, Hirofumi Hamano, Takumi Sakurada, Rie Matsuoka-Ando, Fuka Aizawa, Kenta Yagi, Mitsuhiro Goda, Masayuki Chuma, Toshihiro Koyama, Yuki Izawa-Ishizawa, Hiroaki Yanagawa, Hiromichi Fujino, Yoshihiro Yamanishi and Keisuke Ishizawa : Characterization of Immune Checkpoint Inhibitor-Induced Myasthenia Gravis Using the US Food and Drug Administration Adverse Event Reporting System., Journal of Clinical Pharmacology, Vol.63, No.4, 473-479, 2022. (Summary) 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. (Keyword) Male / United States / Humans / Female / Aged / Immune Checkpoint Inhibitors / United States Food and Drug Administration / Myocarditis / Myasthenia Gravis / Myositis (Link to Publication Site) ● Publication site (DOI): 10.1002/jcph.2187 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36453166 ● Search Scopus @ Elsevier (PMID): 36453166 ● Search Scopus @ Elsevier (DOI): 10.1002/jcph.2187 (DOI: 10.1002/jcph.2187, PubMed: 36453166)
7.	Rie Ando-Matsuoka, Kenta Yagi, Mayu Takaoka, Yuko Sakajiri, Tomokazu Shibata, Ryusuke Sawada, Akinori Maruo, Koji Miyata, Fuka Aizawa, Hirofumi Hamano, Takahiro Niimura, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Satoshi Sakaguchi, Yoshito Zamami, Yoshihiro Yamanishi and Keisuke Ishizawa : Differential effects of proton pump inhibitors and vonoprazan on vascular endothelial growth factor expression in cancer cells., Drug Development Research, Vol.84, No.1, 75-83, 2022. (Summary) 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. (Keyword) Humans / Proton Pump Inhibitors / Endothelial Growth Factors / Molecular Docking Simulation / Peptic Ulcer / Pyrroles / Neoplasms (Tokushima University Institutional Repository) ● Metadata: 118289 (Link to Publication Site) ● Publication site (DOI): 10.1002/ddr.22013 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36484282 ● Search Scopus @ Elsevier (PMID): 36484282 ● Search Scopus @ Elsevier (DOI): 10.1002/ddr.22013 (Tokushima University Institutional Repository: 118289, DOI: 10.1002/ddr.22013, PubMed: 36484282)
8.	Masayuki Chuma, Hirofumi Hamano, Takashi Bando, Masateru Kondo, Naoto Okada, Yuki Izumi, Shunsuke Ishida, Toshihiko Yoshioka, Mizuho Asada, Takahiro Niimura, Yoshito Zamami, Kenshi Takechi, Mitsuhiro Goda, Koji Miyata, Kenta Yagi, Sachiko Kasamo, Yuki Izawa-Ishizawa, Momoyo Azuma, Hiroaki Yanagawa, Yoshikazu Tasaki and Keisuke Ishizawa : Non-recovery of vancomycin-associated nephrotoxicity is related to worsening survival outcomes: Combined retrospective analyses of two real-world databases., Basic & Clinical Pharmacology & Toxicology, Vol.131, No.6, 525-535, 2022. (Summary) 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. (Keyword) Humans / Vancomycin / Retrospective Studies / Anti-Bacterial Agents / Acute Kidney Injury / Drug-Related Side Effects and Adverse Reactions / Risk Factors (Link to Publication Site) ● Publication site (DOI): 10.1111/bcpt.13799 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36169161 ● Search Scopus @ Elsevier (PMID): 36169161 ● Search Scopus @ Elsevier (DOI): 10.1111/bcpt.13799 (DOI: 10.1111/bcpt.13799, PubMed: 36169161)
9.	Shiori Nishiuchi, Kenta Yagi, Hiroumi Saito, Yoshito Zamami, Takahiro Niimura, Koji Miyata, Yoshika Sakamoto, Kimiko Fukunaga, Shunsuke Ishida, Hirofumi Hamano, Fuka Aizawa, Mitsuhiro Goda, Masayuki Chuma, Yuki Izawa-Ishizawa, Hideki Nawa, Hiroaki Yanagawa, Yasunari Kanda and Keisuke Ishizawa : Investigation of drugs for the prevention of doxorubicin-induced cardiac events using big data analysis., European Journal of Pharmacology, Vol.928, No.175083, 2022. (Summary) These findings suggest that doxorubicin-induced cardiac events are suppressed by the administration of mosapride and sirolimus. (Keyword) Animals / apoptosis / Cardiotoxicity / data analysis / Doxorubicin / Mice / Myocytes, Cardiac / Pharmaceutical Preparations / RNA, Messenger / Sirolimus (Tokushima University Institutional Repository) ● Metadata: 117365 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2022.175083 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35659512 ● Search Scopus @ Elsevier (PMID): 35659512 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2022.175083 (Tokushima University Institutional Repository: 117365, DOI: 10.1016/j.ejphar.2022.175083, PubMed: 35659512)
10.	Masaya Kanda, Mitsuhiro Goda, Akiko Maegawa, Toshihiko Yoshioka, Ami Yoshida, Koji Miyata, Fuka Aizawa, Takahiro Niimura, Hirofumi Hamano, Naoto Okada, Takumi Sakurada, Masayuki Chuma, Kenta Yagi, Yuki Izawa-Ishizawa, Hiroaki Yanagawa, Yoshito Zamami and Keisuke Ishizawa : Discovery of preventive drugs for cisplatin-induced acute kidney injury using big data analysis., Clinical and Translational Science, Vol.15, No.7, 1664-1675, 2022. (Summary) 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. (Keyword) Acute Kidney Injury / Animals / Cisplatin / data analysis / Fenofibrate / kidney disease / Mice / Prospective Studies (Tokushima University Institutional Repository) ● Metadata: 117366 (Link to Publication Site) ● Publication site (DOI): 10.1111/cts.13282 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35445533 ● Search Scopus @ Elsevier (PMID): 35445533 ● Search Scopus @ Elsevier (DOI): 10.1111/cts.13282 (Tokushima University Institutional Repository: 117366, DOI: 10.1111/cts.13282, PubMed: 35445533)
11.	Kenta Yagi, Yasutaka Sato, Satoshi Sakaguchi, Mitsuhiro Goda, Hirofumi Hamano, Fuka Aizawa, Mayuko Shimizu, Arisa Inoue-Hamano, Toshihide Nishimori, Masato Tagi, Marina Kanno, Rie Matsuoka-Ando, Toshihiko Yoshioka, Yoshiko Matstubara, Yuki Izawa-Ishizawa, Rieko Shimizu, Akinori Maruo, Yurika Kuniki, Yoshika Sakamoto, Sayuri Itobayashi, Yoshito Zamami, Hiroaki Yanagawa and Keisuke Ishizawa : A web-based survey of educational opportunities of medical professionals based on changes in conference design during the COVID-19 pandemic., Education and Information Technologies, Vol.27, 10371-10386, 2022. (Summary) The online version contains supplementary material available at 10.1007/s10639-022-11032-5. (Link to Publication Site) ● Publication site (DOI): 10.1007/s10639-022-11032-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35464114 ● Search Scopus @ Elsevier (PMID): 35464114 ● Search Scopus @ Elsevier (DOI): 10.1007/s10639-022-11032-5 (DOI: 10.1007/s10639-022-11032-5, PubMed: 35464114)
12.	Masayuki Chuma, Aki Nakamoto, Takashi Bando, Takahiro Niimura, Yutaka Kondo, Hirofumi Hamano, Naoto Okada, Mizuho Asada, Yoshito Zamami, Kenshi Takechi, Mitsuhiro Goda, Koji Miyata, Kenta Yagi, Toshihiko Yoshioka, Yuki Izawa-Ishizawa, Hiroaki Yanagawa, Yoshikazu Tasaki and Keisuke Ishizawa : Association between statin use and daptomycin-related musculoskeletal adverse events: A mixed approach combining a meta-analysis and a disproportionality analysis., Clinical Infectious Diseases, Vol.75, No.8, 1416-1422, 2022. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 117810 (Link to Publication Site) ● Publication site (DOI): 10.1093/cid/ciac128 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35262686 ● Search Scopus @ Elsevier (PMID): 35262686 ● Search Scopus @ Elsevier (DOI): 10.1093/cid/ciac128 (Tokushima University Institutional Repository: 117810, DOI: 10.1093/cid/ciac128, PubMed: 35262686)
13.	Yoshito Zamami, Takahiro Niimura, Takehiro Kawashiri, Mitsuhiro Goda, Yutaro Naito, Keijo Fukushima, Soichiro Ushio, Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Kenta Yagi, Koji Miyata, Kenshi Takechi, Masayuki Chuma, Toshihiro Koyama, Daisuke Kobayashi, Takao Shimazoe, Hiromichi Fujino, Yuki Izawa-Ishizawa and Keisuke Ishizawa : Identification of prophylactic drugs for oxaliplatin-induced peripheral neuropathy using big data., Biomedicine & Pharmacotherapy, Vol.148, 2022. (Summary) 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. (Keyword) Animals / Anticholesteremic Agents / Antineoplastic Agents / Big Data / Databases, Factual / Drug Repositioning / Humans / Hyperalgesia / Japan / Male / Mice / Mice, Inbred BALB C / Oxaliplatin / Peripheral Nervous System Diseases / Pre-Exposure Prophylaxis / Rats / Rats, Sprague-Dawley / Retrospective Studies / Simvastatin (Tokushima University Institutional Repository) ● Metadata: 117414 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2022.112744 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35240525 ● Search Scopus @ Elsevier (PMID): 35240525 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2022.112744 (Tokushima University Institutional Repository: 117414, DOI: 10.1016/j.biopha.2022.112744, PubMed: 35240525)
14.	Mitsuhiro Goda, Masaya Kanda, Toshihiko Yoshioka, Ami Yoshida, Yoichi Murai, Yoshito Zamami, Fuka Aizawa, Takahiro Niimura, Hirofumi Hamano, Naoto Okada, Kenta Yagi, Masayuki Chuma, Yuki Izawa-Ishizawa and Keisuke Ishizawa : Effects of 5-HT₃ receptor antagonists on cisplatin-induced kidney injury., Clinical and Translational Science, 2021. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 116008 (Link to Publication Site) ● Publication site (DOI): 10.1111/cts.13045 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33982438 ● Search Scopus @ Elsevier (PMID): 33982438 ● Search Scopus @ Elsevier (DOI): 10.1111/cts.13045 (Tokushima University Institutional Repository: 116008, DOI: 10.1111/cts.13045, PubMed: 33982438)
15.	Yuki Izawa-Ishizawa, Mitsuhiro Goda, Fuka Aizawa, Yoshito Zamami, Hirofumi Hamano, Kenta Yagi, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : 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, Shikoku Acta Medica, Vol.77, No.1,2, 57-62, 2021. (Summary) 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. (Keyword) aortic dissection / endothelial dysfunction / statin / polyphenol / large medical databases (Tokushima University Institutional Repository) ● Metadata: 116038 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050851320431028352 (Tokushima University Institutional Repository: 116038, CiNii: 1050851320431028352)
16.	Shimon Takahashi, Kenshi Takechi, Natsumi Jozukuri, Takahiro Niimura, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya, Hiroaki Yanagawa and Keisuke Ishizawa : Examination of the antiepileptic effects of valacyclovir using kindling mice- search for novel antiepileptic agents by drug repositioning using a large medical information database., European Journal of Pharmacology, Vol.902, 2021. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 116301 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2021.174099 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33910036 ● Search Scopus @ Elsevier (PMID): 33910036 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2021.174099 (Tokushima University Institutional Repository: 116301, DOI: 10.1016/j.ejphar.2021.174099, PubMed: 33910036)
17.	Kenta Yagi, Marin Mitstui, Yoshito Zamami, Takahiro Niimura, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Masayuki Chuma, Kimiko Fukunaga, Takahiro Shibata, Shunsuke Ishida, Takumi Sakurada, Naoto Okada, Hirofumi Hamano, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : Investigation of drugs affecting hypertension in bevacizumab-treated patients and examination of the impact on the therapeutic effect., Cancer Medicine, 2020. (Summary) PPIs prevent hypertension in bevacizumab-treated patients but may reduce bevacizumab's anti-tumoral effects by inducing VEGF expression. (Tokushima University Institutional Repository) ● Metadata: 116288 (Link to Publication Site) ● Publication site (DOI): 10.1002/cam4.3587 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33231381 ● Search Scopus @ Elsevier (PMID): 33231381 ● Search Scopus @ Elsevier (DOI): 10.1002/cam4.3587 (Tokushima University Institutional Repository: 116288, DOI: 10.1002/cam4.3587, PubMed: 33231381)
18.	Kondo Masateru, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Hosooka Mayuko, Kagimoto Yuu, Saito Naoko, Matsuoka Rie, Yoshito Zamami, Masayuki Chuma, Kenta Yagi, Kenshi Takechi, Koichi Tsuneyama and Keisuke Ishizawa : Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice, International Journal of Molecular Sciences, Vol.21, No.19, 2020. (Tokushima University Institutional Repository) ● Metadata: 115332 (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms21197226 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85091999803 (Tokushima University Institutional Repository: 115332, DOI: 10.3390/ijms21197226, Elsevier: Scopus)
19.	Yasumasa Ikeda, Hiroaki Watanabe, Tetsuya Shiuchi, Hirofumi Hamano, Yuya Horinouchi, Masaki Imanishi, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Deletion of H-ferritin in macrophages alleviates obesity and diabetes induced by high-fat diet in mice, Diabetologia, Vol.63, No.8, 1588-1602, 2020. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 114409 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00125-020-05153-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32430665 ● Summary page in Scopus @ Elsevier: 2-s2.0-85085484596 (Tokushima University Institutional Repository: 114409, DOI: 10.1007/s00125-020-05153-0, PubMed: 32430665, Elsevier: Scopus)
20.	Masaki Imanishi, Yusuke Yamakawa, Keijo Fukushima, Raiki Ikuto, Akiko Maegawa, Yuki Izawa-Ishizawa, Yuya Horinouchi, Masateru Kondo, Masatoshi Kishuku, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Koichiro Tsuchiya, Hiromichi Fujino, Koichi Tsuneyama and Keisuke Ishizawa : Fibroblast-specific ERK5 deficiency changes tumor vasculature and exacerbates tumor progression in a mouse model., Naunyn-Schmiedeberg's Archives of Pharmacology, Vol.393, No.7, 1239-1250, 2020. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00210-020-01859-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32307577 ● Search Scopus @ Elsevier (PMID): 32307577 ● Search Scopus @ Elsevier (DOI): 10.1007/s00210-020-01859-5 (DOI: 10.1007/s00210-020-01859-5, PubMed: 32307577)
21.	Tatsuya Tsuda, Masaki Imanishi, Mizuho Oogoshi, Mitsuhiro Goda, Yoshitaka Kihira, Yuya Horinouchi, Yoshito Zamami, Keisuke Ishizawa, Yasumasa Ikeda, Ichiro Hashimoto, Toshiaki Tamaki and Yuki Izawa-Ishizawa : Rho-associated protein kinase and cyclophilin a are involved in inorganic phosphate-induced calcification signaling in vascular smooth muscle cells., Journal of Pharmacological Sciences, Vol.142, No.3, 109-115, 2020. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 115530 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2019.12.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31882204 ● Search Scopus @ Elsevier (PMID): 31882204 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2019.12.005 (Tokushima University Institutional Repository: 115530, DOI: 10.1016/j.jphs.2019.12.005, PubMed: 31882204)
22.	Hirofumi Hamano, Takahiro Niimura, Yuya Horinouchi, Yoshito Zamami, Kenshi Takechi, Mitsuhiro Goda, Masaki Imanishi, Masayuki Chuma, Yuki Izawa-Ishizawa, Licht Miyamoto, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Keisuke Ishizawa, Toshiaki Tamaki and Yasumasa Ikeda : Proton pump inhibitors block iron absorption through direct regulation of hepcidin via the aryl hydrocarbon receptor-mediated pathway, Toxicology Letters, Vol.318, 86-91, 2020. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 113812 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.toxlet.2019.10.016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31669099 ● Search Scopus @ Elsevier (PMID): 31669099 ● Search Scopus @ Elsevier (DOI): 10.1016/j.toxlet.2019.10.016 (Tokushima University Institutional Repository: 113812, DOI: 10.1016/j.toxlet.2019.10.016, PubMed: 31669099)
23.	Yoshito Zamami, Takahiro Niimura, Toshihiro Koyama, Yuta Shigemi, Yuki Izawa-Ishizawa, Mizuki Morita, Ayako Ohshima, Keisaku Harada, Toru Imai, Hiromi Hagiwara, Naoto Okada, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yutaka Kondo, Koichiro Tsuchiya, Shiro Hinotsu, R Mitsunobu Kano and Keisuke Ishizawa : Search for Therapeutic Agents for Cardiac Arrest Using a Drug Discovery Tool and Large-Scale Medical Information Database., Frontiers in Pharmacology, Vol.10, 2019. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 114461 (Link to Publication Site) ● Publication site (DOI): 10.3389/fphar.2019.01257 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31780928 ● Summary page in Scopus @ Elsevier: 2-s2.0-85075592155 (Tokushima University Institutional Repository: 114461, DOI: 10.3389/fphar.2019.01257, PubMed: 31780928, Elsevier: Scopus)
24.	Yoshito Zamami, Takahiro Niimura, Naoto Okada, Toshihiro Koyama, Keijo Fukushima, Yuki Izawa-Ishizawa and Keisuke Ishizawa : Factors Associated With Immune Checkpoint Inhibitor-Related Myocarditis., JAMA Oncology, 2019. (Link to Publication Site) ● Publication site (DOI): 10.1001/jamaoncol.2019.3113 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31436802 ● Search Scopus @ Elsevier (PMID): 31436802 ● Search Scopus @ Elsevier (DOI): 10.1001/jamaoncol.2019.3113 (DOI: 10.1001/jamaoncol.2019.3113, PubMed: 31436802)
25.	Yasumasa Ikeda, Akiho Satoh, Yuya Horinouchi, Hirofumi Hamano, Hiroaki Watanabe, Mizuki Imao, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Yuki Izawa-Ishizawa, Licht Miyamoto, Hirayama Tasuku, Hideko Nagasawa, Keisuke Ishizawa, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress, The FASEB journal, Vol.33, No.8, 9551-9564, 2019. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 113746 (Link to Publication Site) ● Publication site (DOI): 10.1096/fj.201802724RR (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31145863 ● Search Scopus @ Elsevier (PMID): 31145863 ● Search Scopus @ Elsevier (DOI): 10.1096/fj.201802724RR (Tokushima University Institutional Repository: 113746, DOI: 10.1096/fj.201802724RR, PubMed: 31145863)
26.	Hirofumi Hamano, Marin Mitsui, Yoshito Zamami, Kenshi Takechi, Takahiro Nimura, Naoto Okada, Keijo Fukushima, Masaki Imanishi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasushi Kirino, Toshimi Nakamura, Kazuhiko Teraoka, Yasumasa Ikeda, Hiromichi Fujino, Hiroaki Yanagawa, Toshiaki Tamaki and Keisuke Ishizawa : Irinotecan-induced neutropenia is reduced by oral alkalization drugs: analysis using retrospective chart reviews and the spontaneous reporting database., Supportive Care in Cancer, Vol.27, No.3, 849-856, 2019. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00520-018-4367-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30062585 ● Search Scopus @ Elsevier (PMID): 30062585 ● Search Scopus @ Elsevier (DOI): 10.1007/s00520-018-4367-y (DOI: 10.1007/s00520-018-4367-y, PubMed: 30062585)
27.	Masateru Kondo, Masaki Imanishi, Keijo Fukushima, Raiki Ikuto, Yoichi Murai, Yuya Horinouchi, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : Xanthine Oxidase Inhibition by Febuxostat in Macrophages Suppresses Angiotensin II-induced Aortic Fibrosis., American Journal of Hypertension, Vol.32, No.3, 249-256, 2019. (Summary) Our results suggested that FEB ameliorates Ang II-induced aortic fibrosis via suppressing macrophage-derived TGF-1 expression. (Link to Publication Site) ● Publication site (DOI): 10.1093/ajh/hpy157 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30351343 ● Search Scopus @ Elsevier (PMID): 30351343 ● Search Scopus @ Elsevier (DOI): 10.1093/ajh/hpy157 (DOI: 10.1093/ajh/hpy157, PubMed: 30351343)
28.	Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Toya Hiroki, Nagao Tomoko, Marin Morishita, Koichi Tsuneyama, Yuya Horinouchi, Yoshitaka Kihira, Kenshi Takechi, Yasumasa Ikeda, Koichiro Tsuchiya, Masanori Yoshizumi, Toshiaki Tamaki and Keisuke Ishizawa : Development of a novel aortic dissection mouse model and evaluation of drug efficacy using in-vivo assays and database analyses., Journal of Hypertension, Vol.37, No.1, 73-83, 2019. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 113264 (Link to Publication Site) ● Publication site (DOI): 10.1097/HJH.0000000000001898 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30303488 ● Search Scopus @ Elsevier (PMID): 30303488 ● Search Scopus @ Elsevier (DOI): 10.1097/HJH.0000000000001898 (Tokushima University Institutional Repository: 113264, DOI: 10.1097/HJH.0000000000001898, PubMed: 30303488)
29.	Masaki Imanishi, Yuki Izawa-Ishizawa, T Sakurada, Y Kohara, Yuya Horinouchi, E Sairyo, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yasumasa Ikeda, Hiromichi Fujino, M Yoshizumi, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Nitrosonifedipine, a Photodegradation Product of Nifedipine, Suppresses Pharmacologically Induced Aortic Aneurysm Formation., Pharmacology, Vol.102, No.5-6, 281-286, 2018. (Summary) 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. (Keyword) Aminopropionitrile / Angiotensin II / Animals / Antigens, Differentiation / Antioxidants / Aortic Aneurysm / Chemokine CCL2 / Cyclophilins / Disease Models, Animal / Elastin / Endothelial Cells / Human Umbilical Vein Endothelial Cells / Humans / Male / Matrix Metalloproteinase 2 / Mice / Nifedipine / Nitroso Compounds / Oxidative Stress / Photolysis / Reactive Oxygen Species / Vascular Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1159/000492577 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30253416 ● Summary page in Scopus @ Elsevier: 2-s2.0-85054191604 (DOI: 10.1159/000492577, PubMed: 30253416, Elsevier: Scopus)
30.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Renoprotective effects of a factor Xa inhibitor: fusion of basic research and a database analysis., Scientific Reports, Vol.8, No.1, 2018. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 112445 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-018-29008-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30022146 ● Search Scopus @ Elsevier (PMID): 30022146 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-018-29008-2 (Tokushima University Institutional Repository: 112445, DOI: 10.1038/s41598-018-29008-2, PubMed: 30022146)
31.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The uremic toxin indoxyl sulfate interferes with iron metabolism by regulating hepcidin in chronic kidney disease, Nephrology, Dialysis, Transplantation, Vol.33, No.4, 586-597, 2018. (Tokushima University Institutional Repository) ● Metadata: 110922 (Link to Publication Site) ● Publication site (DOI): 10.1093/ndt/gfx252 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28992067 ● Search Scopus @ Elsevier (PMID): 28992067 ● Search Scopus @ Elsevier (DOI): 10.1093/ndt/gfx252 (Tokushima University Institutional Repository: 110922, DOI: 10.1093/ndt/gfx252, PubMed: 28992067)
32.	Takahiro Niimura, Yoshito Zamami, Toshihiro Koyama, Yuki Izawa-Ishizawa, Masashi Miyake, Tadashi Koga, Keisaku Harada, Ayako Ohshima, Toru Imai, Yutaka Kondo, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki, Shiro Hinotsu, R Mitsunobu Kano and Keisuke Ishizawa : Hydrocortisone administration was associated with improved survival in Japanese patients with cardiac arrest., Scientific Reports, Vol.7, No.1, 2017. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 112397 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-017-17686-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29263333 ● Search Scopus @ Elsevier (PMID): 29263333 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-017-17686-3 (Tokushima University Institutional Repository: 112397, DOI: 10.1038/s41598-017-17686-3, PubMed: 29263333)
33.	Shiho Sato, Yoshito Zamami, Toru Imai, Satoshi Tanaka, Toshihiro Koyama, Takahiro Niimura, Masayuki Chuma, Tadashi Koga, Kenshi Takechi, Yasuko Kurata, Yutaka Kondo, Yuki Izawa-Ishizawa, Toshiaki Sendo, Hironori Nakura and Keisuke Ishizawa : Meta-analysis of the efficacies of amiodarone and nifekalant in shock-resistant ventricular fibrillation and pulseless ventricular tachycardia., Scientific Reports, Vol.7, No.1, 2017. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 112393 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-017-13073-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28978927 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030715238 (Tokushima University Institutional Repository: 112393, DOI: 10.1038/s41598-017-13073-0, PubMed: 28978927, Elsevier: Scopus)
34.	Yasumasa Ikeda, Yuya Horinouchi, Hamano Hirofumi, Hirayama Tasuku, Seiji Kishi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Ken-ichi Aihara, Hideko Nagasawa, Koichiro Tsuchiya and Toshiaki Tamaki : Dietary iron restriction alleviates renal tubulointerstitial injury induced by protein overload in mice, Scientific Reports, Vol.7, No.1, 10621, 2017. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 112368 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-017-11089-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28878231 ● Search Scopus @ Elsevier (PMID): 28878231 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-017-11089-0 (Tokushima University Institutional Repository: 112368, DOI: 10.1038/s41598-017-11089-0, PubMed: 28878231)
35.	Keisuke Oshima, Yasumasa Ikeda, Yuya Horinouchi, Hiroaki Watanabe, Hirofumi Hamano, Yoshitaka Kihira, Seiji Kishi, Yuki Izawa-Ishizawa, Licht Miyamoto, Tasuku Hirayama, Hideko Nagasawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron suppresses erythropoietin expression via oxidative stress-dependent hypoxia-inducible factor-2 alpha inactivation, Laboratory Investigation; a Journal of Technical Methods and Pathology, Vol.97, No.5, 555-566, 2017. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 113749 (Link to Publication Site) ● Publication site (DOI): 10.1038/labinvest.2017.11 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28263291 ● Search Scopus @ Elsevier (PMID): 28263291 ● Search Scopus @ Elsevier (DOI): 10.1038/labinvest.2017.11 (Tokushima University Institutional Repository: 113749, DOI: 10.1038/labinvest.2017.11, PubMed: 28263291)
