Tokushima University / Educator and Researcher Directory --- Ishizawa, Keisuke

Personal Web Page

https://researchmap.jp/read0138449 (researchmap)

Field of Study

○	Pharmacology, Clinical Pharmacology

Subject of Study

○	Drug Discovery for Improvement of Chronic Kidney Disease and Cardiovascular Disease, 安全かつ最適な薬物療法を実践するための副作用マネジメントに関する研究

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.	Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa : 【薬剤疫学】薬剤疫学の応用ドラッグリポジショニング(解説/特集), Aug. 2019.
3.	Masayuki Chuma, 近藤正輝, Kenshi Takechi, Yoshito Zamami, Mitsuhiro Goda, Naoto Okada, Keisuke Ishizawa and Hiroaki Yanagawa : 集中治療患者における臓器系統別評価方法の習得(4)臓器系統別評価3/5 : 感染・炎症・免疫管理 : 敗血症に対する抗菌薬治療を中心に, The Japanese Society of Hospital Pharmacists, Feb. 2019. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520291855946592896 (CiNii: 1520291855946592896)
4.	Naoto Okada, Masayuki Chuma, Yoshito Zamami and Keisuke Ishizawa : 考え方がわかれば解き方がみえてくるクリニカルクエスチョンの解決への道筋, 月刊薬事, 2018.
5.	Yoshito Zamami, Naoto Okada, Kenshi Takechi, Masaki Imanishi and Keisuke Ishizawa : あ，検査値が変わった」そのとき，薬のリスクは?(分担執筆), 株式会社じほう, Jun. 2017.
6.	Keisuke Ishizawa : 徳島大学病院の最新治療がわかる本 : 安全で最適な薬物療法をサポート, 南々社, Aug. 2015.
7.	Licht Miyamoto, 山根萌, 冨田洋輔, Keisuke Ishizawa, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : ヒト腎糸球体内皮細胞における亜硝酸塩によるAMPK-eNOS活性化経路の検討, TOKYO IGAKUSHA, Oct. 2014.
8.	Koichiro Tsuchiya, Keisuke Ishizawa, 智子中西 and 山口巧 : 臨床思考プロセス薬物治療学 -最適治療への論理スパイラル-, 京都廣川書店, Tokyo, Mar. 2013.
9.	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.
10.	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.
11.	Koichiro Tsuchiya, Keisuke Ishizawa, Licht Miyamoto, Yuya Horinouchi, Yasumasa Ikeda, Yoshitaka Kihira, Shuhei Tomita and Toshiaki Tamaki : 腎とフリーラジカル第11集, TOKYO IGAKUSHA, Tokyo, Jan. 2013.
12.	Keisuke Ishizawa, Toshiaki Tamaki and 他 : 疾患モデルの作製と利用-循環器疾患, LIFE-SCIENCE INFORMATION CENTER, Tokyo, Aug. 2010.
13.	田島壮一郎, Koichiro Tsuchiya, 濱本磨以, 久住祥子, Yuya Horinouchi, 八木祐子, 櫻田巧, Keisuke Ishizawa, Yasumasa Ikeda, Yoshitaka Kihira, Shuhei Tomita and Toshiaki Tamaki : 腎とフリーラジカル第10集, TOKYO IGAKUSHA, Tokyo, Jun. 2010.
14.	大西秀樹, Koichiro Tsuchiya, 田島壮一郎, Yuya Horinouchi, 福原弥生, Kunihisa Yamaguchi, Keisuke Ishizawa, Shuhei Tomita and Toshiaki Tamaki : 腎とフリーラジカル第9集, TOKYO IGAKUSHA, Tokyo, Sep. 2008.
15.	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.
16.	Eiji Takeda, Toshiya Okahisa, Yasuko Takahashi, 国清紀子, Akiko Matsumura, Yutaka Nakaya, Masaharu Nishi, Yutaka Taketani, Katsuhiko Yoshimoto, Junji Terao, 美馬福恵, Masami Yoshioka, 山田静恵, Keisuke Ishizawa, 鈴木麗子, chiyo Fujita, Hidekazu Arai, Masashi Kuwahata and Kazuko Okada : 栄養管理のチーム医療, 文光堂, Tokyo, Apr. 2006.
17.	Keisuke Ishizawa, Kazuo Minakuchi and 他 : 南山堂医学大辞典改訂19版, NANZANDO Co.,Ltd., Tokyo, Mar. 2006.

Academic Paper (Judged Full Paper):

1.	Kei Kawada, T Ishida, T Yoshioka, H Fukuda, T Hayashi, Mitsuhiro Goda and Keisuke Ishizawa : Association of non-steroidal anti-inflammatory drug use with encephalopathy development: An analysis using the United States Food and Drug Administration Adverse Event Reporting System (FAERS) and Japanese Adverse Drug Event Report (JADER) databases., Die Pharmazie, Vol.79, No.6, 118-123, 2024. (Summary) Encephalopathy is the most severe complication of various common infections, including influenza and herpes, and it often results in death or severe neurological disability. The risk factors for viral encephalopathy include non-steroidal anti-inflammatory drug (NSAID) use; however, studies on NSAID-related encephalopathy are limited. In this study, we aimed to investigate the characteristics of NSAID-related encephalopathy. We investigated the incidence of NSAID-related encephalopathy using data from the United States Food and Drug Administration Adverse Event Reporting System (FAERS) and Japanese Adverse Drug Event Report (JADER) databases containing reports on spontaneous adverse effects (AEs) published by the Pharmaceuticals and Medical Devices Agency. We used these databases to detect AEs based on reported odds ratios. By separating suspicious drugs, concomitant drugs, and drug interactions involving NSAIDs, we investigated the relationship between encephalopathy pathology and AEs of NSAIDs. Significant encephalopathy signals were detected for loxoprofen and etodolac in the FAERS database and loxoprofen in the JADER database. In the JADER database, significant encephalopathy signals in loxoprofen-treated patients were detected in 70-79-year-old, 80-year-old, influenza viral infection, and herpes virus infection groups. Significant encephalopathy signals in patients with herpes virus infection were detected in the 80-year-old and loxoprofen-treated groups. Regarding the involvement of loxoprofen in the development of encephalopathy, the JADER database listed loxoprofen as a suspect drug, without indicating any concomitant drug interactions. In conclusion, our findings suggest that loxoprofen and etodolac may be associated with viral encephalopathy. Accordingly, prudence is recommended when using loxoprofen in older individuals with viral infections. (Keyword) Adolescent / Adult / Aged / Aged, 80 and over / Child / Female / Humans / Male / Middle Aged / Young Adult / Adverse Drug Reaction Reporting Systems / Anti-Inflammatory Agents, Non-Steroidal / Brain Diseases / Databases, Factual / Japan / Phenylpropionates / United States / United States Food and Drug Administration (Link to Publication Site) ● Publication site (DOI): 10.1691/ph.2024.4506 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38877682 ● Search Scopus @ Elsevier (PMID): 38877682 ● Search Scopus @ Elsevier (DOI): 10.1691/ph.2024.4506 (DOI: 10.1691/ph.2024.4506, PubMed: 38877682)
2.	Kei Kawada, Tomoaki Ishida, Hitoshi Fukuda, Yuki Hyohdoh, Toru Kubo, Tomoyuki Hamada, Yuichi Baba, Toshinobu Hayashi, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Takahiro Niimura, Shinji Abe, Mitsuhiro Goda, Hiroaki Kitaoka and Keisuke Ishizawa : Effects of renin-angiotensin system inhibitor and beta-blocker use on mortality in older patients with heart failure with reduced ejection fraction in Japan., Frontiers in Cardiovascular Medicine, Vol.11, 2024. (Summary) RAS inhibitors prevented all-cause mortality and cardiac death at all ages, whereas beta-blockers had different effects depending on the patient's age. This study suggested that the choice of beta-blockers and RAS inhibitors is more important in older patients with HFrEF than in younger patients with the same condition. (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2024.1377228 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38883984 ● Search Scopus @ Elsevier (PMID): 38883984 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2024.1377228 (DOI: 10.3389/fcvm.2024.1377228, PubMed: 38883984)
3.	Kei Kawada, Tomoaki Ishida, Shumpei Morisawa, Kohei Jobu, Youichirou Higashi, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Takahiro Niimura, Shinji Abe, Mitsuhiro Goda, Mitsuhiko Miyamura and Keisuke Ishizawa : Atractylodes lancea (Thunb.) DC. [Asteraceae] rhizome-derived exosome-like nanoparticles suppress lipopolysaccharide-induced inflammation in murine microglial cells., Frontiers in Pharmacology, Vol.15, 2024. (Summary) Exosome-like nanoparticles (ELNs) mediate interspecies intercellular communications and modulate gene expression. In this study, we isolated and purified ELNs from the dried rhizome of Atractylodes lancea (Thunb.) DC. [Asteraceae] (ALR-ELNs), a traditional natural medicine, and investigated their potential as neuroinflammatory therapeutic agents. ALR-ELN samples were isolated and purified using differential centrifugation, and their physical features and microRNA contents were analyzed through transmission electron microscopy and RNA sequencing, respectively. BV-2 microglial murine cells and primary mouse microglial cells were cultured , and their ability to uptake ALR-ELNs was explored using fluorescence microscopy. The capacity of ALR-ELNs to modulate the anti-inflammatory responses of these cells to lipopolysaccharide (LPS) exposure was assessed through mRNA and protein expression analyses. Overall, BV-2 cells were found to internalize ALR-ELNs, which comprised three microRNAs (ath-miR166f, ath-miR162a-5p, and ath-miR162b-5p) that could have anti-inflammatory activity. Pretreatment of BV-2 cells with ALR-ELN prevented the pro-inflammatory effects of LPS stimulation by significantly reducing the levels of nitric oxide, interleukin-1β, interleukin-6, and tumor necrosis factor-α. Notably, the mRNA levels of , and in BV-2 cells, which increased upon LPS exposure, were significantly reduced following ALR-ELN treatment. Moreover, the mRNA levels of heme oxygenase 1, , and also increased significantly following ALR-ELN treatment. In addition, pretreatment of primary mouse microglial cells with ALR-ELN prevented the pro-inflammatory effects of LPS stimulation by significantly reducing the levels of nitric oxide. Our findings indicate that ALR-ELNs exhibit anti-inflammatory effects on murine microglial cells. Further validation may prove ALR-ELNs as a promising neuroinflammatory therapeutic agent. (Link to Publication Site) ● Publication site (DOI): 10.3389/fphar.2024.1302055 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38738173 ● Search Scopus @ Elsevier (PMID): 38738173 ● Search Scopus @ Elsevier (DOI): 10.3389/fphar.2024.1302055 (DOI: 10.3389/fphar.2024.1302055, PubMed: 38738173)
4.	Naoto Okada, Hirofumi Hamano, Kenta Yagi, Takahiro Niimura, Fuka Aizawa, Mitsuhiro Goda, Yoshito Zamami, Takashi Kitahara and Keisuke Ishizawa : Effect of pre-treatment with EGFR-TKIs on immune checkpoint inhibitor-associated interstitial lung disease in lung cancer patients: Analysis using a Japanese claims database., International Journal of Clinical Pharmacology and Therapeutics, Vol.62, No.2, 69-76, 2024. (Summary) Although further analyses are required to confirm our findings, this study indicated that pre-treatment with EGFR-TKI might not increase the ILD risk after ICI treatment. (Keyword) Humans / Lung Neoplasms / Immune Checkpoint Inhibitors / Carcinoma, Non-Small-Cell Lung / Retrospective Studies / Japan / Lung Diseases, Interstitial / ErbB Receptors / Protein Kinase Inhibitors (Link to Publication Site) ● Publication site (DOI): 10.5414/CP204491 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37969096 ● Search Scopus @ Elsevier (PMID): 37969096 ● Search Scopus @ Elsevier (DOI): 10.5414/CP204491 (DOI: 10.5414/CP204491, PubMed: 37969096)
5.	Iida Midori, Kuniki Yurika, Kenta Yagi, Mitsuhiro Goda, Namba Satoko, Takeshita Jun-ichi, Sawada Ryusuke, Iwata Michio, Yoshito Zamami, Keisuke Ishizawa and Yamanishi Yoshihiro : A network-based trans-omics approach for predicting synergistic drug combinations, Communication. Medicine, Vol.29, No.4, 154, 2024.
6.	Fuka Aizawa, Haruna Kajimoto, Okabayashi Ami, Daishi Moriyama, Kenta Yagi, Takahashi Shimon, sonoda Yuhei, shibata Takahiro, Mitsuhiro Goda, Takahiro Niimura, Yuki Izawa-Ishizawa, Hirofumi Hamano, Kei Kawada, Yoshito Zamami and Keisuke Ishizawa : Statins ameliorate oxaliplatin- and paclitaxel-induced peripheral neuropathy via glutathione-S-transferase, Neurochemistry International, Vol.180, 105863, 2024.
7.	Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Kenta Yagi, Mitsuhiro Goda, Nawa Hideki, Yuya Horinouchi, Nakamura Toshimi, Hakuno Harumasa, Shinomiya Kazuaki, Yoshito Zamami, Masahiko Azuma, Masashi Akaike and Keisuke Ishizawa : Assessing the effects of interprofessional education by hospital pharmacists on pharmaceutical students using a self-evaluation scale, Journal of Pharmaceutical Health Care and Sciences, Vol.10, No.16, 2024.
8.	Okamoto Naoki, Kenta Yagi, Imawaka Sayaka, Takaoka Mayu, Fuka Aizawa, Takahiro Niimura, Mitsuhiro Goda, Miyata Koji, Kei Kawada, Yuki Izawa-Ishizawa, Satoshi Sakaguchi and Keisuke Ishizawa : A Novel Allosteric Inhibitor of BCR-ABL1, Shows Synergistic Effects When Used in Combination with Imatinib with or without Drug Resistance., Pharmacology Research & Perspectives, Vol.12, No.4, e1214, 2024.
9.	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 (Tokushima University Institutional Repository) ● Metadata: 118742 (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 (Tokushima University Institutional Repository: 118742, DOI: 10.18926/AMO/66151, PubMed: 38145933)
10.	Masaki Imanishi, Takahisa Inoue, Keijo Fukushima, Ryosuke Yamashita, Ryo Nakayama, Masataka Nojima, Kosuke Kondo, Yoshiki Gomi, Honoka Tsunematsu, Kohei Goto, Licht Miyamoto, Masafumi Funamoto, Masaya Denda, Keisuke Ishizawa, Akira Otaka, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : CA9 and PRELID2; hypoxia-responsive potential therapeutic targets for pancreatic ductal adenocarcinoma as per bioinformatics analyses., Journal of Pharmacological Sciences, Vol.153, No.4, 232-242, 2023. (Summary) A strong hypoxic environment has been observed in pancreatic ductal adenocarcinoma (PDAC) cells, which contributes to drug resistance, tumor progression, and metastasis. Therefore, we performed bioinformatics analyses to investigate potential targets for the treatment of PDAC. To identify potential genes as effective PDAC treatment targets, we selected all genes whose expression level was related to worse overall survival (OS) in The Cancer Genome Atlas (TCGA) database and selected only the genes that matched with the genes upregulated due to hypoxia in pancreatic cancer cells in the dataset obtained from the Gene Expression Omnibus (GEO) database. Although the extracted 107 hypoxia-responsive genes included the genes that were slightly enriched in angiogenic factors, TCGA data analysis revealed that the expression level of endothelial cell (EC) markers did not affect OS. Finally, we selected CA9 and PRELID2 as potential targets for PDAC treatment and elucidated that a CA9 inhibitor, U-104, suppressed pancreatic cancer cell growth more effectively than 5-fluorouracil (5-FU) and PRELID2 siRNA treatment suppressed the cell growth stronger than CA9 siRNA treatment. Thus, we elucidated that specific inhibition of PRELID2 as well as CA9, extracted via exhaustive bioinformatic analyses of clinical datasets, could be a more effective strategy for PDAC treatment. (Keyword) Humans / Carbonic Anhydrase IX / Antigens, Neoplasm / Carcinoma, Pancreatic Ductal / Pancreatic Neoplasms / Hypoxia / RNA, Small Interfering / Computational Biology / Pancreatic Neoplasms (Tokushima University Institutional Repository) ● Metadata: 119176 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2023.10.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37973221 ● CiNii @ National Institute of Informatics (CRID): 1050018428980929664 ● Search Scopus @ Elsevier (PMID): 37973221 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2023.10.003 (Tokushima University Institutional Repository: 119176, DOI: 10.1016/j.jphs.2023.10.003, PubMed: 37973221, CiNii: 1050018428980929664)
11.	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 (Tokushima University Institutional Repository) ● Metadata: 118743 (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 (Tokushima University Institutional Repository: 118743, DOI: 10.1111/cts.13638, PubMed: 37700528)
12.	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. (Tokushima University Institutional Repository) ● Metadata: 119327 (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 (Tokushima University Institutional Repository: 119327, DOI: 10.1016/j.biopha.2023.115504, PubMed: 37722188)
13.	Mami Neishi, Hirofumi Hamano, Takahiro Niimura, Masaya Denda, Kenta Yagi, Koji Miyata, Tsung-Jen Lin, Tsukasa Higashionna, Mitsuhiro Goda, Yoshito Zamami, Keisuke Ishizawa and Hideki Nawa : Structural characterization of the optical isomers esomeprazole and omeprazole using the JADER and FAERS databases, Toxicology and Applied Pharmacology, Vol.475, 116632, 2023. (Summary) It is unclear whether the s (-) form of esomeprazole (EPZ) has an improved safety profile when compared with its racemic form omeprazole (OPZ). We assessed the potential complications of these optical isomers when combined with cilostazol, clopidogrel, and prasugrel, which are frequently used concomitant medications. Using two adverse event spontaneous reporting databases, Japanese Adverse Drug Event Report (JADER) and FDA Adverse Event Reporting System (FAERS), adverse event names for hemorrhage, venous/arterial embolization, and thrombus were obtained from the Medical Dictionary for Regulatory Activities. Reported odds ratios were calculated using a 2 × 2 contingency table, and a signal was considered present if the lower limit of the 95% confidence interval was >1. In combination with cilostazol, a hemorrhagic signal for OPZ in JADER and arterial emboli and thrombus signals for EPZ were detected in both databases. In combination with clopidogrel, OPZ showed arterial emboli and thrombus signals in JADER and venous/arterial emboli and thrombus signals in FAERS, while EPZ displayed arterial emboli and thrombus signals in FAERS. In contrast, when in combination with prasugrel, there were no adverse event signals in either database. This study has confirmed using big data, that EPZ, the optical isomer and racemic form of omeprazole, has the beneficial characteristics of being less sensitive to CYP, as was intended by its design. (Keyword) Humans / United States / Esomeprazole / Omeprazole / Clopidogrel / Prasugrel Hydrochloride / Cilostazol / Adverse Drug Reaction Reporting Systems / Hemorrhage / Drug-Related Side Effects and Adverse Reactions / Databases, Factual (Link to Publication Site) ● Publication site (DOI): 10.1016/j.taap.2023.116632 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37482254 ● Summary page in Scopus @ Elsevier: 2-s2.0-85165980754 (DOI: 10.1016/j.taap.2023.116632, PubMed: 37482254, Elsevier: Scopus)
14.	Naoto Okada, Takahiro Niimura, Atsuyuki Saisyo, Yoshitaka Kawaguchi, Keisuke Ishizawa and Takashi Kitahara : Pharmacovigilance Study on Eosinophilic Pneumonia Induced by Anti-MRSA Agents: Analysis Based on the FDA Adverse Event Reporting System., Open Forum Infectious Diseases, Vol.10, No.8, ofad414, 2023. (Summary) This study revealed that among the anti-MRSA agents, disproportionality in the occurrence of EP was observed only with DAP. Our results suggest that sex, age, and treatment duration may affect the occurrence of DAP-induced EP. Clinicians should exercise caution regarding EP during DAP administration. (Link to Publication Site) ● Publication site (DOI): 10.1093/ofid/ofad414 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37601729 ● Search Scopus @ Elsevier (PMID): 37601729 ● Search Scopus @ Elsevier (DOI): 10.1093/ofid/ofad414 (DOI: 10.1093/ofid/ofad414, PubMed: 37601729)
15.	Tsukasa Higashionna, Keisaku Harada, Akinari Maruo, Takahiro Niimura, Elizabeth Tan, Thi Quynh Vu, Takayoshi Kawabata, Soichiro Ushio, Hirofumi Hamano, Makoto Kajizono, Yoshito Zamami, Keisuke Ishizawa, Ko Harada, Shiro Hinotsu, R Mitsunobu Kano, Hideharu Hagiya and Toshihiro Koyama : Trends in Head and Neck Cancer Mortality from 1999 to 2019 in Japan: An Observational Analysis., Cancers, Vol.15, No.15, 2023. (Summary) = 156,742). HNC mortality trends were analysed using joinpoint regression models to estimate annual percentage change (APC) and average APC (AAPC). Among men, no significant change was observed in the age-adjusted death rate trend from 1999 to 2014; however, a marked decrease was observed from 2014 to 2019. No changing point was observed in women. Age-adjusted mortality rates continuously decreased over the 21-year period, with an AAPC of -0.7% in men and -0.6% in women. In conclusion, the overall trend in age-adjusted rates of HNC-associated deaths decreased, particularly among men, in the past 5 years. These results will contribute to the formulation of medical policies to develop targeted screening and prevention programmes for HNC in Japan and determine the direction of treatment strategies. (Tokushima University Institutional Repository) ● Metadata: 118887 (Link to Publication Site) ● Publication site (DOI): 10.3390/cancers15153786 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37568602 ● Search Scopus @ Elsevier (PMID): 37568602 ● Search Scopus @ Elsevier (DOI): 10.3390/cancers15153786 (Tokushima University Institutional Repository: 118887, DOI: 10.3390/cancers15153786, PubMed: 37568602)
16.	Takeshi Imakura, Seidai Satou, Kazuya Koyama, Hirohisa Ogawa, Takahiro Niimura, Kojin Murakami, Yuya Yamashita, Keiko Haji, Nobuhito Naito, Kozo Kagawa, Hiroshi Kawano, Yoshito Zamami, Keisuke Ishizawa and Yasuhiko Nishioka : A polo-like kinase inhibitor identified by computational repositioning attenuates pulmonary fibrosis., Respiratory Research, Vol.24, No.1, 148, 2023. (Summary) These findings suggest that targeting PLK1 may be a novel therapeutic approach for pulmonary fibrosis by inhibiting lung fibroblast proliferation without affecting lung epithelial cells. In addition, while in silico screening is useful, it is essential to fully determine the biological activities of candidates by wet-lab validation studies. (Keyword) Mice / Animals / Drug Repositioning / Thiophenes / Benzimidazoles / Lung / Idiopathic Pulmonary Fibrosis / Fibroblasts / Bleomycin (Tokushima University Institutional Repository) ● Metadata: 119057 (Link to Publication Site) ● Publication site (DOI): 10.1186/s12931-023-02446-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37269004 ● Search Scopus @ Elsevier (PMID): 37269004 ● Search Scopus @ Elsevier (DOI): 10.1186/s12931-023-02446-x (Tokushima University Institutional Repository: 119057, DOI: 10.1186/s12931-023-02446-x, PubMed: 37269004)
17.	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)
18.	Satoru Mitsuboshi, Hirofumi Hamano, Yurika Kuniki, Takahiro Niimura, Masayuki Chuma, Soichiro Ushio, Tsung-Jen Lin, Jun Matsumoto, Tatsuaki Takeda, Makoto Kajizono, Yoshito Zamami and Keisuke Ishizawa : Proton Pump Inhibitors and Rhabdomyolysis: Analysis of Two Different Cross-Sectional Databases., The Annals of Pharmacotherapy, 2023. (Summary) The data in 2 separate databases consistently suggest that PPIs may increase the risk of rhabdomyolysis. The evidence for this association should be assessed in further drug safety studies. (Link to Publication Site) ● Publication site (DOI): 10.1177/10600280231156270 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36847276 ● Search Scopus @ Elsevier (PMID): 36847276 ● Search Scopus @ Elsevier (DOI): 10.1177/10600280231156270 (DOI: 10.1177/10600280231156270, PubMed: 36847276)
19.	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)
20.	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)
21.	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)
22.	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)
23.	Hideki Nawa, Hirofumi Hamano, Takahiro Niimura, Koji Miyata, Kenta Yagi, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : Evaluation of the potential complication of interstitial lung disease associated with antifibrotic drugs using data from databases reporting spontaneous adverse effects., Clinical and Translational Science, Vol.15, No.12, 2982-2988, 2022. (Summary) Interstitial lung disease (ILD), as an adverse effect of certain drugs, leads to inflammation and damage in the walls of the alveoli, making it difficult for the alveoli to take up oxygen. Interstitial pneumonia with no identifiable cause is called idiopathic interstitial pneumonia (IIP), and, among the major IIPs, idiopathic pulmonary fibrosis (IPF) is diagnosed in about half of patients. Current treatment options are limited, among which the antifibrotic drugs nintedanib (Ofev) and pirfenidone (Pirespa) are the first-line drugs. In this study, we investigated the incidence of ILD possibly caused by antifibrotic agents using data from the Japanese Adverse Drug Event Report (JADER) database, a database of spontaneous adverse event reports published by the Pharmaceuticals and Medical Devices Agency (PMDA), and the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS), published by the FDA. We used the FAERS and JADER to detect the signals of adverse events on the basis of reporting odds ratios. The relationship between indications and adverse events was clarified by separating indications and adverse events using the spontaneous adverse event reporting database with novel drug involvement. Regarding the involvement of nintedanib and pirfenidone in the development of ILD, JADER and FAERS showed signals for both nintedanib and pirfenidone as suspect drugs, and no signals for nintedanib or pirfenidone as concomitant drug interactions were detected. We highlight this because there are only a few effective drugs for IPF, and effective and safe drug therapies should be implemented by taking into consideration drug-induced ILD. (Keyword) United States / Humans / Pharmaceutical Preparations / Drug-Related Side Effects and Adverse Reactions / Lung Diseases, Interstitial / Databases, Factual / Pyridones / United States Food and Drug Administration / Idiopathic Pulmonary Fibrosis (Tokushima University Institutional Repository) ● Metadata: 118179 (Link to Publication Site) ● Publication site (DOI): 10.1111/cts.13419 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36128688 ● Search Scopus @ Elsevier (PMID): 36128688 ● Search Scopus @ Elsevier (DOI): 10.1111/cts.13419 (Tokushima University Institutional Repository: 118179, DOI: 10.1111/cts.13419, PubMed: 36128688)
24.	Naoto Okada, Akikazu Murakami, Masami Satou, Shingen Nakamura, Shiroh Fujii, Kimiko Sogabe, Mamiko Takahashi, Asami Okada, Akane Abe, Hideki Fujii, Masahiro Abe, Momoyo Azuma and Keisuke Ishizawa : First reported case of Lachnoanaerobaculum gingivalis bacteremia in an acute myeloid leukemia patient with oral mucositis during high dose chemotherapy., Anaerobe, Vol.76, 2022. (Summary) During chemotherapy in patients with oral mucositis, we should consider the possibility of L. gingivalis bacteremia. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.anaerobe.2022.102610 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35811059 ● Search Scopus @ Elsevier (PMID): 35811059 ● Search Scopus @ Elsevier (DOI): 10.1016/j.anaerobe.2022.102610 (DOI: 10.1016/j.anaerobe.2022.102610, PubMed: 35811059)
25.	Takumi Sakurada, Hiroshi Nokihara, Tadashi Koga, Yoshito Zamami, Mitsuhiro Goda, Kenta Yagi, Hirofumi Hamano, Fuka Aizawa, Hirokazu Ogino, Seidai Satou, Yasushi Kirino, Hisatsugu Goto, Yasuhiko Nishioka and Keisuke Ishizawa : Prevention of Pemetrexed-Induced Rash Using Low-Dose Corticosteroids: A Phase II Study., The Oncologist, Vol.27, No.7, e554-e560, 2022. (Summary) Prophylactic administration of low-dose dexamethasone for 5 days from the day after pemetrexed administration resulted in a milder incidence and severity of rash. These findings may provide a standard preventative strategy for pemetrexed-induced rashes. (Trial identifier: UMIN000025666). (Keyword) Adrenal Cortex Hormones / Carcinoma, Non-Small-Cell Lung / Cisplatin / Dexamethasone / Exanthema / Humans / Lung Neoplasms / Mesothelioma, Malignant / Pemetrexed (Tokushima University Institutional Repository) ● Metadata: 117391 (Link to Publication Site) ● Publication site (DOI): 10.1093/oncolo/oyab077 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35325241 ● Search Scopus @ Elsevier (PMID): 35325241 ● Search Scopus @ Elsevier (DOI): 10.1093/oncolo/oyab077 (Tokushima University Institutional Repository: 117391, DOI: 10.1093/oncolo/oyab077, PubMed: 35325241)
26.	Hiroki Yamada, Rio Ohmori, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : A machine learning model using SNPs obtained from a genome-wide association study predicts the onset of vincristine-induced peripheral neuropathy, The Pharmacogenomics Journal, 2022. (Summary) Vincristine treatment may cause peripheral neuropathy. In this study, we identified the genes associated with the development of peripheral neuropathy due to vincristine therapy using a genome-wide association study (GWAS) and constructed a predictive model for the development of peripheral neuropathy using genetic information-based machine learning. The study included 72 patients admitted to the Department of Hematology, Tokushima University Hospital, who received vincristine. Of these, 56 were genotyped using the Illumina Asian Screening Array-24 Kit, and a GWAS for the onset of peripheral neuropathy caused by vincristine was conducted. Using Sanger sequencing for 16 validation samples, the top three single nucleotide polymorphisms (SNPs) associated with the onset of peripheral neuropathy were determined. Machine learning was performed using the statistical software R package "caret". The 56 GWAS and 16 validation samples were used as the training and test sets, respectively. Predictive models were constructed using random forest, support vector machine, naive Bayes, and neural network algorithms. According to the GWAS, rs2110179, rs7126100, and rs2076549 were associated with the development of peripheral neuropathy on vincristine administration. Machine learning was performed using these three SNPs to construct a prediction model. A high accuracy of 93.8% was obtained with the support vector machine and neural network using rs2110179 and rs2076549. Thus, peripheral neuropathy development due to vincristine therapy can be effectively predicted by a machine learning prediction model using SNPs associated with it. (Tokushima University Institutional Repository) ● Metadata: 117583 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41397-022-00282-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35752658 ● Search Scopus @ Elsevier (PMID): 35752658 ● Search Scopus @ Elsevier (DOI): 10.1038/s41397-022-00282-8 (Tokushima University Institutional Repository: 117583, DOI: 10.1038/s41397-022-00282-8, PubMed: 35752658)
27.	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)
28.	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)
29.	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)
30.	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)
31.	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)
32.	Minori Takei, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : A genome-wide association study predicts the onset of dysgeusia due to anti-cancer drug treatment, Biological & Pharmaceutical Bulletin, Vol.45, No.1, 114-117, 2022. (Summary) Dysgeusia is a major side effect of anti-cancer drug treatment. Since dysgeusia significantly lowers the patient's QOL, predicting and avoiding its onset in advance is desirable. Accordingly, aims of the present study were to use a genome-wide association study (GWAS) to identify genes associated with the development of dysgeusia in patients taking anti-cancer drugs and to predict the development of dysgeusia using associated single nucleotide polymorphisms (SNPs). GWAS was conducted on 76 patients admitted to the Department of Hematology, Tokushima University Hospital. Using Sanger sequencing for 23 separately collected validation samples, the top two SNPs associated with the development of dysgeusia were determined. GWAS identified rs73049478 and rs41396146 SNPs on the retinoic acid receptor beta (RARB) gene associated with dysgeusia development due to the administration of anti-cancer drugs. Evaluation of the two SNPs using 23 validation samples indicated that the accuracy rate of rs73049478 was relatively high (87.0%). Thus, the findings of the present study suggest that the rs73049478 SNP of RARB can be used to predict the onset of dysgeusia caused by the administration of anti-cancer drugs. (Keyword) Antineoplastic Agents / Dysgeusia / Genetic Predisposition to Disease / Genome-Wide Association Study / Humans / Pharmaceutical Preparations / Polymorphism, Single Nucleotide / Quality of Life (Tokushima University Institutional Repository) ● Metadata: 117584 (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b21-00745 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34657909 ● CiNii @ National Institute of Informatics (CRID): 1390290617368322560 ● Summary page in Scopus @ Elsevier: 2-s2.0-85123201593 (Tokushima University Institutional Repository: 117584, DOI: 10.1248/bpb.b21-00745, PubMed: 34657909, CiNii: 1390290617368322560, Elsevier: Scopus)
33.	Mami Uchida, Soichiro Ushio, Takahiro Niimura, Kenshi Takechi, Hitoshi Kawazoe, Noriaki Hidaka, Akihiro Tanaka, Hiroaki Araki, Yoshito Zamami, Keisuke Ishizawa, Yoshihisa Kitamura, Toshiaki Sendou, Hiromu Kawasaki, Hiroyuki Namba, Kazuhiko Shibata, Mamoru Tanaka and Shingo Takatori : Renin-Angiotensin-Aldosterone System Inhibitors Prevent the Onset of Oxaliplatin-Induced Peripheral Neuropathy: A Retrospective Multicenter Study and in Vitro Evaluation., Biological & Pharmaceutical Bulletin, Vol.45, No.2, 226-234, 2021. (Summary) Oxaliplatin (OXA) is used in chemotherapy for various cancer types and is associated with acute and chronic neurotoxicity. However, a preventive strategy for OXA-induced peripheral neuropathy (OIPN) and its underlying mechanism remain unclear. We examined the effects of renin-angiotensin-aldosterone system inhibitors (RAASIs) on OIPN by performing a retrospective multicenter study and an in vitro assay. We retrospectively evaluated electronic medical records of 976 patients who underwent one or more courses of OXA-containing regimens at Ehime, Okayama, and Tokushima University Hospitals. The primary endpoint was the incidence of OIPN during or after OXA administration. The effects of RAASIs and OXA on the neurite length in PC12 cells were determined. The combined administration of an OXA-containing regimen and RAASI significantly inhibited the cumulative incidence grade-2 or higher OIPN (log-rank test; p = 0.0001). RAASIs markedly suppressed the development of both acute and chronic OIPN (multivariate analysis; p = 0.017 and p = 0.011). In an in vitro assay, 10 µM OXA suppressed the neurite length; treatment with 1 µM aliskiren, spironolactone, 10 µM candesartan, and enalapril significantly restored neurite length to the control level. Moreover, 1 µM SCH772984 (a selective inhibitor of extracellular signal-regulated kinase, ERK1/2) and 500 µM SQ22536 (a cell-permeable adenylate cyclase (AC) inhibitor) markedly abolished neurite-extending effects of candesartan and enalapril. These results indicate that RAASIs possess preventive or therapeutic effects in acute and chronic OIPN, candesartan and enalapril may increase in the activity of ERK1/2 and AC in PC12 cells. (Keyword) Angiotensin II Type 1 Receptor Blockers / Angiotensin-Converting Enzyme Inhibitors / Animals / Antihypertensive Agents / Antineoplastic Agents / Calcium Channel Blockers / Female / Humans / Male / Neuroprotective Agents / Oxaliplatin / PC12 Cells / Peripheral Nervous System Diseases / Proportional Hazards Models / Rats / Renin-Angiotensin System / Retrospective Studies (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b21-00852 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34803077 ● Search Scopus @ Elsevier (PMID): 34803077 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b21-00852 (DOI: 10.1248/bpb.b21-00852, PubMed: 34803077)
34.	Satoru Mitsuboshi, Takahiro Niimura, Masaya Kanda, Shunsuke Ishida, Yoshito Zamami and Keisuke Ishizawa : Risk of Hematologic Events With Coadministration of Methotrexate and the Breast Cancer Resistance Protein Inhibitor Febuxostat., The Annals of Pharmacotherapy, Vol.56, No.8, 910-915, 2021. (Summary) The breast cancer resistance protein (BCRP) is a key drug transporter found in the liver, kidney, central nervous system, and gastrointestinal tract. Due to the wide expression of BCRP, interactions of other drugs with methotrexate (MTX) may differ in oral and intravenous MTX users, and understanding of these interactions may be useful in preventing severe adverse events. Febuxostat, a urate-lowering drug, inhibits BCRP. The objective of this study was to clarify the differences in the drug-drug interaction profiles of oral and intravenous methotrexate, associated with BCRP. We analyzed the Japanese Adverse Drug Event Report database and compared the frequency of hematologic events in patients taking oral and intravenous MTX, with or without the concomitant use of febuxostat or allopurinol. Hematologic events were defined as pancytopenia and neutropenia. Multiple logistic regression analysis was then used to identify the risk factors for hematologic events in oral and intravenous MTX users. We identified 8 453 oral and 810 intravenous MTX users with 546 and 126 cases of hematologic events, respectively. Compared with those not using febuxostat, a disproportionate number of hematologic events was observed in intravenous MTX users concomitantly using febuxostat ( < 0.01). The multivariate logistic analysis of intravenous MTX users showed that hematologic events were significantly associated with febuxostat use ( < 0.01) and age ≥ 60 years ( < 0.01). Our findings suggest that patients being treated with intravenous MTX who concomitantly use febuxostat may be at an increased risk of hematologic events, presumably due to BCRP-mediated drug-drug interaction. (Keyword) ATP Binding Cassette Transporter, Subfamily G, Member 2 / Allopurinol / Breast Neoplasms / Febuxostat / Female / Gout Suppressants / Humans / Methotrexate / Middle Aged / Neoplasm Proteins (Link to Publication Site) ● Publication site (DOI): 10.1177/10600280211055794 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34726078 ● Search Scopus @ Elsevier (PMID): 34726078 ● Search Scopus @ Elsevier (DOI): 10.1177/10600280211055794 (DOI: 10.1177/10600280211055794, PubMed: 34726078)
35.	Naoto Okada, Yuki Izumi, Aki Nakamoto, Masayuki Chuma, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Hirofumi Hamano, Yoshito Zamami, Momoyo Azuma and Keisuke Ishizawa : Impact of Area Under the Concentration-Time Curve on the Prevalence of Vancomycin-Induced Nephrotoxicity in Combination With Tazobactam/Piperacillin or Cefepime: A Single-Institution Retrospective Study., Clinical Therapeutics, Vol.43, No.11, 1910-1920.e3, 2021. (Summary) VIN risk was higher with VT than with VC, even when the AUC was controlled to the guideline-recommended range. These results strongly suggest that VIN prevention may be difficult with AUC-guided vancomycin dosing in patients receiving VT. (Keyword) Acute Kidney Injury / Anti-Bacterial Agents / Bayes Theorem / Cefepime / Drug Therapy, Combination / Humans / Penicillanic Acid / Piperacillin / Piperacillin, Tazobactam Drug Combination / Prevalence / Retrospective Studies / Vancomycin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.clinthera.2021.09.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34642081 ● Search Scopus @ Elsevier (PMID): 34642081 ● Search Scopus @ Elsevier (DOI): 10.1016/j.clinthera.2021.09.007 (DOI: 10.1016/j.clinthera.2021.09.007, PubMed: 34642081)
36.	Hideki Nawa, Takahiro Niimura, Hirofumi Hamano, Kenta Yagi, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : Evaluation of Potential Complications of Interstitial Lung Disease Associated With Antiandrogens Using Data From Databases Reporting Spontaneous Adverse Effects., Frontiers in Pharmacology, Vol.12, No.655605, 2021. (Summary) From 2002 to 2018, the number of patients with prostate cancer significantly increased from 679,023 to 1276,106 worldwide. Total prostatectomy (including robot-assisted prostatectomy), radiation therapy, and pharmacological treatment are commonly used to treat prostate cancer. The Chief of the Pharmaceutical Safety Division, that is, the Federation of Pharmaceutical Manufacturers' Associations of Japan (FPMAJ), recently called for the revision of package inserts for ethical drugs. However, the pathogenesis of interstitial lung disease (ILD), a serious drug-induced adverse effect, remains unclear. Moreover, there have been no large-scale evaluations of potential complications associated with currently used antiandrogens, which are commonly employed to treat prostate cancer. Hence, ILD, as an adverse event, remains poorly understood. Therefore, we conducted a survey of reports in the Japanese Adverse Drug Event Report (JADER) database to investigate the potential association between the reporting of ILD and antiandrogen drug use in clinical practice. The occurrence of ILD was investigated by evaluating the relationship between antiandrogen drug use and ILD. Adverse event signals were detected with reporting odds ratios (RORs), using data from the JADER and FDA Adverse Event Reporting System (FAERS) databases, for the analysis of post-marketing adverse event reports. The JADER was used to examine the time profile of adverse event occurrence for each drug, whereas the FAERS was used to screen cases of unknown adverse events and analyze their trends of occurrence. The analysis of data from both databases revealed the 95% confidence interval lower limits of ROR for bicalutamide and flutamide to be > 1, and adverse event signals were detected following the use of either drug. While caution should be exercised for drugs that are new to the market, we conclude that drugs with similar therapeutic effects that have been in use for a long period should also be re-examined for potential adverse events. (Link to Publication Site) ● Publication site (DOI): 10.3389/fphar.2021.655605 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34177574 ● Search Scopus @ Elsevier (PMID): 34177574 ● Search Scopus @ Elsevier (DOI): 10.3389/fphar.2021.655605 (DOI: 10.3389/fphar.2021.655605, PubMed: 34177574)
37.	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)
38.	Hideki Nawa, Takahiro Niimura, Kenta Yagi, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : Evaluation of potential complication of interstitial lung disease with abemaciclib and palbociclib treatments., Cancer Reports, 2021. (Summary) Treatment with abemaciclib and palbociclib is associated with a potential complication of interstitial lung disease, regardless of age. (Tokushima University Institutional Repository) ● Metadata: 116289 (Link to Publication Site) ● Publication site (DOI): 10.1002/cnr2.1402 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33939324 ● Search Scopus @ Elsevier (PMID): 33939324 ● Search Scopus @ Elsevier (DOI): 10.1002/cnr2.1402 (Tokushima University Institutional Repository: 116289, DOI: 10.1002/cnr2.1402, PubMed: 33939324)
39.	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)
40.	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)
41.	Tomoko Funahashi, Toshihiro Koyama, Hideharu Hagiya, Ko Harada, Syunya Iinuma, Soichiro Ushio, Yoshito Zamami, Takahiro Niimura, Kazuaki Shinomiya, Keisuke Ishizawa, Toshiaki Sendo, Shiro Hinotsu and R Mitsunobu Kano : Population-Based Observational Study of Adverse Drug Event-Related Mortality in the Super-Aged Society of Japan., Drug Safety, Vol.44, No.5, 531-539, 2021. (Summary) The number of and trend in ADE-related deaths increased in Japan from 1999 to 2016, particularly in the older population. (Link to Publication Site) ● Publication site (DOI): 10.1007/s40264-020-01037-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33826081 ● Search Scopus @ Elsevier (PMID): 33826081 ● Search Scopus @ Elsevier (DOI): 10.1007/s40264-020-01037-9 (DOI: 10.1007/s40264-020-01037-9, PubMed: 33826081)
42.	Mizuho Asada, Takahisa Mikami, Takahiro Niimura, Yoshito Zamami, Yoshihiro Uesawa, Masayuki Chuma and Keisuke Ishizawa : The Risk Factors Associated with Immune Checkpoint Inhibitor-Related Pneumonitis., Oncology, 2021. (Summary) Our data suggest that the risk of ICI-related pneumonitis may increase in certain populations, including younger age (age <60 years) and ICIs users. These patients require careful monitoring. (Link to Publication Site) ● Publication site (DOI): 10.1159/000512633 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33477139 ● Search Scopus @ Elsevier (PMID): 33477139 ● Search Scopus @ Elsevier (DOI): 10.1159/000512633 (DOI: 10.1159/000512633, PubMed: 33477139)
43.	Tashima Hozumi, Endo Yuka, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : Association analysis between adverse drug reactions to cytarabine therapy and single nucleotide polymorphisms in cytarabine metabolic genes in patients with hematopoietic tumor, Personalized Medicine Universe, Vol.10, 1-6, 2021. (Tokushima University Institutional Repository) ● Metadata: 117585 (Link to Publication Site) ● Publication site (DOI): 10.46459/pmu.2021002 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.46459/pmu.2021002 (Tokushima University Institutional Repository: 117585, DOI: 10.46459/pmu.2021002)
44.	Masayuki Chuma, Kenshi Takechi, Kenta Yagi, Satoshi Sakaguchi, Hiroshi Nokihara, Chikako Kane, Yasutaka Sato, Takahiro Niimura, Mitsuhiro Goda, Yoshito Zamami, Keisuke Ishizawa and Hiroaki Yanagawa : Academic investigators' interest in promoting specified clinical trials : Questionnaire survey before and after implementation of the Clinical Trial Act, The Journal of Medical Investigation : JMI, Vol.68, No.1.2, 71-75, 2021. (Summary) Background : Enforcement of the 2018 Clinical Trials Act (CTA) in Japan resulted in strict and complicated regulations surrounding intervention studies. Few Japan-specific measures have been developed to promote intervention studies in Japan despite concerns about CTA's negative influence on such studies. Therefore, this study examined the changes in academic investigators' interest in conducting clinical studies before and after enforcement of the CTA to determine measures to promote specified clinical trials. Methods : We conducted a questionnaire survey with investigators belonging to the Institute of Biomedical Sciences, Tokushima University Graduate School, before and after enforcement of the CTA. Results : Investigators had lesser interest in intervention studies in the post-questionnaire survey (post) group than in the pre-questionnaire survey (pre) group. Their desire for "project management" was significantly higher in the post-group than in the pre-group. Their desire for "support for preparing documents when conducting specified clinical trials" was significantly higher in the group interested in conducting specified clinical trials than that in the not-interested group. Conclusion : We revealed that investigators were highly interested in "project management" and "support for preparing documents when conducting specified clinical trials" after enforcement of the CTA. Measures for these desires may promote specified clinical trials. J. Med. Invest. 68 : 71-75, February, 2021. (Tokushima University Institutional Repository) ● Metadata: 115987 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.68.71 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33994483 ● Search Scopus @ Elsevier (PMID): 33994483 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.68.71 (Tokushima University Institutional Repository: 115987, DOI: 10.2152/jmi.68.71, PubMed: 33994483)
45.	Takayoshi Masuoka, Yuka Yamashita, Katsuya Nakano, Kenshi Takechi, Takahiro Niimura, Masashi Tawa, Qiang He, Keisuke Ishizawa and Takaharu Ishibashi : Chronic Tear Deficiency Sensitizes Transient Receptor Potential Vanilloid 1-Mediated Responses in Corneal Sensory Nerves., Frontiers in Cellular Neuroscience, Vol.14, 598678, 2020. (Summary) Chronic tear deficiency enhances the excitability of corneal cold-sensitive nerves that detect ocular dryness, which can lead to discomfort in patients with dry eye disease (DED). However, changes in corneal nerve excitations through the polymodal nociceptor "transient receptor potential vanilloid 1" (TRPV1) and the potential link between this receptor and symptoms of DED remain unclear. In this study, we examined the firing properties of corneal cold-sensitive nerves expressing TRPV1 and possible contributions of chronic tear deficiency to corneal nerve excitability by TRPV1 activation. The bilateral excision of lacrimal glands in guinea pigs decreased the tear volume and increased the frequency of spontaneous eyeblinks 1-4 weeks after surgery. An analysis of the firing properties of the cold-sensitive nerves was performed by single-unit recordings of corneal preparations 4 weeks after surgery in both the sham-operated and gland-excised groups. Perfusion of the TRPV1 agonist, capsaicin (1 μM), transiently increased the firing frequency in approximately 46-48% of the cold-sensitive nerves characterized by low-background activity and high threshold (LB-HT) cold thermoreceptors in both groups. Gland excision significantly decreased the latency of capsaicin-induced firing in cold-sensitive nerves; however, its magnitude was unchanged. Calcium imaging of cultured trigeminal ganglion neurons from both groups showed that intracellular calcium elevation of corneal neurons induced by a low concentration of capsaicin (0.03 μM) was significantly larger in the gland excision group, regardless of responsiveness to cold. An immunohistochemical study of the trigeminal ganglion revealed that gland excision significantly increased the proportion of corneal neurons enclosed by glial fibrillary acidic protein (GFAP)-immunopositive satellite glial cells. Topical application of the TRPV1 antagonist, A784168 (30 μM), on the ocular surface attenuated eye-blink frequency after gland excision. Furthermore, gland excision enhanced blink behavior induced by a low concentration of capsaicin (0.1 μM). These results suggest that chronic tear deficiency sensitizes the TRPV1-mediated response in the corneal LB-HT cold thermoreceptors and cold-insensitive polymodal nociceptors, which may be linked to dry eye discomfort and hyperalgesia resulting from nociceptive stimuli in aqueous-deficient dry eyes. (Tokushima University Institutional Repository) ● Metadata: 117446 (Link to Publication Site) ● Publication site (DOI): 10.3389/fncel.2020.598678 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33424555 ● Search Scopus @ Elsevier (PMID): 33424555 ● Search Scopus @ Elsevier (DOI): 10.3389/fncel.2020.598678 (Tokushima University Institutional Repository: 117446, DOI: 10.3389/fncel.2020.598678, PubMed: 33424555)
46.	Satoru Mitsuboshi, Takahiro Niimura, Yoshito Zamami and Keisuke Ishizawa : Differences in risk factors for anticoagulant-related nephropathy between warfarin and direct oral anticoagulants: analysis of the Japanese Adverse Drug Event Report database., British Journal of Clinical Pharmacology, 2020. (Summary) Limited information is available on anticoagulant-related nephropathy (ARN). We therefore reviewed the Japanese Adverse Drug Event Report database to investigate kidney injury (KI) in patients administered warfarin or direct oral anticoagulants (DOACs) and sought to clarify the risk factors for ARN. KI risk in warfarin users was associated with male sex (odds ratio [OR], 1.70; 95% confidence interval [CI], 1.35-2.13; P < 0.01) and age 80 years (OR, 1.35; 95% CI, 1.07-1.72; P = 0.01). KI risk in DOAC users was associated with body weight 80 kg (OR, 1.60; 95% CI, 1.01-2.53; P = 0.04) and use of dabigatran (OR, 1.61; 95% CI, 1.09-2.37; P < 0.01). Our findings suggest that risk factors for ARN differ between warfarin and DOACs, and that these risk factors may be associated with bleeding risk. Therefore, the risk of ARN may be decreased by better managing bleeding risk in patients taking anticoagulants. (Link to Publication Site) ● Publication site (DOI): 10.1111/bcp.14688 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33270271 ● Search Scopus @ Elsevier (PMID): 33270271 ● Search Scopus @ Elsevier (DOI): 10.1111/bcp.14688 (DOI: 10.1111/bcp.14688, PubMed: 33270271)
47.	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)
48.	Hiromi Hagiwara, Hidekatsu Fukuta, Hiroya Hashimoto, Takahiro Niimura, Yoshito Zamami, Keisuke Ishizawa, Takeshi Kamiya and Nobuyuki Ohte : A comparison of the safety and effectiveness of prasugrel and clopidogrel in younger population undergoing percutaneous coronary intervention: A retrospective study using a Japanese claims database., Journal of Cardiology, Vol.77, No.3, 285-291, 2020. (Summary) The safety and effectiveness of prasugrel was comparable to that of clopidogrel in real-world Japanese patients scheduled to undergo PCI. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jjcc.2020.10.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34074484 ● Search Scopus @ Elsevier (PMID): 34074484 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jjcc.2020.10.001 (DOI: 10.1016/j.jjcc.2020.10.001, PubMed: 34074484)
49.	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)
50.	Naoto Okada, Rie Matsuoka, Takumi Sakurada, Mitsuhiro Goda, Masayuki Chuma, Kenta Yagi, Yoshito Zamami, Yasuhiko Nishioka and Keisuke Ishizawa : Risk factors of immune checkpoint inhibitor-related interstitial lung disease in patients with lung cancer: a single-institution retrospective study., Scientific Reports, Vol.10, No.1, 2020. (Summary) Immune checkpoint inhibitors (ICIs) elicit antitumour effects by activating the host immunity and cause immune-related adverse events (irAEs). ICI-related interstitial lung disease (ICI-ILD) is a fatal irAE that is difficult to treat; moreover, its incidence is relatively higher in patients with lung cancer. Therefore, early ICI-ILD detection and intervention are important for patient safety. However, a risk assessment method for ICI-ILD has not been established and the prediction of ICI-ILD occurrence is difficult. The aim of our study was to identify the risk factors associated with ICI-ILD. To this end, we retrospectively analysed 102 patients with lung cancer who first received ICI and completed the treatment between April 2016 and December 2019 at Tokushima University Hospital. Nineteen patients had all grades of ICI-ILD and 10 had grade ≥ 3 ICI-ILD. The 30-day mortality rate of patients with grade ≥ 3 ICI-ILD was the highest among all patients (P < 0.01). The multivariate logistic analysis indicated that the performance status ≥ 2 alone and both performance status ≥ 2 and ≥ 50 pack-year were independent risk factors of ICI-ILD of grade ≥ 3 and all grades, respectively. Overall, our study provides insights to predict ICI-ILD occurrence. (Keyword) Adult / Aged / Aged, 80 and over / Antibodies, Monoclonal / Antibodies, Monoclonal, Humanized / B7-H1 Antigen / CTLA-4 Antigen / Carcinoma, Non-Small-Cell Lung / Early Diagnosis / Female / Humans / Immune Checkpoint Inhibitors / Lung Diseases, Interstitial / Lung Neoplasms / Male / Middle Aged / Nivolumab / Programmed Cell Death 1 Receptor / Retrospective Studies / Risk Assessment / Risk Factors (Tokushima University Institutional Repository) ● Metadata: 116635 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-020-70743-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32792640 ● Search Scopus @ Elsevier (PMID): 32792640 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-020-70743-2 (Tokushima University Institutional Repository: 116635, DOI: 10.1038/s41598-020-70743-2, PubMed: 32792640)