36.	Yutaka Fukunaga, Yuki Izawa-Ishizawa, Yuya Horinouchi, Eriko Sairyo, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Yoshiro Abe, Ichiro Hashimoto and Toshiaki Tamaki : Topical Application of Nitrosonifedipine, a Novel Radical Scavenger, Ameliorates Ischemic Skin Flap Necrosis in a Mouse Model., Wound Repair and Regeneration, Vol.25, No.2, 217-223, 2017. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 110118 (Link to Publication Site) ● Publication site (DOI): 10.1111/wrr.12510 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28090711 ● Search Scopus @ Elsevier (PMID): 28090711 ● Search Scopus @ Elsevier (DOI): 10.1111/wrr.12510 (Tokushima University Institutional Repository: 110118, DOI: 10.1111/wrr.12510, PubMed: 28090711)
37.	Yasumasa Ikeda, Mizuki Imao, Akiho Satoh, Hiroaki Watanabe, Hirofumi Hamano, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron-induced skeletal muscle atrophy involves an Akt-forkhead box O3-E3 ubiquitin ligase-dependent pathway, Journal of Trace Elements in Medicine and Biology, Vol.35, No.5, 66-76, 2016. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 113750 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jtemb.2016.01.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27049128 ● Search Scopus @ Elsevier (PMID): 27049128 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jtemb.2016.01.011 (Tokushima University Institutional Repository: 113750, DOI: 10.1016/j.jtemb.2016.01.011, PubMed: 27049128)
38.	Yasumasa Ikeda, Hirofumi Hamano, Akiho Satoh, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Bilirubin exerts pro-angiogenic effects through an Akt-eNOS-dependent pathway, Hypertension Research, Vol.38, No.11, 733-740, 2015. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 113751 (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2015.74 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26134126 ● Summary page in Scopus @ Elsevier: 2-s2.0-84946558014 (Tokushima University Institutional Repository: 113751, DOI: 10.1038/hr.2015.74, PubMed: 26134126, Elsevier: Scopus)
39.	Soichiro Tajima, Yasumasa Ikeda, Hideaki Enomoto, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II alters the expression of duodenal iron transporters, hepatic hepcidin, and body iron distribution in mice, European Journal of Nutrition, Vol.54, No.5, 709-719, 2015. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 113753 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00394-014-0749-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25096756 ● Summary page in Scopus @ Elsevier: 2-s2.0-84937513465 (Tokushima University Institutional Repository: 113753, DOI: 10.1007/s00394-014-0749-1, PubMed: 25096756, Elsevier: Scopus)
40.	Yoshitaka Kihira, Ariunzaya Burentogtokh, Mari Itoh, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia decreases glucagon-like peptide-1 secretion from GLUTag cell line, Biological & Pharmaceutical Bulletin, Vol.38, No.4, 514-521, 2015. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 109948 (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b14-00612 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25832631 ● CiNii @ National Institute of Informatics (CRID): 1390001204631777920 ● Summary page in Scopus @ Elsevier: 2-s2.0-84928951796 (Tokushima University Institutional Repository: 109948, DOI: 10.1248/bpb.b14-00612, PubMed: 25832631, CiNii: 1390001204631777920, Elsevier: Scopus)
41.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Licht Miyamoto, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : A Long-Term High-Fat Diet Changes Iron Distribution in Body, Increasing Iron Accumulation Specifically in the Mouse Spleen, Journal of Nutritional Science and Vitaminology, Vol.61, No.1, 20-27, 2015. (Summary) 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. (Keyword) iron/spleen/diet / high fat/diabetes mellitus / type 2/DMT1 protein (iron transporter) (Link to Publication Site) ● Publication site (DOI): 10.3177/jnsv.61.20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25994136 ● CiNii @ National Institute of Informatics (CRID): 1390282681302013696 ● Summary page in Scopus @ Elsevier: 2-s2.0-84929747372 (DOI: 10.3177/jnsv.61.20, PubMed: 25994136, CiNii: 1390282681302013696, Elsevier: Scopus)
42.	Nhat-Tu Le, Yuichiro Takei, Yuki Izawa-Ishizawa, Kyung-Sun Heo, Hakjoo Lee, V Alan Smrcka, L Benjamin Miller, Ae Kyung Ko, Sara Ture, Craig Morrell, Keigi Fujiwara, Masashi Akaike and Jun-Ichi Abe : Identification of Activators of ERK5 Transcriptional Activity by High-Throughput Screening and the Role of Endothelial ERK5 in Vasoprotective Effects Induced by Statins and Antimalarial Agents., The Journal of Immunology, Vol.193, No.7, 3803-3815, 2014. (Summary) Because ERK5 inhibits endothelial inflammation and dysfunction, activating ERK5 might be a novel approach to protecting vascular endothelial cells (ECs) against various pathological conditions of the blood vessel. We have identified small molecules that protect ECs via ERK5 activation and determined their contribution to preventing cardiac allograft rejection. Using high-throughput screening, we identified certain statins and antimalarial agents including chloroquine, hydroxychloroquine, and quinacrine as strong ERK5 activators. Pitavastatin enhanced ERK5 transcriptional activity and Kruppel-like factor-2 expression in cultured human and bovine ECs, but these effects were abolished by the depletion of ERK5. Chloroquine and hydroxychloroquine upregulated ERK5 kinase activity and inhibited VCAM-1 expression in an ERK5-dependent but MAPK/ERK kinase 5- and Kruppel-like factor 2/4-independent manner. Leukocyte rolling and vascular reactivity were used to evaluate endothelial function in vivo, and we found that EC-specific ERK5 knockout (ERK5-EKO) mice exhibited increased leukocyte rolling and impaired vascular reactivity, which could not be corrected by pitavastatin. The role of endothelial ERK5 in acute cardiac allograft rejection was also examined by heterotopic grafting of the heart obtained from either wild-type or ERK5-EKO mice into allomismatched recipient mice. A robust increase in both inflammatory gene expression and CD45-positive cell infiltration into the graft was observed. These tissue rejection responses were inhibited by pitavastatin in wild-type but not ERK5-EKO hearts. Our study has identified statins and antimalarial drugs as strong ERK5 activators and shown that ERK5 activation is preventive of endothelial inflammation and dysfunction and acute allograft rejection. (Link to Publication Site) ● Publication site (DOI): 10.4049/jimmunol.1400571 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25187658 ● Search Scopus @ Elsevier (PMID): 25187658 ● Search Scopus @ Elsevier (DOI): 10.4049/jimmunol.1400571 (DOI: 10.4049/jimmunol.1400571, PubMed: 25187658)
43.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Masaki Ueno, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya and Toshiaki Tamaki : Smooth muscle cell specific Hif-1 deficiency suppresses angiotensin II-induced vascular remodeling in mice, Cardiovascular Research, Vol.102, No.3, 460-468, 2014. (Summary) 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. (Keyword) Angiotensin II / Animals / Fibrosis / Gene Expression Regulation / Hemodynamics / Hypoxia-Inducible Factor 1, alpha Subunit / Mice / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / phosphorylation / Superoxides / Vascular Remodeling (Tokushima University Institutional Repository) ● Metadata: 106145 (Link to Publication Site) ● Publication site (DOI): 10.1093/cvr/cvu061 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24623277 ● Summary page in Scopus @ Elsevier: 2-s2.0-84901457818 (Tokushima University Institutional Repository: 106145, DOI: 10.1093/cvr/cvu061, PubMed: 24623277, Elsevier: Scopus)
44.	Atsushi Morimoto, Shuhei Tomita, Masaki Imanishi, Go Shioi, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Mitsuru Takaku, Ichiro Hashimoto, Yasumasa Ikeda, Hideki Nakanishi and Toshiaki Tamaki : Overexpressed HIF-2α in Endothelial Cells Promotes Vascularization and Improves Random Pattern Skin Flap Survival., Plastic and Reconstructive Surgery. Global Open, Vol.2, No.4, e132, 2014. (Summary) Specific overexpression of HIF-2 in ECs promoted vascularization and enhanced skin flap survival in vivo in a mouse model. (Tokushima University Institutional Repository) ● Metadata: 106138 (Link to Publication Site) ● Publication site (DOI): 10.1097/GOX.0000000000000083 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25289325 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897362750 (Tokushima University Institutional Repository: 106138, DOI: 10.1097/GOX.0000000000000083, PubMed: 25289325, Elsevier: Scopus)
45.	Yoshitaka Kihira, Mariko Miyake, Manami Hirata, Yoji Hoshina, Kana Kato, Hitoshi Shirakawa, Hiroshi Sakaue, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation., PLoS ONE, Vol.9, No.4, e93856, 2014. (Summary) 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. (Keyword) Adipocytes / Animals / Blotting, Western / Chemokine CCL2 / DNA Primers / Diabetes Mellitus, Type 2 / Gene Deletion / Glucagon-Like Peptide 1 / Glucose Tolerance Test / Hypoxia-Inducible Factor 1, alpha Subunit / Immunohistochemistry / Insulin / Mice / Mice, Knockout / Real-Time Polymerase Chain Reaction / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0093856 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705496 ● Summary page in Scopus @ Elsevier: 2-s2.0-84899440448 (DOI: 10.1371/journal.pone.0093856, PubMed: 24705496, Elsevier: Scopus)
46.	Yasumasa Ikeda, Iori Ozono, Soichro Tajima, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron chelation by deferoxamine prevents renal interstitial fibrosis in mice with unilateral ureteral obstruction, PLoS ONE, Vol.9, No.2, e89355, 2014. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 113752 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0089355 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24586712 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897786390 (Tokushima University Institutional Repository: 113752, DOI: 10.1371/journal.pone.0089355, PubMed: 24586712, Elsevier: Scopus)
47.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Noriko Yamano, Maki Urushihara, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Asami Nuno, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shoji Kagami, Hiroyuki Kobori, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates the progression of type 2 diabetic nephropathy by exerting antioxidative effects, PLoS ONE, Vol.9, No.1, e86335, 2014. (Summary) 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. (Keyword) Animals / Antioxidants / Cell Line / Diabetic Nephropathies / Humans / Male / Mice / Mice, Inbred C57BL / knockout mice / Nifedipine / Nitric Oxide Synthase Type III / Nitroso Compounds / oxidative stress (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0086335 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24489716 ● Summary page in Scopus @ Elsevier: 2-s2.0-84900332178 (DOI: 10.1371/journal.pone.0086335, PubMed: 24489716, Elsevier: Scopus)
48.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Dietary iron restriction inhibits progression of diabetic nephropathy in db/db mice., American Journal of Physiology, Renal Physiology, Vol.304, No.7, F1028-F1036, 2013. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.1152/ajprenal.00473.2012 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23389454 ● Search Scopus @ Elsevier (PMID): 23389454 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00473.2012 (DOI: 10.1152/ajprenal.00473.2012, PubMed: 23389454)
49.	Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Sumiko Yoshida, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Bovine milk-derived lactoferrin exerts proangiogenic effects in an Src-Akt-eNOS-dependent manner in response to ischemia, Journal of Cardiovascular Pharmacology, Vol.61, No.5, 423-429, 2013. (Summary) 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. (Keyword) Animals / Aorta / Cell Movement / Cell Proliferation / Cells, Cultured / Endothelial Cells / Endothelium, Vascular / Enzyme Activation / Hindlimb / Humans / Ischemia / Lactoferrin / Laser-Doppler Flowmetry / Mice / Mice, Inbred C57BL / Milk / Neovascularization, Physiologic / Nitric Oxide Synthase Type III / Phosphorylation / Proto-Oncogene Proteins c-akt / Reperfusion Injury / Signal Transduction / src-Family Kinases (Tokushima University Institutional Repository) ● Metadata: 113754 (Link to Publication Site) ● Publication site (DOI): 10.1097/FJC.0b013e318287d526 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23364610 ● Search Scopus @ Elsevier (PMID): 23364610 ● Search Scopus @ Elsevier (DOI): 10.1097/FJC.0b013e318287d526 (Tokushima University Institutional Repository: 113754, DOI: 10.1097/FJC.0b013e318287d526, PubMed: 23364610)
50.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Yuki Izawa-Ishizawa, Shoko Fujii, Erika Tominaga, Teppei Tsuneishi, Yuya Horinouchi, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Ken-ichi Aihara, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates angiotensin II-induced vascular remodeling via antioxidative effects, Naunyn-Schmiedeberg's Archives of Pharmacology, Vol.386, No.1, 29-39, 2013. (Summary) 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. (Keyword) Angiotensin II / Animals / Antioxidants / Aorta, Thoracic / calcium / Cell Movement / Cell Proliferation / Fibrosis / Male / Mice / Mice, Inbred C57BL / Muscle, Smooth, Vascular / Nifedipine / Nitroso Compounds / oxidative stress / Rats / reactive oxygen species (Link to Publication Site) ● Publication site (DOI): 10.1007/s00210-012-0810-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23149861 ● Summary page in Scopus @ Elsevier: 2-s2.0-84872316103 (DOI: 10.1007/s00210-012-0810-7, PubMed: 23149861, Elsevier: Scopus)
51.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Licht Miyamoto, Shoko Fujii, Hironori Taira, Yoshitaka Kihira, Yasumasa Ikeda, Shuichi Hamano, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II receptor blocker improves tumor necrosis factor-α-induced cytotoxicity via antioxidative effect in human glomerular endothelial cells, Pharmacology, Vol.90, No.5-6, 324-331, 2012. (Summary) 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. (Keyword) Angiotensin II Type 1 Receptor Blockers / apoptosis / Cell Survival / Cells, Cultured / Endothelial Cells / Humans / Imidazoles / Intercellular Adhesion Molecule-1 / Kidney Glomerulus / reactive oxygen species / Tetrazoles / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1159/000343244 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23052181 ● Summary page in Scopus @ Elsevier: 2-s2.0-84867214872 (DOI: 10.1159/000343244, PubMed: 23052181, Elsevier: Scopus)
52.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Takashi Iwase, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya, Masataka Sata, Masashi Akaike, Shigeaki Kato, Toshio Matsumoto and Toshiaki Tamaki : Heparin cofactor II, a serine protease inhibitor, promotes angiogenesis via activation of the AMP-activated protein kinase-endothelial nitric-oxide synthase signaling pathway, The Journal of Biological Chemistry, Vol.287, No.41, 34256-34263, 2012. (Summary) 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. (Keyword) Heparin cofactor II (HCII) / vascular endothelial cells / angiogenesis (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M112.353532 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22904320 ● Search Scopus @ Elsevier (PMID): 22904320 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M112.353532 (DOI: 10.1074/jbc.M112.353532, PubMed: 22904320)
53.	Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Estrogen regulates hepcidin expression via GPR30-BMP6-dependent signaling in hepatocytes, PLoS ONE, Vol.7, No.7, e40465, 2012. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0040465 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22792339 ● Summary page in Scopus @ Elsevier: 2-s2.0-84863827034 (DOI: 10.1371/journal.pone.0040465, PubMed: 22792339, Elsevier: Scopus)
54.	Soichiro Tajima, Yasumasa Ikeda, Kaori Sawada, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : 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., American Journal of Physiology, Endocrinology and Metabolism, Vol.302, No.1, E77-86, 2012. (Summary) 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. (Keyword) ferrum / oxidative stress / obesity (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00033.2011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21917632 ● Search Scopus @ Elsevier (PMID): 21917632 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00033.2011 (DOI: 10.1152/ajpendo.00033.2011, PubMed: 21917632)
55.	Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Basic fibroblast growth factor regulates glucose metabolism through glucose transporter 1 induced by hypoxia-inducible factor-1α in adipocytes, The International Journal of Biochemistry & Cell Biology, Vol.43, No.11, 1602-1611, 2011. (Summary) 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. (Keyword) 3T3-L1 Cells / Adipocytes / Animals / Anoxia / Diabetes Mellitus, Type 2 / Fibroblast Growth Factor 2 / Glucose / Glucose Transporter Type 1 / Glycolysis / Hypoxia-Inducible Factor 1, alpha Subunit / Injections, Intraperitoneal / Insulin / Insulin Receptor Substrate Proteins / Male / Mice / Obesity / Phosphorylation / Proto-Oncogene Proteins c-akt / Signal Transduction / Transcriptional Activation / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biocel.2011.07.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21810481 ● Search Scopus @ Elsevier (PMID): 21810481 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biocel.2011.07.009 (DOI: 10.1016/j.biocel.2011.07.009, PubMed: 21810481)
56.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Narantungalag Dorjsuren, Erika Miki, Yoshitaka Kihira, Yasumasa Ikeda, Shuichi Hamano, Kazuyoshi Kawazoe, Kazuo Minakuchi, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II receptor blocker attenuates PDGF-induced mesangial cell migration in a receptor-independent manner, Nephrology, Dialysis, Transplantation, Vol.25, No.2, 364-372, 2010. (Summary) 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. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Cell Movement / Cells, Cultured / Imidazoles / Male / Mesangial Cells / Platelet-Derived Growth Factor / Rats / Rats, Sprague-Dawley / Signal Transduction / Tetrazoles (Link to Publication Site) ● Publication site (DOI): 10.1093/ndt/gfp520 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19812233 ● Search Scopus @ Elsevier (PMID): 19812233 ● Search Scopus @ Elsevier (DOI): 10.1093/ndt/gfp520 (DOI: 10.1093/ndt/gfp520, PubMed: 19812233)
57.	Hirotsugu Kurobe, Masahisa Urata, Masaki Ueno, Masaaki Ueki, Shiro Ono, Yuki Izawa-Ishizawa, Yayoi Fukuhara, Yu Lei, Adiratna Mat Ripen, Tamotsu Kanbara, Ken-ichi Aihara, Keisuke Ishizawa, Masashi Akaike, Frank J. Gonzalez, Toshiaki Tamaki, Yousuke Takahama, Masanori Yoshizumi, Tetsuya Kitagawa and Shuhei Tomita : Role of Hypoxia-Inducible Factor 1α in T Cells as a Negative Regulator in Development of Vascular Remodeling, Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.30, No.2, 210-217, 2010. (Summary) 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. (Keyword) Animals / Antibody Formation / Arteriosclerosis / Cell Hypoxia / Cell Proliferation / Chemokine CXCL12 / Chemotaxis, Leukocyte / cytokinesis / Disease Models, Animal / Femoral Artery / Hyperplasia / Hypoxia-Inducible Factor 1, alpha Subunit / Immunity, Cellular / immunohistochemistry / Lymphocyte Activation / male / Mice / knockout mice / Nitroimidazoles / Receptors, Antigen, T-Cell / T lymphocytes / Thymus Gland / Time Factors / Tunica Intima (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.109.192666 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20007912 ● Search Scopus @ Elsevier (PMID): 20007912 ● Search Scopus @ Elsevier (DOI): 10.1161/ATVBAHA.109.192666 (DOI: 10.1161/ATVBAHA.109.192666, PubMed: 20007912)
58.	Keisuke Ishizawa, Narantungalag Dorjsuren, Yuki Izawa-Ishizawa, Rika Sugimoto, Yasumasa Ikeda, Yoshitaka Kihira, Kazuyoshi Kawazoe, Shuhei Tomita, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration, The Journal of Endocrinology, Vol.202, No.2, 309-316, 2009. (Summary) 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. (Keyword) Adiponectin / Animals / Cell Movement / Cells, Cultured / Dose-Response Relationship, Drug / Enzyme Inhibitors / Glomerular Mesangium / Imidazoles / Male / Mitogen-Activated Protein Kinase 7 / Phosphorylation / Platelet-Derived Growth Factor / Pyridines / RNA, Small Interfering / Rats / Rats, Sprague-Dawley / Recombinant Proteins / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1677/JOE-08-0469 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19460854 ● Search Scopus @ Elsevier (PMID): 19460854 ● Search Scopus @ Elsevier (DOI): 10.1677/JOE-08-0469 (DOI: 10.1677/JOE-08-0469, PubMed: 19460854)
59.	Yuki Motobayashi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakiko Orino, Kunihisa Yamaguchi, Kazuyoshi Kawazoe, Shuichi Hamano, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 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, Hypertension Research, Vol.32, No.3, 188-193, 2009. (Summary) 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. (Keyword) Adiponectin / Aminoimidazole Carboxamide / Animals / Blotting, Western / Cell Movement / Enzyme Activation / Enzyme Activators / Insulin-Like Growth Factor I / Male / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Myocytes, Smooth Muscle / Oncogene Protein v-akt / Phosphorylation / Rats / Rats, Sprague-Dawley / Ribonucleotides / signal transduction / bcl-Associated Death Protein / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2008.19 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19262481 ● Search Scopus @ Elsevier (PMID): 19262481 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2008.19 (DOI: 10.1038/hr.2008.19, PubMed: 19262481)
60.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Sachiyo Ohnishi, Yuki Motobayashi, Kazuyoshi Kawazoe, Shuichi Hamano, Koichiro Tsuchiya, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : Quercetin Glucuronide Inhibits Cell Migration and Proliferation by Platelet-Derived Growth Factor in Vascular Smooth Muscle Cells, Journal of Pharmacological Sciences, Vol.109, No.2, 257-264, 2009. (Summary) 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. (Keyword) Animals / Antioxidants / Cell Movement / Cell Proliferation / Cells, Cultured / Glucuronides / MAP Kinase Kinase 4 / Male / Muscle, Smooth, Vascular / Platelet-Derived Growth Factor / Quercetin / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.08236FP (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19202317 ● Search Scopus @ Elsevier (PMID): 19202317 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.08236FP (DOI: 10.1254/jphs.08236FP, PubMed: 19202317)
61.	Yasuhisa Kanematsu, Kunihisa Yamaguchi, Hideki Ohnishi, Yuki Motobayashi, Keisuke Ishizawa, Yuki Izawa, Kazuyoshi Kawazoe, Shuji Kondo, Shoji Kagami, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Dietary doses of nitrite restore circulating nitric oxide level and improve renal injury in L-NAME-induced hypertensive rats, American Journal of Physiology, Renal Physiology, Vol.295, No.5, F1457-F1462, 2008. (Summary) 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. (Keyword) Administration, Oral / Animals / blood pressure / Body Weight / Diet / Hemoglobin A, Glycosylated / Hypertension / Kidney / Kidney Diseases / Kidney Glomerulus / Male / NG-Nitroarginine Methyl Ester / Nitrates / nitric oxide / Proteinuria / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1152/ajprenal.00621.2007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18753302 ● Search Scopus @ Elsevier (PMID): 18753302 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00621.2007 (DOI: 10.1152/ajprenal.00621.2007, PubMed: 18753302)
62.	Yuki Izawa, Masanori Yoshizumi, Keisuke Ishizawa, Yoshiko Fujita, Shuji Kondo, Shoji Kagami, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 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, Hypertension Research, Vol.30, No.11, 1107-1117, 2007. (Summary) 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. (Keyword) Animals / Cell Movement / Humans / MAP Kinase Kinase 5 / Male / Mice / Mice, Inbred C57BL / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinase 7 / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Phosphoproteins / Phosphorylation / Platelet-Derived Growth Factor / Protein Tyrosine Phosphatase, Non-Receptor Type 11 / Rats (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.30.1107 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18250560 ● Search Scopus @ Elsevier (PMID): 18250560 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.30.1107 (DOI: 10.1291/hypres.30.1107, PubMed: 18250560)
63.	Yasuhisa Kanematsu, Koichiro Tsuchiya, Hideki Onishi, Yuki Motobayashi, Yuki Izawa, Manabu Ishihara, Keisuke Ishizawa, Shinji Abe, Kazuyoshi Kawazoe and Toshiaki Tamaki : Effects of angiotensin II type 1 receptor blockade on the systemic blood nitric oxide dynamics in Nω-nitro-L-arginine methyl ester-treated rats, Hypertension Research, Vol.29, No.5, 369-374, 2006. (Summary) 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. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Antihypertensive Agents / Blood Pressure / Body Weight / Electron Spin Resonance Spectroscopy / Endothelium, Vascular / Heart Rate / Hemodynamics / Hemoglobins / Hydralazine / Hypertension / Imidazoles / Male / NG-Nitroarginine Methyl Ester / Nitric Oxide / Rats / Rats, Sprague-Dawley / Tetrazoles (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.29.369 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16832158 ● Search Scopus @ Elsevier (PMID): 16832158 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.29.369 (DOI: 10.1291/hypres.29.369, PubMed: 16832158)
64.	Yoshiko Fujita, Masanori Yoshizumi, Yuki Izawa, Nermin Ali, Yasuhisa Kanematsu, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Transactivation of fetal liver kinase-1/kinase-insert domain-containing receptor by lysophosphatidylcholine induces vascular endothelial cell proliferation., Endocrinology, Vol.147, No.3, 1377-1385, 2006. (Summary) 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. (Keyword) atherosclerosis / Benzoquinones / Blotting, Western / Cell Line / Cell Proliferation / Cell Survival / Cells, Cultured / Cinnamates / Disease Progression / Endothelial Cells / Endothelium, Vascular / Humans / Immunoblotting / Immunoprecipitation / Lactams, Macrocyclic / Ligands / Lysophosphatidylcholines / phosphorylation / Protein Structure, Tertiary / Protein-Tyrosine Kinases / Pyrimidines / Quinazolines / Quinones / Transcriptional Activation / Transfection / Vascular Endothelial Growth Factor Receptor-2 (Link to Publication Site) ● Publication site (DOI): 10.1210/en.2005-0644 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16322069 ● Summary page in Scopus @ Elsevier: 2-s2.0-32644452665 (DOI: 10.1210/en.2005-0644, PubMed: 16322069, Elsevier: Scopus)
65.	Yoshiko Fujita, Yuki Izawa, Nermin Ali, Koichiro Tsuchiya, Shuichi Hamano, Toshiaki Tamaki and Masanori Yoshizumi : Pramipexole protects against H2O2-induced PC12 cell death, Naunyn-Schmiedeberg's Archives of Pharmacology, Vol.372, No.4, 257-266, 2006. (Summary) Pramipexole, a novel non-ergot dopamine (DA) agonist, has been successfully applied to the treatment of Parkinson's disease (PD). Although the specific cause of PD remains unknown, recent studies have provided evidence that oxidative stress plays a role in the parthenogenesis of the disease. In the present study, we examined the effect of pramipexole on hydrogen peroxide (H2O2, 100 microM)-induced PC12 cell death, and the intracellular mechanism of this effect. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay revealed that pretreatment of PC12 cells with pramipexole (1-100 microM) resulted in significant protection against H2O2-induced cell death in a concentration-dependent manner. The protective effect of pramipexole was not affected by pretreatment with the DA receptor antagonists sulpiride, spiperone or domperidone, suggesting that the effect of pramipexole is not mediated by DA receptors. In PC12 cells, pramipexole inhibited H2O2-induced lactate dehydrogenase (LDH) leakage, as well as H2O2-induced cytochrome c release and caspase-3 activation with the resultant apoptosis. It was also observed in PC12 cells that H2O2 stimulated phosphorylation of mitogen-activated protein (MAP) kinases, i.e., extracellular signal-regulated kinase1/2 (ERK1/2), c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase. Pramipexole inhibited H2O2-induced JNK and p38 MAP kinase, but not ERK1/2 phosphorylation. Furthermore, in these cells experiments with a fluorescent probe, 2-[6-(4'-amino)phenoxy-3H-xanthen-3-on-9-yl]benzoic acid, revealed that pramipexole, the JNK inhibitor SP600125 and the p38 MAP kinase inhibitor SB203580 inhibited the generation of H2O2-induced reactive oxygen species. Caspase inhibitors Z-DEVD-FMK and Z-IETD-FMK, as well as SP600125 and SB203580, inhibited H2O2-induced PC12 cell death to a similar extent as pramipexole. These results suggest that pramipexole exerts a protective effect against oxidative stress-induced PC12 cell death in part through an inhibition of JNK and p38 MAP kinase. (Keyword) Animals / Antiparkinson Agents / apoptosis / Benzothiazoles / Caspase 3 / Caspases / cell death / Cell Survival / Cytochromes c / Dopamine Agonists / Dopamine Antagonists / hydrogen peroxide / L-Lactate Dehydrogenase / Mitogen-Activated Protein Kinases / Neuroprotective Agents / oxidative stress / PC12 Cells / Rats / Thiazoles (Link to Publication Site) ● Publication site (DOI): 10.1007/s00210-005-0025-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16362428 ● Summary page in Scopus @ Elsevier: 2-s2.0-31144433876 (DOI: 10.1007/s00210-005-0025-2, PubMed: 16362428, Elsevier: Scopus)
66.	Hiroyuki Sakakibara, Kaori Ishida, Yuki Izawa, Yuko Minami, Satomi Saito, Yoshichika Kawai, Veronika Butterweck, Toshiaki Tamaki, Yutaka Nakaya and Junji Terao : Effects of forced swimming stress on rat brain function, The Journal of Medical Investigation : JMI, Vol.52, No.Suppl., 300-3001, 2005. (Summary) Chronic stress has been reported to be an essential factor for depression. In this study, the effect of forced swimming stress on neurotransmitters and cellular signaling pathway contributing to brain functions was investigated using the forced swimming test (FST) in order to understanding of mechanisms to regulate stress signals in brain. Antidepressant drug, imipramine, significantly reduced the immobility time of male rats in the FST by 85% at a dose of 15 mg/kg for 2 weeks. This result indicated that the swimming stress caused a depressed state in the rats without administration of imipramine. Swimming stress significantly lowered the serotonergic ratio and also markedly enhanced the phosphorylation of ERK1/2 in the hypothalamus region compared to the rats without FST. These phenomena may be included in key mechanisms of the development of depression. (Keyword) Animals / Antidepressive Agents, Tricyclic / brain / Chromatography, High Pressure Liquid / Enzyme Activation / Hippocampus / Hydroxyindoleacetic Acid / Imipramine / Immunoblotting / Male / Mitogen-Activated Protein Kinase 3 / Motor Activity / phosphorylation / Rats / Rats, Inbred Strains / Serotonin / signal transduction / Stress, Physiological / Swimming / Time Factors (Tokushima University Institutional Repository) ● Metadata: 111587 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.52.300 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16366521 ● Search Scopus @ Elsevier (PMID): 16366521 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.52.300 (Tokushima University Institutional Repository: 111587, DOI: 10.2152/jmi.52.300, PubMed: 16366521)
67.	Yuki Izawa, Masanori Yoshizumi, Keisuke Ishizawa, Yoshiko Fujita, Shuji Kondo, Shoji Kagami, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : ERK1/2 activation by angiotensin II inhibits insulin-induced glucose uptake in vascular smooth muscle cells, Experimental Cell Research, Vol.308, No.2, 291-299, 2005. (Summary) 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. (Keyword) Angiotensin II / Animals / Blood Vessels / Cell Membrane / Cytoplasm / Enzyme Activation / Enzyme Inhibitors / Glucose / Glucose Transporter Type 4 / Hypertension / Insulin / Insulin Receptor Substrate Proteins / Insulin Resistance / JNK Mitogen-Activated Protein Kinases / Male / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Monosaccharide Transport Proteins / Muscle Proteins / Myocytes, Smooth Muscle / Phosphoproteins / Phosphorylation / Protein Transport / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Rats / Rats, Sprague-Dawley / Serine / Tyrosine (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yexcr.2005.04.028 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15921682 ● Search Scopus @ Elsevier (PMID): 15921682 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yexcr.2005.04.028 (DOI: 10.1016/j.yexcr.2005.04.028, PubMed: 15921682)
68.	Keisuke Ishizawa, Yuki Izawa, Hiroyuki Ito, Chieko Miki, Kayoko Miyama, Yoshiko Fujita, Yasuhisa Kanematsu, Koichiro Tsuchiya, Toshiaki Tamaki, Akira Nishiyama and Masanori Yoshizumi : Aldosterone stimulates vascular smooth muscle cell proliferation via big mitoten-activated protein kinase 1 activation, Hypertension, Vol.46, No.4, 1046-1052, 2005. (Summary) 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. (Keyword) 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt / Aldosterone / Animals / Calcium-Calmodulin-Dependent Protein Kinases / Cell Proliferation / Cells, Cultured / Cycloheximide / Enzyme Activation / flavonoids / Genes, Dominant / MAP Kinase Kinase 5 / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinase 7 / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Protein Synthesis Inhibitors / Rats / Receptors, Mineralocorticoid / Spironolactone / Transfection (Link to Publication Site) ● Publication site (DOI): 10.1161/01.HYP.0000172622.51973.f5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16087789 ● Search Scopus @ Elsevier (PMID): 16087789 ● Search Scopus @ Elsevier (DOI): 10.1161/01.HYP.0000172622.51973.f5 (DOI: 10.1161/01.HYP.0000172622.51973.f5, PubMed: 16087789)
69.	Yasumasa Ikeda, Ken-ichi Aihara, Takashi Sato, Masashi Akaike, Masanori Yoshizumi, Yuki Suzaki, Yuki Izawa-Ishizawa, Mitsunori Fujimura, Shunji Hashizume, Midori Kato, Shusuke Yagi, Toshiaki Tamaki, Hirotaka Kawano, Takahiro Matsumoto, Hiroyuki Azuma, Shigeaki Kato and Toshio Matsumoto : Androgen receptor gene knockout male mice exhibit impaired cardiac growth and exacerbation of angiotensin II-induced cardiac fibrosis., The Journal of Biological Chemistry, Vol.280, No.33, 29661-29666, 2005. (Summary) Androgen has anabolic effects on cardiac myocytes and has been shown to enhance left ventricular enlargement and function. However, the physiological and patho-physiological roles of androgen in cardiac growth and cardiac stress-induced remodeling remains unclear. We aimed to clarify whether the androgen-nuclear androgen receptor (AR) system contributes to the cardiac growth and angiotensin II (Ang II)-stimulated cardiac remodeling by using systemic AR-null male mice. AR knock-out (ARKO) male mice, at 25 weeks of age, and age-matched wild-type (WT) male mice were treated with or without Ang II stimulation (2.0 mg/kg/day) for 2 weeks. ARKO mice with or without Ang II stimulation showed a significant reduction in the heart-to-body weight ratio compared with those of WT mice. In addition, echocardiographic analysis demonstrated impairments of both the concentric hypertrophic response and left ventricular function in Ang II-stimulated ARKO mice. Western blot analysis of the myocardium revealed that activation of extracellular signal-regulated kinases (ERK) 1/2 and ERK5 by Ang II stimulation were lower in ARKO mice than those of WT mice. Ang II stimulation caused more prominent cardiac fibrosis in ARKO mice than in WT mice with enhanced expression of types I and III collagen and transforming growth factor-beta1 genes and with increased Smad2 activation. These results suggest that, in male mice, the androgen-AR system participates in normal cardiac growth and modulates cardiac adaptive hypertrophy and fibrosis during the process of cardiac remodeling under hypertrophic stress. (Keyword) Angiotensin II / Animals / blood pressure / Cardiomegaly / DNA-Binding Proteins / pulmonary fibrosis / Heart Rate / Male / Mice / Mice, Inbred C57BL / Mice, Inbred CBA / knockout mice / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinase 7 / myocardium / RNA, Messenger / Receptors, Androgen / Smad2 Protein / Trans-Activators / Transforming Growth Factor beta / Transforming Growth Factor beta1 / Ventricular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M411694200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15961403 ● Search Scopus @ Elsevier (PMID): 15961403 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M411694200 (DOI: 10.1074/jbc.M411694200, PubMed: 15961403)
70.	Ali Nermin, Masanori Yoshizumi, Yoshiko Fujita, Yuki Izawa, Yasuhisa Kanematsu, Keisuke Ishizawa, Koichiro Tsuchiya, Seiji Yano, Saburo Sone and Toshiaki Tamaki : A Novel Src Kinase Inhibitor, M475271, Inhibits VEGF-Induced Human Umbilical Vein Endothelial Cell Proliferation and Migration, Journal of Pharmacological Sciences, Vol.98, No.2, 130-141, 2005. (Summary) 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. (Keyword) M475271 / vascular endothelial growth factor / human umbilical vein endothelial cell proliferation and migration / angiogenesis (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.FP0040850 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15937404 ● Search Scopus @ Elsevier (PMID): 15937404 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.FP0040850 (DOI: 10.1254/jphs.FP0040850, PubMed: 15937404)
71.	Koichiro Tsuchiya, Yasuhisa Kanematsu, Masanori Yoshizumi, Hideki Ohnishi, Kazuyoshi Kirima, Yuki Izawa, Michiyo Shikishima, Tatsuhiro Ishida, Shuji Kondo, Shoji Kagami, Yoshiharu Takiguchi and Toshiaki Tamaki : Nitrite is an alternative source of NO in vivo, American Journal of Physiology, Heart and Circulatory Physiology, Vol.288, No.5, H2163-H2170, 2005. (Summary) In this study, we investigated whether orally administered nitrite is changed to NO and whether nitrite attenuates hypertension in a dose-dependent manner. We utilized a stable isotope of [15N]nitrite (15NO2-) as a source of nitrite to distinguish between endogenous nitrite and that exogenously administered and measured hemoglobin (Hb)-NO as an index of circulating NO in whole blood using electron paramagnetic resonance (EPR) spectroscopy. When 1 mg/kg Na15NO2 was orally administered to rats, an apparent EPR signal derived from Hb15NO (A(Z) = 23.4 gauss) appeared in the blood. The peak blood HbNO concentration occurred at the first measurement after intake (5 min) for treatment with 1 and 3 mg/kg (HbNO: 4.93 +/- 0.52 and 10.58 +/- 0.40 microM, respectively) and at 15 min with 10 mg/kg (HbNO: 38.27 +/- 9.23 microM). In addition, coadministration of nitrite (100 mg/l drinking water) with N(omega)-nitro-L-arginine methyl ester (L-NAME; 1 g/l) for 3 wk significantly attenuated the L-NAME-induced hypertension (149 +/- 10 mmHg) compared with L-NAME alone (170 +/- 13 mmHg). Furthermore, this phenomenon was associated with an increase in circulating HbNO. Our findings clearly indicate that orally ingested nitrite can be an alternative to L-arginine as a source of NO in vivo and may explain, at least in part, the mechanism of the nitrite/nitrate-rich Dietary Approaches to Stop Hypertension diet-induced hypotensive effects. (Keyword) nitric oxide / hypertension / electron paramagnetic resonance (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpheart.00525.2004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15626692 ● Search Scopus @ Elsevier (PMID): 15626692 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpheart.00525.2004 (DOI: 10.1152/ajpheart.00525.2004, PubMed: 15626692)
72.	Masumi Okamoto, Koichiro Tsuchiya, Yasuhisa Kanematsu, Yuki Izawa, Masanori Yoshizumi, Susumu Kagawa and Toshiaki Tamaki : Nitrite-derived nitric oxide formation following ischemia-reperfusion injyury in kidney., American Journal of Physiology, Renal Physiology, Vol.288, No.1, 182-187, 2005. (Summary) Nitric oxide (NO) is synthesized from l-arginine by nitric oxide synthase (NOS), and nitrite and nitrate are believed to be waste forms of NO. We previously reported an enzyme-independent pathway of NO generation from nitrite in acidic conditions. In this study, we show nitrite-derived NO formation in renal ischemia-reperfusion injury using electron paramagnetic resonance (EPR) spectroscopy. In this experiment, we utilized a stable isotope of [(15)N]nitrite as a source of nitrite to distinguish l-arginine-derived NO from [(15)N]nitrite-derived (15)NO. Intravenous infusion of a stable isotope of [(15)N]nitrite ((15)NO(2)(-)) facilitated the formation of Hb(15)NO during renal ischemia, which demonstrated that the origin of NO was nitrite. The EPR signal of Hb(15)NO in kidney appeared after 40 min of renal ischemia, and renal reperfusion decreased the Hb(15)NO level in the kidney and increased it in blood by contrast. In addition, the amount of HbNO was nitrite concentration dependent, and this formation was NOS independent. Our findings suggest that nitrite can be an alternative source of NO in ischemic kidney and that it binds with hemoglobin and then is spread by the circulation after reperfusion. (Keyword) Animals / Electron Spin Resonance Spectroscopy / Hemoglobins / Kidney / Male / nitric oxide / Nitric Oxide Synthase / Nitrites / Rats / Rats, Sprague-Dawley / Reperfusion Injury (Link to Publication Site) ● Publication site (DOI): 10.1152/ajprenal.00036.2004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15367387 ● Search Scopus @ Elsevier (PMID): 15367387 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00036.2004 (DOI: 10.1152/ajprenal.00036.2004, PubMed: 15367387)
73.	Koichiro Tsuchiya, Yoshiharu Takiguchi, Masumi Okamoto, Yuki Izawa, Yasuhisa Kanematsu, Masanori Yoshizumi and Toshiaki Tamaki : Malfunction of vascular control in lifestyle-related diseases : formation of systemic hemoglobin-nitric oxide Complex(HbNO) From Dietary Nitrite, Journal of Pharmacological Sciences, Vol.96, No.4, 395-400, 2004. (Summary) Nitric oxide (NO) has many physiological functions. It is believed to be produced from L-arginine by nitric oxide synthase (NOS), and nitrite and nitrate are waste forms of it. By the way, nitrate and nitrite are abundant in vegetables and fruits, especially leafy vegetables and pickled vegetables. Orally-ingested nitrate is changed to nitrite by micro-organelles living in the hypopharynx area, and nitrite is expected to change to NO in the stomach due to its low pH. Indeed, some researchers reported that NO is produced in the gastric cavity, although few reports mentioned the physiological meanings of this NO formation. Therefore, we investigated whether the nitrite-derived NO can shift to the circulation and acts like NOS-derived NO does in tissues. We adopted a stable isotope of nitrite (15NO2-) in order to distinguish between the endogenous nitrite and the exogenously administered one and measured nitrosyl hemoglobin (HbNO) as an index of circulating NO using electron paramagnetic resonance spectroscopy. It appeared that the oral administration of 15N-nitrite formed the Hb15NO in rat blood and decreased the blood pressure of chronic L-NAME treated rats. Our findings suggest that the intake of nitrite (or nitrate)-rich foods such as vegetables and fruits would alter the systemic HbNO dynamism, resulting in the improvement of cardiovascular diseases. (Keyword) nitric oxide(NO) / hemoglobin-NO adduct / electron paramagnetic resonance / nitrite (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.FMJ04006X3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15599101 ● Search Scopus @ Elsevier (PMID): 15599101 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.FMJ04006X3 (DOI: 10.1254/jphs.FMJ04006X3, PubMed: 15599101)
74.	Moe Kyaw, Masanori Yoshizumi, Koichiro Tsuchiya, Yuki Izawa, Yasuhisa Kanematsu, Yoshiko Fujita, Nermin Ali, Keisuke Ishizawa, Aiko Yamauchi and Toshiaki Tamaki : 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, Journal of Pharmacological Sciences, Vol.95, No.4, 483-486, 2004. (Summary) 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. (Keyword) Acetylcysteine / Angiotensin II / Animals / Antioxidants / Aorta, Thoracic / Cell Proliferation / Enzyme Activation / Glutathione / JNK Mitogen-Activated Protein Kinases / Male / Mitogen-Activated Protein Kinases / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Rats / Rats, Sprague-Dawley / Signal Transduction / Stereoisomerism / Thymidine / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.SC0040061 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15297771 ● Search Scopus @ Elsevier (PMID): 15297771 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.SC0040061 (DOI: 10.1254/jphs.SC0040061, PubMed: 15297771)
75.	Moe Kyaw, Masanori Yoshizumi, Koichiro Tsuchiya, Yuki Izawa, Yasuhisa Kanematsu and Toshiaki Tamaki : Atheroprotective effects of antioxidants through inhibition of mitogen-activated protein kinases, Acta Pharmacologica Sinica, Vol.25, No.8, 977-985, 2004. (Summary) Reactive oxygen species (ROS) have been known to play an important role in the pathogenesis of atherosclerosis and several other cardiovascular diseases. It is now apparent that ROS induce endothelial cell damage and vascular smooth muscle cell (VSMC) growth and cardiac remodeling, which are associated with hypertension, atherosclerosis, heart failure, and restenosis. Several lines of evidence have indicated that ROS and mitogen-activated protein (MAP) kinases were involved in vascular remodeling under various pathological conditions. Recently, it was also reported that MAP kinases were sensitive to oxidative stress. MAP kinases play an important role in cell differentiation, growth, apoptosis, and the regulation of a variety of transcription factors and gene expressions. Bioflavonoids and polyphenolic compounds are believed to be beneficial for the prevention and treatment of atherosclerosis and cardiovascular diseases. One of the most widely distributed bioflavonoids, 3,3',4',5,7-penta-hydroxyflavone (quercetin) and its metabolite quercetin 3-O-beta-D-glucuronide (Q3GA) inhibited Angiotensin II-stimulated JNK activation and resultant hypertrophy of VSMC. Several studies have suggested that various antioxidants including probucol, N-acetyl-L-cysteine, diphenylene iodonium, Trolox C (vitamin E analogue), and vitamin C inhibit VSMC growth, which is associated with pathogenesis of cardiovascular diseases. Therefore, inhibition of MAP kinases by antioxidant treatment may prove to be a therapeutic strategy for cardiovascular diseases. In contrast, some clinical studies have reported that antioxidant vitamins did not show beneficial effects in coronary artery disease or in a number of high-risk people. Thus, further studies are needed to clarify why antioxidants showed beneficial effects in vitro, whereas less satisfactory results were obtained in some clinical conditions. (Keyword) reactive oxygen species / mitogen-activated protein kinase / antioxidant / vascular smooth muscle cell / atherosclerosis (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15301727 ● Search Scopus @ Elsevier (PMID): 15301727 (PubMed: 15301727)
76.	Keisuke Ishizawa, Masanori Yoshizumi, Koichiro Tsuchiya, Hitoshi Houchi, Kazuo Minakuchi, Yuki Izawa, Yasuhisa Kanematsu, Shoji Kagami, Masao Hirose and Toshiaki Tamaki : 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, Hypertension Research, Vol.27, No.6, 433-440, 2004. (Summary) 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. (Keyword) Animals / Antibodies / Antihypertensive Agents / Cell Movement / Cells, Cultured / Chemokine CCL2 / Culture Media, Conditioned / Endothelin-1 / Glomerular Mesangium / Peptide Fragments / Peptides, Cyclic / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.27.433 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15253109 ● Search Scopus @ Elsevier (PMID): 15253109 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.27.433 (DOI: 10.1291/hypres.27.433, PubMed: 15253109)
77.	Yuki Suzaki, Masanori Yoshizumi, Shoji Kagami, Akira Nishiyama, Yuichi Ozawa, Moe Kyaw, Yuki Izawa, Yasuhisa Kanematsu, Koichiro Tsuchiya and Toshiaki Tamaki : BMK1 is activated in glomeruli of diabetic rats and in mesangial cells by high glucose conditions, Kidney International, Vol.65, No.5, 1749-1760, 2004. (Summary) High glucose causes renal cell injury through various signal transduction pathways, including mitogen-activated protein (MAP) kinases cascades. Big MAP kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a recently identified MAP kinase family member and was reported to be sensitive to osmotic and oxidative stress. However, the role of BMK1 in diabetic nephropathy has not been elucidated yet. We investigated whether BMK1 is activated in the glomeruli of Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus in comparison with the control Long Evans Tokushima Otsuka (LETO) rats. We also examined the effect of high glucose on BMK1 activity in cultured rat mesangial cells. BMK1 and ERK1/2 but not p38 were activated in the glomeruli of OLETF rats, which showed diabetic nephropathy at 52 weeks of age. High glucose, in addition to a high concentration of raffinose, caused rapid and significant activation of BMK1 in rat mesangial cells. MAP kinase/ERK kinase (MEK) inhibitors, U0126 and PD98059, both inhibited BMK1 activation by high glucose in a concentration-dependent manner. Protein kinase C (PKC) inhibition by GF109203X and PKC down-regulation with long-time phorbol myristate acetate (PMA) treatment both inhibited BMK1 and Src kinase activation. Src kinase inhibitors, herbimycin A and PP2, also inhibited high glucose-induced BMK1 activation. PKC inhibitors, Src inhibitors and MEK inhibitors, all inhibited cell proliferation by high glucose. Finally, transfection of dominant-negative MEK5, which is an upstream regulator of BMK1, abolished the BMK1-mediated rat mesangial cell proliferation stimulated by high glucose. In the present study, we demonstrated that high glucose activates BMK1 both in vivo and in vitro. It was suggested that high glucose induces PKC- and c-Src-dependent BMK1 activation. It could not be denied that BMK1 activation is induced through an osmotic stress-sensitive mechanism. BMK1-mediated mesangial cell growth may be involved in the pathogenesis of diabetic nephropathy. (Keyword) Animals / Butadienes / Cells, Cultured / Diabetes Mellitus, Type 2 / Diabetic Nephropathies / Enzyme Activation / Enzyme Inhibitors / Glomerular Mesangium / glucose / MAP Kinase Kinase 5 / Male / Mitogen-Activated Protein Kinase 7 / Nitriles / Organic Chemicals / Protein Kinase C / Protein-Tyrosine Kinases / Rats / Rats, Inbred OLETF (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1523-1755.2004.00576.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15086914 ● Search Scopus @ Elsevier (PMID): 15086914 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1523-1755.2004.00576.x (DOI: 10.1111/j.1523-1755.2004.00576.x, PubMed: 15086914)