51.	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)
52.	Kenji Otsuka, Atsushi Mitsuhashi, Hisatsugu Goto, Masaki Hanibuchi, Kazuya Koyama, Hirohisa Ogawa, Hirokazu Ogino, Atsuro Saijo, Hiroyuki Kozai, Hiroto Yoneda, Makoto Tobiume, Masatoshi Kishuku, Keisuke Ishizawa and Yasuhiko Nishioka : Anti-PD-1 antibody combined with chemotherapy suppresses the growth of mesothelioma by reducing myeloid-derived suppressor cells., Lung Cancer, Vol.146, 86-96, 2020. (Summary) T cells in tumors, the number of Foxp3 (Keyword) Animals / Cell Line, Tumor / Lung Neoplasms / Mesothelioma / Mice / Myeloid-Derived Suppressor Cells / Pemetrexed (Tokushima University Institutional Repository) ● Metadata: 115324 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lungcan.2020.05.023 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32526602 ● Search Scopus @ Elsevier (PMID): 32526602 ● Search Scopus @ Elsevier (DOI): 10.1016/j.lungcan.2020.05.023 (Tokushima University Institutional Repository: 115324, DOI: 10.1016/j.lungcan.2020.05.023, PubMed: 32526602)
53.	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)
54.	Hiromi Hagiwara, Hidekatsu Fukuta, Takahiro Niimura, Yoshito Zamami, Keisuke Ishizawa, Kazunori Kimura, Takeshi Kamiya and Nobuyuki Ohte : Comparison of Hemorrhagic Risk between Prasugrel and Clopidogrel: a Retrospective Study using Adverse Drug Event Reporting Databases., International Journal of Medical Sciences, Vol.17, No.6, 728-733, 2020. (Summary) : The hemorrhagic risk was found to be greater with prasugrel than clopidogrel in real-world patients, including Japanese patients. (Tokushima University Institutional Repository) ● Metadata: 115153 (Link to Publication Site) ● Publication site (DOI): 10.7150/ijms.43168 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32218694 ● Summary page in Scopus @ Elsevier: 2-s2.0-85081614223 (Tokushima University Institutional Repository: 115153, DOI: 10.7150/ijms.43168, PubMed: 32218694, Elsevier: Scopus)
55.	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)
56.	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)
57.	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)
58.	Naoto Okada, Masayuki Chuma, Momoyo Azuma, Shingen Nakamura, Hirokazu Miki, Hirofumi Hamano, Mitsuhiro Goda, Kenshi Takechi, Yoshito Zamami, Masahiro Abe and Keisuke Ishizawa : Effect of serum concentration and concomitant drugs on vancomycin-induced acute kidney injury in haematologic patients: a single-centre retrospective study., European Journal of Clinical Pharmacology, Vol.75, No.12, 1695-1704, 2019. (Summary) We retrospectively analysed 150 haematologic patients to whom VCM was administered between April 2010 and March 2018 at Tokushima University Hospital. VCM-induced AKI was defined according to Kidney Disease Improving Global Outcomes (KDIGO) criteria. Multivariate logistic regression analyses were performed to identify risk factors for VCM-induced AKI. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00228-019-02756-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31511938 ● Search Scopus @ Elsevier (PMID): 31511938 ● Search Scopus @ Elsevier (DOI): 10.1007/s00228-019-02756-4 (DOI: 10.1007/s00228-019-02756-4, PubMed: 31511938)
59.	Takumi Sakurada, Sanako Bando, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Mitsuhiro Goda, Yasushi Kirino, Toshimi Nakamura, Kazuhiko Teraoka, Masami Morimoto, Akira Tangoku and Keisuke Ishizawa : Prophylactic administration of granulocyte colony-stimulating factor in epirubicin and cyclophosphamide chemotherapy for Japanese breast cancer patients: a retrospective study., Cancer Chemotherapy and Pharmacology, Vol.84, No.5, 1107-1114, 2019. (Summary) The incidence of FN in EC therapy among Japanese patients was higher than expected, EC therapy appears to be a high-risk chemotherapy for FN, and prophylactic administration of G-CSF is recommended. Maintaining high therapeutic intensity is associated with a positive prognosis for patients with early breast cancer, and prophylactic administration of G-CSF is likely to be beneficial in treatment involving EC therapy. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00280-019-03948-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31502114 ● Search Scopus @ Elsevier (PMID): 31502114 ● Search Scopus @ Elsevier (DOI): 10.1007/s00280-019-03948-6 (DOI: 10.1007/s00280-019-03948-6, PubMed: 31502114)
60.	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)
61.	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)
62.	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)
63.	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)
64.	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)
65.	Ken Konaka, Takumi Sakurada, Tatsuhiko Saito, Sachiko Mori, Masaki Imanishi, Soji Kakiuchi, Shuji Fushitani and Keisuke Ishizawa : Study on the Optimal Dose of Irinotecan for Patients with Heterozygous Uridine Diphosphate-Glucuronosyltransferase 1A1 (UGT1A1)., Biological & Pharmaceutical Bulletin, Vol.42, No.11, 1839-1845, 2019. (Summary) Uridine 5'-diphospho-glucuronosyltransferase (UGT), a metabolic enzyme of irinotecan active metabolite, has two genetic polymorphisms (UGT1A16 and UGT1A128). In UGT1A1 homozygous or heterozygous patients, metabolism is delayed and the risk of developing adverse effects is increased, and therefore, dose reduction of irinotecan is considered. However, the specific dose reduction rate of irinotecan for heterozygous patients is uncertain. We studied the necessity of irinotecan dose reduction and its optimal dose in UGT1A1 heterozygous patients with lung cancer. Patients with lung cancer treated with irinotecan in the Tokushima University Hospital or Tokushima Municipal Hospital were included in this study. The dose of irinotecan was evaluated based on the relative dose intensity (RDI). The time to treatment failure (TTF) was defined as the period until treatment change, death, or progressive disease based on response evaluation criteria of solid tumors. We targeted 31 patients treated with irinotecan: 12 wild types (WT), 14 heterozygotes, and 1 complex heterozygote and 4 homozygotes. There was no significant difference in the TTF, but the mean RDI during the entire treatment period was significantly different in the wild type (79%), heterozygous (62%), and complex heterozygous and homozygous groups (46%). In addition, the proportion of patients who completed treatment without dose reduction in the WT group tended to be higher than that in the other groups. For lung cancer patients with UGT1A1 heterozygote types who start irinotecan therapy, reducing the initial dose by approximately 20% might be a safer chemotherapy without decreasing the therapeutic effect. (Keyword) Aged / Dose-Response Relationship, Drug / Female / Genotype / Glucuronosyltransferase / Heterozygote / Homozygote / Humans / Irinotecan / Lung Neoplasms / Male / Middle Aged / Polymorphism, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b19-00357 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31685767 ● Search Scopus @ Elsevier (PMID): 31685767 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b19-00357 (DOI: 10.1248/bpb.b19-00357, PubMed: 31685767)
66.	Naoto Okada, Takahiro Niimura, Yoshito Zamami, Hirofumi Hamano, Shunsuke Ishida, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Masaki Imanishi and Keisuke Ishizawa : Pharmacovigilance evaluation of the relationship between impaired glucose metabolism and BCR-ABL inhibitor use by using an adverse drug event reporting database., Cancer Medicine, 2018. (Summary) Breakpoint cluster region-Abelson murine leukemia (BCR-ABL) inhibitors markedly improve the prognosis of chronic myeloid leukemia. However, high treatment adherence is necessary for successful treatment with BCR-ABL inhibitors. Therefore, an adequate understanding of the adverse event profiles of BCR-ABL inhibitors is essential. Although many adverse events are observed in trials, an accurate identification of adverse events based only on clinical trial results is difficult because of strict entry criteria or limited follow-up durations. In particular, BCR-ABL inhibitor-induced impaired glucose metabolism remains controversial. Pharmacovigilance evaluations using spontaneous reporting systems are useful for analyzing drug-related adverse events in clinical settings. Therefore, we conducted signal detection analyses for BCR-ABL inhibitor-induced impaired glucose metabolism by using the FDA Adverse Event Reporting System (FAERS) and Japanese Adverse Drug Event Report (JADER) database. Signals for an increased reporting rate of impaired glucose metabolism were detected only for nilotinib use, whereas these signals were not detected for other BCR-ABL inhibitors. Subgroup analyses showed a clearly increased nilotinib-associated reporting rate of impaired glucose metabolism in male and younger patients. Although FAERS- and JADER-based signal detection analyses cannot determine causality perfectly, our study suggests the effects on glucose metabolism are different between BCR-ABL inhibitors and provides useful information for the selection of appropriate BCR-ABL inhibitors. (Tokushima University Institutional Repository) ● Metadata: 115037 (Link to Publication Site) ● Publication site (DOI): 10.1002/cam4.1920 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30561126 ● Search Scopus @ Elsevier (PMID): 30561126 ● Search Scopus @ Elsevier (DOI): 10.1002/cam4.1920 (Tokushima University Institutional Repository: 115037, DOI: 10.1002/cam4.1920, PubMed: 30561126)
67.	Naoto Okada, Hitoshi Kawazoe, Kenshi Takechi, Yoshihiro Matsudate, Ryo Utsunomiya, Yoshito Zamami, Mitsuhiro Goda, Masaki Imanishi, Masayuki Chuma, Noriaki Hidaka, Koji Sayama, Yoshiaki Kubo, Akihiro Tanaka and Keisuke Ishizawa : Association Between Immune-Related Adverse Events and Clinical Efficacy in Patients with Melanoma Treated With Nivolumab: A Multicenter Retrospective Study., Clinical Therapeutics, Vol.41, No.1, 59-67, 2018. (Summary) Our study indicated that clinical response with nivolumab treatment improves with irAE occurrence in patients with melanoma. Moreover, the early increase in peripheral lymphocyte count may act as a biomarker for predicting the occurrence of irAEs induced by nivolumab. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.clinthera.2018.11.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30528047 ● Summary page in Scopus @ Elsevier: 2-s2.0-85057595502 (DOI: 10.1016/j.clinthera.2018.11.004, PubMed: 30528047, Elsevier: Scopus)
68.	Yoshito Zamami, Y Kouno, T Niimura, Masayuki Chuma, T Imai, M Mitsui, T Koyama, M Kayano, Naoto Okada, H Hamano, Mitsuhiro Goda, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, Y Kondo, Hiroaki Yanagawa, Y Kitamura, T Sendo, Y Ujike and Keisuke Ishizawa : Relationship between the administration of nicardipine hydrochloride and the development of delirium in patients on mechanical ventilation., Die Pharmazie, Vol.73, No.12, 740-743, 2018. (Summary) A history of hypertension is a known risk factor for delirium in patients in intensive care units, but the effect of antihypertensive agents on delirium development is unclear. Nicardipine, a calcium channel blocker, is widely used in ICU as a treatment agent for hypertensive emergency. This study investigated the relationship between the administration of nicardipine hydrochloride and delirium development in patients under mechanical ventilation. We conducted a medical chart review of 103 patients, who were divided into two groups according to the use of nicardipine hydrochloride. The prevalence of delirium was compared with respect to factors such as age, sex, laboratory data, and medical history, by multivariate analysis. 21 patients (20.4 %) were treated with nicardipine hydrochloride in 103 patients. The treatment and non-treatment groups differed significantly in age (72 vs. 65 years) and history of high blood pressure (57% vs. 11%). Multivariate analysis revealed that patients in the treatment group developed delirium significantly less often than those in the non-treatment group (19% vs. 48%). These results suggested that treatment of high blood pressure with nicardipine hydrochloride is a possible method for preventing the development of delirium. (Link to Publication Site) ● Publication site (DOI): 10.1691/ph.2018.8711 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30522561 ● Search Scopus @ Elsevier (PMID): 30522561 ● Search Scopus @ Elsevier (DOI): 10.1691/ph.2018.8711 (DOI: 10.1691/ph.2018.8711, PubMed: 30522561)
69.	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)
70.	Shunsuke Ishida, Kenshi Takechi, Hiroshi Bando, Masaki Imanishi, Yoshito Zamami, Masayuki Chuma, Hiroaki Yanagawa, Yasushi Kirino, Toshimi Nakamura, Kazuhiko Teraoka and Keisuke Ishizawa : Development and pharmacist-mediated use of tools for monitoring atypical antipsychotic-induced side effects related to blood glucose levels., Pharmacoepidemiology and Drug Safety, 2018. (Summary) The results suggested that regardless of pharmacists' experience or skill, the introduction of this tool enables centralization of side effect monitoring and can contribute to proper drug use. (Tokushima University Institutional Repository) ● Metadata: 112203 (Link to Publication Site) ● Publication site (DOI): 10.1002/pds.4656 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30221424 ● Search Scopus @ Elsevier (PMID): 30221424 ● Search Scopus @ Elsevier (DOI): 10.1002/pds.4656 (Tokushima University Institutional Repository: 112203, DOI: 10.1002/pds.4656, PubMed: 30221424)
71.	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)
72.	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)
73.	Naoto Okada, Momoyo Azuma, Masaki Imanishi, Yoshito Zamami, Yasushi Kirino, Toshimi Nakamura, Kazuhiko Teraoka, Masahiro Abe and Keisuke Ishizawa : Potential Usefulness of Early Potassium Supplementation for Preventing Severe Hypokalemia Induced by Liposomal Amphotericin B in Hematologic Patients: A Retrospective Study., Clinical Therapeutics, Vol.40, No.2, 252-260, 2018. (Summary) This study showed that starting administration of a potassium formulation within 2 days from the start of L-AMB administration was a risk reduction factor for L-AMB-induced hypokalemia. This finding indicates that early potassium supplementation should be incorporated into the regimen of hypokalemia management when L-AMB is used. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.clinthera.2017.12.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29305017 ● Search Scopus @ Elsevier (PMID): 29305017 ● Search Scopus @ Elsevier (DOI): 10.1016/j.clinthera.2017.12.006 (DOI: 10.1016/j.clinthera.2017.12.006, PubMed: 29305017)
74.	Takahiro Niimura, Yoshito Zamami, Toru Imai, Tsuyoshi Ito, Hidenori Sagara, Hichiya Hiroyuki, Satoru Esumi, Kenshi Takechi, Masaki Imanishi, Toshihiro Koyama, Manabu Amano, Naomi Kurata, Yoshihisa Kitamura, Hironori Nakura, Toshiaki Sendo and Keisuke Ishizawa : Administration of Kampo medicine through a tube at an advanced critical care center., The Journal of Medical Investigation : JMI, Vol.65, No.1.2, 32-36, 2018. (Summary) n emergency and critical care medical centers, tube administration is employed for patients who have difficulty swallowing oral drugs owing to decreased consciousness or mechanical ventilation. However, tube clogging due to drug injection is a concern. We compared the crushing method with the simple suspension method for the passage of amlodipine, an antihypertensive drug, in combination with rikkunshito, which has been used to treat upper gastrointestinal disorders such as functional dyspepsia and gastroesophageal reflux in emergency and critical care medical centers, to ascertain the effect of Kampo products on the passage of other drugs during tube administration. When the crushing method was employed, poorly water-soluble solid products were formed, while a uniformly dispersed suspension was obtained using the simple suspension method. In addition, the passage rate of amlodipine through the tube was 64% and 93% in the crushing and simple suspension methods, respectively, thereby indicating that the simple suspension method provided more favorable than the crushing method. The results of this study suggested that the passage rate of amlodipine for patients who received Kampo products concurrently was higher when the simple suspension method was used, and an appropriate drug amount might well be able to administered to patients using this method. J. Med. Invest. 65:32-36, February, 2018. (Tokushima University Institutional Repository) ● Metadata: 111388 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.65.32 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29593190 ● Search Scopus @ Elsevier (PMID): 29593190 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.32 (Tokushima University Institutional Repository: 111388, DOI: 10.2152/jmi.65.32, PubMed: 29593190)
75.	Takahiro Niimura, Yoshito Zamami, Toru Imai, Kanako Nagao, Masafumi Kayano, Hidenori Sagara, Mitsuhiro Goda, Naoto Okada, Masayuki Chuma, Kenshi Takechi, Masaki Imanishi, Toshihiro Koyama, Tadashi Koga, Hironori Nakura, Toshiaki Sendo and Keisuke Ishizawa : Evaluation of the Benefits of De-Escalation for Patients with Sepsis in the Emergency Intensive Care Unit., Journal of Pharmacy & Pharmaceutical Sciences, Vol.21, No.1, 54-59, 2018. (Summary) The length of hospital stay after diagnosis was significantly shorter for the de-escalation group than for the non-de-escalation group. In the subgroup analysis, de-escalation for blood culture-positive patients was beneficial in terms of the length of hospital stay and length of antibiotic administration. (Link to Publication Site) ● Publication site (DOI): 10.18433/jpps29737 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29455711 ● Summary page in Scopus @ Elsevier: 2-s2.0-85044119660 (DOI: 10.18433/jpps29737, PubMed: 29455711, Elsevier: Scopus)
76.	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)
77.	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)
78.	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)
79.	Ken Konaka, Kota Moriyama, Takumi Sakurada, Naoto Okada, Masaki Imanishi, Yoshito Zamami, Kazuyoshi Kawazoe, Shuji Fushitani and Keisuke Ishizawa : Kamishoyosan and Shakuyakukanzoto promote recovery from paclitaxel-induced neurite retraction in PC12 cells, Journal of Pharmaceutical Health Care and Sciences, Vol.3, 20, 2017. (Summary) In chemotherapy, the full round of treatment must be completed as scheduled to achieve the strongest therapeutic effect. However, peripheral neuropathy, a severe side effect of the chemotherapeutic agent paclitaxel, can force the premature discontinuation of treatment. As some kampo practitioners have suggested that it may be possible to counteract such side effects, we analyzed the effects of Kamishoyosan, Shakuyakukanzoto, and Goshajinkigan in an in vitro model of paclitaxel-induced peripheral neuropathy. Paclitaxel-treated PC12 cells were assessed for neurite length and performed Western blot analysis for growth-associated protein-43 (GAP-43) and light neurofilament protein (NF-L) levels in the presence of nerve growth factor (NGF); they were re-assessed, with additional testing for acetylcholinesterase levels, after application of one of the kampo. We also compared phosphorylation of extracellular signal-regulated kinase (Erk)1/2 and Akt via Western blot analysis. About effect of kampo to anticancer efficacy, we confirmed cell cytotoxicity in A549 cells using MTT assay. Addition of Kamishoyosan or Shakuyakukanzoto, but not Goshajinkigan, significantly improved neurite length and GAP-43 and NF-L levels from paclitaxel-treated PC12 cells, relative to those of only NGF-treated PC12 cells. The promoting effect of Kamishoyosan and Shakuyakukanzoto in neurite outgrowth is confirmed when NGF promoted neurite outgrowth, and it was inhibited partially when Erk1/2 and Akt were blocked by Erk1/2 inhibitor or Akt inhibitor alone. Furthermore, neurite outgrowth induced by TJ24 and TJ68 was inhibited more strongly when Erk1/2 inhibitor and Akt inhibitor were treated at the same time. NGF with Kamishoyosan or Shakuyakukanzoto promoted the proportion of phosphorylated Erk1/2 and phosphorylated Akt compare with NGF only. On the other hand, Kamishoyosan or Shakuyakukanzoto didn't influence cytotoxicity of paclitaxel in A549 cells. Kamishoyosan or Shakuyakukanzoto promotes neurite outgrowth with NGF via increasing the proportion of phosphorylated Erk1/2 and phosphorylated Akt in PC12 cells. The effect applies to recovery from paclitaxel-induced axonal involvement and might promote recovery from paclitaxel-induced neuropathy without influence of anticancer effect of paclitaxel. (Tokushima University Institutional Repository) ● Metadata: 114522 (Link to Publication Site) ● Publication site (DOI): 10.1186/s40780-017-0090-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28748102 ● Search Scopus @ Elsevier (PMID): 28748102 ● Search Scopus @ Elsevier (DOI): 10.1186/s40780-017-0090-y (Tokushima University Institutional Repository: 114522, DOI: 10.1186/s40780-017-0090-y, PubMed: 28748102)
80.	Kenshi Takechi, Hiroaki Yanagawa, Yoshito Zamami, Keisuke Ishizawa, Akihiro Tanaka and Hiroaki Araki : Evaluation of factors associated with the achievement of an optimal teicoplanin trough concentration ., International Journal of Clinical Pharmacology and Therapeutics, 2017. (Summary) These results suggested that patients with decreased renal function (eGFR. (Link to Publication Site) ● Publication site (DOI): 10.5414/CP203009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28655381 ● Search Scopus @ Elsevier (PMID): 28655381 ● Search Scopus @ Elsevier (DOI): 10.5414/CP203009 (DOI: 10.5414/CP203009, PubMed: 28655381)
81.	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)
82.	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)
83.	Kenshi Takechi, Yurika Yoshioka, Hitoshi Kawazoe, Mamoru Tanaka, Shingo Takatori, Miwako Kobayashi, Ichiro Matsuoka, Hiroaki Yanagawa, Yoshito Zamami, Masaki Imanishi, Keisuke Ishizawa, Akihiro Tanaka and Hiroaki Araki : Psychiatric patients with antipsychotic drug-induced hyperprolactinemia and menstruation disorders, Biological & Pharmaceutical Bulletin, Vol.40, No.10, 1775-1778, 2017. (Summary) Treatment with antipsychotic drugs has been associated with hyperprolactinemia. The same antipsychotic drugs have also been associated with side effects such as menstruation disorders. The aim of this study was to evaluate the prevalence of hyperprolactinemia and menstruation disorders in women undergoing antipsychotic treatment. We performed a retrospective chart review study of psychiatric patients who underwent laboratory testing for serum prolactin (PRL) level between March 2011 and March 2015 in Ehime University Hospital. Patients presenting with and without menstruation disorders were evaluated to determine if they presented concomitant hyperprolactinemia. Patients with menstrual disorders had a significant increase in serum PRL level with a mean of approximately 90 ng/mL. Those with menstrual disorders presented increased PRL levels by 2-fold that of patients without menstrual disorder. However, there was no significant difference in the equivalent dose of chlorpromazine between these two groups. Additionally, about 70% of patients with menstrual disorders received risperidone treatment. The receiver operating characteristic curve showed that the optimal cutoff point of serum PRL level associated with the development of menstrual disorders was 60 ng/mL. Based on these results, we concluded that patients with menstrual disorders presented increased serum PRL, and that most of them underwent treatment with risperidone. (Keyword) Adolescent / Adult / Antipsychotic Agents / Female / Humans / Hyperprolactinemia / Menstruation Disturbances / Mental Disorders / Prolactin / Young Adult (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b17-00053 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28966250 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030761013 (DOI: 10.1248/bpb.b17-00053, PubMed: 28966250, Elsevier: Scopus)
84.	Yoshito Zamami, Toru Imai, Masaki Imanishi, Kenshi Takechi, Naoko Shiraishi, Toshihiro Koyama, Hidenori Sagara, Yasukazu Shiino, Toshiaki Sendo and Keisuke Ishizawa : Evaluation of pharmaceutical lifesaving skills training oriented pharmaceutical intervention., Journal of Pharmaceutical Health Care and Sciences, Vol.2, No.1, 21, 2016. (Summary) Our high-performance patient simulator-based lifesaving skills training program not only increased the participants' understanding of the training content but also increased their confidence in their ability to perform pharmaceutical interventions. Therefore, the pharmaceutical lifesaving skills training program we developed will contribute to the education of emergency care pharmacists who can perform pharmaceutical interventions for emergency patients. (Tokushima University Institutional Repository) ● Metadata: 114521 (Link to Publication Site) ● Publication site (DOI): 10.1186/s40780-016-0054-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27606071 ● Search Scopus @ Elsevier (PMID): 27606071 ● Search Scopus @ Elsevier (DOI): 10.1186/s40780-016-0054-7 (Tokushima University Institutional Repository: 114521, DOI: 10.1186/s40780-016-0054-7, PubMed: 27606071)
85.	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)
86.	Naoto Okada, Takeshi Hanafusa, Shinji Abe, Chiemi Sato, Toshimi Nakamura, Kazuhiko Teraoka, Masahiro Abe, Kazuyoshi Kawazoe and Keisuke Ishizawa : Evaluation of the risk factors associated with high-dose chemotherapyinduced dysgeusia in patients undergoing autologous hematopoietic stem cell transplantation: Possible usefulness of cryotherapy in dysgeusia prevention, Supportive Care in Cancer, Vol.24, No.9, 3979-3985, 2016. (Summary) Dysgeusia is one of the sporadic adverse effects induced by chemotherapy, but it remains poorly understood. The aim of this study was to retrospectively identify the risk factors related with dysgeusia in patients undergoing autologous hematopoietic stem cell transplantation (AHSCT). Forty-eight patients with myeloma or lymphoma undergoing AHSCT were enrolled in this study. Data regarding dysgeusia and symptoms were collected by interviews conducted by medical workers. Patient characteristics and unfavorable effects induced by dysgeusia were obtained from medical records and analyzed. Logistic regression analysis was performed to identify the risk factors related with dysgeusia. Of the 48 patients, 20 (42 %) had dysgeusia after AHSCT. The total period of parenteral nutrition (TPN) administration and period of decreased oral intake in the dysgeusia group were statistically longer than those in the non-dysgeusia group. Multivariate analyses revealed that oral mucositis (odds ratio: 30.3; p < 0.01) and the type of chemotherapy prior to AHSCT (odds ratio: 6.56; p < 0.05) were independent risk factors, while oral cryotherapy was the independent suppressive factor of dysgeusia (odds ratio: 0.14; p < 0.05). Our study showed that dysgeusia after AHSCT led to the decrease in oral intake and extended the TPN administration period. Moreover, MEAM or LEED chemotherapy and oral mucositis were independent risk factors for dysgeusia in patients undergoing AHSCT, while oral cryotherapy was an independent suppressive factor for dysgeusia. Therefore, oral cryotherapy should be implemented into the regimen of supportive care management in patients undergoing AHSCT. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00520-016-3244-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27129837 ● Search Scopus @ Elsevier (PMID): 27129837 ● Search Scopus @ Elsevier (DOI): 10.1007/s00520-016-3244-9 (DOI: 10.1007/s00520-016-3244-9, PubMed: 27129837)
87.	Naoto Okada, Shuji Fushitani, Momoyo Azuma, Shingen Nakamura, Toshimi Nakamura, Kazuhiko Teraoka, Hiroyoshi Watanabe, Masahiro Abe, Kazuyoshi Kawazoe and Keisuke Ishizawa : Clinical evaluation of pharmacist interventions in patients treated with anti-methicillin-resistant Staphylococcus aureus agents in a hematological ward, Biological & Pharmaceutical Bulletin, Vol.39, No.2, 295-300, 2015. (Summary) The therapeutic effects of anti-methicillin-resistant Staphylococcus aureus (MRSA) agents, vancomycin (VCM), teicoplanin (TEIC), and arbekacin (ABK), depend on their concentrations in blood. Therefore, therapeutic drug monitoring (TDM) is important when these antibiotics are used. In the hematological ward at Tokushima University Hospital, pharmacists have ordered the measurement of blood VCM, TEIC, and ABK concentrations to promote the use of TDM in accordance with an agreed protocol since 2013. Moreover, the infection control team includes several medical disciplines and has advised on the optimal treatment using VCM, TEIC, and ABK since 2013. This study aimed to investigate the clinical effectiveness of these pharmacist interventions. We retrospectively studied 145 cases in which patients were treated with VCM, TEIC, or ABK between January 2012 and December 2013 in the hematological ward at Tokushima University Hospital. The patients were divided into a control group (71 cases) and an intervention group (74 cases), and their clinical outcomes were compared. The rate of achievement of effective drug concentrations significantly increased in the intervention group (74%), compared to the rate in the control group (55%). Moreover, univariate and multivariate Cox proportional hazard regression revealed that pharmacist intervention and appropriate concentrations of anti-MRSA agents were independent factors associated with reduced hospitalization periods in patients with lymphoma. Our study revealed that proactive pharmacist intervention may improve the therapeutic effect of anti-MRSA agents in hematology ward patients. (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b15-00774 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26830489 ● Search Scopus @ Elsevier (PMID): 26830489 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b15-00774 (DOI: 10.1248/bpb.b15-00774, PubMed: 26830489)
88.	Naoto Okada, Hiroyoshi Watanabe, Shoji Kagami and Keisuke Ishizawa : Ifosfamide and etoposide chemotherapy may interact with warfarin, enhancing the warfarin-induced anticoagulant response, International Journal of Clinical Pharmacology and Therapeutics, Vol.54, No.1, 58-61, 2015. (Summary) To report a case of warfarin-response enhancement during administration of ifosfamide and etoposide chemotherapy. A 15-yearold boy with rhabdomyosarcoma was treated with a regimen of alternating cycles of vincristine, doxorubicin, and cyclophosphamide (VDC) chemotherapy and ifosfamide and etoposide (IE) chemotherapy. During VDC chemotherapy, occlusion of the left middle cerebral artery occurred, and warfarin was started. On day 3 of IE chemotherapy, the patient's international normalized ratio (INR) transiently increased from baseline 2.61 to 5.45. The INR returned to normal within 3 days after warfarin discontinuation. An increase in INR was observed between days 1 and 3 of subsequent cycles of IE chemotherapy but not during VDC chemotherapy. This INR increase was also observed during concomitant use of aprepitant, an inducer of the CYP2C9. There are no reports describing the interaction between warfarin and IE chemotherapy because coadministration of warfarin and IE chemotherapy is unusual. The Drug Interaction Probability Scale score of this interaction was 7, and it is probable that the enhancement of the warfarin response was caused by an interaction with IE chemotherapy. Moreover, in the present case, the enhancement of warfarin response was observed during concomitant use of aprepitant, which has been reported to weaken the warfarin response. Therefore, this interaction may be quite powerful and may increase the risk of warfarin toxicity. A patient who was administered both warfarin and IE chemotherapy experienced a rapid increase in INR, suggesting that INR should be closely monitored in patients receiving warfarin with IE chemotherapy. (Keyword) Adolescent / Anticoagulants / Cytochrome P-450 CYP2C9 Inhibitors / Drug Interactions / Etoposide / Humans / Ifosfamide / International Normalized Ratio / Male / Rhabdomyosarcoma / Warfarin (Link to Publication Site) ● Publication site (DOI): 10.5414/CP202426 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26587904 ● Search Scopus @ Elsevier (PMID): 26587904 ● Search Scopus @ Elsevier (DOI): 10.5414/CP202426 (DOI: 10.5414/CP202426, PubMed: 26587904)
89.	Ken Konaka, Kouta Moriyama, Naoto Okada, Takahiro Nishisako, Masayuki Shono, Kazuyoshi Kawazoe and Keisuke Ishizawa : Ephedra protects vascular endothelium cells from vinorelbine-induced cytotoxicity by preserving endothelial nitric oxide synthase activity, Traditional & Kampo Medicine, Vol.2, No.2, 74-80, 2015. (Link to Publication Site) ● Publication site (DOI): 10.1002/tkm2.1024 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1002/tkm2.1024 (DOI: 10.1002/tkm2.1024)
90.	Takumi Sakurada, Souji Kakiuchi, Soichiro Tajima, Yuya Horinouchi, Ken Konaka, Naoto Okada, Hirotaka Nishisako, Toshimi Nakamura, Kazuhiko Teraoka, Kazuyoshi Kawazoe, Hiroaki Yanagawa, Yasuhiko Nishioka and Keisuke Ishizawa : Pemetrexed-induced rash may be prevented by supplementary corticosteroids, Biological & Pharmaceutical Bulletin, Vol.38, No.11, 1752-1756, 2015. (Summary) Pemetrexed, a chemotherapeutic drug, is highly active in non-small cell lung cancer and malignant pleural mesothelioma. Unfortunately, rashes are more commonly associated with pemetrexed than other chemotherapies, and it is recommended that patients receive corticosteroids (8 mg/d of dexamethasone) for 3 d, including the day of pemetrexed administration (day 1). However, the efficacy of corticosteroids in this context has not been fully verified. In this retrospective study, we evaluated the medical records of 78 patients who received pemetrexed between April 2009 and March 2014, to confirm whether supplementary corticosteroids prevented rash development. The incidence of rash was lower in the 47 patients who received supplementary corticosteroids (after day 1) compared with the incidence among the 31 patients who did not receive supplementary corticosteroids (19.1% vs. 38.7%). The average cutoff dosage of supplementary corticosteroids on day 2 and day 3 was 1.5 mg/d of dexamethasone, as calculated using the receiver operating characteristic curve, and the odds ratio was 0.33 (95% confidence interval: 0.12-0.94). Administration of ≥1.5 mg of corticosteroids on day 2 and day 3 significantly reduced the severity of the rash compared to no supplementary treatment (grades 2/3, 13.3% vs. 33.3%, p<0.05). However, increasing the dose of corticosteroids had no additional effect on rash development. These results suggest that ≥1.5 mg of supplementary dexamethasone on day 2 and day 3 (in addition to day 1) may be necessary for preventing pemetrexed-induced rash, but high doses of dexamethasone (e.g., 8 mg/d) are unnecessary. (Keyword) Adrenal Cortex Hormones / Adult / Aged / Aged, 80 and over / Anti-Inflammatory Agents / Antineoplastic Agents / Area Under Curve / Dexamethasone / Exanthema / Female / Humans / Male / Middle Aged / Neoplasms / Odds Ratio / Pemetrexed / ROC Curve / Retrospective Studies / Severity of Illness Index / Treatment Outcome (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b15-00435 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26521826 ● Summary page in Scopus @ Elsevier: 2-s2.0-84946902360 (DOI: 10.1248/bpb.b15-00435, PubMed: 26521826, Elsevier: Scopus)
91.	Kazuki Maeda, Rumi Katashima, Keisuke Ishizawa and Hiroaki Yanagawa : Japanese Physicians' Views on Drug Post-Marketing Surveillance., Journal of Clinical Medicine Research, Vol.7, No.12, 956-960, 2015. (Summary) Registration trials leading to the approval of drugs are paramount in drug development. After approval, continuous efforts are necessary to ensure proper use of the approved drugs. In Japan, post-marketing surveillance (PMS) by drug companies is conducted in accordance with good post-marketing study practice (GPSP). Although the global standard for pharmacovigilance is incorporated into GPSP, attention has recently been focused on disassociating them. In this study, we examined physicians' views on PMS with the aim of conducting PMS more effectively. We retrospectively reviewed records between 2009 and 2013 from the institutional review board of Tokushima University Hospital, an academic hospital in rural Japan. The annual number of times PMS was performed was then determined. Next, we assessed physicians' attitudes toward drug PMS, including ethical issues, in a cross-sectional study using a questionnaire designed for this study. Five- and two-point scales were used. The questionnaire was distributed in 2014 to 221 physicians listed as investigators in PMS contracts. Of the 221 physicians, 103 (46.6%) responded to the questionnaire. About 50% of the respondents had experience writing PMS reports. Many of the physicians considered PMS to be important but burdensome. Furthermore, from the viewpoint of research ethics, many physicians considered it improper within the present PMS framework to collect and provide data beyond the scope of routine clinical practice without obtaining informed consent in the case of extra blood sampling, provision of images, monitoring and controlled studies. Beyond practical factors such as workload, attention should be given to establishing an ethical infrastructure and globally harmonized system with regard to the Japanese PMS system. Given the limitations of this single-institution study, further research is needed to collect information for developing a suitable infrastructure. (Link to Publication Site) ● Publication site (DOI): 10.14740/jocmr2328w (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26566409 ● Search Scopus @ Elsevier (PMID): 26566409 ● Search Scopus @ Elsevier (DOI): 10.14740/jocmr2328w (DOI: 10.14740/jocmr2328w, PubMed: 26566409)
92.	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)
93.	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)
94.	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)
95.	Takumi Sakurada, Souji Kakiuchi, Soichiro Tajima, Yuya Horinouchi, Naoto Okada, Hirotaka Nishisako, Toshimi Nakamura, Kazuhiko Teraoka, Kazuyoshi Kawazoe, Hiroaki Yanagawa, Yasuhiko Nishioka, Kazuo Minakuchi and Keisuke Ishizawa : Characteristics and risk factors of interstitial lung disease induced by chemotherapy for lung cancer, The Annals of Pharmacotherapy, Vol.49, No.4, 398-404, 2015. (Summary) Drug-induced interstitial lung disease (DILD) is generally a serious adverse effect and almost always necessitates the discontinuation of the offending drug. Cancer pharmacotherapy is strongly associated with DILD, and the risk of DILD has been suggested to be higher in patients with lung cancer because of preexisting pneumonic disease. The aim of this retrospective study was to identify the risk factors and prognostic factors for early death from interstitial lung disease (ILD) induced by chemotherapy for lung cancer. The medical records of 459 patients who underwent chemotherapy for lung cancer between April 2007 and March 2013 were analyzed with regard to patient background and DILD development, initial symptoms, and prognosis. A total of 33 patients (7.2%) developed chemotherapy-induced ILD. The most frequently observed initial symptom was dyspnea (94.3%). Preexisting ILD was identified as a risk factor for DILD (odds ratio [OR] = 5.38; 95% CI = 2.47-11.73; P < 0.01). Among the 33 patients who developed DILD, 10 patients suffered an early death despite steroid therapy. Poor prognostic factors included epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) use (OR = 9.26; 95% CI = 1.05-82.0; P < 0.05) and 2 or more prior chemotherapy regimens (OR = 6.95; 95% CI = 1.14-42.3; P < 0.05). Many lung cancer patients have coexisting ILD, and these patients have a high risk of developing chemotherapy-induced ILD. In addition, patients with DILD who underwent EGFR-TKI therapy and 2 or more prior chemotherapy regimens had a higher risk of fatal outcome. (Keyword) Adult / Aged / Aged, 80 and over / Antineoplastic Agents / Female / Humans / Lung Diseases, Interstitial / Lung Neoplasms / Male / Middle Aged / Odds Ratio / Prognosis / Retrospective Studies / Risk Factors (Link to Publication Site) ● Publication site (DOI): 10.1177/1060028014566446 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25565405 ● Summary page in Scopus @ Elsevier: 2-s2.0-84924872993 (DOI: 10.1177/1060028014566446, PubMed: 25565405, Elsevier: Scopus)
96.	Licht Miyamoto, Yuko Yagi, Aya Hatano, Kazuyoshi Kawazoe, Keisuke Ishizawa, Kazuo Minakuchi, Shuhei Tomita and Koichiro Tsuchiya : Spontaneously hyperactive MEK-Erk pathway mediates paradoxical facilitation of cell proliferation in mild hypoxia, Biochimica et Biophysica Acta (BBA) - General Subjects, Vol.1850, No.4, 640-646, 2015. (Summary) Oxygen is important for common eukaryotic cells to generate ATP. Pathophysiological conditions such as ischemic diseases cause tissue hypoxia. In addition, oxygen availability in deep tissues is supposed to be far lower than surrounding atmosphere even in healthy animals, and the oxygen partial pressures in most normal tissues are estimated to be around 40-50mmHg, so-called mild hypoxia. Recent studies have demonstrated that mild hypoxia has distinct effects on living cells from severe hypoxia. For instance, mild hypoxia was reported to promote cell reprogramming. Although severe hypoxia is known to inhibit cell proliferation, mild hypoxia has been paradoxically demonstrated to increase cell proliferation. However, it has not been clarified by which molecular mechanisms mild hypoxia evokes the discontinuous increment of cell proliferation. We established experimental conditions showing the opposite influences of mild and severe hypoxia on cell proliferation using undifferentiated Caco2 human colon carcinoma cells in order to clarify the underlying molecular mechanism. The basal activity of Erk, which is a typical mediator of mitogenic signals, is spontaneously increased specifically in cells exposed to mild hypoxia, and inhibition of MEK, an upstream kinase of the Erk, completely inhibited the mild hypoxia-induced enhancement of cell proliferation. Spontaneous hyperactivation of the MEK-Erk pathway by mild hypoxia should be the plausible molecular mechanism of the paradoxical promotion of cell proliferation. Our findings will provide clues to the molecular basis of mild hypoxia-evoked phenomena such as cell reprogramming. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbagen.2014.12.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25497211 ● Summary page in Scopus @ Elsevier: 2-s2.0-84921044624 (DOI: 10.1016/j.bbagen.2014.12.006, PubMed: 25497211, Elsevier: Scopus)
97.	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)
98.	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)
99.	Yuko Imamura, Shuhei Tomita, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : HIF-2α/ARNT complex regulates hair development via induction of p21Waf1/Cip1 and p27Kip1, The FASEB journal, Vol.28, No.6, 2517-2524, 2014. (Summary) The hypoxia-inducible factors HIF-1α or HIF-2α form heterodimeric complexes with the aryl hydrocarbon receptor nuclear translocator (ARNT). HIF-1α/ARNT and HIF-2α/ARNT complexes activate hypoxia-inducible genes that play critical roles in angiogenesis, anaerobic metabolism, and other processes in response to O2 deprivation. HIF-2α is known to regulate the function and/or differentiation of stem cells by activating the POU domain transcription factor Oct4; however, the precise underlying mechanism is unknown. This study examined the role of HIF-2α/ARNT in hair development using conditional-knockout mice, in which Arnt was specifically deleted in keratinocytes. In wild-type mice, HIF-2α and ARNT were highly expressed in the precortex above the hair matrix, an area containing differentiating stem cells. An analysis of hair size and type in these mice showed that loss of ARNT decreased the production of zigzag hairs, corresponding to reduced expression of HIF-2α and induction of the mammalian cyclin-dependent kinase inhibitors p21(Waf1/Cip1) and p27 (Kip1). The results suggest that the HIF-2α/ARNT complex regulates hair follicle differentiation via induction of p21(Waf1/Cip1) and possibly p27(Kip1), as p27(Kip1) expression was not altered in ARNT knockout mice. The findings provide insight into a possible mechanism underlying hair growth disorders and can be useful for future studies on hair follicle response to insults, such as chemotherapy and ionizing radiation.-Imamura, Y., Tomita, S., Imanishi, M., Kihira, Y., Ikeda, Y., Ishizawa, K., Tsuchiya, K., Tamaki, T. HIF-2α/ARNT complex regulates hair development via induction of p21(Waf1/Cip1) and p27(Kip1). (Keyword) Animals / Aryl Hydrocarbon Receptor Nuclear Translocator / Basic Helix-Loop-Helix Transcription Factors / cell differentiation / Cells, Cultured / Cyclin-Dependent Kinase Inhibitor p21 / Cyclin-Dependent Kinase Inhibitor p27 / Hair / Hair Follicle / Hypoxia-Inducible Factor 1, alpha Subunit / Keratinocytes / Mice / knockout mice (Link to Publication Site) ● Publication site (DOI): 10.1096/fj.13-244079 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24599965 ● Summary page in Scopus @ Elsevier: 2-s2.0-84901845393 (DOI: 10.1096/fj.13-244079, PubMed: 24599965, Elsevier: Scopus)
100.	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)
101.	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)
102.	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)
103.	Licht Miyamoto, Masashi Watanabe, Chiaki Taoka, Mai Kono, Yosuke Tomida, Tsuyoshi Matsushita, Masaki Kamiya, Hatsuhiko Hattori, Keisuke Ishizawa, Shinji Abe, Hisao Nemoto and Koichiro Tsuchiya : A novel prodrug strategy for extremely hydrophobic agents; - Conjugation to symmetrically branched glycerol trimer improves pharmacological and pharmacokinetic properties of fenofibrate, Molecular Pharmaceutics, Vol.10, No.7, 2723-2729, 2013. (Summary) Management of a lipophilic-hydrophilic balance is a key element in drug design to achieve desirable pharmacokinetic characters. Therefore we have created unique modular molecules, symmetrically branched oligoglycerols (BGL), as an alternative way to endow hydrophobic molecules with sufficient hydrophilicity. We have successfully demonstrated amelioration of the water solubility and thermal stability of several hydrophobic agents by covalent conjugation to BGL so far. However, it has not been clarified whether the molecular modification by BGL also improves the pharmacological and/or pharmacokinetic properties indeed. Recently, we synthesized a novel BGL-prodrug derivative of fenofibrate, which is an antihyperlipidemic agent and one of the most hydrophobic medicinal compounds currently used clinically, by conjugating fenofibric acid to symmetrically branched glycerol trimer (BGL003), the simplest BGL. We have previously demonstrated that the hydrophilicity and water solubility of fenofibrate are improved more than 2000 times just by conjugation to the BGL003. To verify our hypothesis that the prodrug strategy with BGL should improve pharmacological efficacy and pharmacokinetic properties of extremely hydrophobic agents such as fenofibrate by the rise in hydrophilicity, we evaluated the BGL003-prodrug derivative of fenofibrate (FF-BGL) using rodent models. Here we demonstrate that the lipid-lowering effects of fenofibrate are much potentiated by chemical conjugation to BGL003 without exhibiting significant toxicity. Plasma concentration of fenofibric acid, an active metabolite of fenofibrate, after single oral administration of FF-BGL was more than 3 times higher than that of fenofibrate, in accordance. In fasting rats, plasma concentration of fenofibric acid after fenofibrate administration was curtailed into less than half of that in ad libitum-fed rats, while FF-BGL showed about the same plasma level even in the starving rats. This is the first report showing that BGL-prodrug improves pharmacological and pharmacokinetic properties as well as hydrophilicity of highly hydrophobic compounds. Furthermore, prodrug strategy using BGL suggests the possibility of diminishing the food-drug interaction effects, which should be advantageous for promoting drug compliance. BGL will be a suitable prodrug strategy to ameliorate physical, pharmacological, and pharmacokinetic characteristics of extremely hydrophobic compounds. (Link to Publication Site) ● Publication site (DOI): 10.1021/mp400133j (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23672178 ● Search Scopus @ Elsevier (PMID): 23672178 ● Search Scopus @ Elsevier (DOI): 10.1021/mp400133j (DOI: 10.1021/mp400133j, PubMed: 23672178)