78.	Moe Kyaw, Masanori Yoshizumi, Koichiro Tsuchiya, Shoji Kagami, Yuki Izawa, Yoshiko Fujita, Nermin Ali, Yasuhisa Kanematsu, Kazunori Toida, Kazunori Ishimura and Toshiaki Tamaki : Src and Cas are essentially but differentially involved in angiotensin II-stimulated migration of vascular smooth muscle cell via extracellur signal-regulated kinase 1/2 and c-Jun NH2-terminal kinase activation, Molecular Pharmacology, Vol.65, No.4, 832-841, 2004. (Summary) Angiotensin II (Ang II) plays an important role in several cardiovascular diseases associated with vascular smooth muscle cell (VSMC) growth and migration. Src activity is known to be required for the migration of a number of cell types. p130Cas was reported to be essential for cell migration and actin filament reorganization. Mitogen-activated protein (MAP) kinases were also reported to be critical regulatory factors for growth and migration of VSMC. However, precise intracellular mechanisms involving c-Src, p130Cas, and MAP kinases in Ang II-stimulated migration of VSMC have not been well elucidated. Here we demonstrated that Ang II rapidly and significantly stimulated tyrosine phosphorylation of Src and Cas and their association in rat aortic smooth muscle cells (RASMC). Ang II-stimulated tyrosine phosphorylation of Src and Cas and activation of ERK1/2 and JNK, but not p38, were potently inhibited by Src family tyrosine kinase inhibitors, herbimycin A (HA) and PP2. Ang II-stimulated Src and Cas association, tyrosine phosphorylation of Cas, and activation of ERK1/2 and JNK were suppressed in kinase-inactive Src (KI Src)-overexpressed RASMC. Ang II-stimulated JNK activation but not ERK1/2 activation was blocked in substrate domain-deleted Cas (DeltaSD Cas)-overexpressed RASMC. In addition, HA, PP2, ERK1/2 inhibitor, 2'-amino-3'-methoxyflavone (PD98059) and JNK inhibitor, and anthra[1,9-cd]pyrazol-6(2H)-one (SP600125) significantly inhibited Ang II-stimulated migration of RASMC. Ang II-induced colocalization of Src and Cas and migration were inhibited in both KI Src- and DeltaSD Cas-overexpressed RASMC. These findings suggest that Src and Cas are essentially but differentially involved in Ang II-stimulated migration of VSMC through the activation of ERK1/2 and JNK. (Keyword) Angiotensin II / Animals / Cell Adhesion / Cell Movement / Cells, Cultured / Cellular Apoptosis Susceptibility Protein / Enzyme Activation / Genes, src / JNK Mitogen-Activated Protein Kinases / Male / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinases / Muscle, Smooth, Vascular / phosphorylation / Rats / Rats, Sprague-Dawley / Tyrosine / Vinculin / src-Family Kinases (Link to Publication Site) ● Publication site (DOI): 10.1124/mol.65.4.832 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15044612 ● Search Scopus @ Elsevier (PMID): 15044612 ● Search Scopus @ Elsevier (DOI): 10.1124/mol.65.4.832 (DOI: 10.1124/mol.65.4.832, PubMed: 15044612)
79.	Masanori Yoshizumi, Yoshiko Fujita, Yuki Izawa, Yuki Suzaki, Moe Kyaw, Nermin Ali, Koichiro Tsuchiya, Shoji Kagami, Seiji Yano, Saburo Sone and Toshiaki Tamaki : Ebselen inhibits tumor necrosis factor-α-induced c-jun N-terminal kinase activation and adhesion molecule expression in endothelial cells, Experimental Cell Research, Vol.292, No.1, 1-10, 2004. (Summary) Tumor necrosis factor-alpha (TNF-alpha) stimulates expression of endothelial cell (EC) genes that may promote atherosclerosis in part by an activation of mitogen-activated protein (MAP) kinases. Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one), a selenoorganic compound, is effective for acute ischemic stroke; however, its effect on EC has not yet been elucidated. We examined the effect of ebselen on TNF-alpha-induced MAP kinase activation and adhesion molecule expression in cultured human umbilical vein endothelial cells (HUVEC). Extracellular signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 were rapidly and significantly activated by TNF-alpha in HUVEC. TNF-alpha-induced JNK activation was inhibited by ebselen, whereas ERK1/2 and p38 were not affected. Apoptosis signal-regulated kinase 1 (ASK1) was suggested to be involved in TNF-alpha-induced JNK activation because transfection of kinase-inactive ASK1 inhibited TNF-alpha-induced JNK activation. Ebselen inhibited TNF-alpha-induced TNF receptor-associated factor 2 (TRAF2)-ASK1 complex formation and phosphorylation of stress-activated protein kinase ERK kinase 1 (SEK1), which is an upstream signaling molecule of JNK. Finally, TNF-alpha-induced activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) activation and resultant intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions were inhibited by ebselen. Specific inhibitors for JNK and NF-kappaB also inhibited TNF-alpha-induced ICAM-1 and VCAM-1 expressions in HUVEC. These findings suggest that ebselen prevents TNF-alpha-induced EC activation through the inhibition of TRAF2-ASK1-SEK1 signaling pathway, which leads to JNK activation. Inhibition of JNK by ebselen may imply its usefulness for the prevention of atherosclerosis relevant to EC activation. (Keyword) Azoles / Cell Adhesion Molecules / Cells, Cultured / Endothelium, Vascular / Enzyme Activation / Humans / Intercellular Adhesion Molecule-1 / JNK Mitogen-Activated Protein Kinases / MAP Kinase Kinase 4 / Mitogen-Activated Protein Kinase Kinases / Mitogen-Activated Protein Kinases / NF-kappa B / Organoselenium Compounds / Phosphorylation / Time Factors / Transcription Factor AP-1 / Tumor Necrosis Factor-alpha / Umbilical Veins / Vascular Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yexcr.2003.08.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14720501 ● CiNii @ National Institute of Informatics (CRID): 1571980076667609856 ● Search Scopus @ Elsevier (PMID): 14720501 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yexcr.2003.08.003 (DOI: 10.1016/j.yexcr.2003.08.003, PubMed: 14720501, CiNii: 1571980076667609856)
80.	Nermin Ali, Masanori Yoshizumi, Koichiro Tsuchiya, Moe Kyaw, Yoshiko Fujita, Yuki Izawa, Shinji Abe, Yasuhisa Kanematsu, Shoji Kagami and Toshiaki Tamaki : Ebsalen inhibits p38MAP kinase-mediated endothelial cell death by hydrogen peroxide., European Journal of Pharmacology, Vol.485, No.1-3, 127-135, 2004. (Summary) Ebselen (2-phenyl-1, 2-benzisoselenazol-3[2H]-one) is a seleno-organic compound exhibiting both glutathione peroxidase and antioxidant activity. Although it has been reported that ebselen is effective against hydrogen peroxide (H(2)O(2))-induced cell death in several cell types, its effect on endothelial cell damage has not yet been elucidated. In the present study, we examined the effect of ebselen on H(2)O(2)-induced human umbilical vein endothelial cells (HUVECs) death, and its intracellular mechanism. Our findings showed that pretreatment of HUVECs with ebselen resulted in a significant recovery from H(2)O(2)-induced cell death in a concentration-dependent manner. In addition to the inhibition of lactate dehydrogenase (LDH) leakage, ebselen inhibited H(2)O(2)-induced cytochrome c release and caspase-3 activation and the resultant apoptosis in HUVECs. Moreover, it was observed that H(2)O(2) significantly stimulated activation of mitogen-activated protein (MAP) kinases, i.e., p38 MAP kinase, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK1/2). Ebselen inhibited H(2)O(2)-induced p38 MAP kinase, but not JNK or ERK1/2 activation. Furthermore, SB203580 (4-[4-fluorophenyl]-2-[4-methylsulfinylphenyl]-5-[4-pyridyl]-1H-imidazole), a specific p38 MAP kinase inhibitor, inhibited H(2)O(2)-induced p38 MAP kinase phosphorylation, cytochrome c release, caspase-3 activation, as well as cell death in HUVECs. These findings suggest that ebselen attenuates H(2)O(2)-induced endothelial cell death through the inhibition of signaling pathways mediated by p38 MAP kinase, caspase-3, and cytochrome c release. Thus, inhibition of p38 MAP kinase by ebselen may imply its usefulness for prevention and/or treatment of endothelial cell dysfunction, which was suggested to be the first step in the development of atherosclerosis. (Keyword) Azoles / cell death / Cell Survival / Dose-Response Relationship, Drug / Endothelial Cells / Enzyme Inhibitors / Humans / hydrogen peroxide / Mitogen-Activated Protein Kinases / Organoselenium Compounds / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2003.11.079 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14757132 ● Search Scopus @ Elsevier (PMID): 14757132 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2003.11.079 (DOI: 10.1016/j.ejphar.2003.11.079, PubMed: 14757132)

Academic Paper (Unrefereed Paper):

1.	Yuki Izawa-Ishizawa, Yoshimi Bando, Satsuki Sumitani, Akira Tangoku and Mari Haku : 研究に関する男女共同参画・ダイバーシティの推進状況に関するアンケート調査-全国の集計結果との比較から見える徳島大学の現状-, 徳島大学人と地域共創センター紀要, Vol.31, 17-32, 2022. (Summary) 本調査では，全国ダイバーシティネットワークの幹事機関である大阪大学と，日本学術会議科学者委員会男女共同参画分科会・同アンケート検討小分科会が共同で実施した「大学・研究機関における男女共同参画・ダイバーシティの推進状況調査」のうち「大学・研究機関における男女共同参画の推進状況に対する意見・感想」について，徳島大学回答分(男性60 件，女性21 件)のみ抽出されたデータを用いて，本学における男女共同参画・ダイバーシティ推進に関する研究者の意識調査を実施した．男女別に集計し，公開されている全国集計結果(計10，105 件)と比較検討することで，全国における本学の位置付けについて分析した．調査項目は， 1 ．男女共同参画の推進(全般) 2 ．男女共同参画の取り組み 3 ．ワークライフバランス・育児支援サービス 4 ．ダイバーシティ対応 5 ．ハラスメント防止体制 6 ．医学系の6 項目にわたる．全国と徳島での回答差，また男女間の回答差から，現在の徳島大学の研究者における男女共同参画に対する意識について考察する． (Keyword) ダイバーシティ推進 / 男女共同参画 / 女性研究者支援 (Tokushima University Institutional Repository) ● Metadata: 116860 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050010293735891072 (Tokushima University Institutional Repository: 116860, CiNii: 1050010293735891072)
2.	Yoshiko Fujita, Masanori Yoshizumi, Yuki Izawa, Yasuhisa Kanematsu and Toshiaki Tamaki : Lysophosphatidylcholine(LPC)transactivates vascular endothelial growth factor(VEGF) receptor via c-Src in HUVEC, Shikoku Acta Medica, Vol.61, No.3,4, 91-94, 2005. (Summary) One of the major lipid components of oxidized low density lipoprotein, lysophosphatidylcholine(LPC)is involved in numerous biological processes as a bioactive lipid molecule and has beenshown to be involved in the progression of atherosclerosis. As counter-ligands, G2A and GPR4wereidentified with high binding affinity for LPC that are belonging to orphan G-protein-coupledreceptors(GPCRs)at plasma membranes. Although several GPCR ligands transactivate receptortyrosine kinases (RTKs), such as epidermal growth factor receptor, transactivation of RTK byLPC has not yet been reported. Here we observed for the first time that LPC treatment inducestyrosyl phosphorylation of vascular endothelial growth factor(VEGF)receptor2(fetal liverkinase-1/kinase-insert domain-containing receptor, Flk-1/KDR)in human umbilical vein endothelialcells(HUVEC). VEGF receptor tyrosine kinase inhibitors, SU1498and VTKi inhibited Flk-1/KDRtransactivation by LPC. Furthermore, we examined the effect of the Src family kinases inhibitors,Herbimycin A and PP2 on LPC-induced Flk-1/KDR transactivation. Herbimycin A and PP2inhibited Flk-1/KDR transactivation in HUVEC, suggesting that c-Src is involved in LPC-inducedFlk-1/KDR transactivation. Kinase-inactive(KI)Src transfection also inhibited LPC-induced Flk-1/KDR transactivation. In addition, LPC activated extracellular signal-regulated kinase1/2and Akt,which are downstream effectors of Flk-1/KDR, and these were inhibited by SU1498，VTKi,Herbimycin A, PP2and KI Src transfection in HUVEC. LPC-mediated HUVEC proliferation wasshown to be secondary to transactivation because it was suppressed by SU1498，VTKi, HerbimycinA, PP2and KI Src transfection. It is concluded that c-Src-mediated Flk-1/KDR transactivation byLPC may have important implications for the progression of atherosclerosis. (Keyword) LPC / endothelial cells / Flk-1 / KDR / c-Src / atherosclerosis (Tokushima University Institutional Repository) ● Metadata: 47262 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050845762393810304 (Tokushima University Institutional Repository: 47262, CiNii: 1050845762393810304)

Review, Commentary:

1.	Hirofumi Hamano, Yoshito Zamami, Soichiro Ushio, Takahiro Niimura, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa : [Development of Preventive Methods for Drug-induced Cardiotoxicity Using a Large-scale Medical Information Database]., Journal of the Pharmaceutical Society of Japan, Vol.144, No.3, 257-264, 2024. (Summary) 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. (Keyword) Humans / Cardiotoxicity / Myocarditis / quality of life / Doxorubicin / Neoplasms (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.23-00164-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38432934 ● Search Scopus @ Elsevier (PMID): 38432934 ● Search Scopus @ Elsevier (DOI): 10.1248/yakushi.23-00164-2 (DOI: 10.1248/yakushi.23-00164-2, PubMed: 38432934)
2.	Yoshito Zamami, Hirofumi Hamano, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa : Drug-Repositioning Approaches Based on Medical and Life Science Databases., Frontiers in Pharmacology, Vol.12, No.752174, Nov. 2021. (Tokushima University Institutional Repository) ● Metadata: 116895 (Link to Publication Site) ● Publication site (DOI): 10.3389/fphar.2021.752174 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.3389/fphar.2021.752174 (Tokushima University Institutional Repository: 116895, DOI: 10.3389/fphar.2021.752174)
3.	Masaki Imanishi, Keisuke Ishizawa, TAKUMI SAKURADA, Yuki Izawa-Ishizawa, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Drug development for cardiorenal disease based on oxidative stress control, Journal of the Pharmaceutical Society of Japan, Vol.134, No.6, 715-719, Jun. 2014. (Summary) 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. (Keyword) oxidative stress / chronic kidney disease / cardiovascular disease / nitrosonifedipine (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.13-00255-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24882646 ● Search Scopus @ Elsevier (PMID): 24882646 ● Search Scopus @ Elsevier (DOI): 10.1248/yakushi.13-00255-4 (DOI: 10.1248/yakushi.13-00255-4, PubMed: 24882646)
4.	櫻田巧, Keisuke Ishizawa, Masaki Imanishi, 藤井聖子, 谷口順平, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineはangiotensin IIによるマウス血管リモデリングを抑制する, 腎とフリーラジカル, Vol.11, 78-81, Jan. 2013.
5.	Masanori Yoshizumi, Keisuke Ishizawa, Yuki Izawa and Toshiaki Tamaki : Intracellular signal transduction of vascular injury in insulin resistance, Folia Pharmacologica Japonica, Vol.128, No.3, 147-151, Sep. 2006. (Summary) 近年，メタボリック症候群の疾患概念が確立され，本邦でもその診断基準が発表された．メタボリック症候群の根底にはインスリン抵抗性が存在するといわれるが，高血圧，動脈硬化などの血管病にインスリン抵抗性がどのように関っているかは未だ明らかではない．我々はこの数年，血管病の発症，進展に関わるインスリン抵抗性の細胞内情報伝達機構について研究を行なってきた．糖尿病モデル動物のOLETFラットを用いた検討では，アンジオテンシンII受容体拮抗薬の投与が末梢での糖利用臓器のインスリン抵抗性を改善させ，レニン-アンジオテンシン系のメタボリック症候群への関与が示唆された．培養血管平滑筋細胞を用いた細胞内情報伝達機構の検討では，アンジオテンシンII刺激によって活性化されるMAPキナーゼの一つ，ERK1/2がインスリン抵抗性の発現に関与していることが明らかになった．また，血管リモデリング進展過程のひとつである血管平滑筋細胞の遊走において，SrcチロシンキナーゼやCasアダプタータンパクが細胞内分子として重要な役割を果たしていることを見いだした．血管病におけるインスリン抵抗性に関わる標的分子の探求は，今後も増加することが予想されるメタボリックシンドローム治療のための創薬に有用な情報をもたらすことが期待される．<br> (Keyword) メタボリックシンドローム / インスリン抵抗性 / アンジオテンシンII / MAPキナーゼ / 血管平滑筋細胞 (Link to Publication Site) ● Publication site (DOI): 10.1254/fpj.128.147 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16971777 ● CiNii @ National Institute of Informatics (CRID): 1390001204271623040 ● Search Scopus @ Elsevier (PMID): 16971777 ● Search Scopus @ Elsevier (DOI): 10.1254/fpj.128.147 (DOI: 10.1254/fpj.128.147, PubMed: 16971777, CiNii: 1390001204271623040)

Proceeding of International Conference:

1.	Takahiro Niimura, Koji Miyata, Kenta Yagi, Fuka Aizawa, Kei Kawada, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa : Evaluation of cardiovascular toxicity profile of ALK inhibitors using adverse event reporting database., ASCPT 2024 Annual Meeting Colorado Springs March 2024, Colorado Springs, Mar. 2024.
2.	Koji Miyata, Yuki Izawa-Ishizawa, Honoka Nishi, Shuto Itokazu, Tatsumi Miyata, Kaito Tsujinaka, Masateru Kondo, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : Fluoroquinolones attribute aortic diseases through endothelial dysfunction., ASCPT 2024 Annual Meeting, Colorado Springs, Mar. 2024.
3.	Kei Kawada, Ishida Tomoaki, Morisawa Shumpei, Jobu Kohei, Higasi Youichirou, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Takahiro Niimura, Shinji Abe, Mitsuhiro Goda and Keisuke Ishizawa : Atractylodes lancea Rhizome-derived Exosome-like Nanoparticles Suppress Lipopolysaccharide-induced Inflammation in Murine Microglial Cells, 81st FIP World Congress of Pharmacy and Pharmaceutical Sciences., Brisbane, Sep. 2023.
4.	Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Hirofumi Hamano, Ishida Shunsuke, Takahiro Niimura, Kondo Masateru, Bando Takashi, Yuki Izawa-Ishizawa, Tasaki Yoshikazu and Keisuke Ishizawa : Identification of prophylactic drug for vancomycin- associated nephrotoxicity using big data analysis., 19th World Congress of Basic & Clinical Pharmacology (WCP2023), Glasgow, Jul. 2023.
5.	Mitsuhiro Goda, Kanda Masaya, Yoshioka Toshihiko, Miyata Koji, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Sakurada Takumi and Yuki Izawa-Ishizawa : Discovery of preventive drugs for cisplatin-induced acute kidney injury., 19th World Congress of Basic & Clinical Pharmacology (WCP2023), Glasgow, Jul. 2023.
6.	Miyata Koji, Yuki Izawa-Ishizawa, Takahiro Niimura, Hirofumi Hamano, Fuka Aizawa, Kenta Yagi, Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa : Investigation of PDE5 Inhibitors and Artery Diseases Using Real-World Database, 19th World Congress of Basic & Clinical Pharmacology (WCP2023), Glasgow, Jul. 2023.
7.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Mitsuhiro Goda, Naoto Okada, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : Development of therapeutic agents using drug discovery tools and large-scale medical information, FIP2019, Abu Dhabi, Sep. 2019.
8.	Niimura Takahiro, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : Nicorandil improve prognosis of cardiac arrest patient: A large-scale medical information analysis, FIP2019, Abu Dhabi, Sep. 2019.
9.	Mitsuhiro Goda, Kazuhito Saike, Takahiro Niimura, Masaya Kanda, Kenshi Takechi, Masayuki Chuma, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : Effect of new preventive medicine on cisplatin-induced acute kidney injury, EACPT2019, Stockholm, Jun. 2019.
10.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Utilizing Real-World Big Data in the Search for New Renoprotective Drugs, Joint Hypertension 2018 Scientific Sessions, Sep. 2018.
11.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : Drug repositioning for post cardiopulmonary resuscitation syndrome using large-scale medical claims, FIP2018, グラスゴー, Sep. 2018.
12.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Renoprotective effects of edoxaban, a factor Xa inhibitor, 18th World Congress of Basic and Clinical Pharmacology, Jul. 2018.
13.	Yuki Izawa-Ishizawa, Masaki Imanishi, kotoko suzuki, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Koichiro Tsuchiya, Toshiaki Tamaki, Keisuke Ishizawa and Yasumasa Ikeda : The effect of quercetin on aortic aneurysms in mice, WCP2018, Jul. 2018.
14.	濱野裕章, Yasumasa Ikeda, Yuya Horinouchi, Yoshito Zamami, Masaki Imanishi, Yuki Izawa-Ishizawa, Licht Miyamoto, Koichiro Tsuchiya, Keisuke Ishizawa and Toshiaki Tamaki : Proton Pump Inhibitor Involves Abnormality of Iron Metabolism through Hepcidin Regulation, 18th World Congress of Basic and Clinical Pharmacology, Jul. 2018.
15.	Yoshito Zamami, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Toshiaki Tamaki and Keisuke Ishizawa : Search for drugs that attenuate the anti tumor effect of bevacizumab using adverse event database, 18th World Congress of Basic and Clinical Pharmacology, Jul. 2018.
16.	Yoshito Zamami, Takahiro Niimura, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Krino Yashishi, Nakamura Toshimi, Teraoka Kazuhiko and Keisuke Ishizawa : Drug repositioning research aimed at improving the survival rate of patients with cardiopulmonary arrest using large-scale medical claims database, ASHPMidyear2017Clinical Meeting&Exhibition, Dec. 2017.
17.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The effect of iron on skeletal muscle atrophy in chronic kidney disease., Free Radical Biology and Medicine, Vol.112, No.1, 204-205, Dec. 2017. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.freeradbiomed.2017.10.323 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.freeradbiomed.2017.10.323 (DOI: 10.1016/j.freeradbiomed.2017.10.323)
18.	hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Indoxyl Sulfate Disturbs Normal Iron Metabolism via Hepcidin Upregulation in Chronic Kidney Disease, ASN Kidney Week 2017 Annual Meeting, Nov. 2017.
19.	Yuya Horinouchi, Yasumasa Ikeda, Masaki Imanishi, Yoshito Zamami, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Direct activated factor X inhibitor attenuates renal fibrosis on unilateral ureteral obstruction-induced nephrotoxicity., 53rd Congress of the European Societies of Toxicology (eurotox2017), Sep. 2017.
20.	Yuya Horinouchi, Yasumasa Ikeda, Masaki Imanishi, Yoshito Zamami, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : FACTOR XA INHIBITOR ATTENUATES RENAL INTERSTITIAL FIBROSIS IN MICE WITH UNILATERAL URETERAL OBSTRUCTION, THE 13TH CONGRESS OF THE EUROPEAN ASSOCIATION FOR CLINICAL PHARMACOLOGY AND THERAPEUTICS(EACPT2017), Jun. 2017.
21.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 田淵正樹, Masaki Imanishi, Mai Takata, Eriko Sairyo, Yoshito Zamami, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : NITROSONIFEDIPINE, A NOVEL ANTIOXIDANT, AMELIORATES NEUROLOGICALSYMPTOMS AND PROLONGS THE SURVIVAL IN A MALIGNANT STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS, 27th European Meeting on Hypertension and Cardiovascular Protection, Jun. 2017.
22.	Masaki Imanishi, Kyohei Tanaka, Raiki Ikutoh, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : THE EFFECTS OF FEBUXOSTAT ON ANGIOTENSIN II-INDUCED VASCULAR REMODELING, 27th European Meeting on Hypertension and Cardiovascular Protection, Jun. 2017.
23.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa and Toshiaki Tamaki : IRON RESTRICTION PREVENTS RENAL TUBULOINTERSTITIAL INJURY INDUCED BY ALBUMIN OVERLOAD IN MICE, 54th ERA-EDTA Congress, Madrid, Jun. 2017.
24.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa and Toshiaki Tamaki : DIRECT FACTOR XA INHIBITOR PREVENTS RENAL INTERSTITIAL FIBROSIS IN MICE WITH UNILATERAL URETERAL OBSTRUCTION, 54th ERA-EDTA Congress, Madrid, Jun. 2017.
25.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Indoxyl Sulfate Involves Abnormality of Iron Metabolism through Hepcidin Regulation, Experimental Bioogy 2017, Chicago, Apr. 2017.
26.	Ota Kazuma, Yoshitaka Kihira, Kishibuchi Reina, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda and Toshiaki Tamaki : Disruption of hypoxia-inducible factor-1a deteriorates renal ischemia-reperfusion injury through dysregulation of Kv2.2-induced apoptosis in tubules., ASN KIDNEY WEEK 2016, Chicago, Nov. 2016.
27.	Yoshito Zamami, Mitsui Marin, Moriguchi Hiroshi, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Kawasaki Hiromu, Toshiaki Tamaki and Keisuke Ishizawa : Search for a preventative therapy for Bevacizumab-induced hypertension using the drug repositioning approach, 7th Scientific Meeting of Asian Society for Vascular Biology, Oct. 2016.
28.	Yutaka Fukunaga, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Ichiro Hashimoto : Topical Application of Nitrosonifedipine, a Novel Free Radical Scavenger, Ameliorate the Ischemic Skin Flap Necrosis, Plastic Surgery THE MEETING 2016, Los Angeles, Sep. 2016.
29.	Yuki Izawa-Ishizawa, Masaki Imanishi, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : The effects of pitavastatin, a lipid-lowering agent, against aortic dissection model mice induced by L-NAME, a nitric oxide synthase inhibitor., The 9th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide/16th Annual Scientific Meeting of the Nitric Oxide Society of Japan., May 2016.
30.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa and Toshiaki Tamaki : The new insight of iron on tissue damage in metabolic disorders., The 9th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide/16th Annual Scientific Meeting of the Nitric Oxide Society of Japan., May 2016.
31.	Yasumasa Ikeda, Keisuke Oshima, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The Involvement of Iron Supplementation on Erythropoietin Expression, Experimental Biology 2016, Apr. 2016.
32.	Yasumasa Ikeda, Hamano Hirofumi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Bilirubin Enhances Ischimia-induced Angiogenesis Through Akt-eNOS-Dependent Signaling Pathway, American Heart Association Scientific Sessions 2015, Orlando, Nov. 2015.
33.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Toya Hiroki, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Novel aortic dissection model by pharmacologically-induced endothelial dysfunction, 17th International Congress on Atherosclerosis 2015, Amsterdam, May 2015.
34.	Yasumasa Ikeda, Yusuke Kanai, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The Effects of Bilirubin on Angiogenesis in Mice with Hindlimb Ischemia, Experimental Biology 2015, Boston, Mar. 2015.
35.	Keisuke Ishizawa, Kohara Yusuke, Sakurada Takumi, Toya Hiroki, Iki Yutaka, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates the progression of aortic aneurysms by exerting antioxidative effects, ESC Congress 2014, Barcelona, Sep. 2014.
36.	Yasumasa Ikeda, Soichiro Tajima, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Ferritin induces IL-1 production through inflammasome activation via NF-B-dependent manner in macrophages, Experimental Biology 2014, San Diego, Apr. 2014.
37.	Nhat-Tu Le, Yuichiro Takei, Yuki Izawa-Ishizawa, Kyung-Sun Heo, Hakjoo Lee, Alan V. Smrcka, Benjamin Miller, Kyung Ae Ko, Craig Morrell, Keigi Fujiwara, Masashi Akaike and Jun-ichi Abe : A HMG-CoA Reductase Inhibitor (statin) Directly Activates Endothelial Erk5 And Prevents Endothelial Dysfunction And Acute Cardiac Allograft Rejection, AHA scientific sessions 2013, Nov. 2013.
38.	Keisuke Ishizawa, Noriko Yamano, Hiroyuki Kobori, Maki Urushihara, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine prevents the progression of diabetic nephropathy via attenuating the expression of intrarenal angiotensinogen and oxidative stress, High Blood Pressure Research 2013 Scientific Sessions, Sep. 2013.
39.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakiko Doi, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Rho-kinase is involved in inorganic phosphate-induced ERK1/2 activation in vascular smooth muscle cells, World Biotechnology Congress 2013, Jun. 2013.