104.	Yoshinori Iba, Koushi Watanabe, Kiyokazu Ozaki, Osamu Aozasa, Keisuke Ishizawa, Tetsuro Matsuura, Hiroshi Oyama and Tohru Masukawa : Altered gene expression profiles associated with enhanced skin inflammation induced by 12-O-tetradecanoylphorbol-13-acetate in streptozotocin-diabetic mice, International Immunopharmacology, Vol.15, No.3, 614-619, 2013. (Summary) To examine the mechanisms of diabetes-enhanced inflammation, ear inflammation was induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in streptozotocin (STZ)-injected diabetic and control mice. The inflammatory response was determined from ear thickness and histology. The mRNA expression of several inflammation-related genes 8, 24 and 32h after TPA treatment was determined by quantitative real-time RT-PCR. Ear thickness did not differ between the two groups at 8h, but was greater in the diabetic mice than control mice at 24 and 32h (late phase). STZ-diabetic conditions variously affected TPA-induced gene expression. The changes 8h after TPA treatment probably reflected transcriptional regulation, and the genes were divided into three groups, up-regulated (IL-6, MCP-1, HO-1 and SOCS3), unregulated (IL-1beta, TNF-alpha and IL-10) and down-regulated (RANTES) genes. TPA-induced gene expression of cytokines, except for RANTES, peaked at 8h and significantly declined in the late phase in control mice, while the expression of IL-1beta and TNF-alpha did not decline in the late phase in the diabetic mice. This result indicated the destabilization process for these mRNA, a type of post-transcriptional regulation, to be impaired under STZ-induced diabetic conditions; however, TPA-induced gene and protein expression of TTP, an RNA-binding protein involved in mRNA decay, were adversely enhanced in the diabetic mice. These findings suggested that STZ-induced diabetes affected the transcriptional and post-transcriptional control of TPA-induced inflammation, and greater mRNA levels of IL-1beta and TNF-alpha in the late phase were probably responsible for the diabetes-enhanced inflammation. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.intimp.2013.01.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23339930 ● Search Scopus @ Elsevier (PMID): 23339930 ● Search Scopus @ Elsevier (DOI): 10.1016/j.intimp.2013.01.007 (DOI: 10.1016/j.intimp.2013.01.007, PubMed: 23339930)
105.	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)
106.	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)
107.	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)
108.	Licht Miyamoto, Masashi Watanabe, Yosuke Tomida, Mai Kono, Shoko Fujii, Tsuyoshi Matsushita, Hatsuhiko Hattori, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : Acute oral toxicity evaluation of symmetrically branched glycerol trimer in ddY mice, The Journal of Toxicological Sciences, Vol.37, No.6, 1253-1259, 2012. (Summary) Lipophilic-hydrophilic balance is a quite important determinant of pharmacokinetic properties of pharmaceuticals. Thus it is a key step to successfully manage lipophilic-hydrophilic balance in drug design. We have designed unique modular molecules, symmetrically branched oligoglycerols (BGL) as an alternative means to endow hydrophobic molecules with much hydrophilicity. We have succeeded in improving the water-solubility of several hydrophobic medicinal small molecules and thermal stability of artificial protein by covalent conjugation to BGL. We have also demonstrated that a representative BGL, symmetrically branched glycerol trimer (BGL003) does not exhibit significant cytotoxicity against human hepatocarcinoma HepG2 cells. However, there have been no reports suggesting whether BGL could be used in safety in vivo. Therefore, evaluation of acute oral toxicity of BGL003 in healthy mice was conducted. Here we demonstrate that an oral administration of BGL003 did not exhibit acute lethal toxicity up to 3,000 mg/kg. Body weight, food intake, blood glucose levels and weights of tissues were not affected by a short-term repetitive administration of increasing doses of BGL003. Biochemical indications related to hepatic disorders and tissue damage were unchanged, either. A single administration study revealed that 50% lethal dose of BGL003 should be more than 2,000 mg/kg. BGL003 will be safe and suitable approach to improve hydrophilicity of hydrophobic compounds. (Keyword) Hydrophilicity / Lipophilicity / Branched oligoglycerols / Acute oral toxicity / Mice (Link to Publication Site) ● Publication site (DOI): 10.2131/jts.37.1253 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23208440 ● CiNii @ National Institute of Informatics (CRID): 1390282679880737408 ● Search Scopus @ Elsevier (PMID): 23208440 ● Search Scopus @ Elsevier (DOI): 10.2131/jts.37.1253 (DOI: 10.2131/jts.37.1253, PubMed: 23208440, CiNii: 1390282679880737408)
109.	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)
110.	Licht Miyamoto, Masashi Watanabe, Mai Kono, Tsuyoshi Matsushita, Hatsuhiko Hattori, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : Cytotoxicity evaluation of symmetrically branched glycerol trimer in human hepatocellular carcinoma HepG2 cells, The Journal of Toxicological Sciences, Vol.37, No.5, 1059-1063, 2012. (Keyword) Hydrophilicity / Lipophilicity / Cytotoxicity / Branched oligoglycerols / HepG2 / Fenofibrate (Link to Publication Site) ● Publication site (DOI): 10.2131/jts.37.1059 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23038013 ● CiNii @ National Institute of Informatics (CRID): 1390282679882410752 ● Search Scopus @ Elsevier (PMID): 23038013 ● Search Scopus @ Elsevier (DOI): 10.2131/jts.37.1059 (DOI: 10.2131/jts.37.1059, PubMed: 23038013, CiNii: 1390282679882410752)
111.	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)
112.	Hisao Nemoto, Masaki Kamiya, Aki Nakamoto, Tsuyoshi Matsushita, Kosuke Matsumura, Hatsuhiko Hattori, Tomoyuki Kawamura, Chiaki Taoka, Shinji Abe, Keisuke Ishizawa, Licht Miyamoto and Koichiro Tsuchiya : Synthesis of highly water-soluble fibrate derivatives via BGLation, Bioorganic & Medicinal Chemistry Letters, Vol.22, No.20, 6425-6428, 2012. (Summary) Three water-soluble fibrates (fenofibrate, bezafibrate and chlofibrate) conjugated with a symmetrically branched glyceryl trimer (BGL003) were synthesized, and an evaluation of the fenofibrate-BGL003 conjugate as a candidate for anti-hyperlipemia drug was carried out using rats. The water-solubility of the fenofibrate-BGL003 conjugate was several thousand times greater than that of the original fenofibrate. The lipid-lowering effects of the fenofibrate-BGL003 conjugate were as strong as those of the same grams of fenofibrate. The actual active species of fenofibrate, fenofibric acid, was detected in rats' blood, but neither the fenofibrate-BGL003 conjugate nor fenofibrate was detected, probably due to enzymatic hydrolysis of the ester bond. The plasma concentration of fenofibric acid derived from the fenofibrate-BGL003 conjugate was five times higher than that derived from fenofibrate 4h after administration. (Keyword) Animals / Bezafibrate / Clofibrate / Fenofibrate / Hypolipidemic Agents / Male / Rats / Rats, Sprague-Dawley / Solubility / Triglycerides / Water (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bmcl.2012.08.057 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22975299 ● Search Scopus @ Elsevier (PMID): 22975299 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bmcl.2012.08.057 (DOI: 10.1016/j.bmcl.2012.08.057, PubMed: 22975299)
113.	Hisao Nemoto, Ayato Katagiri, Masaki Kamiya, Tomoyuki Kawamura, Tsuyoshi Matsushita, Kosuke Matsumura, Tomohiro Itou, Hatsuhiko Hattori, Miho Tamaki, Keisuke Ishizawa, Licht Miyamoto, Shinji Abe and Koichiro Tsuchiya : Synthesis of paclitaxel-BGL conjugates, Bioorganic & Medicinal Chemistry, Vol.20, No.18, 5559-5567, 2012. (Summary) Four kinds of symmetrically branched oligoglyceryl trimeric (BGL003)-paclitaxel conjugates and a corresponding heptameric (BGL007) conjugate were synthesized. Molecular weights of all the compounds were less than two times that of paclitaxel. The anti-tumor activity of the most water-soluble BGL003 conjugate was examined and found to be preserved in spite of the chemical modification that is displacement of the N3'-debenzoyl residue with the BGL003 succinyl residue. (Keyword) Animals / Antineoplastic Agents, Phytogenic / Cell Line, Tumor / Dose-Response Relationship, Drug / Glycerol / Humans / Male / Mice / Mice, Inbred BALB C / Mice, Nude / Molecular Conformation / Molecular Weight / Neoplasms, Experimental / Paclitaxel / Solubility / Structure-Activity Relationship / Xenograft Model Antitumor Assays (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bmc.2012.07.031 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22892212 ● Search Scopus @ Elsevier (PMID): 22892212 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bmc.2012.07.031 (DOI: 10.1016/j.bmc.2012.07.031, PubMed: 22892212)
114.	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)
115.	Akira Shigenaga, Keiji Ogura, Hiroko Hirakawa, Jun Yamamoto, Koji Ebisuno, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Akira Otaka : Development of a reduction-responsive amino acid that induces peptide bond cleavage in hypoxic cells, ChemBioChem, Vol.13, 968-971, 2012. (Summary) Hypoxia-responsive amino acids are indispensable in the preparation of hypoxic tumor-specific peptidyl prodrugs. In this paper, the design and synthesis of a reduction-responsive amino acid that induces peptide bond cleavage after reduction of the nitro group are described. Application to hypoxia-responsive peptide bond cleavage system is also reported. (Keyword) Amides / Amino Acids / Cell Hypoxia / Fluorescence Resonance Energy Transfer / Molecular Structure / Oxidation-Reduction / Peptides / Prodrugs (Tokushima University Institutional Repository) ● Metadata: 111913 (Link to Publication Site) ● Publication site (DOI): 10.1002/cbic.201200141 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22505188 ● Search Scopus @ Elsevier (PMID): 22505188 ● Search Scopus @ Elsevier (DOI): 10.1002/cbic.201200141 (Tokushima University Institutional Repository: 111913, DOI: 10.1002/cbic.201200141, PubMed: 22505188)
116.	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)
117.	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)
118.	Shuhei Tomita, Yoshitaka Kihira, Masaki Imanishi, Yayoi Fukuhara, Yuko Imamura, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Pathophysiological Response to Hypoxia From the Molecular Mechanisms of Malady to Drug Discovery: Inflammatory Responses of Hypoxia-Inducible Factor 1 (HIF-1) in T Cells Observed in Development of Vascular Remodeling, Journal of Pharmacological Sciences, Vol.115, No.4, 433-439, 2011. (Summary) Recent studies have shown that the cellular immune response to the hypoxic microenvironment constructed by vascular remodeling development modulates the resulting pathologic alterations. A major mechanism mediating adaptive responses to reduced oxygen availability is the regulation of transcription by hypoxia-inducible factor 1 (HIF-1). Impairment of HIF-1-dependent inflammatory responses in T cells causes an augmented vascular remodeling induced by arterial injury, which is shown as prominent neointimal hyperplasia and increase in infiltration of inflammatory cells at the adventitia in mice lacking Hif-1α specifically in T cells. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice have shown enhanced production of cytokines in activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. This minireview shows that HIF-1α in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of the T cell-mediated immune response and suggests potential new therapeutic strategies that target HIF-1α. (Keyword) Animals / Anoxia / Drug Discovery / Humans / Hypoxia-Inducible Factor 1, alpha Subunit / Immunity, Cellular / Reperfusion Injury / T lymphocytes / Vasculitis (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.10R22FM (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21422726 ● Summary page in Scopus @ Elsevier: 2-s2.0-79955046642 (DOI: 10.1254/jphs.10R22FM, PubMed: 21422726, Elsevier: Scopus)
119.	Keisuke Ishizawa, Masanori Yoshizumi, Yoshichika Kawai, Junji Terao, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Pharmacology in health food: Metabolism of quercetin in vivo and its protective effect against arteriosclerosis, Journal of Pharmacological Sciences, Vol.115, No.4, 466-470, 2011. (Summary) Quercetin, a member of the bioflavonoids family, has been proposed to have anti-atherogenic, anti-inflammatory, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. It was recently demonstrated that quercetin 3-O-β-D-glucuronide (Q3GA) is one of the major quercetin conjugates in human plasma, in which the aglycone could not be detected. Although most of the in vitro pharmacological studies have been carried out using only the quercetin aglycone form, experiments using Q3GA would be important to discover the preventive mechanisms of cardiovascular diseases by quercetin in vivo. Therefore we examined the effects of the chemically synthesized Q3GA, as an in vivo form, on vascular smooth muscle cell (VSMC) disorders related to the progression of arteriosclerosis. Platelet-derived growth factor-induced cell migration and proliferation were inhibited by Q3GA in VSMCs. Q3GA attenuated angiotensin II-induced VSMC hypertrophy via its inhibitory effect on JNK and the AP-1 signaling pathway. Q3GA scavenged 1,1-diphenyl-2-picrylhydrazyl radical measured by the electron paramagnetic resonance method. In addition, immunohistochemical studies with monoclonal antibody 14A2 targeting the Q3GA demonstrated that the positive staining specifically accumulates in human atherosclerotic lesions, but not in the normal aorta. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may have preventative effects on arteriosclerosis relevant to VSMC disorders. (Keyword) Animals / Antioxidants / Arteriosclerosis / Cell Movement / Cell Proliferation / Drug Evaluation, Preclinical / Free Radicals / Health Food / Humans / Hypertrophy / Muscle, Smooth, Vascular / Quercetin / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.10R38FM (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21436601 ● Search Scopus @ Elsevier (PMID): 21436601 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.10R38FM (DOI: 10.1254/jphs.10R38FM, PubMed: 21436601)
120.	Yuya Horinouchi, Koichiro Tsuchiya, Chiaki Taoka, Soichiro Tajima, Yoshitaka Kihira, Yuko Matsuda, Kozo Shishido, Masahiro Yoshida, Shuichi Hamano, Kazuyoshi Kawazoe, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita and Toshiaki Tamaki : Antioxidant effects of photodegradation product of nifedipine, Chemical & Pharmaceutical Bulletin, Vol.59, No.2, 208-214, 2011. (Summary) Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nifedipine is unstable under light and reportedly decomposes to a stable nitrosonifedipine (NO-NIF). NO-NIF has no antihypertensive effect, and it has been recognized as a contaminant of nifedipine. The present study for the first time demonstrated that NO-NIF changed to a NO-NIF radical in a time-dependent manner when it interacted with human umbilical vein endothelial cells (HUVECs). The electron paramagnetic resonance (EPR) signal of NO-NIF radicals in HUVECs showed an asymmetric pattern suggesting that the radicals were located in the membrane. The NO-NIF radicals had radical scavenging activity for 1,1-diphenyl-2-picrylhydrazyl, whereas neither NO-NIF nor nifedipine did. In addition, the NO-NIF radical more effectively quenched lipid peroxides than NO-NIF or nifedipine. Furthermore, NO-NIF attenuated the superoxide-derived free radicals in HUVECs stimulated with LY83583, and suppressed iron-nitrilotriacetic acid (Fe-NTA)-induced cytotoxicity in rat pheochromocytoma (PC12) cells. Our findings suggest that NO-NIF is a candidate for a new class of antioxidative drugs that protect cells against oxidative stress. (Keyword) Animals / Antioxidants / Cells, Cultured / Endothelial Cells / Humans / Nifedipine / PC12 Cells / Photolysis / Rats (Link to Publication Site) ● Publication site (DOI): 10.1248/cpb.59.208 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21297301 ● Summary page in Scopus @ Elsevier: 2-s2.0-79551489998 (DOI: 10.1248/cpb.59.208, PubMed: 21297301, Elsevier: Scopus)
121.	Yayoi Fukuhara, Koichiro Tsuchiya, Yuya Horinouchi, Soichiro Tajima, Yoshitaka Kihira, Shuichi Hamano, Kazuyoshi Kawazoe, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita and Toshiaki Tamaki : Protective effect of photodegradation product of nifedipine against tumor necrosis factor alpha-induced oxidative stress in human glomerular endothelial cells, The Journal of Medical Investigation : JMI, Vol.58, No.1, 2, 118-126, 2011. (Summary) Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nitrosonifedipine (NO-NIF) is metabolically and photochemically produced from nifedipine, and NO-NIF has been recognized as a contaminant of nifedipine because it has no antihypertensive effect. Treatment of tumor necrosis factor-α (TNF-α) suppressed the cell viability and facilitated the expression of Inter-Cellular Adhesion Molecule 1(ICAM-1) in human glomerular endothelial cells (HGECs) though, pretreatment of NO-NIF significantly recovered the TNF-α-induced cell damage to the same extent as Trolox-C did, and suppressed the ICAM-1 expression in a concentration dependent manner. In addition, NO-NIF inhibited the cell toxicity induced by cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, as effective as Trolox-c. These data suggest that NO-NIF is a candidate for a new class of antioxidative drug that protect cells against oxidative stress in glomerular endothelial cells. (Keyword) Antioxidants / Benzene Derivatives / Cell Survival / Cells, Cultured / Endothelial Cells / Humans / Intercellular Adhesion Molecule-1 / Kidney Glomerulus / Nifedipine / Nitroso Compounds / oxidative stress / Tumor Necrosis Factor-alpha (Tokushima University Institutional Repository) ● Metadata: 72667 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.58.118 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21372496 ● CiNii @ National Institute of Informatics (CRID): 1390001204242892288 ● Search Scopus @ Elsevier (PMID): 21372496 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.58.118 (Tokushima University Institutional Repository: 72667, DOI: 10.2152/jmi.58.118, PubMed: 21372496, CiNii: 1390001204242892288)
122.	Yasumasa Ikeda, Soichiro Tajima, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine promotes angiogenesis via the activation of vascular endothelial cell function., Atherosclerosis, Vol.215, No.2, 339-347, 2011. (Summary) BACKGROUND: Deferoxamine (DFO), an iron chelator for disorders of excess iron, upregulates the expression of angiogenic factors, such as vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2), indicating that it affects angiogenesis. Herein, we clarify the effect and mechanism of action of DFO on angiogenesis. METHODS AND RESULTS: In an in vitro study, DFO increased endothelial nitric oxide synthesis (eNOS) phosphorylation in human aortic endothelial cells (HAECs), which were inhibited by the phosphatidylinositol 3-kinase inhibitor LY294002. Tube formation, cell proliferation, and cell migration in HAECs were promoted by DFO, which were significantly reduced by LY294002. In an in vivo study, DFO promoted blood flow recovery in response to the hindlimb ischemia in mice with unilateral hindlimb surgery. The density of capillaries and arterioles in ischemic muscle was higher in DFO-treated mice compared to vehicle-treated mice. Endothelial cell proliferation increased and oxidative stress and apoptosis decreased in ischemic muscles of DFO-treated mice. The phosphorylation of Akt and eNOS on the ischemic side was elevated and urinary nitric oxide/nitric dioxide (NOx) excretion was higher in DFO-treated mice compared to vehicle-treated mice. The effect of DFO on angiogenesis was abolished in eNOS-deficient mice with hindlimb ischemia. CONCLUSION: These findings indicate that DFO promotes revascularization via the activation of vascular endothelial cell function by an Akt-eNOS-dependent mechanism. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2011.01.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21315355 ● Search Scopus @ Elsevier (PMID): 21315355 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2011.01.009 (DOI: 10.1016/j.atherosclerosis.2011.01.009, PubMed: 21315355)
123.	Soichiro Tajima, Koichiro Tsuchiya, Yuya Horinouchi, Keisuke Ishizawa, Yasumasa Ikeda, Yoshitaka Kihira, Masayuki Shono, Kazuyoshi Kawazoe, Shuhei Tomita and Toshiaki Tamaki : Effect of angiotensin II on iron-transporting protein expression and subsequent intracellular labile iron concentration in human glomerular endothelial cells, Hypertension Research, Vol.33, No.7, 713-721, 2010. (Summary) Angiotensin II (Ang II)-induced endothelial injury, which is associated with atherosclerosis, is believed to be mediated by intracellular reactive oxygen species (ROS) through stimulation of nicotinamide adenine dinucleotide phosphate oxidase (NOX). Iron is essential for the amplification of oxidative stress. In this study, we investigated whether Ang II altered iron metabolism and whether the Ang II-induced endothelial injury is attributable to changes in iron metabolism of human glomerular endothelial cells (HGECs). When 90% iron-saturated human transferrin (90% Tf) was applied to HGECs without Ang II, the labile ferrous iron level was same as the effect of control in spite of a significant increase in the total cellular iron concentration. Treatment with Ang II and 30% Tf or 90% Tf significantly (P<0.01) increased the intracellular iron concentration, as well as labile ferrous iron and protein oxidation levels, compared with the effect of separate administration of each compound. Ang II treatment facilitated the protein expression of the Tf receptor, divalent metal transporter 1, and ferroportin 1 in a dose- and time-dependent manner. It was also found that simultaneous exposure of HGECs to Ang II and 90% Tf accelerated hydroxyl radical production, as shown by using an electron paramagnetic resonance spectrometer. These results suggest that Ang II not only induces production of ROS by NOX activation but also iron incorporation followed by an increase in labile iron in HGECs. Both of these events may participate in the progression of oxidative stress because of endothelial cell dysfunction through ferrous iron-mediated ROS generation. (Keyword) Angiotensin II / Cation Transport Proteins / Endothelial Cells / Humans / Hydroxyl Radical / Iron / Kidney Glomerulus / oxidation and reduction / Receptors, Transferrin / Transferrin (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2010.63 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20431588 ● Summary page in Scopus @ Elsevier: 2-s2.0-77954369377 (DOI: 10.1038/hr.2010.63, PubMed: 20431588, Elsevier: Scopus)
124.	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)
125.	Koichiro Tsuchiya, Shuhei Tomita, Keisuke Ishizawa, Shinji Abe, Yasumasa Ikeda, Yoshitaka Kihira and Toshiaki Tamaki : Dietary nitrite ameliorates renal injury in l-NAME-induced hypertensive rats, Nitric Oxide: Biology and Chemistry, Vol.22, No.2, 98-103, 2010. (Summary) Nitric oxide (NO) has numerous important functions in the kidney, and long-term blockage of nitric oxide synthases in rats by L-NAME results in severe hypertension and progressive kidney damage. On the other hand, NO production seems to be low in patients with chronic kidney disease (CKD), and NO deficiency may play a role in CKD progression. In this review, we summarized the mechanisms of amelioration of renal injury induced by L-NAME treated rats by treatment of nitrite. First, we demonstrate whether orally-administrated nitrite-derived NO can shift to the circulation. When 3mg/kg body weight Na(15)NO(2) was orally administered to rats, an apparent EPR signal derived from Hb(15)NO (A(z)=23.4 gauss) appeared in the blood, indicating that orally ingested nitrite can be a source of NO in vivo. Next, in order to clarify the capacity of nitrite to prevent renal disease, we administered low-dose nitrite (LDN: 0.1mg of sodium nitrite in 1L of drinking water), medium-dose nitrite (MDN: 1mg sodium nitrite/L, which corresponds to the amount of nitrite ingested by vegetarians), or high-dose nitrite (HDN: 10mg sodium nitrite/L) to rats simultaneously with L-NAME (1 g l-NAME/L) for 8 weeks, then examined the blood NO level as a hemoglobin-NO adduct (iron-nitrosyl-hemoglobin) using electron paramagnetic resonance spectroscopy, urinary protein excretion, and renal histological changes at the end of the experiment. It was found that oral administration of MDN and HDN but not LDN increased the blood iron-nitrosyl-hemoglobin concentration to the normal level, ameliorated the L-NAME-induced proteinuria, and reduced renal histological damage. The findings demonstrate that chronic administration of a mid-level dietary dose of nitrite restores the circulating iron-nitrosyl-hemoglobin levels reduced by L-NAME and that maintenance of the circulating iron-nitrosyl-hemoglobin level in a controlled range protects against L-NAME-induced renal injury. Taking these findings together, we propose that dietary supplementation of nitrite is a potentially useful nonpharmacological strategy for maintaining circulating NO level in order to prevent or slow the progression of renal disease. It had been believed that nitrite could result in intragastric formation of nitrosamines, which had been linked to esophageal and other gastrointestinal cancers. However, there is no positive association between the intake of nitrate or nitrite and gastric and pancreatic cancer by recent researches. Furthermore, nitrate-derived NO formation pathway is a possible mechanism for the hypotensive effect of vegetable- and fruit-rich diets, which may explain, at least in part, the mechanism of the Dietary Approach to Stop Hypertension (DASH) diet-induced hypotensive and organ-protective effects. Further research is needed to investigate the interaction between nitrite-nitrate intakes and human health. (Keyword) Animals / Diet / Hypertension / Kidney Diseases / NG-Nitroarginine Methyl Ester / Rats / Sodium Nitrite (Link to Publication Site) ● Publication site (DOI): 10.1016/j.niox.2009.12.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20005970 ● Search Scopus @ Elsevier (PMID): 20005970 ● Search Scopus @ Elsevier (DOI): 10.1016/j.niox.2009.12.002 (DOI: 10.1016/j.niox.2009.12.002, PubMed: 20005970)
126.	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)
127.	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)
128.	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)
129.	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)
130.	Keisuke Ishizawa, Kunihisa Yamaguchi, Yuya Horinouchi, Yayoi Fukuhara, Soichiro Tajima, Shuichi Hamano, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Toward drug discovery for overcoming CKD: Development of drugs on endothelial cell protection for overcoming CKD, Journal of Pharmacological Sciences, Vol.109, No.1, 14-19, 2009. (Summary) Chronic kidney disease (CKD) is becoming a major public health problem worldwide. It is important to protect endothelial function in CKD treatment because injury of the endothelium is a critical event for the generation and progression of CKD. Recently, clinical studies showed that nifedipine, an antihypertensive drug, acts as a protective agent of endothelial cells (ECs). Nifedipine is reported to partially decompose to a nitrosonifedipine that has high reactivity against lipid-derived radicals in vitro. However, it is still unclear whether nitrosonifedipine is a biologically active agent against endothelial injury. We observed that nitrosonifedipine was converted to radical form by reaction with cultured ECs. The cumene hydroperoxide mediated cytotoxity was reduced by nitrosonifedipine in cultured human glomerular ECs (HGECs). Also nitrosonifedipine suppressed the expression of TNF-alpha-induced intercellular cell adhesion molecule-1 in HGECs. Chronic administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) caused systemic arterial hypertension, endothelial injury, and renal dysfunction. In L-NAME-induced hypertensive rats, nitrosonifedipine treatment improved not only the acetylcholine-induced vasodilation of the aortic rings, but also renal dysfunction such as increasing the levels of serum creatinine and urinary protein excretion. Our preliminary data suggest that nitrosonifedipine is a new and useful drug for the treatment of CKD involving ameliorating effects on EC disorder. (Keyword) Animals / Cells, Cultured / Drug Discovery / Endothelial Cells / Humans / Kidney Failure, Chronic / Molecular Structure / Nifedipine / Nitroso Compounds / Vasodilator Agents (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.08R08FM (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19151535 ● Search Scopus @ Elsevier (PMID): 19151535 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.08R08FM (DOI: 10.1254/jphs.08R08FM, PubMed: 19151535)
131.	Hideki Ohnishi, Satoshi Iwanaga, Kazuyoshi Kawazoe, Keisuke Ishizawa, Sakiko Orino, Shuhei Tomita, Koichiro Tsuchiya, Yasuhisa Kanematsu, Nagakatsu Harada, Kazuhiro Mori, Tomoko Tsuchihashi, Yasuko Ishikawa and Toshiaki Tamaki : Effect of iron-quercetin complex on reduction of nitrite in in vitro and in vivo systems, Journal of Agricultural and Food Chemistry, Vol.56, No.21, 10092-10098, 2008. (Summary) This study investigated whether reducing agents such as quercetin and iron(II) facilitate formation of nitric oxide (NO) gas from orally ingested nitrite in an vivo study. When 3 mg/kg Na (15)NO2 was orally administered to rats with or without iron(II) or quercetin, Hb (15)NO, which is indicative of systemic (15)NO, was detected in the blood, with the maximum blood concentration of Hb (15)NO at 15 min after nitrite or nitrite plus quercetin treatment, whereas after administration of nitrite plus iron(II) or nitrite plus iron(II) and quercetin, the time was shortened to 10 min. Interestingly, iron(II), quercetin, or iron(II) plus quercetin did not affect the total amount of Hb (15)NO generated from orally administered Na (15)NO2. However, the systemic nitrite concentration was significantly decreased in the presence of iron(II) or iron(II) plus quercetin. These results may indicate that iron(II) is critical to the generation of NO gas from nitrite, whereas quercetin contributed little under the in vivo experimental conditions. (Keyword) Animals / Antioxidants / Iron / Male / Nitrates / Nitric Oxide / Nitrites / Oxidation-Reduction / Quercetin / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1021/jf801010j (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18831560 ● Search Scopus @ Elsevier (PMID): 18831560 ● Search Scopus @ Elsevier (DOI): 10.1021/jf801010j (DOI: 10.1021/jf801010j, PubMed: 18831560)
132.	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)
133.	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)
134.	Ali Nermin, Masanori Yoshizumi, Seiji Yano, Saburo Sone, Hideki Ohnishi, Keisuke Ishizawa, Yasuhisa Kanematsu, Koichiro Tsuchiya and Toshiaki Tamaki : The novel Src kinase inhibitor M475271 inhibits VEGF-induced vascular endothelial-cadherin and β-catenin phosphorylation but increases their association, Journal of Pharmacological Sciences, Vol.102, No.1, 112-120, 2006. (Summary) M475271, 4-quinazolinamine, N-(2-chloro-5-methoxyphenyl)-6-methoxy-7-[(1-methyl-4-piperidinyl) methoxy]-(9Cl), is a new anilinoquinazoline derivative that displays selective inhibition of Src kinase activity and tumor growth in vivo. Vascular endothelial growth factor (VEGF)-induced angiogenesis plays a pivotal role in tumor growth and metastasis. Vascular endothelial (VE)-cadherin is an endothelial cell-specific adhesion molecule that can interact with the cytoskeleton via several anchoring molecules such as beta-catenin. Here, we examined the effect of M475271 on VE-cadherin and beta-catenin phosphorylation and association. We also examined its effect on VEGF-induced human umbilical vein endothelial cell (HUVEC) proliferation, migration, and tube formation. The findings reveal pretreatment with M475271 significantly inhibits VEGF-induced VE-cadherin and beta-catenin phosphorylation. However, M475271 significantly increases VE-cadherin and beta-catenin association compared to the VEGF-treated group. Confocal laser microscopic examination confirmed the augmentation effect of M475271 on VE-cadherin and beta-catenin association. Finally, M475271 was shown to have inhibitory effects comparable to those of PP2 and Herbimycin A on VEGF-induced HUVEC proliferation, migration, and tube formation. These findings suggest that M475271 attenuates VEGF-induced angiogenesis by maintaining cell-cell junction stability. Although the involvement of other signaling molecules cannot be ruled out, M475271 has potential as a drug for the inhibition of the angiogenesis needed for tumor growth and metastasis. (Keyword) M475271 / vascular endothelial growth factor (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.FP0060357 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16974068 ● Search Scopus @ Elsevier (PMID): 16974068 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.FP0060357 (DOI: 10.1254/jphs.FP0060357, PubMed: 16974068)
135.	Shinji Abe, Hideki Ohnishi, Koichiro Tsuchiya, Keisuke Ishizawa, Mayumi Torii, Yasuhisa Kanematsu, Kazuyoshi Kawazoe, Kazuo Minakuchi, Masanori Yoshizumi and Toshiaki Tamaki : Calcium and reactive oxygen species mediated Zn²⁺-induced apoptosis in PC12 cells, Journal of Pharmacological Sciences, Vol.102, No.1, 103-111, 2006. (Summary) The release of excessive Zn(2+) from presynaptic boutons into extracellular regions contributes to neuronal apoptotic events, which result in neuronal cell death. However, the mechanisms of Zn(2+)-induced neuronal cell death are still unclear. Therefore, we investigated the dynamics of intracellular Zn(2+), calcium, and reactive oxygen species in PC12 cells. The addition of Zn(2+) produced cell death in a concentration- and time-dependent manner. (45)Ca(2+) influx occurred just after the treatment with Zn(2+), although subsequent hydroxyl radical (()OH) production did not begin until 3 h after Zn(2+) exposure. ()OH production was significantly attenuated in Ca(2+)-free medium or by L-type Ca(2+) channel antagonist treatment, but it was independent of the intracellular Zn(2+) content. Dantrolene treatment had no protective effects against Zn(2+)-induced cell death. Treatment with N-acetyl-L-cysteine blocked ()OH generation and subsequent cell death. These data indicate that Ca(2+) influx and subsequent ()OH production are critical events in Zn(2+)-induced toxicity in PC12 cells. (Keyword) Acetylcysteine / Animals / Apoptosis / Bisbenzimidazole / Calcium / Calcium Channel Blockers / Calcium Channels, L-Type / Calcium Radioisotopes / Cell Survival / Dantrolene / Fluorescent Dyes / Free Radical Scavengers / Hydroxyl Radical / PC12 Cells / Rats / Reactive Oxygen Species / Spectrophotometry, Atomic / Zinc (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.FP0060342 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16990703 ● Search Scopus @ Elsevier (PMID): 16990703 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.FP0060342 (DOI: 10.1254/jphs.FP0060342, PubMed: 16990703)
136.	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)
137.	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)
138.	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)
139.	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)
140.	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)
141.	生田雅子, 会田真規, Keisuke Ishizawa, Kazuo Minakuchi, Koichiro Tsuchiya, Masaru Kihara and Aiko Yamauchi : 徳島大学病院におけるTPN処方設計支援ソフトの使用評価と改良, Japanese Journal of Pharmaceutical Health Care and Sciences, Vol.31, No.4, 279-286, 2005. (Summary) Fluid therapy is a fundamental treatment for almost all inpatients, and nutritional therapy is the most important type of such therapy. Currently, total parenteral nutrition (TPN) is widely used to provide complete nutritional support but 30-40% of TPN recipients are considered to in a malnourished state due to inappropriate TPN prescriptions. Computer-assisted TPN prescription systems are thought to be useful to clinical professionals in solving this problem because they can perform complicated calculations that make it easy to draw up correct TPN prescriptions. So, we made a prototype system for aiding the preparation of TPN prescriptions based on Microsoft^[ !R] EXCEL and it was tested by physicians, pharmacists, dietitians and nurses engaged in TPN therapy at Tokushima University Hospital. We also had them fill out a questionnaire on the system in which they rated it for ease of operation and usefulness according to a scoring system in which 5 indicated full marks. Our Computer-Assisted TPN Prescription System was improved on the basis of the questionnaire results and is now being effectively used by the nutrition support team (NST) in Tokushima University Hospital. (Keyword) computer-assisted TPN prescription system / calculation software / TPN (total parenteral nutrition) / fluid therapy / questionnaire (Link to Publication Site) ● Publication site (DOI): 10.5649/jjphcs.31.279 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679753550336 ● Search Scopus @ Elsevier (DOI): 10.5649/jjphcs.31.279 (DOI: 10.5649/jjphcs.31.279, CiNii: 1390282679753550336)
142.	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)
143.	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)
144.	Mami Azuma, Hitoshi Houchi, Hirotaka Nishisako, Keisuke Ishizawa, Koichiro Tsuchiya, Kazuhiko Teraoka, Toshitaka Ikehara, Takenori Kusumi and Kazuo Minakuchi : Inhibitory action of novel arginine derivative on catecholamine secretion evoked by acetylcholine from cultured bovine adrenal chromaffin cells, Journal of Cardiovascular Pharmacology, Vol.42, No.Suppl. 1, S15-S18, 2003. (Summary) A novel product, 4-amino-5-guanidinopentanoic acid 15-[(4-aminobutyl)-3-aminopropylcarbamoyl] pentadecyl ester (Arg-HSA-Spm), was synthesized based on ptilomycalin A, which is one of the extracts from marine sponge. Arg-HSA-Spm contains arginine in its chemical structure. The pharmacological action of Arg-HSA-Spm on catecholamine secretion from cultured bovine adrenal chromaffin cells was examined. Arg-HSA-Spm inhibited catecholamine secretion stimulated by the physiological secretagog acetylcholine. This inhibitory action of Arg-HSA-Spm on catecholamine secretion induced by 10(-4) M acetylcholine was dose-dependent from 10(-8) M to 10(-5) M. In the presence of 3 x 10(-7) M Arg-HSA-Spm, the stimulation of catecholamine secretion observed by increasing acetylcholine up to 10(-3) M did not reach the maximal level observed without Arg-HSA-Spm. Arg-HSA-Spm at 10(-5) M suppressed both the increase in intracellular free Ca2+ level and the influx of 45Ca2+ induced by 10(-4) M acetylcholine. The Arg-HSA-Spm-induced suppression of intracellular free Ca2+ level, the influx of 45Ca2+ and catecholamine secretion were not observed in the presence of extracellular K+ at 56 mM. The results presented in this study suggested that Arg-HSA-Spm may inhibit the influx of extracellular Ca2+ into the cells, probably through its blocking action related to acetylcholine receptors, resulting in the inhibition of catecholamine secretion in adrenal chromaffin cells. (Keyword) Acetylcholine / Adrenal Medulla / Alkaloids / Animals / Arginine / calcium / Calcium Radioisotopes / Carbamates / Catecholamines / Cattle / Cells, Cultured / Chromaffin Cells / Dose-Response Relationship, Drug / Guanidines / Spermidine (Link to Publication Site) ● Publication site (DOI): 10.1097/00005344-200312001-00005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14871022 ● Search Scopus @ Elsevier (PMID): 14871022 ● Search Scopus @ Elsevier (DOI): 10.1097/00005344-200312001-00005 (DOI: 10.1097/00005344-200312001-00005, PubMed: 14871022)
145.	Masanori Yoshizumi, Toshiaki Kogame, Yuki Suzaki, Yoshiko Fujita, Moe Kyaw, Kazuyoshi Kirima, Keisuke Ishizawa, Koichiro Tsuchiya, Shoji Kagami and Toshiaki Tamaki : Ebselen attenuates oxidative styress-induced apoptosis via the inhibition of the c jun N-terminal kinase and activator protein-1 signaling pathway in PC12 cells., British Journal of Pharmacology, Vol.136, No.7, 1023-1032, 2002. (Summary) 1: Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one) is a selenoorganic compound exhibiting both glutathione peroxidase activity and antioxidant activity. Although it has been reported that ebselen is effective for oxidative stress-induced neuronal damage both in vivo and clinically, the precise mechanisms of the efficacy have not yet been elucidated. Thus, we hypothesized that ebselen may affect reactive oxygen species-induced mitogen-activated protein (MAP) kinase activation in cultured PC12 cells. 2: Our findings showed that hydrogen peroxide (H(2)O(2)) stimulated rapid and significant activation of extracellular signal-regulated kinase (ERK)1/2, c-Jun N-terminal kinase (JNK) and p38 in PC12 cells, which is a model of catecholamine-containing neurons. 3: H(2)O(2)-induced JNK activation was inhibited by ebselen, whereas ERK1/2 and p38 activation by H(2)O(2) were not affected by ebselen. 4: Inhibition by ebselen of H(2)O(2)-induced hydroxyl radical generation in PC12 cells was observed using electron paramagnetic resonance measurements. Ebselen also inhibited H(2)O(2)-induced increases in DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK, composed of the c-Jun homo/heterodimer. 5: Finally, pretreatment of cells with ebselen resulted in a significant recovery from cell death including apoptosis by H(2)O(2) in PC12 cells. 6 These findings suggest that ebselen attenuates oxidative stress-induced neuronal cell death through the inhibition of the JNK and AP-1 signalling pathway. Thus, inhibition of JNK by ebselen may imply its usefulness for treatment of ischaemic cerebral diseases relevant to neuronal cell death. (Keyword) Analysis of Variance / Animals / Antioxidants / Apoptosis / Azoles / Cell Survival / DNA Fragmentation / Electron Spin Resonance Spectroscopy / Enzyme Activation / Hydrogen Peroxide / JNK Mitogen-Activated Protein Kinases / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinases / Organoselenium Compounds / Oxidative Stress / PC12 Cells / Rats / Reactive Oxygen Species / Signal Transduction / Time Factors / Transcription Factor AP-1 / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1038/sj.bjp.0704808 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12145102 ● Search Scopus @ Elsevier (PMID): 12145102 ● Search Scopus @ Elsevier (DOI): 10.1038/sj.bjp.0704808 (DOI: 10.1038/sj.bjp.0704808, PubMed: 12145102)
146.	Keisuke Ishizawa, Masanori Yoshizumi, Koichiro Tsuchiya, Eiko Takishita, Yutaka Nakaya, Kazuhiro Kishi, Yousuke Ebina, Hitoshi Houchi, Kazuo Minakuchi and Toshiaki Tamaki : Effects of losartan in combination with or without exercise on insulin resistance in Otsuka Long-Evans Tokushima Fatty rats., European Journal of Pharmacology, Vol.430, No.2-3, 359-367, 2001. (Summary) Hypertension often complicates type 2 diabetes mellitus, and angiotensin converting enzyme inhibitor treatment has been shown to improve insulin resistance in such cases. However, the effect of angiotensin II type-1 (AT(1)) receptor antagonists on insulin resistance is still controversial. To gain further information on this effect, we examined the effect of losartan on insulin resistance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus. Losartan administration alone lowered systolic blood pressure, but did not improve oral glucose tolerance test or insulin resistance in OLETF rats. However, the administration of losartan with exercise significantly improved both systolic blood pressure and insulin resistance relative to control OLETF rats. On the other hand, losartan treatment, regardless of exercise, increased glucose uptake in excised soleus muscle and fat cells. To explore the beneficial effect of losartan on skeletal muscle glucose uptake, we examined intracellular signaling of soleus muscle. Although Akt activity and glucose transporter type 4 (GLUT4) expressions were not affected by losartan with or without exercise, extracellular signal-regulated kinase (ERK1/2) and p38 mitogen-activated protein (MAP) kinase activities were increased by both interventions. These results indicate that angiotensin AT(1) receptor antagonist improved local insulin resistance, but not systemic insulin resistance. These findings may explain the controversy over the effect of angiotensin AT(1) receptor antagonists on insulin resistance in clinical use. The enhancing effect of angiotensin AT(1) receptor antagonist on skeletal muscle glucose uptake may be attributable to MAP kinase activation or other mechanisms rather than phosphatidylinositol 3-kinase activation. (Keyword) Adipocytes / Animals / Antihypertensive Agents / Blood Glucose / Blood Pressure / Blotting, Western / Body Weight / Deoxyglucose / Diabetes Mellitus, Type 2 / Enzyme Activation / Glucose / Glucose Tolerance Test / Glucose Transporter Type 4 / Heart Rate / Insulin / Insulin Resistance / JNK Mitogen-Activated Protein Kinases / Losartan / Male / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinases / Monosaccharide Transport Proteins / Muscle Proteins / Muscle, Skeletal / Phosphorylation / Physical Conditioning, Animal / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Rats / Rats, Inbred OLETF / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1016/S0014-2999(01)01405-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11711055 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035798388 (DOI: 10.1016/S0014-2999(01)01405-4, PubMed: 11711055, Elsevier: Scopus)
147.	Yukio Sugimoto, Keisuke Ishizawa, Kouichi Saitou, Genzo Suzuki, Tadatsugu Tarumi, Hiroto Nakahara, Yasushi Kirino and Chiaki Kamei : Effect of mometasone furoate by topical application on allergic rhinitis model in rats, Pharmacology, Vol.61, No.2, 91-95, 2000. (Summary) The effects of mometasone furoate on experimental allergic rhinitis in rats were studied in comparison with that of fluticasone propionate. Topical application of both drugs inhibited dose-dependently the increase of nasal symptoms (sneezing and nasal rubbing) after antigen challenge to the nasal cavity of actively sensitized rats. Mometasone furoate and fluticasone propionate at concentrations of 0.01 or 0.1% significantly inhibited both nasal rubbing and sneezing 1 h after topical application of both drugs. The relative potencies of mometasone furoate in nasal rubbing and sneezing compared to fluticasone propionate were 5.01 and 6.87, respectively. Mometasone furoate (0.02%) and fluticasone propionate (0.1%) significantly inhibited the increase of antigen-induced nasal rubbing even 6 h after topical application, indicating that both drugs have a long-lasting effect. (Keyword) Administration, Topical / Androstadienes / Animals / Anti-Allergic Agents / Disease Models, Animal / Male / Outcome Assessment (Health Care) / Pregnadienediols / Rats / Rats, Wistar / Rhinitis (Link to Publication Site) ● Publication site (DOI): 10.1159/000028386 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10940782 ● Search Scopus @ Elsevier (PMID): 10940782 ● Search Scopus @ Elsevier (DOI): 10.1159/000028386 (DOI: 10.1159/000028386, PubMed: 10940782)
148.	Keisuke Ishizawa, Zhong Chen, Chihiro Okuma, Yukio Sugimoto, Yoko Fujii and Chiaki Kamei : Participation of GABAergic and histaminergic systems in inhibiting amygdaloid kindled seizures, The Japanese Journal of Pharmacology, Vol.82, No.1, 48-53, 2000.
149.	Yukio Sugimoto, Yoshinori Iba, Keisuke Ishizawa, Genzo Suzuki and Chiaki Kamei : Effects of levocabastine on lipid mediator release from guinea pig lung fragments, Acta Medica Okayama, Vol.53, No.6, 271-274, 1999. (Summary) The effects of levocabastine, a novel histamine H1-receptor antagonist, on lipid mediator release induced by antigen-antibody reaction from actively sensitized guinea pig lung fragments were studied. Levocabastine dose-dependently inhibited the release of leukotriene C4 from guinea pig lung fragments induced by antigen. A significant effect was observed with levocabastine at a concentration of 10(-4) M. On the other hand, levocabastine produced no effect on the release of leukotriene E4 or thromoboxane B2. From these findings, it was concluded that levocabastine may be useful for relieving the nasal obstruction in allergic rhinitis caused by inhibition of leukotriene C4 release. (Keyword) Animals / Antigens / Guinea Pigs / Histamine H1 Antagonists / In Vitro Techniques / Leukotriene C4 / Leukotriene E4 / Lung / Male / Piperidines / Thromboxane B2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10631382 ● Search Scopus @ Elsevier (PMID): 10631382 (PubMed: 10631382)
150.	Masafumi Fukinaga, Keisuke Ishizawa and Chiaki Kamei : Anticonvulsant properties of 1,4-benzodiazepine derivatives in amygdaloid-kindled seizures and their chemical structure-related anticonvulsant action, Pharmacology, Vol.57, No.5, 233-241, 1998. (Summary) The effects of 14 different 1,4-benzodiazepines on amygdaloid-kindled seizures and their chemical structure-related anticonvulsive actions were studied. The prophylactic effects of 1, 4-benzodiazepines on amygdaloid-kindled seizures were also examined. Male Wistar strain rats were used in this study. Rats were anesthetized with pentobarbital sodium (35 mg/kg i.p.) and bipolar electrodes were implanted into the right amygdala. The stimulating parameters were 1 ms pulse duration, 60 Hz frequency and a 1 s duration at an intensity just sufficient to induce afterdischarge (AD). All the 1,4-benzodiazepines depressed both seizure stage and AD duration of amygdaloid-kindled seizures. Of the 1, 4-benzodiazepines, prazepam, flutoprazepam and flurazepam with a long alkyl chain at position 1 were less effective than the drugs having a hydrogen or methyl group at the same position. Nitrazepam, nimetazepam, flunitrazepam and clonazepam which have a nitro group at position 7 showed more potent antiepileptic activity than the drugs with a chloro group. Certain 1,4-benzodiazepines caused inhibition of the development of amygdaloid-kindled seizures. The existence of a hydrogen or methyl group at position 1 and a nitro group at position 7 is important for exhibiting potent anticonvulsant activity in amygdaloid-kindled seizures. Introduction of an oxygen group at position 2 is also necessary for high activity. 1,4-benzodiazepines had not only therapeutic but also prophylactic effects on amygdaloid-kindled seizures. (Keyword) Amygdala / Analysis of Variance / Animals / Anti-Anxiety Agents / Anticonvulsants / Benzodiazepines / Dose-Response Relationship, Drug / Electric Stimulation / Kindling, Neurologic / Male / Rats / Rats, Wistar / Seizures / structureactivity relationship (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9742288 ● CiNii @ National Institute of Informatics (CRID): 1571135651705617792 ● Search Scopus @ Elsevier (PMID): 9742288 (PubMed: 9742288, CiNii: 1571135651705617792)
151.	Hiroshi Kakinoki, Keisuke Ishizawa, Masatumi Fukunaga, Yoko Fujii and Chiaki Kamei : The effects of histamine H3-receptor antagonists on amygdaloid kindled seizures in rats, Brain Research Bulletin, Vol.46, No.5, 461-465, 1998.
152.	Chiaki Kamei, Keisuke Ishizawa, Hiroshi Kakinoki and Masafumi Fukunaga : Histaminergic mechanisms in amygdaloid-kindled seizures in rats, Epilepsy Research, Vol.30, No.3, 187-194, 1998.

Academic Paper (Unrefereed Paper):

1.	Miku Kita, Jun Yamamoto, Koji Ebisuno, Chiaki Komiya, Akira Shigenaga, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Akira Otaka : Development of hydrogen peroxide-responsive amide bond cleavage device, Peptide Science 2013, 203-204, 2014.
2.	Akira Shigenaga, Keiji Ogura, Hiroko Hirakawa, Jun Yamamoto, Koji Ebisuno, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Akira Otaka : Design and synthesis of hypoxia-responsive amino acid which causes peptide bond cleavage in hypoxic cells, Peptide Science 2012, 135-136, 2013. (Keyword) hypoxia-responsive / peptide bond cleavage / prodrug / stimulus-responsive / trimethyl lock (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1570854176180146304 (CiNii: 1570854176180146304)
3.	Keisuke Ishizawa : 2型糖尿病治療に対する標的分子としてのHIF-1αの可能性, Farumashia, Vol.47, No.2, 160-161, 2011.
4.	Yuki Minami, Toshitaka Ikehara, Keiko Hosokawa, Hisao Yamaguchi, Keisuke Ishizawa, Masayuki Shono, Kazuyoshi Kawazoe, Kazuo Minakuchi, Kazuo Yoshizaki, Yohsuke Kinouchi and Hiroshi Miyamoto : Effect of time-varying magnetic field on cell volume regulation of adrenal chromaffin cells, The Journal of Japan Biomagnetism and Bioelectromagnetics Society, Vol.19, No.1, 156-157, 2006.