40.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : The effect of dietary iron restriction against diabetic nephropathy in db/db mice, Experimental Biology 2013, Apr. 2013.
41.	Yusaku Maeda, Shuhei Tomita, Masaki Murakami, Hirotsugu Kurobe, Masaki Imanishi, Yasushi Yoshida, Yoichiro Hirata, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Tetsuya Kitagawa, Masataka Sata and Toshiaki Tamaki : Deficiency of Hypoxia Inducible Factor-1a in SM-22a-Expressing Bone Marrow-Derived Cells Alleviates Neointimal Formation Following Wire-induced Vascular Formation, American Heart Association Scientific Sessions 2012, Nov. 2012.
42.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Iron Restriction Prevents the Progression of Diabetic Nephropathy in db/db Mice, American Heart Association Scientific Sessions 2012, Nov. 2012.
43.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible Factor-1a in Vascular Smooth Muscle Cells Regulates Angiotensin -induced Vascular Remodeling and AT1 Receptor Expression in Mouse Aortic Media, American Heart Association Scientific Sessions 2012, Nov. 2012.
44.	Hideaki Enomoto, Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Protective Effects of Iron-Restricted Food against Diabetic Nephropathy in db/db Mice, American Heart Association High Blood Pressure Research 2012, Sep. 2012.
45.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine, a Photodegradation Product of Nifedipine, Prevents the Progression of Diabetic Nephropathy in Type II Diabetic Mice, American Heart Association High Blood Pressure Research 2012, Sep. 2012.
46.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible factor-1a deficiency in smooth muscle cell attenuates angiotensin -induced vascular remodeling in mice, ISOTT (International Society on Oxygen Transport to Tissue) 2012, Aug. 2012.
47.	Takumi Sakurada, Keisuke Ishizawa, Shoko Fujii, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Effects of nitrosonifedipine, a photodegradation product of nifedipine, on diabetic nephropathy in type II diabetic mice, Experimental Biology 2012, Apr. 2012.
48.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Iron restriction prevents progression of diabetic nephropathy, KEYSTONE SYMPOSIA 40th ANNIVERSARY 1972-2012 Complications of Diabetes: Mechanisms of Injury and Failure of Repair, Mar. 2012.
49.	Yusaku Maeda, Shuhei Tomita, Masaki Murakami, Hirotsugu Kurobe, Masaki Imanishi, Yasushi Yoshida, Yoichiro Hirata, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Tetsuya Kitagawa, Masataka Sata and Toshiaki Tamaki : Deficiency of Hypoxia Inducible Factor-1 in SM-22-Expressing Bone Marrow-Derived Cells Alleviates Neointimal Formation Following Wire-induced Vascular Formation, AHA SCIENTIFIC SESSIONS 2012, 2012.
50.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible Factor-1 in Vascular Smooth Muscle Cells Regulates Angiotensin -induced Vascular Remodeling and AT1 Receptor Expression in Mouse Aortic Media, AHA SCIENTIFIC SESSIONS 2012, 2012.
51.	Fujii Shoko, Keisuke Ishizawa, Takumi Sakurada, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine, a Photodegradation Product of Nifedipine, Prevents the Progression of Diabetic Nephropathy in Type II Diabetic Mice, HIGH BLOOD PRESSURE RESEARCH 2012 SCIENTIFIC SESSIONS, 2012.
52.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible factor-1 deficiency in smooth muscle cell attenuates angiotensin II-induced vascular remodeling in mice, The International Society on Oxygen Transport to Tissue 2012, 2012.
53.	Takumi Sakurada, Keisuke Ishizawa, Shoko Fujii, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Effects of nitrosonifedipine, a photodegradation product of nifedipine, on diabetic nephropathy in type II diabetic mice, Experimental Biology 2012, 2012.
54.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Smooth Muscle Cell-Specific Hypoxia-Inducible Factor-1a Deficiency Attenuates Angiotensin II-Induced Vascular Remodeling in Mice, AHA scientific sessions 2011, Orlando, Nov. 2011.
55.	Soichiro Tajima, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : Inhibition of Adipocyte Hypertrophy by Deferoxiamine Diabetic KKAy mice, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
56.	Kazuyuki Yamaguchi, Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : Glucose Metabolism of Adipocytes is Regulated by Basic Fibroblast Growth Factor via Hypoxia-inducible Factor-1a, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
57.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible Factor-1a Deficiency in Smooth Muscle Cells Suppresses Angiotensin -induced Vascular Remodeling in Mice, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
58.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Yoshitaka Kihira, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Shuhei Tomita, Masataka Sata, Masashi Akaike, Shigeki Kato, Toshio Matsumoto and Toshiaki Tamaki : Heparin Cofactor Promotes Angiogenesis via an AMPK-eNOS Signaling Pathway, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
59.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin -induced Vascular Remodeling is Improved by Nitrosonifedipine, a Possible New Class Drug Against Oxidative Stress, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
60.	Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitorosonifedipine is a new class drug to improves angiotensin II-induced vascular remodeling, European Society of Cardiology Congress 2011, Aug. 2011.
61.	Shuhei Tomita, Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Characterization on mice lacking HIF1a gene in renal ischemia-reperfusion injury, ISOTT (International Society on Oxygen Transport to Tissue) 2011, Washington, D.C., Jul. 2011.
62.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Smooth Muscle Cell-specific Hypoxia-inducible Factor-1a Deficiency Attenuates Angiotensin II-induced Vascular Remodeling In Mice, AHA SCIENTIFIC SESSIONS 2011, 2011.
63.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakurada Takumi, Masaki Imanishi, Fujii Shoko, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II-induced Vascular Remodeling Is Improved By Nitrosonifedipine, A Possible New Class Drug, HIGH BLOOD PRESSURE RESEARCH 2011 SCIENTIFIC SESSIONS, 2011.
64.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible Factor-1 Deficiency In Smooth Muscle Cells Suppresses Angiotensin II-induced Vascular Remodeling In Mice, HIGH BLOOD PRESSURE RESEARCH 2011 SCIENTIFIC SESSIONS, 2011.
65.	Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitorosonifedipine is a new class drug to improve angiotensin II-induced vascular remodeling, ESC Congress 2011, 2011.
66.	Keisuke Ishizawa, Masaki Imanishi, Yuya Horinouchi, Yayoi Fukuhara, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Yoshitaka Kihira, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitroso-nifedipine is a new class drug to protect endothelial function for overcoming organ damage, International Society of Hypertension 2010, Vancouver, Sep. 2010.
67.	Hirotsugu Kurobe, M Urata, Yuki Izawa, Y Fukuhara, Tamotsu Kanbara, K Aihara, F Gonzalez and T Matsumoto : Hif-1α In T Cells Pathway Plays A Crucial Role In The Progression Of Arteriosclerosis And Artery Intimal Thickening, Scientific Sessions 2007, Florida, Nov. 2007.
68.	Keisuke Ishizawa, Narantungalag Dorjsuren, Yuki Izawa-Ishizawa, Teppei Tsuneishi, Yuki Motobayashi, Hideki Ohnishi, Kunihisa Yamaguchi, Koichiro Tsuchiya and Toshiaki Tamaki : Inhibitory effects of olmesartan on TNF-α-induced cytotoxicity in human glomerular endothelial cells, 40th ASN annual meeting, San Francisco, Nov. 2007.
69.	Hirotsugu Kurobe, M Urata, Yuki Izawa, Y Fukuhara, Tamotsu Kanbara, K Aikhara, T Tamaki, T Matsumoto, Tetsuya Kitagawa, M Yoshizumi and S Tomita : HIF-1 signaling pathway plays a crucial role in the progression of atherosclerosis, The 76th Congress of the European Atherosclerosis Society, Helsinki, Jun. 2007.
70.	Hiroyuki Sakakibara, Yuki Izawa, Jun-ichiro Nakajima, Shujiro Seo, Toshiaki Tamaki, Yoshichika Kawai and Junji Terao : Antidepressant effects of polyphenol rich herbal medicine, Ginkgo biloba, extracts in behavioral models, 232 nd American Chemical Society Meeting & Exposition, San Francisco, Sep. 2006.
71.	Hirotsugu Kurobe, Yuki Izawa, Y Fukuhara, Tamotsu Kanbara, A Kurushima, Ken-ichi Aihara, Masashi Akaike, Masashi Kano, Takashi Kitaichi, Yutaka Masuda, Hiroyuki Azuma, Toshiaki Tamaki, Toshio Matsumoto, Tetsuya Kitagawa, Shuhei Tomita and Masanori Yoshizumi : HIF-ARNT transcriptional system in Tcells has a pivotal role in vascular inflammation and remodeling, XIL International Symposium on Atherosclerosis, Italy, Jun. 2006.
72.	Hirotsugu Kurobe, Yuki Izawa, Yayoi Fukuhara, Tamotsu Kanbara, Ken-ichi Aihara, Masashi Akaike, Hiroyuki Azuma, Tetsuya Kitagawa, Toshiaki Tamaki, Toshio Matsumoto, Masaki Ueno, Shuhei Tomita and Masanori Yoshizumi : T Cell-specific HIF-1α-deficient Mice, but Not ARNT-deficient Mice, Exhibit Exacerbated Inflammation and Vascular Remodeling in Response to Cuff Injury, American Heart Association 2005 Scientifc Sessions, Dallas, Nov. 2005.
73.	Toshiaki Tamaki, Yasuhisa Kanematsu, Yuki Izawa, Hideki Ohnishi, Yuki Motobayashi, Shoji Kagami and Koichiro Tsuchiya : Chronic oral administration of nitrite restores circulating NO level and improves renal injury in L-NAME treated rats, 38th ASN annual meeting, Philadelphia, Nov. 2005.
74.	Keisuke Ishizawa, Rika Sugimoto, Yuki Izawa, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : The inhibitory effect of adiponectin on migration and proliferation induced by PDGF in rat mesangial cells, 38th ASN annual meeting, Philadelphia, Nov. 2005.
75.	Hiroyuki Sakakibara, Kaori Ishida, Yuki Izawa, Yuko Minami, Satomi Saito, Yoshichika Kawai, Butterweck Veronika, Toshiaki Tamaki, Yutaka Nakaya and Junji Terao : Effects of Ginkgo biloba Extract on Rat brain Function, 2nd International Conference on Polyphenols and Health, California Davis, Davis, Oct. 2005.
76.	Hiroyuki Sakakibara, Kaori Ishida, Yuki Izawa, Yuko Minami, Saito Saromi, Yoshichika Kawai, Butterweck Veronika, Toshiaki Tamaki, Yutaka Nakaya and Junji Terao : Effects of forced swimming stress on rat brain function, 2005 COE International Conference ''Biological Mechanism for Stress Control'', Tokushima, Aug. 2005.
77.	Keisuke Ishizawa, Rika Sugimoto, Yuki Izawa, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Adiponectin inhibits PDGF-induced migration and proliferation in rat mesangial cells, 第10回アディポサイエンス研究会シンポジウム(第10回記念国際シンポジウム), Osaka, Aug. 2005.
78.	Toshiaki Tamaki, Masumi Okamoto, Yasuhisa Kanematsu, Yuki Izawa, Shoji Kagami, Shuji Kondo, Masanori Yoshizumi and Koichiro Tsuchiya : Dietary dose of nitrite attenuates L-NAME-induced renal injury in rats, 3rd World Congress of Nephrology, Singapore, Jun. 2005.
79.	Masanori Yoshizumi, Keisuke Ishizawa, Yuki Izawa, Chieko Miki, Yoshiko Fujita, Yasuhisa Kanematsu, Koichiro Tsuchiya and Toshiaki Tamaki : Aldosterone stimulates vascular smooth muscle cell proliferation through big mitogen-activated protein kinase1 activation, 16th scientific meeting of the interamerican society of hypertension, Cancun, Mexico, Apr. 2005.
80.	Toshiaki Tamaki, Masumi Okamoto, Yasuhisa Kanematsu, Yuki Izawa, Shoji Kagami, Shuji Kondo, Maki Shimizu, Masanori Yoshizumi and Koichiro Tsuchiya : Nitrite-derived nitric oxide formation following ischemia-reperfusion injury in rat kidney, 37th ASN annual meeting, St. Louis, MO, Oct. 2004.

Proceeding of Domestic Conference:

1.	Kenta Yagi, Sayaka Imawaka, Mayu Takaoka, Naoki Okamoto, Fuka Aizawa, Takahiro Niimura, Mitsuhiro Goda, Kei Kawada, Yuki Izawa-Ishizawa and Keisuke Ishizawa : Bcr-Abl 阻害剤に対する慢性骨髄性白血病細胞の耐性獲得メカニズムの探索, 第144回日本薬理学会近畿部会, Mar. 2024.
2.	Yuki Izawa-Ishizawa, Koji Miyata, Kaito Tsujinaka, Shuto Itokazu, Tatsumi Miyata, Masateru Kondoh, Takahiro Niimura, Toshihiko Yoshioka, Fuka Aizawa, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : フルオロキノロン系抗菌薬による大動脈疾患リスクに関する2つの矛盾, 第144回日本薬理学会近畿部会, Mar. 2024.
3.	Fuka Aizawa, Ami Okabayashi, Daishi Moriyama, Kenta Yagi, Takahiro Niimura, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Kei Kawada and Keisuke Ishizawa : HMG-CoA還元酵素阻害剤はGST を介して抗がん剤誘発性機械的刺激応答閾値低下を改善する, 第144回日本薬理学会近畿部会, Mar. 2024.
4.	Tatsumi Miyata, Yuki Izawa-Ishizawa, Koji Miyata, Shuto Itokazu, Kaito Tsujinaka, Himeno Fukuoka, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : レボフロキサシンの血管炎症への影響, 第268回徳島医学会, Mar. 2024.
5.	Shuto Itokazu, Yuki Izawa-Ishizawa, Koji Miyata, Tatsumi Miyata, Masateru Kondoh, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : 杜仲葉エキスによる大動脈疾患発症抑制効果の検討, 第268回徳島医学会, Mar. 2024.
6.	Koji Miyata, Yuki Izawa-Ishizawa, Honoka Nishi, Shuto Itokazu, Tatsumi Miyata, Kaito Tsujinaka, Masateru Kondoh, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : フルオロキノロン系抗菌薬に関連した大動脈瘤解離には内皮障害が関与する, 第97回日本薬理学会年会第44回日本臨床薬理学会学術総会, Dec. 2023.
7.	Kei Kawada, 石田智滉, 福田仁, 兵頭勇己, 浜田知幸, 久保亨, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Takahiro Niimura, Mitsuhiro Goda and Keisuke Ishizawa : 機械学習解析を用いた心不全治療薬の年齢別有効性の検討―高知急性非代償性心不全レジストリ研究より―, 第97回日本薬理学会年会第44回日本臨床薬理学会学術総会, Dec. 2023.
8.	杉本祐悟, Mitsuhiro Goda, 石田朋奈, 加納菜々, Masaya Kanda, Toshihiko Yoshioka, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Kei Kawada, Yuki Izawa-Ishizawa and Keisuke Ishizawa : SGLT2阻害薬によるシスプラチン誘発腎障害の抑制効果, 第62回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2023.
9.	Kenta Yagi, Takahiro Niimura, Satoshi Sakaguchi, Fuka Aizawa, Kei Kawada, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa : リアルワールドデータの医療への活用に向けて, 第62回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2023.
10.	Kei Kawada, 石田智滉, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Takahiro Niimura, Shinji Abe, Mitsuhiro Goda and Keisuke Ishizawa : 植物由来細胞外膜小胞を用いた抗神経炎症治療薬の開発, 次世代を担う若手のための創薬・医療薬理シンポジウム2023, Aug. 2023.
11.	Kei Kawada, 石田智滉, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Takahiro Niimura, Shinji Abe, Mitsuhiro Goda and Keisuke Ishizawa : 植物由来細胞外膜小胞を用いた抗神経炎症治療薬の開発, 次世代を担う若手のための創薬・医療薬理シンポジウム2023, Aug. 2023.
12.	Toshihiko Yoshioka, Mitsuhiro Goda, Tomona Ishida, Yugo Sugimoto, 神田将哉, 櫻田巧, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa : シスプラチン誘発腎障害に対するバルプロ酸ナトリウムの予防効果, 次世代を担う若手のための創薬・医療薬理シンポジウム2023, Aug. 2023.
13.	Yugo Sugimoto, Mitsuhiro Goda, Tomona Ishida, 加納菜々, 神田将哉, Toshihiko Yoshioka, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa : 慢性骨髄性白血病の薬剤耐性に有用な薬剤の探索, 次世代を担う若手のための創薬・医療薬理シンポジウム2023, Aug. 2023.
14.	友近七海, Fuka Aizawa, SONODA Yuhei, NISHIBASHI Ayaka, MIYAUCHI Kanaho, Mitsuhiro Goda, Kenta Yagi, Takahiro Niimura, Yuki Izawa-Ishizawa, 朝田瑞穂, 植沢芳広 and Keisuke Ishizawa : 実験的多発性硬化症モデルマウスに対するウルソデオキシコール酸の治療効果の検討, 次世代を担う若手のための創薬・医療薬理シンポジウム2023, Aug. 2023.
15.	Honoka Nishi, Fuka Aizawa, Yuki Izawa-Ishizawa, TSUJINAKA Kaito, MIYATA Koji, Toshihiko Yoshioka, Masateru Kondoh, Shuto Itokazu, MIYATA Tatsumi, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa : 血管新生阻害剤による大動脈解離発症のリスク因子解明, 次世代を担う若手のための創薬・医療薬理シンポジウム2023, Aug. 2023.
16.	森山大嗣, Fuka Aizawa, Ami Okabayashi, Mitsuhiro Goda, Kenta Yagi, Takahiro Niimura, Yuki Izawa-Ishizawa and Keisuke Ishizawa : 抗がん剤誘発性末梢神経障害に対するスタチン系薬剤の有効性ならびに作用標的の検討, 次世代を担う若手のための創薬・医療薬理シンポジウム2023, Aug. 2023.
17.	Kazushi Uchida, Hiroto Unten, Hirofumi Hamano, Takahiro Niimura, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 免疫チェックポイント阻害剤関連心筋炎モデルマウスの作製とモデルマウスを用いた予防薬探索, 次世代を担う若手のための創薬・医療薬理シンポジウム2023, Aug. 2023.
18.	Takahiro Niimura, MIYATA Koji, Kenta Yagi, Fuka Aizawa, Hirofumi Hamano, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : 有害事象報告データベースを活用したALK阻害薬の心血管毒性プロファイル解明, 生体機能と創薬シンポジウム2023, Aug. 2023.
19.	Toshihiko Yoshioka, Mitsuhiro Goda, Yugo Sugimoto, Tomona Ishida, 神田将哉, 櫻田巧, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa : シスプラチン誘発腎障害に対するバルプロ酸ナトリウムの予防効果, 生体機能と創薬シンポジウム2023, Aug. 2023.
20.	BANDO Hiroshi, Mitsuhiro Goda, Takahiro Niimura, 新田侑生, Masayuki Chuma, 北川航平, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, 櫻田巧 and Keisuke Ishizawa : 大規模医療情報データベース解析を基盤としたラモトリギンの皮膚障害発現リスクに影響する薬剤の探索, 生体機能と創薬シンポジウム2023, Aug. 2023.
21.	Toshihiko Yoshioka, Mitsuhiro Goda, 神田将哉, Yugo Sugimoto, Yuki Izawa-Ishizawa, Kenta Yagi, Fuka Aizawa, MIYATA Koji, Takahiro Niimura, 櫻田巧, 桐野靖 and Keisuke Ishizawa : バルプロ酸ナトリウムのシスプラチン誘発腎障害予防薬としての可能性, 第267回徳島医学会学術集会, Aug. 2023.
22.	神田将哉, Mitsuhiro Goda, 吉岡俊彦, Yugo Sugimoto, 櫻田巧, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa : MATE型輸送体を標的とするシスプラチン誘発腎障害予防戦略の開発, 第32回霧島神経薬理フォーラム, Aug. 2023.
23.	Fuka Aizawa, Ami Okabayashi, Daishi Moriyama, Kenta Yagi, Mitsuhiro Goda, Takahiro Niimura, Yuki Izawa-Ishizawa and Keisuke Ishizawa : 抗がん剤誘発性末梢神経障害に対するHMG-CoA還元酵素阻害剤の多面的作用, 第2回あべの薬理学懇話会, Aug. 2023.
24.	Fuka Aizawa, Ami Okabayashi, Daishi Moriyama, Kenta Yagi, 高橋志門, Takahiro Niimura, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa : スタチンはOxaliplatin および Paclitaxel 誘発性末梢神経障害を改善する, 医療薬学フォーラム2023 / 第31回クリニカルファーマシーシンポジウム, Jul. 2023.
25.	Kei Kawada, 石田智滉, 常風興平, 森沢惇平, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Takahiro Niimura, Shinji Abe, Mitsuhiro Goda and Keisuke Ishizawa : 植物由来Exosome-like Nanoparticles (ELNs)の医療への応用 -蒼朮由来ELNsによる抗神経炎症作用の検討-, 第143回日本薬理学会近畿部会, Jun. 2023.
26.	OKAMOTO Naoki, Kenta Yagi, Sayaka Imawaka, Mayu Takaoka, Yurika Kuniki, Yuki Izawa-Ishizawa, Fuka Aizawa, Takahiro Niimura, Mitsuhiro Goda and Keisuke Ishizawa : 慢性骨髄性白血病に対する新規分子標的治療薬の耐性メカニズムの探索, 第143回日本薬理学会近畿部会, Jun. 2023.
27.	Yoshika Sakamoto, Nanami Tomochika, Takahiro Niimura, Mitsuhiro Goda, Fuka Aizawa, Kenta Yagi, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : スニチニブ誘発心毒性に対する新規予防薬の探索と作用機序の検討, 日本医療薬学会第6回フレッシャーズ・カンファランス, Jun. 2023.
28.	Hiroto Unten, Kazushi Uchida, Hirofumi Hamano, Takahiro Niimura, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 免疫チェックポイント阻害剤関連心筋炎モデルマウスの確立と病理組織像の評価, 日本医療薬学会第6回フレッシャーズ・カンファランス, Jun. 2023.
29.	Yoshito Zamami, Hirofumi Hamano, 牛尾聡一郎, Takahiro Niimura, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa : 大規模医療情報データベースを用いた薬剤性心毒性の予防法の開発, 日本薬学会第143年会, Mar. 2023.
30.	Kenta Yagi, Mayu Takaoka, 吉武愛哉, 丸尾陽成, Rie Andou, Fuka Aizawa, Takahiro Niimura, Yuki Izawa-Ishizawa, Hirofumi Hamano, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : プロトンポンプ阻害剤およびボノプラザンがVEGF発現に与える影響, 日本薬学会第143年会, Mar. 2023.
31.	Mitsuhiro Goda, 糸林小友理, 神田将哉, 吉岡俊彦, 杉本祐悟, 石田朋奈, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Yuki Izawa-Ishizawa, Takumi Sakurada, 桐野靖 and Keisuke Ishizawa : バルプロ酸ナトリウムのシスプラチン誘発腎障害に対する予防効果の作用機序解明, 日本薬学会第143年会, Mar. 2023.
32.	Takahiro Niimura, Hiroto Unten, Hirofumi Hamano, Kazushi Uchida, Nanami Tomochika, MIYATA Koji, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 遺伝子改変マウスを用いた免疫チェックポイント阻害剤関連心筋炎の病態モデル開発, 日本薬学会第143年会, Mar. 2023.
33.	MIYATA Koji, Yuki Izawa-Ishizawa, Hirofumi Hamano, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa : ホスホジエステラーゼ5阻害剤に関連した動脈疾患, 日本薬学会第143年会, Mar. 2023.
34.	Fuka Aizawa, Kenta Yagi, Takahiro Niimura, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa and Keisuke Ishizawa : データサイエンス×基礎によるCIPN支持療法薬の創出, 日本薬学会第143年会, Jan. 2023.
35.	Takahiro Niimura, Hiroto Unten, Hirofumi Hamano, Kazushi Uchida, MIYATA Koji, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Yuki Izawa-Ishizawa, Yoshito Zamami and 石澤啓介 : PD-1ノックアウトマウスを用いた免疫チェックポイント阻害剤関連心筋炎の新規病態モデル開発, 第32回日本循環薬理学会, Jan. 2023.
36.	八木健太, Fuka Aizawa, Takahiro Niimura, Yuki Izawa-Ishizawa, Hirofumi Hamano, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : VEGF発現にプロトンポンプ阻害剤が与える影響, 第32回日本循環薬理学会, Jan. 2023.
37.	Mitsuhiro Goda, Masaya Kanda, Toshihiko Yoshioka, Fuka Aizawa, 櫻田巧, 小川敦, Takahiro Niimura, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa : がん薬物療法に伴う腎障害とその予防, 第96回日本薬理学会年会/第43回日本臨床薬理学学術総会シンポジウム6, Nov. 2022.
38.	Mitsuhiro Goda, Fuka Aizawa, Kenta Yagi, Takahiro Niimura, 櫻田巧, 小川敦, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 医療ビッグデータ解析と基礎研究を融合した研究手法によるハイブリッド創薬, 第96回日本薬理学会年会/第43回日本臨床薬理学学術総会日本臨床薬理学会共催シンポジウム(シンポジウム41), Nov. 2022.
39.	Kenta Yagi, 丸尾陽成, 石田俊介, 鍛治園誠, Fuka Aizawa, MIYATA Koji, Takahiro Niimura, Yuki Izawa-Ishizawa, Hirofumi Hamano, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : ベバシズマブ治療継続にプロトンポンプ阻害剤，ボノプラザンが与える影響, 第32回日本医療薬学会年会, Sep. 2022.
40.	山川裕介, Kenta Yagi, Toshihiko Yoshioka, 佐藤真希, 丸尾陽成, MIYATA Koji, Fuka Aizawa, Yurika Kuniki, Takahiro Niimura, Satoshi Sakaguchi, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : 慢性骨髄性白血病患者における Bcr-Abl 阻害剤治療期間とアルコール摂取の関連, 第32回日本医療薬学会年会, Sep. 2022.
41.	Mitsuhiro Goda, Masaya Kanda, 吉岡俊彦, Takahiro Niimura, 櫻田巧, 小川敦, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 薬物療法の最適化を目指すリアルワールドデータ駆動型臨床薬理学研究, 第32回日本医療薬学会年会シンポジウム32, Sep. 2022.
42.	Fuka Aizawa, Ami Okabayashi, Daishi Moriyama, SONODA Yuhei, Shimon Takahashi, Takahiro Niimura, Mitsuhiro Goda, Yoshito Zamami, Toshihiko Yoshioka, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa : 臨床薬理の視点で実践する創薬研究:抗がん剤有害事象をターゲットとしたトランスレーショナルリサーチ, 第32回日本医療薬学会年会シンポジウム55, Sep. 2022.
43.	Fuka Aizawa, Ami Okabayashi, Daishi Moriyama, SONODA Yuhei, Shimon Takahashi, NITTA Ayaka, Mitsuhiro Goda, Kenta Yagi, Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa and Keisuke Ishizawa : スタチンの pleiotropic effects: 抗がん剤誘発性末梢神経障害抑制作用の検討, 次世代を担う若手のための創薬・医療薬理シンポジウム2022, Aug. 2022.
44.	神田将哉, Mitsuhiro Goda, Toshihiko Yoshioka, 小川敦, 石田俊介, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 医療ビッグデータ解析を基盤としたシスプラチン誘発腎障害予防薬の探索, 次世代を担う若手のための創薬・医療薬理シンポジウム2022, Aug. 2022.
45.	Takashi Bandoh, Masayuki Chuma, Mitsuhiro Goda, Tomomi Tani, Yurika Kuniki, 小川敦, 櫻田巧, Fuka Aizawa, Takahiro Niimura, 八木健太, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 医療ビッグデータ解析および基礎研究を融合したバンコマイシン関連腎障害に対する予防薬探索, 次世代を担う若手のための創薬・医療薬理シンポジウム2022, Aug. 2022.
46.	MIYATA Koji, Yuki Izawa-Ishizawa, TSUJINAKA Kaito, Kohei Ohmine, Honoka Nishi, Shuto Itokazu, Takahiro Niimura, Masateru Kondoh, Fuka Aizawa, Hirofumi Hamano, Kenta Yagi, Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa : フルオロキノロン系抗菌薬に関連した動脈瘤・解離の病態解明, 次世代を担う若手のための創薬・医療薬理シンポジウム2022, Aug. 2022.
47.	Sayuri Itobayashi, Mitsuhiro Goda, Yugo Sugimoto, 石田朋奈, 神田将哉, Toshihiko Yoshioka, 小川敦, 櫻田巧, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : シスプラチン誘発急性腎障害に対するバルプロ酸ナトリウムの予防効果, 次世代を担う若手のための創薬・医療薬理シンポジウム2022, Aug. 2022.
48.	Yurika Kuniki, Kenta Yagi, Mayu Takaoka, OKAMOTO Naoki, Hirofumi Hamano, Fuka Aizawa, Takahiro Niimura, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 慢性骨髄性白血病に対する既存承認薬とALDH阻害剤併用の有効性, 次世代を担う若手のための創薬・医療薬理シンポジウム2022, Aug. 2022.
49.	Toshihiko Yoshioka, Mitsuhiro Goda, Sayuri Itobayashi, Yugo Sugimoto, Tomona Ishida, 神田将哉, 小川敦, 櫻田巧, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 薬剤性腎障害予防を志向したドラッグリポジショニング研究, 第31回霧島神経薬理フォーラム, Aug. 2022.
50.	MIYATA Koji, Yuki Izawa-Ishizawa, TSUJINAKA Kaito, Kohei Ohmine, Honoka Nishi, Shuto Itokazu, Takahiro Niimura, 近藤正輝, Fuka Aizawa, Hirofumi Hamano, Kenta Yagi, Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa : 関連した動脈瘤・動脈解離:医療ビッグデータ解析と基礎薬理学実験によるアプローチ, 第29回市大フォーラム, Aug. 2022.
51.	Mitsuhiro Goda, 神田将哉, Toshihiko Yoshioka, Ami Yoshida, Sayuri Itobayashi, Takahiro Niimura, 櫻田巧, 小川敦, Naoto Okada, Fuka Aizawa, Kenta Yagi, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 遺伝子発現および大規模医療情報データベースを活用したシスプラチン関連腎障害に対する予防薬の探索, 第51回日本心脈管作動物質学会学術集会, Jul. 2022.
52.	Sayuri Itobayashi, Mitsuhiro Goda, Ami Yoshida, Yugo Sugimoto, Masaya Kanda, Toshihiko Yoshioka, 櫻田巧, Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 抗がん剤誘発急性腎障害に対するバルプロ酸ナトリウムの影響, 医療薬学フォーラム2022/第30回クリニカルファーマシーシンポジウム, Jul. 2022.
53.	Kenta Yagi, Mayu Takaoka, 丸尾陽成, Fuka Aizawa, Takahiro Niimura, Yuki Izawa-Ishizawa, Hirofumi Hamano, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : プロトンポンプ阻害剤，ボノプラザンが抗VEGF療法に与える影響, 医療薬学フォーラム2022/第30回クリニカルファーマシーシンポジウム, Jul. 2022.
54.	Yoshika Sakamoto, Nanami Tomochika, Takahiro Niimura, Mitsuhiro Goda, Fuka Aizawa, Kenta Yagi, Shiori Nishiuchi, 生田賢治, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 医療ビッグデータを活用したスニチニブ誘発心毒性に対する予防薬の探索, 医療薬学フォーラム2022/第30回クリニカルファーマシーシンポジウム, Jul. 2022.
55.	Kohei Ohmine, 近藤正輝, Mitsuhiro Goda, Honoka Nishi, MIYATA Koji, TSUJINAKA Kaito, Hirofumi Hamano, Fuka Aizawa, Kenta Yagi, Yoshito Zamami, Keisuke Ishizawa and Yuki Izawa-Ishizawa : 大動脈瘤，解離に対する杜仲葉エキスの抑制効果の検討, 医療薬学フォーラム2022/第30回クリニカルファーマシーシンポジウム, Jul. 2022.
56.	Yurika Kuniki, Kenta Yagi, Mayu Takaoka, OKAMOTO Naoki, Hirofumi Hamano, Mitsuhiro Goda, Takahiro Niimura, Fuka Aizawa, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 慢性骨髄性白血病に対するBCR-ABL阻害剤とALDH阻害剤併用による抗腫瘍効果増強の検討, 医療薬学フォーラム2022/第30回クリニカルファーマシーシンポジウム, Jul. 2022.
57.	MIYATA Koji, Yuki Izawa-Ishizawa, 近藤正輝, TSUJINAKA Kaito, Kohei Ohmine, 西穂香, Shuto Itokazu, Takahiro Niimura, Fuka Aizawa, Hirofumi Hamano, Kenta Yagi, Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa : フルオロキノロン系抗菌薬による血管毒性の病態解明, 第141回日本薬理学会近畿部会, Jul. 2022.
58.	Rie Andou, Kenta Yagi, OKAMOTO Naoki, Mayu Takaoka, Fuka Aizawa, Hirofumi Hamano, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : 各種プロトンポンプ阻害剤のがん細胞におけるVEGF発現に与える影響, 日本薬学会第142年会, Mar. 2022.
59.	Sayuri Itobayashi, Mitsuhiro Goda, Ami Yoshida, Yugo Sugimoto, Masaya Kanda, Toshihiko Yoshioka, 櫻田巧, Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : シスプラチン誘発腎障害に対するバルプロ酸ナトリウムの有効性の検証, 日本薬学会第142年会, Mar. 2022. (Keyword) data analysis / kidney disease
60.	Fuka Aizawa, Haruna Kajimoto, Daishi Moriyama, Ami Okabayashi, Mitsuhiro Goda, Hirofumi Hamano, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : リアルワールドデータに基づく抗がん剤支持療法の開発;スタチン系薬剤による末梢神経障害治療および予防効果の検証, 第95回日本薬理学会年会, Mar. 2022. (Keyword) data analysis
61.	Toshihiko Yoshioka, Mitsuhiro Goda, Masaya Kanda, Ami Yoshida, Sayuri Itobayashi, Yugo Sugimoto, Yuki Izawa-Ishizawa, Kenta Yagi, Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Yoshito Zamami and Keisuke Ishizawa : シスプラチン誘発急性腎障害に対するバルプロ酸ナトリウムの影響, 第95回日本薬理学会年会, Mar. 2022. (Keyword) data analysis / kidney disease
62.	MIYATA Koji, Yuki Izawa-Ishizawa, Masateru Kondoh, TSUJINAKA Kaito, Kohei Ohmine, Honoka Nishi, Fuka Aizawa, Hirofumi Hamano, Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa : 杜仲葉エキスによる大動脈解離発症抑制効果の検討, 第95回日本薬理学会年会, Mar. 2022.
63.	Yoshika Sakamoto, Nanami Tomochika, Hirofumi Hamano, Mitsuhiro Goda, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Akihito Nakamura, Shiori Nishiuchi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 大規模医療情報データベースを用いたスニチニブ誘発心不全に対する予防薬の探索, 第95回日本薬理学会年会, Mar. 2022.
64.	Yurika Kuniki, Kenta Yagi, Rina Yoshida, OKAMOTO Naoki, Rie Andou, 山川裕介, Hirofumi Hamano, Mitsuhiro Goda, Takahiro Niimura, Fuka Aizawa, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 慢性骨髄性白血病に対するBCR-ABL阻害剤とALDH阻害剤併用による抗腫瘍効果, 第95回日本薬理学会年会, Mar. 2022.
65.	Mitsuhiro Goda, Masaya Kanda, Toshihiko Yoshioka, Takahiro Niimura, 櫻田巧, 小川敦, Naoto Okada, Fuka Aizawa, Kenta Yagi, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 医療ビッグデータ解析と基礎研究を融合した研究手法による抗がん剤誘発副作用に対する予防法の探索, 日本臨床腫瘍薬学会学術大会2022 シンポジウム 12, Mar. 2022. (Keyword) data analysis
66.	Shiori Nishiuchi, Hiroumi Saito, Takahiro Niimura, Yoshito Zamami, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Hirofumi Hamano, Yuki Izawa-Ishizawa and Keisuke Ishizawa : ドキソルビシン誘発心筋症に対する予防薬探索を目的としたドラッグリポジショニング研究, 第42回日本臨床薬理学会学術総会, Dec. 2021.
67.	MIYATA Koji, 坂東寛, Mitsuhiro Goda, Masayuki Chuma, 新田侑生, 田崎嘉一, Toshihiko Yoshioka, 小川淳, Yoshito Zamami, Hirofumi Hamano, Yuki Izawa-Ishizawa and Keisuke Ishizawa : ラモトリギンの皮膚障害リスクに影響する因子の探索, 第42回日本臨床薬理学会学術総会, Dec. 2021. (Keyword) data analysis
68.	Rie Andou, Kenta Yagi, OKAMOTO Naoki, Fuka Aizawa, Hirofumi Hamano, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : ボノプラザンががん細胞のVEGF発現に与える影響に関する検討, 第140回日本薬理学会近畿部会, Nov. 2021.
69.	Ami Yoshida, Mitsuhiro Goda, Yugo Sugimoto, Hikari Yagita, Masaya Kanda, Toshihiko Yoshioka, 櫻田巧, Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : シスプラチン誘発腎障害に対する新規予防候補薬の効果, 第140回日本薬理学会近畿部会, Nov. 2021. (Keyword) kidney disease / data analysis
70.	Kohei Ohmine, Masateru Kondoh, Mitsuhiro Goda, Honoka Nishi, MIYATA Koji, TSUJINAKA Kaito, Hirofumi Hamano, Fuka Aizawa, Kenta Yagi, Yoshito Zamami, Keisuke Ishizawa and Yuki Izawa-Ishizawa : 杜仲茶エキスによる大動脈疾患発症抑制効果の検討, 第140回日本薬理学会近畿部会, Nov. 2021.
71.	Toshihiko Yoshioka, Mitsuhiro Goda, Masaya Kanda, Ami Yoshida, Sayuri Itobayashi, Yugo Sugimoto, Yuki Izawa-Ishizawa, Kenta Yagi, Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Yoshito Zamami and Keisuke Ishizawa : シスプラチン誘発腎障害に対する杜仲葉エキスの効果, 第60回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2021. (Keyword) kidney disease / data analysis
72.	Ami Yoshida, Mitsuhiro Goda, Yugo Sugimoto, Hikari Yagita, Masaya Kanda, Toshihiko Yoshioka, Takumi Sakurada, Yuki Izawa-Ishizawa, Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Kenta Yagi, Yoshito Zamami and Keisuke Ishizawa : シスプラチン誘発腎障害に対する新規予防薬の探索, 第60回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2021. (Keyword) data analysis / kidney disease
73.	Haruna Kajimoto, Daishi Moriyama, Fuka Aizawa, Takahiro Niimura, Yoshito Zamami, Mitsuhiro Goda, Kenta Yagi, Hirofumi Hamano, Yuki Izawa-Ishizawa and Keisuke Ishizawa : FAERS解析を活用したオキサリプラチン誘発末梢神経障害に対する予防薬の検討, 第60回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2021. (Keyword) data analysis
74.	Shimon Takahashi, Kenshi Takechi, JOHZUKURI Natsumi, Hirofumi Hamano, Fuka Aizawa, Kenta Yagi, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa : 大規模医療情報データベースを用いたドラッグリポジショニングによるバラシクロビルの抗てんかん作用の検討, 第60回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2021. (Keyword) data analysis
75.	Fuka Aizawa, Haruna Kajimoto, Daishi Moriyama, Takahiro Niimura, Mitsuhiro Goda, NITTA Ayaka, Shimon Takahashi, Hirofumi Hamano, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 医療ビッグデータを基盤とした迅速かつ安全ながん支持療法の開発, 第31回日本医療薬学会年会, Oct. 2021. (Keyword) data analysis
76.	Yoshito Zamami, Takahiro Niimura, Hirofumi Hamano, Mitsuhiro Goda, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa : リアルワールドデータを活用したドラッグリポジショニング研究, 第31回日本医療薬学会年会, Oct. 2021. (Keyword) data analysis
77.	Masaya Kanda, Mitsuhiro Goda, Toshihiko Yoshioka, Ami Yoshida, Takahiro Niimura, Takumi Sakurada, Atsushi Ogawa, Naoto Okada, Fuka Aizawa, Yoshito Zamami, Kenta Yagi, Hirofumi Hamano, Yuki Izawa-Ishizawa and Keisuke Ishizawa : 抗がん剤副作用予防のための大規模医療情報データベース解析を活用したリバーストランスレーショナルリサーチ, 第31回日本医療薬学会年会, Oct. 2021. (Keyword) data analysis / kidney disease
78.	Mitsuhiro Goda, Masaya Kanda, Toshihiko Yoshioka, Ami Yoshida, Takahiro Niimura, Takumi Sakurada, Atsushi Ogawa, Naoto Okada, Fuka Aizawa, Kenta Yagi, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 大規模医療情報データベースを活用した抗がん剤副作用に対する予防法の確立, 第60回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2021. (Keyword) data analysis / kidney disease
79.	Yuki Izawa-Ishizawa : 薬物有害事象の発現リスクにおける性差分析, 日本学術会議公開シンポジウムジェンダード・イノベーション ∼一人ひとりが主役の研究開発が新しい未来を拓く∼, Aug. 2021.
80.	TSUJINAKA Kaito, Yuki Izawa-Ishizawa, Takahiro Niimura, Toshihiko Yoshioka, Mitsuhiro Goda, Masateru Kondoh, Kohei Ohmine, Honoka Nishi, MIYATA Koji, Hirofumi Hamano, Fuka Aizawa, Kenta Yagi, Yoshito Zamami and Keisuke Ishizawa : 血管新生阻害剤における大動脈解離発症の関連要因解明, 第50回日本心脈管作動物質学会, Jul. 2021.
81.	Haruna Kajimoto, Daishi Moriyama, Fuka Aizawa, Takahiro Niimura, Yoshito Zamami, Mitsuhiro Goda, Kenta Yagi, Hirofumi Hamano, Yuki Izawa-Ishizawa and Keisuke Ishizawa : オキサリプラチン誘発末梢神経障害に対するスタチン系薬剤の予防効果, 第139回日本薬理学会近畿部, Jun. 2021. (Keyword) data analysis / kidney disease
82.	Tomomi Tani, Masayuki Chuma, Mitsuhiro Goda, Takashi Bandoh, Masateru Kondoh, Yurika Kuniki, Hirofumi Hamano, Takahiro Niimura, Naoto Okada, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa : 大規模医療情報および遺伝子発現データベースを活用したバンコマイシン関連腎障害に対する予防薬の探索とソの有用性の検討, 第139回日本薬理学会近畿部, Jun. 2021. (Keyword) data analysis / kidney disease
83.	Masaya Kanda, Mitsuhiro Goda, Toshihiko Yoshioka, Ami Yoshida, Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Kenta Yagi, Hirofumi Hamano, Naoto Okada and Keisuke Ishizawa : シスプラチン誘発急性腎障害に対する各種5-HT3受容体拮抗薬併用の影響, 第94回日本薬理学会年会, Mar. 2021.
84.	Fuka Aizawa, Yoshito Zamami, Takahiro Niimura, Takehiro Kawashiri, Mitsuhiro Goda, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa : HMG-CoA還元酵素阻害剤はGSTを介してオキサリプラチン誘発末梢神経障害を抑制する, 第94回日本薬理学会年会, Mar. 2021.
85.	Yuki Izawa-Ishizawa, Miho Mitsunari, Yoshimi Bando, Satsuki Sumitani, Akira Tangoku and Mari Haku : 研究に関する男女共同参画・ダイバーシティの推進状況に関するアンケート調査 -全国の集計結果との比較から見える徳島大学の現状-, 第262回徳島医学会学術集会(令和2年度冬期), Mar. 2021.
86.	Takahiro Niimura, Yoshito Zamami, 川尻雄大, Mitsuhiro Goda, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa : 基礎研究と臨床研究の融合による薬剤性末梢神経障害に対する予防薬探索, 日本薬学会第141年会, Mar. 2021. (Keyword) data analysis
87.	Takashi Bandoh, Masayuki Chuma, Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenta Yagi, Hirofumi Hamano, Naoto Okada, 泉侑希, 桐野靖, 中村敏己 and Keisuke Ishizawa : 大規模医療情報データベースを活用したバンコマイシン関連腎障害に対する薬剤性腎障害原因薬剤の多剤併用における影響, 日本薬学会第141年会, Mar. 2021. (Keyword) data analysis
88.	Fuka Aizawa, Haruna Kajimoto, Daishi Moriyama, Takahiro Niimura, Yoshito Zamami, Hirofumi Hamano, Mitsuhiro Goda, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa : オキサリプラチン誘発末梢神経障害に対するHMG-CoA還元酵素阻害剤の影響, 第262回徳島医学会学術集会, Mar. 2021.
89.	Mitsuhiro Goda, Yoshito Zamami, Takahiro Niimura, 萱野純史, Hirofumi Hamano, Naoto Okada, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, 桐野靖, 中村敏己 and Keisuke Ishizawa : 大規模医療情報データベースを活用した抗がん剤副作用予防のためのリバーストランスレーショナルリサーチ, 日本薬学会第140年会, Mar. 2021.
90.	Yoshika Sakamoto, Yoshito Zamami, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa : 大規模医療情報データベースを用いたドキソルビシン誘発心筋症に対する予防薬の探索, 日本薬学会第141年会大学院生・学生シンポジウム, Mar. 2021. (Keyword) data analysis
91.	Keisuke Ishizawa, Mitsuhiro Goda, Masayuki Chuma, Kenta Yagi, Yuki Izawa-Ishizawa and Yoshito Zamami : 有害事象自発報告データベースを活用した抗がん剤副作用に対する予防法の探索, 第41回日本臨床薬理学会学術総会学術委員会企画シンポジウム5, Dec. 2020.
92.	Fuka Aizawa, Mitsuhiro Goda, Masaya Kanda, Toshihiko Yoshioka, Ami Yoshida, Takahiro Niimura, Kenta Yagi, Hirofumi Hamano, Naoto Okada, Yoshito Zamami, Yuki Izawa-Ishizawa and Keisuke Ishizawa : シスプラチンと5-HT3受容体拮抗薬併用が腎機能障害に与える影響, 第30回日本循環薬理学会, Nov. 2020.
93.	Yuki Izawa-Ishizawa, Yoshito Zamami, Niimura Takahiro, Mitsuhiro Goda, Kenta Yagi, Masayuki Chuma, Masaki Imanishi and Keisuke Ishizawa : New strategy for Cardio-Oncology study; the combination of big data analysis and basic research, 第79回日本癌学会学術集会シンポジウム8, Oct. 2020.
94.	Masateru Kondoh, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kotoko Suzuki, Rie Matsuoka, Yoshito Zamami, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : 薬剤誘発性急性大動脈疾患に対するケルセチンの抑制効果, 第137回日本薬理学会近畿部会, Jun. 2020.
95.	Tatsuya Tsuda, Mitsuhiro Goda, Yuya Horinouchi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa, Ichiro Hashimoto and Yuki Izawa-Ishizawa : 血管平滑筋細胞石灰化シグナルにおけるRhoキナーゼーサイクロフィリンA経路の関与, 第260回徳島医学会学術集会(令和元年度冬期), Feb. 2020.
96.	Mitsuhiro Goda, Masaya Kanda, 前川晃子, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Kenshi Takechi, Hirofumi Hamano, Naoto Okada, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : 大規模医療情報データベースを活用したシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証, 第40回日本臨床薬理学会学術総会, Dec. 2019.
97.	Takahiro Niimura, Yoshito Zamami, Yutaroh Naitoh, 川尻雄大, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda and Keisuke Ishizawa : 抗がん剤誘発末梢神経障害の予防薬開発を目的とした医療ビッグデータ解析および基礎研究, 第40回日本臨床薬理学会学術総会, Dec. 2019.
98.	Yoshito Zamami, Takahiro Niimura, 川尻雄大, Mitsuhiro Goda, 相澤風花, Naoto Okada, 濱野裕章, Kenshi Takechi, Masayuki Chuma, Yuki Izawa-Ishizawa, Hiroaki Yanagawa and Keisuke Ishizawa : 大規模医療情報を活用した多施設共同臨床研究の提案, 第3回臨床薬理学集中講座フォローアップ・セミナー, Dec. 2019.
99.	Tatsuya Tsuda, Yuki Izawa-Ishizawa, Yoshiro Abe and Ichiro Hashimoto : 血管内皮細胞特異的ERK5欠損の皮弁生着に対する影響の検討, 第28回日本形成外科学会基礎学術集会, Nov. 2019.
100.	Yuki Izawa-Ishizawa : 男女がともに活躍できる徳島大学を目指すAWAサポートセンターの取組み, 日本医療薬学会第29回年会, Nov. 2019.
101.	Mitsuhiro Goda, 神田将哉, 前川晃子, Ami Yoshida, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Kenshi Takechi, Yasumasa Ikeda and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたシスプラチン誘発腎障害に対する新規予防薬探索, 第29回日本循環薬理学会・第55回高血圧関連疾患モデル学会合同学術集会, Nov. 2019.
102.	Takahiro Niimura, Yoshito Zamami, Hiroumi Saito, 神田将哉, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : 大規模医療情報を活用した抗がん剤誘発心筋症予防薬の探索, 第29回日本循環薬理学会・第55回高血圧関連疾患モデル学会合同学術集会, Nov. 2019.
103.	鈴木琴子, Yuki Izawa-Ishizawa, Mitsuhiro Goda, 近藤正輝, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : ケルセチンによる薬剤誘発性急性大動脈疾患発症抑制効果の検討, 第58回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2019.
104.	Hiroumi Saito, Takahiro Niimura, Yoshito Zamami, Masaya Kanda, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : 大規模医療情報データベースを活用したドキソルビシン誘発心筋炎に対する予防薬の探索, 第58回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2019.
105.	内藤優太朗, Yoshito Zamami, Takahiro Niimura, 川尻雄大, 相澤風花, Shiori Nishiuchi, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, 島添隆雄, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : 大規模医療情報データベースを活用したオキサリプラチン誘発末梢神経障害に対する予防薬探索, 第58回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2019.
106.	JOHZUKURI Natsumi, Shimon Takahashi, Kenshi Takechi, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Yuya Horinouchi, Hirofumi Hamano, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : ドラッグリポジショニングによる大規模医療情報データベースを用いた新規抗てんかん薬の探索研究, 第58回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2019.
107.	村井陽一, Mitsuhiro Goda, 神田将哉, Takahiro Niimura, Ami Yoshida, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Hirofumi Hamano, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : シスプラチンと各種5-HT3受容体拮抗薬の併用による腎機能への影響, 第58回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2019.
108.	Masaya Kanda, Mitsuhiro Goda, Akiko Maegawa, Takahiro Niimura, Ami Yoshida, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Kenshi Takechi, Hirofumi Hamano, 岡田直人, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたシスプラチン誘発腎障害の予防薬探索, 第58回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2019.
109.	相澤風花, Yoshito Zamami, 内藤優太郎, Takahiro Niimura, 川尻雄大, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuki Izawa-Ishizawa, 小林大介, 島添隆雄, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : オキサリプラチン誘発末梢神経障害に対する新規予防薬の有効性に関する基礎的検証, 第58回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2019.
110.	Masaya Kanda, Mitsuhiro Goda, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Hirofumi Hamano, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : シスプラチン誘発腎障害に対する各種 5-HT3 受容体拮抗薬の影響, 第29回日本医療薬学会年会, Nov. 2019.
111.	定作奈津美, Shimon Takahashi, Kenshi Takechi, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : ビッグデータを活用した新規抗てんかん薬の検討, 第29回日本医療薬学会年会, Nov. 2019.