Academic Letter:

1.	Satoru Mitsuboshi, Takahiro Niimura, Fuka Aizawa, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : Atenolol and mortality events in patients with chronic kidney disease: Analysis of data from the Japanese Adverse Drug Event Report database., Basic & Clinical Pharmacology & Toxicology, Vol.130, No.4, 553-556, 2022. (Keyword) Adrenergic beta-Antagonists / Atenolol / Drug-Related Side Effects and Adverse Reactions / Female / Humans / Hypertension / Japan / Male / Renal Insufficiency, Chronic (Link to Publication Site) ● Publication site (DOI): 10.1111/bcpt.13717 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35174631 ● Summary page in Scopus @ Elsevier: 2-s2.0-85125109476 (DOI: 10.1111/bcpt.13717, PubMed: 35174631, Elsevier: Scopus)
2.	Satoru Mitsuboshi, Takahiro Niimura, Masaki Yoshino, Yoshika Sakamoto, Yoshito Zamami and Keisuke Ishizawa : Fluoropyridmidine use and hypertriglyceridemia among Japanese patients: analysis of adverse event database., International Journal of Clinical Pharmacy, Vol.44, No.1, 260-263, 2021. (Summary) Background The association between fluoropyrimidines except for capecitabine and the risk of hypertriglyceridemia is unclear. Objective To investigate hypertriglyceridemia in patients receiving fluoropyrimidines. Method This observational study used anonymized patient data recorded in the open-access Japanese Adverse Drug Event Report database. All fluoropyrimidine and taxane users were investigated. Results We identified 29,451 fluoropyrimidine users and 21,266 taxane users. Disproportionality for both hypertriglyceridemia and an increase in serum triglyceride levels was observed in fluoropyrimidine users compared with in taxane users (reporting odds ratio, 6.74; 95% confidence interval [CI] 2.05-22.17; P < .001). Multivariate logistic analysis showed that both hypertriglyceridemia and an increase in serum triglyceride levels among fluoropyrimidines users were significantly associated with doxifluridine use (odds ratio [OR] 42.50; 95% CI 5.34-338.00; P < .001), tegafur use (OR 9.56; 95% CI 2.08-43.90; P < .001), capecitabine use (OR 12.30; 95% CI 2.67-56.80; P < .001), and breast cancer (OR 5.61; 95% CI 1.07-29.50; P = .042). Conclusion This study suggests that the use of tegafur and doxifluridine is associated with an increased risk of hypertriglyceridemia similar to that with the use of capecitabine; in particular, fluoropyrimidine users with breast cancer may have a high risk of hypertriglyceridemia. (Keyword) Antineoplastic Combined Chemotherapy Protocols / Capecitabine / Fluorouracil / Humans / Hypertriglyceridemia / Japan / Tegafur (Link to Publication Site) ● Publication site (DOI): 10.1007/s11096-021-01324-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34482500 ● Search Scopus @ Elsevier (PMID): 34482500 ● Search Scopus @ Elsevier (DOI): 10.1007/s11096-021-01324-0 (DOI: 10.1007/s11096-021-01324-0, PubMed: 34482500)