112.	Masayuki Chuma, Mitsuhiro Goda, Takahiro Niimura, Yoshito Zamami, Kenshi Takechi, Yuki Izawa-Ishizawa, 濱野裕章, 石田俊介, Takahiro Niimura, Masateru Kondoh, Takashi Bandoh, Naoto Okada, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたバンコマイシン関連腎障害の予防薬探索とその有用性の検討, 第13回日本腎臓病薬物療法学会学術集会・総会, Nov. 2019.
113.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, 小山敏広, Hirofumi Hamano, Naoto Okada, Mitsuhiro Goda, Naoto Okada, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 大規模医療情報データベースを活用した周術期領域における薬剤疫学研究, 第29回日本医療薬学会年会シンポジウム9, Nov. 2019.
114.	Mitsuhiro Goda, Yoshito Zamami, Takahiro Niimura, Kenshi Takechi, Masayuki Chuma, 萱野純史, Hirofumi Hamano, Naoto Okada, 島添隆雄, Yuki Izawa-Ishizawa, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 大規模医療情報データベースを活用したオキサリプラチン誘発末梢神経障害に対する予防薬探索, 第29回日本医療薬学会年会シンポジウム12, Nov. 2019.
115.	Nori Sato, Yuki Izawa-Ishizawa, 百田佳織, 橋本采佳, Shinsuke Katoh and Koichi Sairyo : 男女共同参画の現状と未来運動器診療を生涯継続するための私の決断, The Journal of the Chugoku-Shikoku Orthopaedic Association, Vol.31, No.3, 297, Oct. 2019. (Keyword) 労働衛生女性医師女性の権利整形外科医ヒト
116.	Takahiro Niimura, Yoshito Zamami, Takahiro Niimura, Yutaroh Naitoh, 川尻雄大, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda and Keisuke Ishizawa : 医療ビッグデータ解析と基礎研究を融合した抗がん剤誘発末梢神経障害の予防薬開発, 次世代を担う創薬・医療薬理シンポジウム2019, Aug. 2019.
117.	Takahiro Niimura, Yoshito Zamami, Takahiro Niimura, 内藤優太朗, 川尻雄大, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda and Keisuke Ishizawa : 医療ビッグデータ解析と基礎研究を融合した抗がん剤誘発末梢神経障害の予防薬開発, 生体機能と創薬シンポジウム2019, Aug. 2019.
118.	齊藤広海, Yoshito Zamami, Takahiro Niimura, Masaya Kanda, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : 大規模医療情報データベースを活用したドキソルビシン誘発心筋炎にたいする予防薬の探索, 第30回霧島神経薬理フォーラム, Aug. 2019.
119.	新村貴博, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報を用いたニコランジルの心肺停止後予後改善効果の検討, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
120.	Yutaroh Naitoh, Takahiro Niimura, Yoshito Zamami, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda and Keisuke Ishizawa : オキサリプラチン誘発末梢神経障害の予防薬探索を目的としたドラッグリポジショニング研究, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
121.	齊藤広海, 新村貴博, Yoshito Zamami, Masaya Kanda, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : 医療ビッグデータ解析を活用したドキソルビシン誘発心筋炎に対する予防薬探索研究, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
122.	JOHZUKURI Natsumi, Shimon Takahashi, Kenshi Takechi, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報データベースを活用した新規抗てんかん薬の探索研究, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
123.	Mitsuhiro Goda, 斉家和仁, Akiko Maegawa, Masaya Kanda, Ami Yoshida, Yoichi Murai, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Kenshi Takechi, Hirofumi Hamano, Naoto Okada, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : 医療ビッグデータを活用したシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証, 第4回中四国臨床薬理学会, Jul. 2019.
124.	新村貴博, Yoshito Zamami, 川尻雄大, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたオキサリプラチン誘発末梢神経障害の予防薬探索, 第4回中四国臨床薬理学会, Jul. 2019.
125.	Kotoko Suzuki, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Masateru Kondoh, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : 薬剤誘発性急性大動脈疾患に対するケルセチンの効果, 第135回日本薬理学会近畿部会, Jun. 2019.
126.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 医療ビッグデータ解析と基礎研究を融合した薬剤性副作用の機序解明および治療薬の開発, 第29回日本医療薬学会年会シンポジウム13, Mar. 2019.
127.	Kenshi Takechi, Masayuki Chuma, 石田俊介, 坂東寛, Yoshito Zamami, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa and Hiroaki Yanagawa : 向精神薬の副作用対策を基盤とした臨床研究とその活用, 第139回日本薬学会年会一般シンポジウムS48, Mar. 2019.
128.	近藤正輝, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : キサンチンオキシダーゼ阻害剤による新規血管線維化抑制機構の検討, 日本薬学会第139年会大学院生シンポジウムGS03, Mar. 2019.
129.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Masaki Imanishi, Keijo Fukushima, Mitsuhiro Goda, Kenshi Takechi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全関連骨格筋萎縮における鉄代謝異常, 第92回日本薬理学会年会, Mar. 2019.
130.	Yasumasa Ikeda, Akiho Satoh, Yuya Horinouchi, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron accumulation negatively regulates skeletal muscle myogenesis, 第92回日本薬理学会年会, Mar. 2019.
131.	Mitsuhiro Goda, Masaya Kanda, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, 濱野裕章, 生田賢治, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda, Yasushi Kirino, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : ビッグデータを用いたシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証, 日本薬学会第139年会, Mar. 2019.
132.	Mitsuhiro Goda, Masaya Kanda, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, 濱野裕章, 生田賢治, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda, Yasushi Kirino, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : シスプラチン誘発腎障害に対する新規予防薬の有効性の基礎的検証, 日本臨床腫瘍薬学会学術大会2019, Mar. 2019.
133.	Mitsuhiro Goda, 神田将哉, 新村貴博, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, 濱野裕章, 生田賢治, Naoto Okada, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda and Keisuke Ishizawa : シスプラチン誘発腎障害に対する新規予防薬の有効性の検証, 第92回日本薬理学会年会, Mar. 2019.
134.	鈴木琴子, Yuki Izawa-Ishizawa, Masateru Kondoh, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Kenshi Takechi, Mitsuhiro Goda, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : 薬物誘発性大動脈瘤または大動脈解離モデルマウスに対するケルセチンの効果, 第92回日本薬理学会年会, Mar. 2019.
135.	新村貴博, Yoshito Zamami, 川尻雄大, Mitsuhiro Goda, Naoto Okada, 萱野純史, 小山敏広, Masaki Imanishi, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, 小林大介, 島添隆雄 and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたオキサリプラチン誘発末梢神経障害の予防薬探索, 第92回日本薬理学会年会学生セッション, Mar. 2019.
136.	Yoshito Zamami, Takahiro Niimura, 川尻雄大, Mitsuhiro Goda, Naoto Okada, Hirofumi Hamano, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, 島添隆雄 and Keisuke Ishizawa : 大規模医療情報データベースを活用した抗がん剤誘発副作用に対する予防薬の探索, 第92回日本薬理学会年会年会企画シンポジウム, Mar. 2019.
137.	Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Watanabe, Hirofumi Hamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : マクロファージフェリチン欠損は肥満・糖尿病における脂肪炎症を抑制する, 第48回日本心脈管作動物質学会, Feb. 2019.
138.	藤本望, 村田梨菜, Keiji Murakami, Hideki Fujii, Licht Miyamoto, 井上貴久, Koichiro Tsuchiya, Yasumasa Ikeda, Yuki Izawa-Ishizawa and Shuichi Hamano : 唾液中の硝酸イオンが口腔細菌に与える影響について·, 第42回徳島県医学検査学会, Dec. 2018.
139.	Yuki Izawa-Ishizawa : 新規大動脈解離モデルマウスの開発と予防薬の探索, 第4回四国オープンイノベーションワークショップin徳島, Dec. 2018.
140.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Hiroumi Saito, Masaki Imanishi, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報データベースおよび遺伝子発現データベースを活用した薬剤性心筋炎に対する予防薬の探索, 第28回日本医療薬学会年会シンポジウム, Nov. 2018.
141.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Hirofumi Hamano, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Kenshi Takechi, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : リアルワールドビッグデータを活用した新規腎保護薬の探索, 第28回日本医療薬学会年会, Nov. 2018.
142.	Yoshito Zamami, Yuki Izawa-Ishizawa, 新村貴博, Masaki Imanishi, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 救急・集中治療領域において大規模医療情報データベースを活用したトランスレーショナルリサーチ, 第29回霧島神経薬理フォーラム, Nov. 2018.
143.	桂明里, Licht Miyamoto, 服部真奈, 津田勝範, 森崎実友, Yuki Izawa-Ishizawa and Koichiro Tsuchiya : 青黛含有成分による細胞増殖活性の検討, 第134回日本薬理学会近畿部会, Nov. 2018.
144.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Masaki Imanishi, Keijo Fukushima, Mitsuhiro Goda, Kenshi Takechi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全関連サルコペニアにおける鉄の関与, 第134回日本薬理学会近畿部会, Nov. 2018.
145.	斉家和仁, Mitsuhiro Goda, 伊勢諒, 新村貴博, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Naoto Okada, Kenshi Takechi, Masaki Imanishi, Yasumasa Ikeda, 演野裕章, Yuya Horinouchi, Koichiro Tsuchiya and Keisuke Ishizawa : シスプラチン誘発腎障害に対する脂質異常症治療薬の影響, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
146.	生藤来希, Masaki Imanishi, 山川祐介, Keijo Fukushima, 前川晃子, Yuya Horinouchi, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino and Koichiro Tsuchiya : 大腸がん増大におけるがん関連線維芽細胞由来ERKSの役割, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
147.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Yuki Izawa-Ishizawa, Hiromichi Fujino and Toshiaki Tamaki : リアルワールドデータを活用した新規腎保護薬の探索, 第48回日本腎臓学会西部学術大会, Sep. 2018.
148.	Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Watanabe, Hirofumi Hamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Yoshito Zamami, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : マクロファージ鉄の肥満・糖尿病における役割第42回日本鉄バイオサイエンス学会学術集会 2018/9/2 石川県金沢医科大学病院北辰講堂, 第42回日本鉄バイオサイエンス学会学術集会, Sep. 2018.
149.	新村貴博, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報を活用した新規心肺蘇生後脳症治療薬の探索, 第29回霧島神経薬理フォーラム, Aug. 2018.
150.	Yuki Izawa-Ishizawa, Yu Kagimoto, Masaki Imanishi, Yusuke Iwata, Kotoko Suzuki, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : 第40回徳島医学会賞受賞講演動脈硬化性疾患発症に対するケルセチンの効果, 第257回徳島医学会学術集会(平成30年度夏季), Aug. 2018.
151.	Yoshito Zamami, 新村貴博, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : 医療情報データベースを活用した抗がん剤誘発副作用に対する予防薬の探索研究, 第21回日本医薬品情報学会総会・学術大会, Jul. 2018.
152.	Masaki Imanishi, Masateru Kondoh, 山川裕介, 生藤来希, 村井陽一, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Keijo Fukushima, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : Angiotensin II誘発性心臓線維化は線維芽細胞特異的ERK5欠損マウスにおいて亢進される, 第133回日本薬理学会近畿部会, Jun. 2018.
153.	Yoshito Zamami, Marin Mitsui, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Keijo Fukushima, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを活用したベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究, 日本薬学会第138年会, Mar. 2018.
154.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニング手法を用いた心肺蘇生後脳症治療薬の探索, 日本薬学会第138年会, Mar. 2018.
155.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa and Toshiaki Tamaki : Factor Xa Inhibitor Exerts a Protective Effect against Renal Injury, 第82回日本循環器学会学術集会, Mar. 2018.
156.	Yoshito Zamami, Marin Mitsui, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : 有害事象自発報告データベースを活用したベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究, 日本臨床腫瘍薬学会学術大会2018, Mar. 2018.
157.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Hirofumi Hamano, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 大規模医療情報データベース解析と基礎研究の融合による新規腎保護薬の探索, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
158.	Yuki Izawa-Ishizawa, Yu Kagimoto, Masaki Imanishi, Yusuke Iwata, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : マウス大動脈瘤形成に対するケルセチンの効果, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
159.	Masaki Imanishi, Masateru Kondoh, Kyohei Tanaka, Raiki Ikutoh, Yoichi Murai, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Febuxostatの尿酸合成抑制作用とは独立した血管線維化抑制機構の解明, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
160.	Kenshi Takechi, Yoshito Zamami, Masaki Imanishi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Toshiaki Tamaki, Keisuke Ishizawa and Hiroaki Yanagawa : てんかん誘発性精神症状の行動学的解析および治療薬の探索と作用機序の解明, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
161.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用した心肺停止患者に対するニコランジルの有効性に関する検討, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
162.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 第Xa因子阻害剤の腎保護効果, 第47回日本心脈管作動物質学会, Feb. 2018.
163.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Yuki Izawa-Ishizawa, Hiromichi Fujino and Toshiaki Tamaki : 医療ビッグデータを活用した腎保護薬の探索, 2017年度肥満・糖尿病クラスター・ミニリトリート, Feb. 2018.
164.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 第Xa因子阻害薬の腎保護効果, 第10回心・血管クラスター・ミニリトリート, 2017.
165.	Sakiko Hino, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用した薬剤性腎障害に対する予防薬の探索, 西日本医学生学術フォーラム2017, Dec. 2017.
166.	Yusuke Iwata, Yuki Izawa-Ishizawa, Yu Kagimoto, Kotoko Suzuki, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : マウス大動脈瘤形成に対するケルセチンの効果, 西日本医学生学術フォーラム2017, Dec. 2017.
167.	Yuki Izawa-Ishizawa, Yu Kagimoto, Masaki Imanishi, Yuya Horinouchi, Kotoko Suzuki, Yusuke Iwata, Yoshito Zamami, Kenshi Takechi, Yasumasa Ikeda, Toshiaki Tamaki and Keisuke Ishizawa : ケルセチンによる動脈硬化性疾患発症に対する予防効果の検討, 第27回日本循環薬理学会, Dec. 2017.
168.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を用いて新規心肺蘇生後症候群治療薬の開発を志向したドラッグリポジショニング研究, 第38回日本臨床薬理学会学術総会, Dec. 2017.
169.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 臨床薬理学集中講座修了後の研究活動∼大規模医療情報を活用したドラッグリポジショニング研究を中心に∼, 第38回日本臨床薬理学会学術総会臨床薬理学集中講座フォローアップ・セミナー, Dec. 2017.
170.	Hiroaki Watanabe, Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 肥満・糖尿病におけるマクロファージ鉄制御機構の検討, 第132回日本薬理学会近畿部会, Nov. 2017.
171.	Takahiro Niimura, Yoshito Zamami, 小山敏広, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニングを切り口とした心肺蘇生後症候群治療薬の探索研究, 第27回日本医療薬学会年会, Nov. 2017.
172.	Yoshito Zamami, 小山敏広, Yuki Izawa-Ishizawa, Takahiro Niimura, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, 桐野靖, 中村敏己, 寺岡和彦, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用して心肺停止患者の生存率向上を志向したドラッグリポジショニング研究, 第27回日本医療薬学会年会, Nov. 2017.
173.	Marin Mitsui, Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを基にしたベバシズマブと相互作用を起こす薬剤の探索研究, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
174.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 心肺停止患者の予後に与えるニコランジルの影響-大規模レセプト情報を用いた検討, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
175.	Shiori Urushizaki, Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用して新規心肺蘇生後症候群治療薬の開発を志向したドラッグリポジショニング研究, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
176.	Yu Kagimoto, Yuki Izawa-Ishizawa, Mayuko Hosohka, Naoko Saito, Kotoko Suzuki, Masaki Imanishi, Yuya Horinouchi, Yoshito Zamami, Kenshi Takechi, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 急性大動脈解離易発症マウスにおけるquercetinの効果, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
177.	Kyohei Tanaka, Masaki Imanishi, Masateru Kondoh, Raiki Ikutoh, Yoichi Murai, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : フェブキソスタットの尿酸合成抑制剤作用とは独立した血管線維化抑制作用の検討, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
178.	Hiroaki Watanabe, Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 肥満・糖尿病におけるマクロファージ鉄の役割の検討, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
179.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎臓病における尿毒素蓄積によるヘプシジン制御と鉄代謝破綻のメカニズムの解明, 第41回日本鉄バイオサイエンス学会学術集会, Sep. 2017.
180.	Yasumasa Ikeda, Yuya Horinouchi, Hirofumi Hamano, 平山祐, Seiji Kishi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Ken-ichi Aihara, Hideko Nagasawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄摂取制限による尿細管間質障害の抑制効果の検討, 第41回日本鉄バイオサイエンス学会学術集会, Sep. 2017.
181.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全における尿毒素蓄積はヘプシジンを介した鉄代謝恒常性破綻に関与する, 大阪市大フォーラム, Aug. 2017.
182.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 心肺蘇生後症候群治療薬の開発を目的としたドラッグリポジショニング研究-大規模医療情報を活用した検討-, 第255回徳島医学会学術集会, Aug. 2017.
183.	Yoshito Zamami, Yuki Izawa-Ishizawa, 桐野靖, Marin Mitsui, Shiori Urushizaki, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを切り口としたベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究, 医療薬学フォーラム2017 第25回クリニカルファーマシーシンポジウム, Jul. 2017.
184.	Yuya Horinouchi, Yasumasa Ikeda, Masaki Imanishi, Yoshito Zamami, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 経口FXa阻害剤の腎線維化抑制効果, 医療薬学フォーラム2017 第25回クリニカルファーマシーシンポジウム, Jul. 2017.
185.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 第Xa因子阻害剤は腎間質線維化を抑制する, 第131回日本薬理学会近畿部会, Jun. 2017.
186.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : インドキシル硫酸蓄積はヘプシジン制御を介して鉄代謝恒常性破綻に関与する, 第131回日本薬理学会近畿部会, Jun. 2017.
187.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa and Toshiaki Tamaki : Inhibitory effect of dietary iron restriction on albumin-induced renal tubulointerstitial injury, 第60回日本腎臓学会学術総会, May 2017.
188.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : インドキシル硫酸はヘプシジンを介した鉄代謝異常に関与する, 第60回日本腎臓学会学術総会, May 2017.
189.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : FXa阻害剤は腎間質線維化を抑制する, 第60回日本腎臓学会学術総会, May 2017.
190.	Marin Mitsui, Yoshito Zamami, Yuki Izawa-Ishizawa, Shiori Urushizaki, 桐野靖, Kazuhito Saike, Hiroshi Moriguchi, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを基にしたベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究, 日本薬学会第137年会, Mar. 2017.
191.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : FXa 阻害剤の片側尿管結紮モデルマウスにおける腎間質線維化抑制作用, 日本薬学会第137年会, Mar. 2017.
192.	Raiki Ikutoh, Masaki Imanishi, Kyohei Tanaka, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : アンジオテンシンII 誘発性血管リモデリングに対するキサンチンオキシダーゼ阻害剤の影響, 日本薬学会第137年会, Mar. 2017.
193.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Factor Xa inhibitor attenuates renal fibrosis in mice with unilateral ureteral obstruction, 第90回日本薬理学会年会, Mar. 2017.
194.	Masaki Imanishi, Kyohei Tanaka, Raiki Ikuto, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Febuxostat suppresses angiotensin II-induced aortic fibrosis, 第90回日本薬理学会年会, Mar. 2017.
195.	Masaki Imanishi, 田中恭平, 生藤来希, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : フェブキソスタットはアンジオテンシンII誘発性大動脈繊維化を抑制する, 第90回日本薬理学会年会(長崎), Mar. 2017.
196.	Yuki Izawa-Ishizawa, Mayuko Hosooka, Naoko Saito, Masaki Imanishi, Yuya Horinouchi, Yoshito Zamami, Kenshi Takechi, Yasumasa Ikeda, Koichiro Tsuchiya, Keisuke Ishizawa and Toshiaki Tamaki : The effect of quercetin on the aortic dissection onset via its endothelial protective effect in mice, 第90回日本薬理学会年会, Mar. 2017.
197.	Koichiro Tsuchiya, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Yuya Horinouchi, Licht Miyamoto and Toshiaki Tamaki : 鉄ストレスと代謝性疾患-鉄ストレスによる疾患と，鉄ストレスによる治療, 日本薬学会第137年会, Mar. 2017.
198.	Yoshito Zamami, Yuki Izawa-Ishizawa, 桐野靖, 三井茉綸, 漆崎汐里, 斉家和仁, 森口浩史, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを切り口としたベバシズマブと相互作用を起こす薬剤の探索研究, 第46回日本心脈管作動物質学会年会, Feb. 2017.
199.	Masaki Imanishi, 田中恭平, 生藤来希, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Angiotensin II誘発性血管リモデリングに対するfebuxostatの効果, 第46回日本心脈管作動物質学会, Feb. 2017.
200.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Akiho Satoh, Keisuke Oshima, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全における尿毒素蓄積が生体内鉄代謝に与える影響の検討, 第46回日本心脈管作動物質学会, Feb. 2017.
201.	Yuki Izawa-Ishizawa, 細岡真由子, 斎藤尚子, 鍵本優有, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ケルセチンによるマウス大動脈解離発症予防効果の検討, 第46回日本心脈管作動物質学会年会, Feb. 2017.
202.	Yuki Izawa-Ishizawa, Yutaka Fukunaga, 西良恵理子, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya, Ichiro Hashimoto and Toshiaki Tamaki : ニトロソニフェジピンは虚血性皮弁モデルにおいて皮弁壊死を抑制する, 第26回日本循環薬理学会, Dec. 2016.
203.	細岡真由子, Yuki Izawa-Ishizawa, 斎藤尚子, Masaki Imanishi, Yoshito Zamami, Licht Miyamoto, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : Quercetin による血管内皮細胞保護効果の検討, 第130回日本薬理学会近畿部会, Nov. 2016.
204.	Akiho Satoh, Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Mizuki Imao, Hiroaki Watanabe, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 鉄欠乏が骨格筋に与える作用の検討, 第55回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2016.
205.	Yutaka Fukunaga, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Ichiro Hashimoto : 虚血性皮弁壊死モデルにおける抗酸化薬ニトロソニフェジピンの壊死抑制効果, 第25回日本形成外科学会基礎学術集会, Sep. 2016.
206.	三井茉綸, Yoshito Zamami, 漆崎汐里, 斉家和仁, 森口浩史, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニングを切り口としたベバシズマブ誘発高血圧に対する予防薬の探索研究, 第27回霧島神経薬理フォーラム(福岡), Aug. 2016.
207.	Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, 田淵正樹, Toshiaki Tamaki and Keisuke Ishizawa : 脳卒中後の神経症状増悪に対するニトロソニフェジピンの効果, 第46回日本神経精神薬理学会年会( ソウル), Jul. 2016.
208.	Yuki Izawa-Ishizawa, 細岡真由子, 斎藤尚子, Yuya Horinouchi, Masaki Imanishi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ケルセチン代謝産物Q3GAの血管内皮膚細胞に対する短期及び長期効果の検討, 第129回日薬理学会学会近畿部会( 広島), Jun. 2016.
209.	Yasumasa Ikeda, 佐藤明穂, Yuya Horinouchi, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 骨格筋分化における鉄の役割, 第129回日薬理学会学会近畿部会 (広島), Jun. 2016.
210.	Yasumasa Ikeda, Keisuke Oshima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄は低酸素誘導因子を抑制してエリスロポエチン発現を低下させる, 第59回日本腎臓学会学術総会, Jun. 2016.
211.	細岡真由子, Yuki Izawa-Ishizawa, 斎藤尚子, Licht Miyamoto, Masaki Imanishi, Yoshito Zamami, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : ケルセチン生体内代謝産物 quercetin -3-O-β-Dglucuronideによる血管内皮細胞保護効果, 日本薬学会第136年会(横浜), Mar. 2016.
212.	鍵本優有, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 無機リン刺激による血管平滑筋細胞石灰化におけるrho-kinase 及び cyclophilinA の関与, 日本薬学会第136年会(横浜), Mar. 2016.
213.	Hiroaki Watanabe, Yasumasa Ikeda, Hirofumi Hamano, Akiho Satoh, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 慢性腎臓病におけるヘプシジン制御メカニズムの検討, 日本薬学会第136年会(横浜), Mar. 2016.
214.	佐藤明穂, Yasumasa Ikeda, Yuya Horinouchi, 濱野裕章, 今尾瑞季, 渡邉大晃, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Toshiaki Tamaki, Licht Miyamoto and Koichiro Tsuchiya : 鉄過剰による骨格筋分化抑制作用の解明, 日本薬学会第136年会(横浜), Mar. 2016.
215.	Yasumasa Ikeda, Keisuke Oshima, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron Supplementation Suppressed Erythropoietin Expression through HIF-dependent Pathway, The 80th Annual Scientific Meeting of the Japanese Circulation Society, Mar. 2016.
216.	太田和馬, Yoshitaka Kihira, 岸渕麗奈, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 電位依存性カリウムチャネルKv2.2は腎虚血再灌流障害の軽減に関与する, 第89回日本薬理学会年会(神奈川), Mar. 2016.
217.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : HIF-1aはアポトーシス制御因子Bcl-2及びCHAC1の発現制御を介して腎虚血再灌流障害からの回復に関与する, 第89回日本薬理学会年会(神奈川), Mar. 2016.
218.	斎藤尚子, Yuki Izawa-Ishizawa, 細岡真由子, Yoshitaka Kihira, Masaki Imanishi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ケルセチン代謝物Q3GAによる血管内皮細胞保護効果の検討, 第89回日本薬理学会年会(神奈川), Mar. 2016.
219.	青木友里, Yuki Izawa-Ishizawa, 高田真衣, 田渕正樹, Masaki Imanishi, Yoshito Zamami, 福永豊, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Keisuke Ishizawa and Toshiaki Tamaki : 神経突起伸長および脳卒中後神経症状に対するニトロソニフェジピンの効果, 第89回日本薬理学会年会(神奈川), Mar. 2016.
220.	大島啓亮, Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄のエリスロポエチン発現への影響の検討, 第89回日本薬理学会年会(神奈川), Mar. 2016.
221.	佐藤明穂, Yasumasa Ikeda, Yuya Horinouchi, 濱野裕章, 今尾瑞季, 渡邉大晃, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄欠乏に伴う骨格筋萎縮メカニズム, 第89回日本薬理学会年会(神奈川), Mar. 2016.