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.	Yoshito Zamami, Masaki Imanishi, Kenshi Takechi and Keisuke Ishizawa : Pharmacological approach for drug repositioning against cardiorenal diseases., The Journal of Medical Investigation : JMI, Vol.64, No.3.4, 197-201, 2017. (Summary) New applications of approved clinically used drugs are being discovered. Drug repositioning is a proposed strategy for developing these drugs as therapeutic agents for different diseases. Currently, approximately 2000 drugs are used in Japan. However, the compound targets and pathways involved in the pharmacological actions of 70-80% of these drugs have not been adequately clarified. Pharmacological examination of approved drugs is an important task in drug repositioning and vital for improving drug development efficiency. This review reports that angiotensin II type 1 receptor blockers show receptor-independent effects against reactive oxygen species generation in renal cells. Additionally, nitrosonifedipine has an antioxidative effect and protects endothelial cells against oxidative stress, and pioglitazone has multiple effects that improve dysfunctions in vascular control regulated by adrenergic and calcitonin gene-related peptide-containing nerves in animal models of diabetes. These data suggest that some approved drugs could be useful for treating cardiorenal diseases. Since cardiorenal diseases are likely to have chronic pathological conditions and require chronic drug administration, highly safe drugs are needed. Compared to newly developed drugs, drug repositioning of approved drugs with safety information is considered a particularly useful technique for searching new treatments for cardiorenal diseases. J. Med. Invest. 64: 197-201, August, 2017. (Tokushima University Institutional Repository) ● Metadata: 111115 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.64.197 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28954981 ● Search Scopus @ Elsevier (PMID): 28954981 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.197 (Tokushima University Institutional Repository: 111115, DOI: 10.2152/jmi.64.197, PubMed: 28954981)
4.	Yoshito Zamami, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, T Koyama and Keisuke Ishizawa : Drug repositioning research to improve the survival rate after cardiopulmonary arrest - utilizing large scale Medical Claims Database -, Journal of the Pharmaceutical Society of Japan, Vol.137, No.12, 1439-1442, 2017. (Summary) Approximately 100000 people suffer cardiopulmonary arrest in Japan every year, and the aging of society means that this number is expected to increase. Worldwide, approximately 100 million develop cardiac arrest annually, making it an international issue. Although survival has improved thanks to advances in cardiopulmonary resuscitation, there is a high rate of postresuscitation encephalopathy after the return of spontaneous circulation, and the proportion of patients who can return to normal life is extremely low. Treatment for postresuscitation encephalopathy is long term, and if sequelae persist then nursing care is required, causing immeasurable economic burdens as a result of ballooning medical costs. As at present there is no drug treatment to improve postresuscitation encephalopathy as a complication of cardiopulmonary arrest, the development of novel drug treatments is desirable. In recent years, new efficacy for existing drugs used in the clinical setting has been discovered, and drug repositioning has been proposed as a strategy for developing those drugs as therapeutic agents for different diseases. This review describes a large-scale database study carried out following a discovery strategy for drug repositioning with the objective of improving survival rates after cardiopulmonary arrest and discusses future repositioning prospects. (Keyword) Databases, Factual / Drug Repositioning / Heart Arrest / Humans / Hypoxia-Ischemia, Brain / Japan / Research Design / Survival Rate (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.17-00139-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29199254 ● Summary page in Scopus @ Elsevier: 2-s2.0-85037339843 (DOI: 10.1248/yakushi.17-00139-3, PubMed: 29199254, Elsevier: Scopus)
5.	Naoto Okada and Keisuke Ishizawa : 今求められているNSTと薬剤師の役割: 臨床・研究・教育を柱とするNST活動の実践, 薬事新報, Vol.2921, 1306-1310, Dec. 2015.
6.	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)
7.	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.
8.	Keisuke Ishizawa : Drug Discovery for Improvement of Chronic Kidney Disease and Cardiovascular Disease, Journal of the Pharmaceutical Society of Japan, Vol.131, No.9, 1347-1352, Sep. 2011. (Summary) Chronic kidney disease (CKD) has been increasingly recognized as a major public health problem in the world. Recent studies have showed that CKD is an independent risk factor for the occurrence of cardiovascular disease (CVD). Reactive oxygen species (ROS), generated by reduction-oxidation actions, have been generated by reduction-oxidation actions, recognized as the important chemical mediators that regulate signal transduction in various cells including vascular smooth muscle cells (VSMC) and mesangial cells (MC). It has been showed that increase in ROS generation may relate to a risk for CVD and CKD. In addition, ROS mediate activation of mitogen-activated protein (MAP) kinases, extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase, p38, and big MAP kinase 1, in various cells leading to change in gene expressions. Control of the oxidative stress and ROS-mediated alterations of signaling molecules including MAP kinases may provide new therapeutic strategy against CKD and CVD. In this review, we summarize mainly our data regarding the pharmacological effects of renin-angiotensin-aldosterone system blockers, bioflavonoids and adiponectin in VSMC and MC. Also we review the data on a possible new class drug against oxidative stress to improve CKD and CVD. (Keyword) oxidative stress / chronic kidney disease / cardiovascular disease / mitogen-activated protein kinase / renin-angiotensin-aldosterone system (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.131.1347 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282681104589184 ● Search Scopus @ Elsevier (DOI): 10.1248/yakushi.131.1347 (DOI: 10.1248/yakushi.131.1347, CiNii: 1390282681104589184)
9.	Keisuke Ishizawa, Kazuo Minakuchi and Toshiaki Tamaki : 医療人としての薬剤師育成教育の実践, Medicine and Drug Journal, Vol.43, No.3, 871-874, Mar. 2007.
10.	Toshiaki Tamaki, Kunihisa Yamaguchi and Keisuke Ishizawa : 薬理作用から見た健康食品, Shikoku Acta Medica, Vol.63, No.5,6, 170-171, 2007. (Tokushima University Institutional Repository) ● Metadata: 110195 (Tokushima University Institutional Repository: 110195)
11.	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)
12.	Keisuke Ishizawa and Kazuo Minakuchi : 栄養管理における薬剤師の役割, 調剤と情報, Vol.11, No.1, 95-100, Jan. 2005.
13.	Keisuke Ishizawa and Kazuo Minakuchi : 大学病院におけるNST活動と薬剤師, 薬事新報, Vol.2332, 902-905, Oct. 2004.
14.	Keisuke Ishizawa, Hitoshi Houchi and Kazuo Minakuchi : 大学病院における栄養支援チーム(NST)と薬剤師, Journal of Japnese Society of Hospital Pharmacists, Vol.40, No.10, 1245-1248, Oct. 2004. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1573950401508262400 (CiNii: 1573950401508262400)

Proceeding of International Conference:

1.	Iida Midori, Yamanishi Yoshihiro, Kuniki Yurika, Kenta Yagi, Mitsuhiro Goda, Namba Satoko, Takeshita Jun-ichi, Sawada Ryusuke, Iwata Michio, Yoshito Zamami and Keisuke Ishizawa : A Computational Method for Predicting Synergistic Drug Combinations Using Network Propagation and Trans-OmicsAnalysis, 1st Asia&Pacific Bioinformatics Joint Conference JSBi, GIW, InCoB, APBC, and ISCB-Asia, Okinawa, Oct. 2024.
2.	Kenta Yagi, Fuka Aizawa, Takahiro Niimura, Mitsuhiro Goda, Kei Kawada, Yuki Izawa-Ishizawa and Keisuke Ishizawa : Exploration of drugs that affect treatment with anti-VEGF drugs, 30th Congress of the Federation of Asian Pharmaceutical Associations; FAPA2024, Seoul, Oct. 2024.
3.	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.
4.	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.
5.	Fuka Aizawa, okabayashi Ami, moriyama daishi, Kenta Yagi, takahashi shimon, Takahiro Niimura, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa : HMG-CoA reductase inhibitor ameliorate platinum and taxane induced peripheral neuropathy: basic and medical database analysis, 81st FIP World Congress of Pharmacy and Pharmaceutical Sciences., Brisbane, Sep. 2023.
6.	Kenta Yagi, Fuka Aizawa, Takahiro Niimura, Maruo Akinori, Yuki Izawa-Ishizawa, Hirofumi Hamano, Mitsuhiro Goda, Yoshito Zamami and Keisuke Ishizawa : Impact of Supportive Care Drugs on Treatment Effectiveness in Cancer Chemotherapy, 81st FIP World Congress of Pharmacy and Pharmaceutical Sciences., Brisbane, Sep. 2023.
7.	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.
8.	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.
9.	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.
10.	Imakura Takeshi, Seidai Satou, Kazuya Koyama, Hirohisa Ogawa, Takahiro Niimura, Murakami Kojin, Yuya Yamashita, Keiko Haji, Nobuhito Naito, Kozo Kagawa, Hiroshi Kawano, Yoshito Zamami, Keisuke Ishizawa and Yasuhiko Nishioka : Computational drug repositioning and wet-lab validation approach identifies polo-like kinase inhibitors as potential therapeutics for pulmonary fibrosis, ERS International Congress 2022, Barcelona, Sep. 2022.
11.	Takeshi Imakura, Seidai Satou, Kazuya Koyama, Hirohisa Ogawa, Takahiro Niimura, Kojin Murakami, Yuya Yamashita, Keiko Haji, Nobuhito Naito, Kozo Kagawa, Hiroshi Kawano, Yoshito Zamami, Keisuke Ishizawa and Yasuhiko Nishioka : Computational Drug Repositioning Approach Identifies Polo-Like KinaseInhibitors as Potential Therapeutics for Pulmonary Fibrosis, ATS 2022 International Conference, San Francisco, May 2022.
12.	Imakura Takeshi, Seidai Satou, Kazuya Koyama, Takahiro Niimura, Kohjin Murakami, Yuya Yamashita, Takahashi Naoki, Nobuhito Naito, Kozo Kagawa, Hiroshi Kawano, Yoshito Zamami, Keisuke Ishizawa and Yasuhiko Nishioka : Polo-like kinase inhibitors identified by computational repositioning attenuates bleomycin-induced pulmonary fibrosis in mice, APSR 2021, Kyoto and online, Nov. 2021.
13.	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.
14.	Masayuki Chuma, Masateru Kondo, Yoshito Zamami, Kenshi Takechi, Mitsuhiro Goda, Naoto Okada, Akitomo Shibata, Mizuho Asada, Jun Oto, Hiroaki Yanagawa and Keisuke Ishizawa : Successful dose adjustment of vancomycin utilizing cystatin C in septic patients with bacterial meningitis: A case report, FIP2019, Abu Dhabi, Sep. 2019.
15.	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.
16.	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.
17.	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.
18.	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.
19.	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.
20.	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.
21.	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.
22.	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.
23.	Ishida Shunsuke, Bando Hiroshi, Kenshi Takechi, Masaki Imanishi, Yoshito Zamami, Krino Yashishi, Nakamura Toshimi, Teraoka Kazuhiko and Keisuke Ishizawa : Development and clinical application of management tool to monitor side effects for atypical antipsychotics, ASHPMidyear2017Clinical Meeting&Exhibition, フロリダ, Dec. 2017.
24.	Kenshi Takechi, Yoshito Zamami, Masaki Imanishi, Hiroaki Yanagawa and Keisuke Ishizawa : Psychiatric patients with antipsychotic drug-induced hyperprolactinemia and menstruation disorders, ASHPMidyear2017Clinical Meeting&Exhibition, フロリダ, Dec. 2017.
25.	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.
26.	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)
27.	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.
28.	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.
29.	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.
30.	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.
31.	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.
32.	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.
33.	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.
34.	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.
35.	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.
36.	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.
37.	Naoto Okada, Shuji Fushitani, Takumi Sakurada and Keisuke Ishizawa : Pharmacist interventions can improve clinical outcomes in patients treated with anti-methicillin-resistant Staphylococcus aureus agents in a hematological ward, 50th ASHP Midyear Clinical Meeting, New Orleans, Dec. 2015.
38.	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.
39.	Wenting Xu, Licht Miyamoto, Haruna Aihara, Tomomi Yamaoka, Keisuke Ishizawa, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : The Mechanism of Citrus sudachi Peel Extract Exerts Lipid Reducing Effect in Cells, 2015.10.19-22 The 10th IAGG Asia / Oceania Congress of Gerontology and Geriatrics 2015, Chiang Mai, Oct. 2015.
40.	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.
41.	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.
42.	Hatano Aya, Licht Miyamoto, Yamane Megumi, Takenokuma Kazuya, Kono Mai, Keisuke Ishizawa and Koichiro Tsuchiya : Dietary nitrite ameliorates glucose tolerance and hyperlipidemia in diet-induced obesity rats., ASMRM 2014, Taipei, Nov. 2014.
43.	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.
44.	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.
45.	Licht Miyamoto, Yamane Megumi, Tomida Yosuke, Takenokuma Kazuya, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : Significance of AMPK in renal protective and metabolic actions of nitrite, international conference of food science, Kyoto, Mar. 2014.
46.	Licht Miyamoto, Tomida Y, Takenokuma K, Yamane M, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : Dietary nitrite ameliorates glucose and lipid metabolism in high fat diet-fed rats., 2014 Keystone Symposia Conference, Jan. 2014.
47.	Miku Kita, Jun Yamamoto, Koji Ebisuno, Chiaki Komiya, Akira Shigenaga, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Akira Otaka : Development of hydrogen peroxide-responsive amide bond cleavage device, 4th Asia-Pacific International Peptide Symposium, 50th Japanese Peptide Symposium, Suita, Nov. 2013.
48.	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.
49.	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.
50.	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.
51.	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.
52.	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.
53.	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.
54.	Licht Miyamoto, Kono Mai, Nakagawa Takeo, Hattori Hatsuhiko, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : A Novel Hydrophilic Derivative of Probucol Ameliorates Glucose Tolerance and Insulin Sensitivity Independently of the Canonical Potency of Probucol., 48th Annual Meeting of the European Association for the Study of Diabetes, Oct. 2012.
55.	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.
56.	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.
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 cell attenuates angiotensin -induced vascular remodeling in mice, ISOTT (International Society on Oxygen Transport to Tissue) 2012, Aug. 2012.
58.	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.
59.	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.
60.	Licht Miyamoto, Mai Kono, Takeo Nakagawa, Hatsuhiko Hattori, Hisao Nemoto, Keisuke Ishizawa, Yoshiyuki Yoshimura and Koichiro Tsuchiya : A Hydrophilic Derivative of Probucol, Probucol-(glutaric branched-triglycerol)2 (ProBGL2) Ameliorates Glucose Tolerance and Insulin Sensitivity by Independent Mechanism of the Canonical Potency of Probucol in HFD-fed mice, Keystone symposiaon Molecular and Cellular Biology, Jan. 2012.
61.	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.
62.	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.
63.	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.
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 cell attenuates angiotensin II-induced vascular remodeling in mice, The International Society on Oxygen Transport to Tissue 2012, 2012.
65.	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.
66.	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.
67.	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.
68.	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.
69.	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.
70.	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.
71.	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.
72.	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.
73.	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.
74.	Yasumasa Ikeda, Soichiro Tajima, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Estrogen action on iron metabolism, ENDO 2011: The 93rd Annual Meeting & Expo, Boston, Jun. 2011.
75.	Masaki Imanishi, Soichiro Tajima, Yoshitaka Kihira, Keisuke Ishizawa, Shuji Kondo, Shoji Kagami, Shuhei Tomita, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Increment intracellular labile iron enhances Angiotensin-induced intracellular adhesion molecule-1 (ICAM-1) expression in human glomerular endothelial cells, World congress of Nephrology 2011, Vancouver, Apr. 2011.
76.	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.
77.	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.
78.	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.
79.	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.
80.	Masaki Imanishi, Soichiro Tajima, Yoshitaka Kihira, Keisuke Ishizawa, Shuji Kondo, Shoji Kagami, Shuhei Tomita, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : INCREMENT INTRACELLULAR LABILE IRON ENHANCES ANGIOTENSIN II-INDUCED INTRACELLULAR ADHESION MOLECULE-1 (ICAM-1) EXPRESSION IN HUMAN GLOMERULAR ENDOTHELIAL CELLS, World Congress of Nephrology 2011, 2011.
81.	Ayato Katagiri, Hatsuhiko Hattori, Kohsuke Yoshitoimi, Keisuke Ishizawa, Koichiro Tsuchiya and Hisao Nemoto : Modification of Medicines by using Branched Oligo-Glycerols (BGL), Pachifichem 2010, Honolulu, Dec. 2010.
82.	Kohsuke Yoshitomi, Hatsuhiko Hattori, Ayato Katagiri, Keisuke Ishizawa, Koichiro Tsuchiya and Hisao Nemoto : Water-solubilization of Highly Hydrophobic Medicines by using Branched Oligo-Glycerols (BGL), Pachifichem 2010, Honolulu, Dec. 2010.
83.	Toshiaki Tamaki, Kunihisa Yamaguchi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Shuji Kondo, Shoji Kagami and Shuhei Tomita : Global gene expression analyses in renal ischemia-reperfusion injury (IRI) from mice lucking Hif-1a gene, ASN RENAL WEEK 2010 EXHIBIT, Nov. 2010.
84.	Koichiro Tsuchiya, Yuya Horinouchi, Soichiro Tajima, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Yoshiyuki Yoshimura, Shuhei Tomita, Shuichi Hamano and Toshiaki Tamaki : Antioxidant effects of photodegradation product of nifedipine, 17th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2010), Nov. 2010.
85.	Shuhei Tomita, Masahisa Urata, Yayoi Fukuhara, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Tetsuya Kitagawa and Toshiaki Tamaki : Endothelial-targeted hypoxia-inducible factor-1b (HIF-1b) loss-of function alleviates the monocrotaline-induced pulmonary hypertension in mice, American Heart Association Scientific Sessions 2010, Chicago, Nov. 2010.
86.	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.
87.	Soichiro Tajima, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : IRON DERIVATION AMELIORATES GLUCOSE TOLERANCE THROUGH REDUCTION OF OXIDATIVE STRESS AND INFLAMMATION IN DIABETIC KKAY MICE, 2010 American Physiological Society Conference Inflammation, Immunity and Cardiovascular Disease, Aug. 2010.
88.	Yoshitaka Kihira, Shuhei Tomita, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Basic fibroblast growth factor upregulates hypoxia inducible factor 1 and glucose transporter 1 in adipose cells, The 16th World Congress of Basic and Clinical Pharmacology (WorldPharma 2010), Copenhagen, Jul. 2010.
89.	Soichiro Tajima, Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Toshiaki Tamaki and Koichiro Tsuchiya : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, The 6th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide, Jun. 2010.
90.	Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Toshiaki Tamaki and Koichiro Tsuchiya : Metabolism of quercetin in vivo and its protective effect against cardiovascular diseases, 2nd International On-Board Symposium: Human Health, Energy and Environment, May 2010.
91.	Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, XX World Congress ISHR 2010 KYOTO, May 2010.
92.	Toshiaki Tamaki, Kunihisa Yamaguchi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Shuhei Tomita : Amelioration of acute tubular necrosis in ischemic acute renal failure was impaired in mice lucking hypoxia inducible factor-1 gene, ISN (International Society of Nephrology) nexus sympojium 2010, Apr. 2010.
93.	Souichiro Tajima, Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Toshiaki Tamaki and Koichiro Tsuchiya : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, The 6th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide, Kyoto, Apr. 2010.
94.	Koichiro Tsuchiya, Soichiro Tajima, Keisuke Ishizawa, Shuhei Tomita, Yoshitaka Kihira, Yasumasa Ikeda, Yoshiyuki Yoshimura, Shuichi Hamano and Toshiaki Tamaki : Effect of Angiotensin II on the intracellular labile iron concentration in HGECs, 16th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2009), Nov. 2009.
95.	Yasumasa Ikeda, Kaori Sato, David Pimentel, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Flora Sam, Toshiaki Tamaki and Kenneth Walsh : LKB1 gene in myocytes plays a critical role to regulate the coordinated cardiac growth and capillary development, American Heart Association Scientific Sessions 2009, Orlando, Nov. 2009.
96.	Yasumasa Ikeda, Kaori Sato, David Pimentel, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Flora Sam, Toshiaki Tamaki and Kenneth Walsh : LKB1 gene in myocytes plays a critical role to regulate the coordinated cardiac growth and capillary development, American Heart Association Scientific Sessions 2009, Orlando, Nov. 2009.
97.	Kunihisa Yamaguchi, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya, Shuji Kondo, Shoji Kagami and Toshiaki Tamaki : Hypoxia-Inducible Factor-1α ameliorates ischemic acute renal failure and has a relation with a recovery from acute tubular necrosis, 41th ASN annual meeting, Philadelphia, Nov. 2008.
98.	Toshiaki Tamaki, Keisuke Ishizawa, Kunihisa Yamaguchi, Shuji Kondo, Shoji Kagami, Fukuhara Yayoi, Yuya Horinouchi and Koichiro Tsuchiya : Nitoroso-nifedipine is a new class drug to protect kidney against oxidative stress, 41th ASN annual meeting, Philadelphia, Nov. 2008.
99.	Koichiro Tsuchiya, Soichiro Tajima, Mai Hamamoto, Hideki Ohnishi, Yuki Motobayashi, Yuya Horinouchi, Kunihisa Yamaguchi, Keisuke Ishizawa, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : Effect of angiotensin II on iron (II) turnover in HGEC, Biomedical Redox Navigation (EPR2008), Fukuoka, Sep. 2008.
100.	Yuya Horinouchi, Koichiro Tsuchiya, Keisuke Ishizawa, Soichiro Tajima, Yuki Motobayashi, Kunihisa Yamaguchi, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : Endotherial cell protective activity of nitrosonifedipine, Biomedical Redox Navigation (EPR2008), Fukuoka, Sep. 2008.
101.	Yuki Motobayashi, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Sakiko Orino, Dorjsuren Narantungalag, Kunihisa Yamaguchi, Kazuo Minakuchi and Toshiaki Tamaki : Inhibitory effects of adiponectin on cell migration induced by insulin-like growth factor-1 in vascular smooth muscle cells, The IXth World Conference on Clinical Pharmacology and Therapeutics, Québec City, Jul. 2008.
102.	Toshiaki Tamaki, Kunihisa Yamaguchi, Narantungalag Dorjsuren, Yayoi Fukuhara, Yuya Horinouchi, Yuki Motobayashi, Koichiro Tsuchiya and Keisuke Ishizawa : Olmesartan inhibits the TNF-α-induced cytotoxicity in human glomerular endothelial cells, ISN Nexus Symposium on Diabetes & the Kidney, Dublin, Jun. 2008.
103.	Yasushi Kirino, Toshimi Nakamura, Hirotaka Nishisako, Natsuko Ise, Keisuke Ishizawa, Toshihide Kujime, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Kazuo Minakuchi : Dosase adjustment and monitoring the side effects of the anticancer drug in Tokushima University Dental Hospital, 42nd ASHP Midyear Clinical Meeting & Exhibition, Las Vegas, Dec. 2007.
104.	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.
105.	Maki Urushihara, Masanori Takamatsu, Maki Shimizu, Shuji Kondo, Akiko Kitamura, Yukiko Kinoshita, Keisuke Ishizawa, Toshiaki Tamaki and Shoji Kagami : The role of extracellular signal regulated kinase 5 in the accumulation of collagen matrix in rat mesangioproliferative glomerulonephritis, 40th ASN annual meeting, San Francisco, CA, Nov. 2007.
106.	Keisuke Ishizawa, Erika Miki, Arisa Hironaga, Koichiro Tsuchiya, Maki Urushihara, Shoji Kagami and Toshiaki Tamaki : Angiotensin II receptor blocker inhibits PDGF-induced cell migration in rat mesangial cells, 39th ASN annual meeting 2006, San Diego, Nov. 2006.
107.	Koichiro Tsuchiya, Yuya Horinouchi, Yasuhisa Kanematsu, Shinji Abe, Hideki Ohnishi, Soichiro Tajima, Keisuke Ishizawa, Toshiaki Tamaki and Yoshiharu Takiguchi : Production of nitrosonifedipine radical from nifedipine and its antioxidative activity in cultured cells, 13th annual meeting of society of free radical and biology of medicine, Denver, Nov. 2006.
108.	Koichiro Tsuchiya, Yasuhisa Kanematsu, Keisuke Ishizawa, Shinji Abe, Hideki Ohnishi, Soichiro Tajima, Kazuyoshi Kawazoe, Yoshiharu Takiguchi and Toshiaki Tamaki : Dietary nitrite is an alternative source of NO in vivo, International Society for Radical Research 13th Biennial Congress, Davos, Switzerland, Aug. 2006.
109.	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.
110.	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.
111.	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.