222.	濱野裕章, Yasumasa Ikeda, 渡邉大晃, 佐藤明穂, 大島啓亮, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 尿毒素は慢性腎不全におけるヘプシジン発現に関与する, 第89回日本薬理学会年会(神奈川), Mar. 2016.
223.	Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Licht Miyamoto, Yoshito Zamami, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Development of endothelial dysfunction-induced aortic dissection model and search for a preventive strategy, 第89回日本薬理学会年会(神奈川), Mar. 2016.
224.	Masaki Imanishi, Keisuke Ishizawa, 小原佑介, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニフェジピン光分解産物による血管リモデリング抑制効果, 第252回徳島医学会学術集会(平成27年度冬期), Feb. 2016.
225.	Keisuke Oshima, Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄のエリスロポエチン発現への影響の検討, 第45回日本心脈管作動物質学会, Feb. 2016.
226.	Masaki Imanishi, Keisuke Ishizawa, 小原佑介, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンによる抗大動脈瘤機序の検討, 第45回日本心脈管作動物質学会, Feb. 2016.
227.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 鍵本優有, 斎藤尚子, 高田真衣, Yoshitaka Kihira, Masaki Imanishi, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 高リン刺激は血管平滑筋細胞においてrho-kinase-cyclophilin A経路を活性化させる, 第45回日本心脈管作動物質学会, Feb. 2016.
228.	Yasumasa Ikeda, 濱野裕章, 渡邉大晃, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎臓病におけるヘプシジン制御メカニズムの検討, 第25回日本循環薬理学会, Dec. 2015.
229.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 高田真衣, 田渕正樹, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは悪性脳卒中易発性高血圧自然発症ラットの生命予後を改善する, 第25回日本循環薬理学会, Dec. 2015.
230.	斎藤尚子, Yuki Izawa-Ishizawa, Keisuke Ishizawa, 戸谷紘基, Masaki Imanishi, 鍵本優有, 細岡真由子, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈解離発症における内皮障害の関与, 第25回日本循環薬理学会, Dec. 2015.
231.	Hirofumi Hamano, Yasumasa Ikeda, Yuya Horinouchi, Akiho Satoh, Hiroaki Watanabe, Keisuke Oshima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全における尿毒素によるヘプシジン制御機構, 第128回日本薬理学会近畿部会, Nov. 2015.
232.	今尾瑞季, Yasumasa Ikeda, 佐藤明穂, 濱野裕章, Yuya Horinouchi, Licht Miyamoto, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 鉄蓄積によって引き起こされる骨格筋萎縮のメカニズム, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2015.
233.	高田真衣, Keisuke Ishizawa, 田渕正樹, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 悪性脳卒中易発性高血圧自然発症ラットの神経症状に対するニトロソニフェジピンの効果, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2015.
234.	戸谷紘基, Keisuke Ishizawa, Yuki Izawa-Ishizawa, 細岡真由子, 鍵本優有, 斎藤尚子, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 大動脈解離発症における内皮障害の関与の検討, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2015.
235.	Yasumasa Ikeda, 佐藤明穂, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄欠乏は骨格筋量減少の原因となる, 第39回日本鉄バイオサイエンス学会学術集会, Aug. 2015.
236.	Ariunzaya Burentogtokh, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : YC1 increased adiponectin expression in 3T3-L1 adipocytes, 次世代を担う創薬・医療薬理シンポジウム2015, Aug. 2015.
237.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 大越瑞穂, 土肥紗希子, Yoshitaka Kihira, Yasumasa Ikeda and Toshiaki Tamaki : 血管石灰化シグナルにおけるRhoキナーゼおよびサイクロフィリンAの関与, 第47回日本動脈硬化学会総会・学術集会, Jul. 2015.
238.	Yasumasa Ikeda, Kanai Yusuke, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Bilirubin Promotes Ischemic-Induced Revascularization through Akt-eNOS Pathway, 第79回日本循環器学会学術集会, Apr. 2015.
239.	Yoshitaka Kihira, 岸渕麗奈, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 腎虚血再灌流障害において低酸素誘導因子が制御する因子の探索, 日本薬学会第135年会(神戸), Mar. 2015.
240.	Mai Takata, Keisuke Ishizawa, 田渕正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 悪性脳卒中易発性高血圧自然発症ラットに対するニトロソニフェジピンの効果, 日本薬学会第135年会(神戸), Mar. 2015.
241.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ビリルビンは虚血後血管新生を促進する, 第88回日本薬理学会年会(愛知), Mar. 2015.
242.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 田渕正樹, Mai Takata, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは悪性脳卒中易発性高血圧自然発症ラットの生存期間を延長させる, 第88回日本薬理学会年会(愛知), Mar. 2015.
243.	Hiroki Toya, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Yusuke Kohara, Tomoko Nagao, 今西正樹, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈解離発症における血管内皮機能障害の関与, 第88回日本薬理学会年会(愛知), Mar. 2015.
244.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible factor-1 participates in induction of apoptosis in renal reperfusion injury, 第88回日本薬理学会年会(愛知), Mar. 2015.
245.	Mizuho Ogoshi, Yuki Izawa-Ishizawa, Sakiko Doi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管平滑筋細胞において無機リンによる石灰化シグナルにはRho-kinaseおよびcyclophilin Aが関与する, 第88回日本薬理学会年会(愛知), Mar. 2015.
246.	Burentogtokh Ariunzaya, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia decreases glucagon-like peptide-1 secretion from glutag cell lines, 第88回日本薬理学会年会(愛知), Mar. 2015.
247.	Yasumasa Ikeda, 金井佑亮, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ビリルビンの血管新生促進作用の検討, 第44回日本心脈管作動物質学会, Feb. 2015.
248.	Yasumasa Ikeda, 金井佑亮, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ビリルビンは血管内皮細胞を活性化させて，虚血後血管新生を促進する, 第24回循環薬理学会, Dec. 2014.
249.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 長尾朋子, 戸谷紘基, 小原佑介, 細岡真由子, 高田真衣, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 新規薬剤誘発性大動脈解離モデルを用いたスタチンの効果の検討, 第24回循環薬理学会, Dec. 2014.
250.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 低酸素誘導因子の機能不全は腎虚血再灌流障害からの回復を阻害する, 第36回生体膜と薬物の相互作用シンポジウム, Nov. 2014.
251.	Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 高脂肪食誘発肥満に対する脂肪特異的低酸素誘導因子欠損の影響, 第36回生体膜と薬物の相互作用シンポジウム, Nov. 2014.
252.	長尾朋子, Keisuke Ishizawa, 戸谷紘基, 小原佑介, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : HMG-CoA 還元酵素阻害薬の大動脈解離に対する効果, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
253.	長尾朋子, Keisuke Ishizawa, 戸谷紘基, 小原佑介, 今西正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : HMG-CoA 還元酵素阻害薬の大動脈解離に対する効果, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
254.	小原佑介, Keisuke Ishizawa, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, 今西正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈瘤形成に対する新規抗酸化薬の効果, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
255.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 低酸素誘導因子の腎虚血再灌流障害に対する役割, 第126回日本薬理学会近畿部会, Oct. 2014.
256.	長尾朋子, Keisuke Ishizawa, 戸谷紘基, 小原佑介, 今西正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈解離に対するピタバスタチンの効果, 第126回日本薬理学会近畿部会, Oct. 2014.
257.	Yasumasa Ikeda, 今尾瑞季, 佐藤明穂, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄による骨格筋萎縮メカニズムの検討, 日本鉄バイオサイエンス学会第38回学術集会, Sep. 2014.
258.	小原佑介, Keisuke Ishizawa, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは大動脈瘤の形成を抑制する, 次世代を担う創薬・医療薬理シンポジウム 2014, Aug. 2014.
259.	戸谷紘基, Keisuke Ishizawa, 小原佑介, 長尾朋子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管内皮障害を介する新規大動脈解離モデルの作製, 次世代を担う創薬・医療薬理シンポジウム 2014, Aug. 2014.
260.	小原佑介, Keisuke Ishizawa, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 薬剤誘導性大動脈瘤モデルに対するニトロソニフェジピンの効果, 第125回日本薬理学会近畿部会, Jun. 2014.
261.	Yasumasa Ikeda, 田島壮一郎, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : アンジオテンシンIIは鉄吸収制御と生体内鉄分布変化に関与する, 第125回日本薬理学会近畿部会, Jun. 2014.
262.	今西正樹, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya and Toshiaki Tamaki : 血管リモデリングにおける低酸素誘導因子HIF-1αの役割, 日本薬学会第134年会, Mar. 2014.
263.	Yoshitaka Kihira, Ariunzaya BURENTOGTOKH, Mari Itoh, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 腸管L細胞のグルカゴン様ペプチド-1分泌に対する低酸素の影響, 日本薬学会第134年会, Mar. 2014.
264.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Noriko Yamano, 布あさ美, 今西正樹, 櫻田巧, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates the progression of renal disease associated with endothelial dysfunction independently of eNOS, 第87回日本薬理学会年会, Mar. 2014.
265.	Mizuki Imao, Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The mechanism of sj=keletal muscle atroph induced by iron, 第87回日本薬理学会年会, Mar. 2014.
266.	Yuki Izawa-Ishizawa, Le Nhat-Tu, 竹井雄一郎, Heo Kyung-Sun, Lee Hakjoo, Smrcka Alan, Miller Benjamin, Ko Kyung-Ae, Ture Sara, Morrell Craig, 藤原敬己, Masashi Akaike, Toshiaki Tamaki and 阿部純一 : Anti-inflammatory effects of statins and anti-malarial agents via endothelial ERK5 activation, 第87回日本薬理学会年会, Mar. 2014.
267.	Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : アンジオテンシンIIは十二指腸鉄輸送体発現とマクロファージ鉄量を増加させる, 第43回日本心脈管作動物質学会, Feb. 2014.
268.	Masaki Imanishi, Shuhei Tomita, Hirotsugu Kurobe, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 薬剤誘導性大動脈瘤モデルにおける平滑筋由来hypoxia-inducible factor-1αの役割, 第23回日本循環薬理学会, Dec. 2013.
269.	Yoshitaka Kihira, Shuhei Tomita, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 肥満に伴う脂肪組織炎症に対する低酸素誘導因子の役割, 第124回日本薬理学会近畿部会, Nov. 2013.
270.	布あさ美, Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, 櫻田巧, Masaki Imanishi, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : ニトロソニフェジピンは血管内皮機能を改善することで糖尿病性腎症の進展を抑制する, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
271.	Yuta Suzuki, Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 平滑筋由来HIF-1 αがアンジオテンシンII 誘発血管リモデリングに関与するメカニズム, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
272.	Masaki Murakami, Yusaku Maeda, Shuhei Tomita, Masaki Imanishi, Yoshitaka Kihira, Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管傷害モデルに伴う血管リモデリングにおける骨髄由来細胞のHIF1 αの役割, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
273.	Mariko Miyake, Yoshitaka Kihira, Shuhei Tomita, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 脂肪細胞の低酸素誘導因子欠損による耐糖能改善メカニズムの解析, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
274.	Yasumasa Ikeda, 田島壮一郎, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : フェリチンの炎症惹起作用, 第37回日本鉄バイオサイエンス学会, Sep. 2013.
275.	Masaki Murakami, Shuhei Tomita, Yusaku Maeda, Masaki Imanishi, Noriko Yamano, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管傷害モデルに伴う血管リモデリング形成過程には，傷害部位に動員される骨髄由来細胞のHIFが関与する, 次世代を担う創薬・医療薬理シンポジウム2013, Aug. 2013.
276.	Noriko Yamano, Keisuke Ishizawa, 小堀浩幸, Maki Urushihara, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病性腎症における腎内局所アンジオテンシノーゲンに対するニトロソニフェジピンの効果, 第123回日本薬理学会近畿部会, Jul. 2013.
277.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 血管平滑筋細胞のhypoxia-inducible factor-1αがangiotensinⅡ誘発血管リモデリング形成に関与するメカニズムの解析, 第34回日本炎症・再生医学会, Jul. 2013.
278.	Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, 櫻田巧, Masaki Imanishi, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは血管内皮保護作用を示して糖尿病性腎症進展を抑制する, 第56回日本腎臓学会学術総会, May 2013.
279.	Masaki Imanishi, Keisuke Ishizawa, Takumi Sakurada, Yuki Izawa-Ishizawa, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 酸化ストレスに起因する心腎血管障害の克服を目指す新規治療薬開発, 日本薬学会第133年会, Mar. 2013.
280.	Koichiro Tsuchiya, Yasumasa Ikeda, 田島壮一郎, Yoshitaka Kihira, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Licht Miyamoto, Noriko Yamano and Toshiaki Tamaki : 糖尿病に対する鉄の関与とキレート療法, 日本薬学会第133年会, Mar. 2013.
281.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible factor-1a; in vascular smooth muscle cells contributes to AT1 receptor expression in angiotensin II-induced vascular remodeling in mice, 第86回日本薬理学会年会, Mar. 2013.
282.	Mari Itoh, Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : Secretion of glucagon-like peptide-1 from Intestinal L cell in hypoxia, 第86回日本薬理学会年会, Mar. 2013.
283.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, Takumi Sakurada, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : The influence of angiotensin II on duodenal iron absorption, 第86回日本薬理学会年会, Mar. 2013.
284.	Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Bovine lactoferrin stimulated angiogenesis in response to ischemic hindlimb, 第86回日本薬理学会年会, Mar. 2013.
285.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakiko Doi, Masaki Imanishi, Takumi Sakurada, Noriko Yamano, Yusuke Kohara, Tomoko Nagao, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Y-27632, a rho-kinase inhibitor, inhibits inorganic phosphate-induced ERK1/2 phosphorylation and ALP activity in vascular smooth muscle cells, 第86回日本薬理学会年会, Mar. 2013.
286.	Iori Ohzono, Yasumasa Ikeda, Souichirou Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The Effects of Iron chelatoion against Renal Fibrosis in Unilateral Ureteral Obstruction Mice Model, 第86回日本薬理学会年会, Mar. 2013.
287.	Yoji Hoshina, Yoshitaka Kihira, Shuhei Tomita, Mariko Miyake, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Adipocyte-specific hypoxia-inducible factor-1alpha knockout stimulated GLP-1 and insulin secretions in mice, 第86回日本薬理学会年会, Mar. 2013.
288.	Noriko Yamano, Keisuke Ishizawa, Shoko Fujii, Asami Nuno, Masaki Imanishi, Takumi Sakurada, Yuta Suzuki, Furi Endo, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Effects of nitrosonifedipine on the diabetic nephropathy with the endothelial dysfunction, 第86回日本薬理学会年会, Mar. 2013.
289.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Low Iron Diet Limits Development of Diabetic Nephropathy In db/db Mice, 第77回日本循環器学会学術集会, Mar. 2013.
290.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Noriko Yamano, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは血管内皮細胞障害を伴う糖尿病性腎症の進展を抑制する, 第42回日本心脈管作動物質学会, Feb. 2013.
291.	田島壮一郎, Yasumasa Ikeda, Hideaki Enomoto, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : 鉄制限食によってdb/dbマウスの糖尿病性腎症進展は抑制される, 第42回日本心脈管作動物質学会, Feb. 2013.
292.	Sakiko Doi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Yusuke Kohara, Tomoko Nagao, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 無機リン刺激による血管平滑筋細胞石灰化におけるRho-kinaseの関与, 第42回日本心脈管作動物質学会, Feb. 2013.
293.	Yoshitaka Kihira, Shuhei Tomita, Mariko Miyake, Yoji Hoshina, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 脂肪細胞特異的低酸素誘導因子欠損マウスに観察される耐糖能の改善にはglucagon-like peptide-1が関与する, 第42回日本心脈管作動物質学会, Feb. 2013.
294.	Keisuke Ishizawa, Masaki Imanishi, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Angiotensin II慢性投与はhypoxia-inducible factor-1αを介して血管リモデリングを惹起する, 第33回日本臨床薬理学会学術総会, Dec. 2012.
295.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 血管平滑筋細胞のhypoxia-inducible factor-1αがangiotensinⅡ誘発血管リモデリング形成に寄与するメカニズムの解析, 第22回日本循環薬理学会, Nov. 2012.
296.	Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄吸収機構におけるAngiotensinⅡの効果の検討, 第122回日本薬理学会近畿部会, Nov. 2012.
297.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Nifedipine 光分解産物であるnitrosonifedipine は糖尿病性腎症進展を抑制する, 第51回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
298.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 血管平滑筋細胞におけるHIF-1αのangiotensinⅡ誘発血管リモデリング形成およびAT1受容体発現への関与;平滑筋特異的HIF-1α遺伝子欠損マウスを用いた検討 The Role of HIF-1α in angiotensin Ⅱ-induced Vascular Remodeling and AT1 Receptor Expression in Vascular Smooth Muscle Cells, 第35回日本高血圧学会総会, Sep. 2012.
299.	Asami Nuno, Keisuke Ishizawa, Shoko Fujii, 櫻田巧, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病性腎症進展に対するニトロソニフェジピンの抑制作用, 次世代を担う創薬・医療薬理シンポジウム2012, Sep. 2012.
300.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensinⅡ誘発血管リモデリングにおける血管平滑筋細胞内HIFシグナルの解析, 次世代を担う創薬・医療薬理シンポジウム2012, Sep. 2012.
301.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, 櫻田巧, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 十二指腸からの鉄吸収に対するAngiotensinⅡの影響, 第36回日本鉄バイオサイエンス学会学術集会, Sep. 2012.
302.	Yusaku Maeda, Shuhei Tomita, Masaki Murakami, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 血管傷害モデルに伴う血管リモデリング形成過程には，傷害部位に動員される骨髄由来細胞のHIFが関与する, 第121回日本薬理学会近畿部会, Jun. 2012.
303.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 平滑筋特異的hypoxia-inducible factor-1α欠損がangiotensin II誘発血管リモデリング形成に及ぼす影響, 第121回日本薬理学会近畿部会, Jun. 2012.
304.	Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yuki Izawa-Ishizawa, Licht Miyamoto, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine はangiotensin II 誘発のマウス血管リモデリングを改善する, 第65回日本酸化ストレス学会学術集会, Jun. 2012.
305.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病モデルマウスにおいてニトロソニフェジピンは腎症の進展を抑制する, 第55回日本腎臓学会学術総会, Jun. 2012.
306.	Mariko Miyake, Yoshitaka Kihira, Manami Hirata, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 脂肪細胞における低酸素誘導因子1a欠損は高脂肪食負荷による耐糖能異常の発現を抑制する, 日本薬学会第132年会, Mar. 2012.
307.	Asami Nuno, Keisuke Ishizawa, 藤井聖子, Yuki Izawa-Ishizawa, Masaki Imanishi, Takumi Sakurada, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 2型糖尿病性腎症に対するニトロソニフェジピンの効果, 日本薬学会第132年会, Mar. 2012.
308.	Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Bovine Lactoferin Promotes Angiogenesis Via Akt-eNOS Dependent Pathway in Vascular Endothelial Cells, 第76回日本循環器学会学術集会, Mar. 2012.
309.	Hideaki Enomoto, Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Protective effect of dietary iron restriction on diabetic nephropathy, 第85回日本薬理学会年会, Mar. 2012.
310.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Accumulated iron storage in high fat diet-induced obese and diabetic mice, 第85回日本薬理学会年会, Mar. 2012.
311.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine prevents the progression of diabetic nephropathy in type 2 diabetic mice, 第85回日本薬理学会年会, Mar. 2012.
312.	Shuhei Tomita, Mitsuru Takaku, Noriko Yamano, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Preoperative stabilization of HIF-1 by systemic introduction of dimethyloxalylglycine (DMOG), improves skin flap survival, 第85回日本薬理学会年会, Mar. 2012.
313.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : The inhibitory effects of smooth muscle cell-specific hypoxia-inducible factor-1a deficiency on angiotensin 2-induced vascular remodeling in mice, 第85回日本薬理学会年会, Mar. 2012.
314.	Manami Hirata, Yoshitaka Kihira, Mariko Miyake, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : High fat diet-induced inflammation in adipose tissues is reduced in adipocyte-specific hypoxia-inducible factor-1a knockout mice, 第85回日本薬理学会年会, Mar. 2012.
315.	Keisuke Ishizawa, Shoko Fujii, Asami Nuno, Yuki Izawa-Ishizawa, Masaki Imanishi, Takumi Sakurada, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineは2型糖尿病モデルマウスにおける腎症進展を抑制する, 第41回心脈管作動物質学会, Feb. 2012.
316.	Yoshitaka Kihira, Mariko Miyake, Manami Hirata, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 肥満に伴う耐糖能異常の発現に対する脂肪細胞の低酸素誘導因子の役割, 第41回心脈管作動物質学会, Feb. 2012.
317.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : The alternation of iron metabolism in high fat diet-induced obese and diabetic mice, 第34回日本分子生物学会年会, Dec. 2011.
318.	Yasumasa Ikeda, Hideaki Enomoto, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病腎症進展における鉄除去の効果, 腎と高血圧update, Dec. 2011.
319.	Mitsuru Takaku, Shuhei Tomita, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Hideki Nakanishi and Toshiaki Tamaki : PHD阻害剤の虚血皮弁生存拡大に対する効果, 第21回日本循環薬理学会, Dec. 2011.
320.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : AngiotensinⅡ誘発性血管リモデリングは平滑筋特異的HIF-1α遺伝子欠損により抑制される, 第34回日本高血圧学会総会, Oct. 2011.
321.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : AngiotensinⅡ誘発性血管リモデリングは平滑筋特異的HIF-1α遺伝子欠損により抑制される, 第34回日本高血圧学会総会, Oct. 2011.
322.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Takumi Sakurada, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 肥満の脂肪組織における鉄の役割, 第35回日本鉄バイオサイエンス学会学術集会, Sep. 2011.
323.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Jumpei Taniguchi, Shoko Fujii, Asami Nuno, Yuta Suzuki, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineによるマウス血管リモデリング抑制機構の解明, 次世代を担う創薬・医療薬理シンポジウム2011, Aug. 2011.
324.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible factor-1a in vascular smooth muscle cells contributes to the development of angiotensin -induced vascular remodeling, 第43回日本動脈硬化学会総会・学術集会, Jul. 2011.
325.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensisⅡ誘発血管リモデリングは血管平滑筋細胞のhypoxia-inducible factor-1αを介して形成される, 第119回日本薬理学会近畿部会, Jul. 2011.
326.	Yuki Izawa-Ishizawa, Taichi Murakami, 岸史, Motokazu Matsuura, 近藤直樹, Seiji Kishi, Kojiro Nagai, Hideharu Abe and Toshio Doi : LDL吸着が複数回奏功した難治性ネフローゼ症候群の1例, 日本内科学会第104会四国地方会, May 2011.
327.	Hirotsugu Kurobe, Yuki Izawa, Yayoi Fukumura, Tamotsu Kanbara, Atsushi Kurushima, Ken-ichi Aihara, Masashi Akaike, Masashi Kano, Takashi Kitaichi, Yutaka Masuda, Hiroyuki Azuma, Toshiaki Tamaki, Toshio Matsumoto, Tetsuya Kitagawa, Shuhei Tomita and Masanori Yoshizumi : HIF-ARNT transcriptional system in T cells has a pivotal role in vascular in flammation and remodeling., 第70回日本循環器学会学術総会, Mar. 2006.
328.	Hirotsugu Kurobe, Shuhei Tomita, Yuki Izawa, 福原弥生, Tamotsu Kanbara, Ken-ichi Aihara, Masashi Akaike, Tetsuya Kitagawa, Toshio Matsumoto, Masanori Yoshizumi and Toshiaki Tamaki : T細胞特異的HIF1αKOマイスではカフモデルにて血管リモデリングが促進される, 第15回日本循環薬理学会, Nov. 2005.

Et cetera, Workshop:

1.	池田裕美子, 斎藤尚子, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : ケルセチンによる血管保護効果の検討, 西日本医学生学術フォーラム(第5回医学研究学生フォーラム), Dec. 2016.
2.	Yoshito Zamami, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニング手法を用いた新規循環器治療薬の探索研究, 第23回大阪市大フォーラム, Aug. 2016.
3.	Yuki Izawa-Ishizawa : 「基礎」という選択，仕事と子育て, 第4回医学研究学生フォーラム, Dec. 2015.
4.	Yuki Izawa-Ishizawa : グローカルな視点から女性研究者支援を考える, 四国5大学連携女性研究者活躍推進シンポジウム2015, Dec. 2015.
5.	Yuki Izawa-Ishizawa : A Mom Takes "Research Leave" in Rochester, NY, Japanese Journal of Circulation Research, Vol.37, No.2, 83-84, May 2014.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

Gendered innovation in cancer chemotherapy - real world data driven pharmacological research (Project/Area Number: 22K06863 )
Elucidation of the relationship between infectious diseases and aortic diseases by big data analysis and in vivo experiments (Project/Area Number: 21H02646 )
Construction of a Synergy Effect Exploration Method and Its Application to Medical Information Databases (Project/Area Number: 20H05798 )
Establishment of optimal supportive care for prevention of drug-induced kidney injury using medical big data (Project/Area Number: 20K07132 )
Elucidation of the role of ERK5 and the mechanism of epithelial-mesenchymal transition for cancer metastasis control (Project/Area Number: 19K07321 )
Elucidation of pathophysiology of aortic dissection and development of the preventive strategies by medical big data and novel model mice (Project/Area Number: 18K06686 )
Effect of glucagon on antidiabetic effect induced by nitrite (Project/Area Number: 16K08550 )
Clarification of ERK5-mediated endothelial mesenchymal transition suppression mechanism and its application to the prevention of arteriosclerosis (Project/Area Number: 16K08549 )
Development of novel aortic dissection model based on vascular endothelial dysfunction and elucidation of pathophysiological mechanisms (Project/Area Number: 15K07967 )
Physiological role of dietary nitrite (Project/Area Number: 15H02898 )
The role of ERK5 in diabetic vascular calcification mediated by endothelial-to-mesenchymal transition (Project/Area Number: 26860172 )
The role of cyclophilin A in diabetic vascular calcification (Project/Area Number: 24790254 )
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