Proceeding of Domestic Conference:

1.	竹内大平, 吉岡俊彦, Kenta Yagi, 馬場彩花, 竹原恵美, 藤本啓介, Hiroyuki Sumitomo, Shin-ichi Sakamoto, Naoki Miyamoto, Atsushi Morishita, Naoya Kawakita, Hiroaki Toba, Keisuke Ishizawa and Hiromitsu Takizawa : JCOG0802/WJOG4607Lの結果を踏まえた肺癌術後他疾患罹患のリアルワールドデータ検証, 第77回日本胸部外科学会定期学術集会, Nov. 2024.
2.	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.
3.	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.
4.	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.
5.	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.
6.	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.
7.	福田仁, Takahiro Niimura, Kei Kawada, 石田智滉, 川西裕, 門田知倫, Mitsuhiro Goda, 安藤里英, Keisuke Ishizawa and 上羽哲也 : クラゾセンタンの体液貯留リスク因子の探索 -Japanese Adverse Drug Event Report (JADER)より-, 第41回SAH/スパズム・シンポジウム, Mar. 2024.
8.	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.
9.	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.
10.	Kei Kawada, 石田智滉, Mitsuhiro Goda and Keisuke Ishizawa : 基礎研究の力で明らかになる新たな真実:clinical questionの解決に向けて, 第33回医療薬学会年会, Nov. 2023.
11.	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.
12.	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.
13.	神農麻里奈, 小川敦, 鈴木加奈, 萱野純史, Masaya Kanda, Kaito Tsujinaka, Takashi Bandoh, Ayaka Nitta, 椋田千晶, Fuka Aizawa, Kei Kawada, 櫻田巧, 桐野靖, Mitsuhiro Goda and Keisuke Ishizawa : 処方提案受容率向上を目指した栄養輸液設計ツールの検討, 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.
14.	Keisuke Ishizawa : 医療における薬理学舎の矜持, 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.	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.
16.	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.
17.	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.
18.	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.
19.	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.
20.	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.
21.	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.
22.	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.
23.	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.
24.	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.
25.	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.
26.	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.
27.	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.
28.	Naoto Okada, Taro Shimizu, Hidenori ANDO, Tatsuhiro Ishida, Keisuke Ishizawa and 北原隆志 : 血液腫瘍患者における抗PEG抗体価の定量評価によるPEG修飾G-CSF関連有害事象の予測, 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.
29.	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.
30.	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.
31.	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.
32.	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.
33.	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.
34.	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.
35.	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.
36.	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.
37.	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.
38.	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.
39.	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.
40.	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.
41.	Satoshi Sakaguchi, 佐藤康敬, 石田光代, 前田和輝, 二見明香里, Kenta Yagi, 沖良祐, Koji Fujita, Hiroaki Yanagawa, Yuishin Izumi, Ryuji Kaji and Keisuke Ishizawa : 高用量メチルコバラミンの筋萎縮性側索硬化症に対する第III相試験の被験者及び家族におけるアンケート調査, 第43回日本臨床薬理学会学術総会, Nov. 2022.
42.	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.
43.	Keisuke Ishizawa : Data-driven pharmacological research for cardiovascular disease associated with cancer chemotherapy., 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33, Nov. 2022.
44.	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.
45.	Keisuke Ishizawa : Significance of Pharmacology in Clinical Practice - Learning the Basics and Applying the Basics., 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.
46.	Naoto Okada, Shingen Nakamura, Taro Shimizu, Hidenori ANDO, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Mitsuhiro Goda, Tatsuhiro Ishida and Keisuke Ishizawa : 免疫不全リスクを有する患者における新型コロナワクチンによる抗体獲得能に関連する因子の検討, 第32回日本医療薬学学会, Sep. 2022.
47.	BANDO Hiroshi, Mitsuhiro Goda, 新田侑生, Masayuki Chuma, 小川敦, 櫻田巧, 桐野靖 and Keisuke Ishizawa : 医療ビッグデータを用いたラモトリギン皮膚障害リスクに影響する併用薬の探索と多施設診療情報による検証, 第32回日本医療薬学会年会, Sep. 2022.
48.	Naoto Okada, Shingen Nakamura, Taro Shimizu, Hidenori ANDO, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Mitsuhiro Goda, Tatsuhiro Ishida and Keisuke Ishizawa : 免疫不全リスクを有する患者における新型コロナワクチンによる抗体獲得能に影響を与える因子の検討, 第32回日本医療薬学会年会, Sep. 2022.
49.	椋田千晶, 小川敦, Mitsuhiro Goda, Toshihiko Yoshioka, Takahiro Niimura, 牛尾聡一郎, 江角悟, Naoto Okada, Yoshito Zamami and Keisuke Ishizawa : 有害事象自発報告データベースを用いたダントロレン誘発高カリウム血症に影響を与える因子の解析, 第32回日本医療薬学会年会, Sep. 2022.
50.	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.
51.	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.
52.	Naoto Okada, Mitsuhiro Goda and Keisuke Ishizawa : 【How to 編】臨床研究はじめの一歩:研究の「種」の見つけ方と育て方, 第32回日本医療薬学会年会シンポジウム3, Sep. 2022.
53.	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.
54.	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.
55.	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.
56.	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.
57.	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.
58.	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.
59.	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.
60.	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.
61.	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.
62.	Koji MIYATA, Yuki Izawa-Ishizawa, Kaito TSUJINAKA, 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.
63.	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.
64.	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.
65.	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.
66.	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.
67.	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.
68.	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.
69.	Hiroto Unten, Hirofumi Hamano, Takahiro Niimura, Nanami Tomochika, Shiori Nishiuchi, Mitsuhiro Goda, Kenta Yagi, 相澤風花, Yoshito Zamami 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性心筋症に対する予防薬の開発, 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シンポジウム 2, Jul. 2022.
70.	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.
71.	Hiroto Unten, Hirofumi Hamano, Takahiro Niimura, Kazushi Uchida, Nanami Tomochika, MIYATA Koji, 石田俊介, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Yoshito Zamami and Keisuke Ishizawa : 免疫チェックポイント阻害剤関連心筋炎の解析に適した実験的病態モデルの開発, 第141回日本薬理学会近畿部会, Jul. 2022.
72.	Takeshi Imakura, Seidai Satou, Kazuya Koyama, Takahiro Niimura, Kojin Murakami, Yuya Yamashita, Keiko Haji, Kozo Kagawa, Hiroshi Kawano, Yoshito Zamami, Keisuke Ishizawa and Yasuhiko Nishioka : In silico解析により同定されたPLK阻害剤のブレオマイシン誘発肺線維症モデルマウスにおける効果の検討, 第62回日本呼吸器学会学術講演会, Apr. 2022.
73.	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.
74.	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
75.	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
76.	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
77.	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.
78.	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.
79.	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.
80.	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
81.	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.
82.	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
83.	Hiroki Yamada, Rio Ohmori, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : ゲノムワイド関連解析によるビンクリスチン副作用発現関連遺伝子の同定と機械学習を用いた副作用発現予測モデルの構築, 第60回日本薬学会中国四国支部学術大会, Nov. 2021.
84.	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.
85.	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
86.	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.
87.	Naoto Okada, Aki Nakamoto, 泉侑希, Masayuki Chuma, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Hirofumi Hamano, Yoshito Zamami, Momoyo Azuma and Keisuke Ishizawa : タゾバクタム・ピペラシリン併用時における血中濃度時間曲線下面積に基づくバンコマイシン誘発腎障害の評価, 第15回日本腎臓病薬物療法学会学術集会・総会2021, Nov. 2021.
88.	Takeshi Imakura, Seidai Satou, Kazuya Koyama, Takahiro Niimura, Kohjin Murakami, Naoki Takahashi, Kozo Kagawa, Yoshito Zamami, Keisuke Ishizawa and Yasuhiko Nishioka : In silico 解析を用いた肺線維症に対する新規治療薬の探索, 第1回日本びまん性肺疾患研究会, Oct. 2021.
89.	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
90.	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
91.	Tomomi Tani, Masayuki Chuma, Mitsuhiro Goda, Takashi Bandoh, Masateru Kondoh, Yurika Kuniki, Hirofumi Hamano, Takahiro Niimura, Naoto Okada, Fuka Aizawa, Kenta Yagi and Keisuke Ishizawa : ビッグデータ解析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その有用性の検討, 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
92.	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
93.	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
94.	Hiroto Unten, Hirofumi Hamano, Takahiro Niimura, Nanami Tomochika, Shiori Nishiuchi, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Yoshito Zamami and Keisuke Ishizawa : Exploration of prophylactic drugs against doxorubicin-induced cardiomyopathy using largescale medical databases, 第15回次世代を担う若手のための医療薬科学シンポジウム, Oct. 2021.
95.	Hirofumi Hamano, Yoshito Zamami, Kazushi Uchida, MIYATA Koji, Yuya Miwa, Akihito Nakamura, 生田賢治, 泉侑希, Mitsuhiro Goda and Keisuke Ishizawa : Development of an Experimental Disease Model Suitable for the Analysis of Cancer Immunotherapy-Associated Myocarditis, 第15回次世代を担う若手のための医療薬科学シンポジウム, Oct. 2021.
96.	TSUJINAKA Kaito, Naoto Okada, 藤原範子, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Hirofumi Hamano, 櫻田巧, 桐野靖, Yoshito Zamami, Momoyo Azuma and Keisuke Ishizawa : 医療従事者におけるインフルエンザ暴露後予防目的におけるオセルタミビルのアドヒアランス解析, 第31回日本医療薬学会年会, Oct. 2021.
97.	Naoto Okada, Aki Nakamoto, 泉侑希, Masayuki Chuma, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Hirofumi Hamano, Yoshito Zamami, Momoyo Azuma and Keisuke Ishizawa : タゾバクタム・ピペラシリン併用時のバンコマイシン誘発腎障害は血中濃度時間曲線下面積を指標とした TDMによって回避可能か?, 第31回日本医療薬学会年会, Oct. 2021.
98.	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
99.	Kenta Yagi, Mitsuhiro Goda, Hirofumi Hamano, Satoshi Sakaguchi, Hiroaki Yanagawa and Keisuke Ishizawa : 臨床研究における倫理指針と個人情報の基礎知識, 第31回日本医療薬学会年会, Oct. 2021.
100.	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
101.	Hirofumi Hamano, Yoshito Zamami, Mitsuhiro Goda, Fuka Aizawa, Kenta Yagi and Keisuke Ishizawa : データサイエンスと基礎研究手法の融合, 第31回日本医療薬学会年会, Oct. 2021. (Keyword) data analysis
102.	Masayuki Chuma, Aki Nakamoto, Takashi Bandoh, Takahiro Niimura, Naoto Okada, Fuka Aizawa, Hirofumi Hamano, Kenta Yagi, Mitsuhiro Goda, Yoshito Zamami, Keisuke Ishizawa and Yoshikazu Tasaki : メタアナリシスとデータベース解析の融合によるハイインパクトエビデンスの創出, 第31回日本医療薬学会年会, Oct. 2021. (Keyword) data analysis
103.	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
104.	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
105.	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.
106.	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
107.	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
108.	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.
109.	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.
110.	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
111.	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
112.	坂東寛, Mitsuhiro Goda, Yoshito Zamami, 桐野靖, 中村敏己 and Keisuke Ishizawa : 医療ビッグデータを用いた併用薬によるラモトリギンの皮膚障害リスクの検証, 日本薬学会第141年会, Mar. 2021.
113.	Fuka Aizawa, Yoshito Zamami, Hirofumi Hamano, Naoto Okada, 林明希, Kenta Yagi, Mitsuhiro Goda, 桐野靖, 中村敏己 and Keisuke Ishizawa : COVID-19感染拡大に伴うオンライン型薬学実務実習の導入, 日本薬学会第141年会, Mar. 2021.
114.	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.
115.	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.
116.	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
117.	尾崎領彦, Atsushi Mitsuhashi, Hiroto Yoneda, Kenji Otsuka, Hiroshi Nokihara, Yasuhiko Nishioka, 櫻田巧 and Keisuke Ishizawa : ペメトレキセド投与後の皮疹に対するデキサメタゾン予防投与の効果の検討, 第18回日本臨床腫瘍学会学術集会, Feb. 2021.
118.	Minori Takei, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : 機械学習による遺伝情報を用いた抗がん剤投与の味覚障害発現予測モデルの構築, 第59回中国四国支部学術大会, Dec. 2020.
119.	Yuka Endoh, Hozumi Tashima, 岡田直人, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : ゲノム情報を用いた機械学習によるシタラビン投与後の副作用発現予測モデルの構築, 第59回中国四国支部学術大会, Dec. 2020.
120.	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.
121.	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.
122.	Atsushi Mitsuhashi, 櫻田巧, Mitsuhiro Goda, Yoshito Zamami, Hiroto Yoneda, Kenji Otsuka, Hiroshi Nokihara, Keisuke Ishizawa and Yasuhiko Nishioka : ペメトレキセド投与後の皮疹に対する低用量デキサメタゾン予防効果の検討, 第61回日本肺癌学会学術集会, Nov. 2020.
123.	櫻田巧, Atsushi Mitsuhashi, Hiroto Yoneda, Kenji Otsuka, Mitsuhiro Goda, Yoshito Zamami, Keisuke Ishizawa, Hiroshi Nokihara and Yasuhiko Nishioka : ペメトレキセド投与後の皮疹に対する低用量のステロイド予防投与の前向き臨床試験, 第58回日本癌治療学会学術集会, Oct. 2020.
124.	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.
125.	泉侑希, Shunsuke Ishida, 長谷川結美, 武智研志, Mitsuhiro Goda, Yoshito Zamami, 桐野靖, 中村敏己, 寺岡和彦, Shusuke Yagi, Masataka Sata and Keisuke Ishizawa : 高齢者の薬物療法管理ツールを活用した薬剤業務の効率化, 第84回日本循環器学会学術集会, Jul. 2020.
126.	Naoto Okada, 神農麻里奈, Shingen Nakamura, Hirokazu Miki, Hiroyoshi Watanabe, Mitsuhiro Goda, Masayuki Chuma, Kenshi Takechi, Yoshito Zamami, 桐野靖, 中村敏己, Kazuhiko Teraoka, Masahiro Abe and Keisuke Ishizawa : 血液凝固因子製剤の在庫適正化に向けた取り組みによる薬剤廃棄額の削減効果, Journal of Japnese Society of Hospital Pharmacists, Vol.56, No.7, 803-808, Jul. 2020. (Summary) 血友病治療に用いる血液凝固因子製剤(coagulation factor:以下，CF)は高価である一方で，在庫流動性が低いという製剤的性質を有するが，これまで適切な在庫管理法の報告はない．徳島大学病院は2017年4月から，診療科と連携したCFの在庫適正化の取り組みを開始した．取り組み開始前である2015年4月~2017年3月の期間と，取り組み開始後である2017年4月~2019年3月の期間における血友病患者数，CF調剤薬剤数に差はなかったが，取り組み開始後のCF廃棄額は取り組み開始前と比較して78.4 (Keyword) 血液凝固因子(治療的利用) / 血友病A(薬物療法) / 病院在庫管理 / ヒト / 新生児 / 乳児(1~23ヶ月) / 幼児(2~5) / 小児(6~12) / 青年期(13~18) / 成人(19~44) / 中年(45~64) / 高齢者(65~79) / 男 / 女
127.	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.
128.	Yuka Endoh, Hozumi Tashima, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : 機械学習を用いたゲノム情報によるシタラビン投与の副作用発現予測モデルの構築, 日本薬学会第140年会, Mar. 2020.
129.	Minori Takei, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : 遺伝情報を用いた機械学習による抗がん剤投与の味覚障害発現予測モデルの構築, 日本薬学会第140年会, Mar. 2020.
130.	Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Mitsuhiro Goda, Yoshito Zamami, Licht Miyamoto, Keisuke Ishizawa and Koichiro Tsuchiya : The involvement of ferroptosis on cisplatin-induced nephrotoxicity, 第93回日本薬理学会年会, Mar. 2020.
131.	遠藤優香, 田島穂澄, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : 機械学習を用いたゲノム情報によるシタラビン投与の副作用発現予測モデルの構築, 日本薬学会年会要旨集, 26M-am07S, Mar. 2020. (Keyword) Cytarabine(毒性・副作用) / 皮膚疾患(化学的誘発) / リスク評価 / 機械学習 / ヒト
132.	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.
133.	Hirofumi Hamano, Yasumasa Ikeda, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Kenshi Takechi, Masayuki Chuma, Yoshito Zamami, Yuya Horinouchi, Licht Miyamoto, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン誘発性腎障害を予防する既存薬物の同定, 第260回徳島医学会学術集会(令和元年度冬期), Feb. 2020.
134.	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.
135.	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.
136.	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.
137.	Yasumasa Ikeda, Yuya Horinouchi, Hirofumi Hamano, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン腎障害における鉄依存性細胞死の検討, 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会, Nov. 2019.
138.	Hirofumi Hamano, Yasumasa Ikeda, Yuya Horinouchi, Mitsuhiro Goda, Yoshito Zamami, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : プロトンポンプ阻害剤はヘプシジンを介して鉄代謝異常に関与する, 第29回日本医療薬学会年会, Nov. 2019.
139.	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.
140.	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.
141.	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.
142.	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.
143.	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.
144.	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.
145.	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.
146.	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.
147.	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.
148.	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.
149.	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.
150.	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.
151.	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.
152.	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.
153.	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.
154.	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.
155.	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.
156.	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.
157.	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.
158.	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.
159.	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.
160.	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.
161.	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.
162.	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.
163.	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.
164.	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.
165.	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.
166.	Yuto Tanigaki, Yuta Yamaguchi, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : ゲノムワイド関連解析を用いたテイコプラニン・バンコマイシン投与による皮疹発現および血中濃度関連遺伝子座の同定, 日本薬学会第139年会, Mar. 2019.
167.	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.
168.	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.
169.	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.
170.	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.
171.	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.
172.	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.
173.	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.
174.	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.
175.	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.
176.	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.
177.	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.
178.	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.
179.	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.
180.	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.
181.	Rio Ohmori, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : ゲノムワイド関連解析を用いたビンクリスチンによる末梢神経障害発現関連遺伝子の同定, 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.
182.	Yuta Yamaguchi, Yuto Tanigaki, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Youichi Sato : CYP遺伝子多型とバンコマイシンの副作用発現及び血中濃度との関連解析, 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.
183.	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.
184.	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.
185.	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.
186.	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.
187.	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.
188.	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.
189.	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.
190.	櫻田巧, Masaki Imanishi, Yoshito Zamami, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : 腎機能がペメトレキセド治療における安全性に影響を与えるか, 日本臨床腫瘍薬学会学術大会2018, Mar. 2018.
191.	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.
192.	高橋志門, 城ヶ瀧里奈, 高橋撤多, Kenshi Takechi, Yoshito Zamami, 相良英憲 and Keisuke Ishizawa : PTSDモデルラットにおける文脈的恐怖記憶の消去に対する治療薬の探索, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
193.	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.
194.	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.
195.	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.
196.	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.
197.	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.
198.	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.
199.	Yoshito Zamami, 近藤正輝, 阿部奈都美, Masayuki Chuma, 今井徹, Kenshi Takechi, Masaki Imanishi, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : 集中治療における薬剤師教育, 第45回日本集中治療医学会学術集会委員会企画4(CP4)「集中治療における薬剤師のポジションを考える」, Feb. 2018.
200.	石田俊介, 坂東寛, Kenshi Takechi, Yoshito Zamami, Masaki Imanishi, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : 副作用モニタリング管理ツールの開発と業務効率化, 平成29年度大学病院情報マネジメント部門連絡会議, Feb. 2018.
201.	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.
202.	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.
203.	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.
204.	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.
205.	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.
206.	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.
207.	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.
208.	石田俊介, 坂東寛, Kenshi Takechi, Yoshito Zamami, Masaki Imanishi, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : 抗精神病薬を対象とする副作用モニタリング管理ツールの開発と臨床評価, 第27回日本医療薬学会年会, Nov. 2017.
209.	濱野裕章, 三井茉綸, Yoshito Zamami, Takahiro Niimura, Kenshi Takechi, 岡田直人, 今西正樹, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : アルカリ化剤はイリノテカン誘発性好中球減少症を予防する, 第27回日本医療薬学会年会, Nov. 2017.
210.	岡田直人, Yoshito Zamami, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : リポソーム化アムホテリシン B 製剤による低カリウム血症発現に関与する因子の同定:予防的カリウム製剤投与の有用性, 第27回日本医療薬学会年会, Nov. 2017.
211.	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.
212.	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.
213.	石田俊介, 坂東寛, Kenshi Takechi, Yoshito Zamami, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : 管理ツール導入による臨床検査値を指標とした副作用モニタリングへの効果, 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.
214.	濱野裕章, 三井茉綸, Yoshito Zamami, Takahiro Niimura, Kenshi Takechi, 岡田直人, Masaki Imanishi, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : アルカリ化剤はイリノテカン誘発性好中球減少症を予防する, 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.
215.	岡田直人, 東桃代, Masaki Imanishi, Yoshito Zamami, 桐野靖, 中村敏己, 寺岡和彦, 安倍正博 and Keisuke Ishizawa : リポソーム化アムホテリシンB製剤による低カリウム血症の発現関連因子の同定, 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.
216.	柴田高洋, Masaki Imanishi, Yoshito Zamami, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : PCR法によるSCCmec タイピングを利用した動向調査から探る来院者とMRSAの院内伝播の関連性, 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.
217.	合田光寛, 高橋沙矢佳, 長田武, Masaki Imanishi, Kenshi Takechi, Yoshito Zamami, 桐野靖, 中村敏己, 寺岡和彦, 大塚正人 and Keisuke Ishizawa : シスプラチン誘発腎障害に対するSGLT2阻害薬の影響, 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.
218.	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.
219.	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.
220.	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.
221.	Yuto Tanigaki, Youichi Sato, Yuta Yamaguchi, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Aiko Yamauchi : テイコプラニン投与による副作用発現および血中濃度とCYP遺伝子多型との関連解析, 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.
222.	Hozumi Tashima, Youichi Sato, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Aiko Yamauchi : シタラビン投与による副作用発現と代謝経路関連遺伝子多型の関連解析, 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.
223.	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.
224.	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.
225.	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.
226.	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.
227.	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.
228.	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.
229.	Masahiko Azuma, Masami Nagamune, Takashi Iwata, Kazuyoshi Kawazoe, Keisuke Ishizawa, Yutaka Taketani, Yasuhiko Nishioka and Masashi Akaike : 徳島大学における担当患者を用いた多職種連携教育の取り組み, 第49回日本医学教育学会大会, Aug. 2017.
230.	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.
231.	Rio Ohmori, Youichi Sato, Misaki Kiguchi, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Aiko Yamauchi : ビンクリスチンによる副作用発現とMDR1遺伝子多型との関連性, 第20回日本医薬品情報学会総会・学術大会, Jul. 2017.
232.	Yuta Yamaguchi, Youichi Sato, Yuto Tanigaki, Naoto Okada, Shingen Nakamura, Kumiko Kagawa, Shiroh Fujii, Hirokazu Miki, Keisuke Ishizawa, Masahiro Abe and Aiko Yamauchi : バンコマイシン投与による副作用発現及び血中濃度とCYP遺伝子多型との関連解析, 第20回日本医薬品情報学会総会・学術大会, Jul. 2017.
233.	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.
234.	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.
235.	坂東寛, 石田俊介, Kenshi Takechi, Masaki Imanishi, Yoshito Zamami, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 薬剤師がマネジメントする非定型抗精神病薬における副作用モニタリングの効果, 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.
236.	石田俊介, Masaki Imanishi, Yoshito Zamami, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 医薬品管理モニタリングツールを活用した周術期における医薬品管理業務の効率化, 第20回日本医薬品情報学会総会・学術大会, Jul. 2017.
237.	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.
238.	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.
239.	中本亜樹, 岡田直人, 濱野裕章, Sonoko Yasui, 西麻希, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka, Yasuhiro Hamada and Keisuke Ishizawa : 頭頸部癌に対する化学放射線療法における CDDP 単独療法及び 52FU+CDDP 療法による副作用発現の比較, 第11回日本緩和医療薬学会年会, Jun. 2017.
240.	坂東左奈子, 櫻田巧, Naoto Okada, Masaki Imanishi, Yoshito Zamami, Kazuhiko Teraoka, 中村敏己 and Keisuke Ishizawa : エピルビシン，シクロフォスファミド投与による持続型G-CSF製剤の有効性の検討, 第42回日本外科系連合学会学術集会, Jun. 2017.
241.	井上貴久, 櫻田巧, 柴田高洋, Naoto Okada, Yoshito Zamami, 今西正樹, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 抗EGFR抗体薬の投与による低Mg血症発現率の比較検討, 第42回日本外科系連合学会学術集会, Jun. 2017.
242.	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.
243.	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.
244.	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.
245.	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.
246.	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.
247.	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.
248.	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.
249.	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.
250.	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.
251.	井上貴久, 櫻田巧, 柴田高洋, Naoto Okada, Yoshito Zamami, 今西正樹, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 抗EGFR抗体薬における副作用としての低Mg血症発現率の比較検討, 日本薬学会年会要旨集, No.4, 172, Mar. 2017.
252.	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.
253.	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.
254.	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.
255.	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.
256.	Yoshito Zamami, 近藤正輝, 阿部奈都美, Masaki Imanishi, Kenshi Takechi, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 薬剤師と考える感染症治療抗MRSA薬による抗菌薬治療, Journal of the Japanese Society of Intensive Care Medicine, Vol.24, No.Suppl., SS4-1, Feb. 2017.
257.	Masaki Imanishi, 松永慎司, Keisuke Ishizawa, Toshiaki Tamaki and Shuhei Tomita : 大動脈瘤形成における平滑筋由来HIF-1αの役割, 第26回日本循環薬理学会, Dec. 2016.
258.	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.
259.	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.
260.	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.
261.	中本亜樹, 野裕章, Naoto Okada, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : DPP-4阻害薬ーDPP-4阻害薬間の切り替えによるLDL-Cの変動, 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.
262.	木宿昌俊, Masaki Imanishi, 中村敏己, Kazuhiko Teraoka, Keisuke Ishizawa and 中村敏己 : 消化器外科病棟における専任薬剤師のチーム医療参画に対する評価, 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.
263.	井上貴久, 柴田高洋, 櫻田巧, Naoto Okada, Yoshito Zamami, Masaki Imanishi, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 抗EGFR抗体薬の使用における低Mg血症の発現率の比較検討, 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.
264.	坂東左奈子, Naoto Okada, 櫻田巧, Masaki Imanishi, Yoshito Zamami, Kazuhiko Teraoka, 中村敏己 and Keisuke Ishizawa : 乳がん患者におけるエピルビシン，シクロフォスファミド投薬による持続型G-CSF製剤の有効性の検討, 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.
265.	桑原絵美, Naoto Okada, 高瀬友佳子, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 徳島大学病院におけるニボルマブの適正使用に向けた取り組み, 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.
266.	田岡寛之, 中本亜紀, 桐野靖, 中村敏己, Kazuhiko Teraoka, 伏谷秀治 and Keisuke Ishizawa : 頭頸部癌の放射線化学療法による口腔粘膜障害，口腔内痛に対する半夏瀉心湯含嗽の効果, 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.
267.	濱野裕章, 中本亜紀, 桐野靖, 中村敏己, Kazuhiko Teraoka, 伏谷秀治 and Keisuke Ishizawa : 高ビリルビン血症を伴う膵癌患者におけるGEM+nabPTX療法施行時の副作用発現状況, 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.
268.	石田俊介, 坂東寛, 坂本久美子, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 抗精神病薬を対象にした臨床検査値を指標とする副作用モニタリング管理ツール導入による効果, 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.
269.	櫻田巧, Naoto Okada, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : ペメトレキセドによる骨髄抑制のリスク因子解析, 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.
270.	Naoto Okada, 中本亜紀, 田中里奈, 泉侑希, Shinji Abe, Chiemi Sato, Keisuke Ishizawa and Kazuyoshi Kawazoe : qSOFAスコアを用いたカンジダ血漿の重症度分類の有用性, 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.
271.	伊勢夏子, Kenshi Takechi, 前田和輝, 宮本登志子, 片島るみ, 阿部真治, 今西正樹, Yoshito Zamami, Keisuke Ishizawa and Hiroaki Yanagawa : 薬学病院実務実習の受講者における臨床研究・治験に関する意識と実習による変化, Japanese Journal of Clinical Pharmacology and Therapeutics, Vol.47, No.Suppl., S315, Oct. 2016. (Keyword) 疫学研究特性臨床試験意識調査臨床・臨地実習薬学大学教育 *臨床研究ヒト
272.	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.
273.	三井茉綸, Yoshito Zamami, Masaki Imanishi, Kenshi Takechi and Keisuke Ishizawa : オーストラリアのがん病棟における薬剤師業務に対する患者満足度調査, 第26回日本医療薬学会年会, Sep. 2016.
274.	小中健, 櫻田巧, Masaki Imanishi, Yoshito Zamami, Keisuke Ishizawa and 伏谷秀治 : 肺がん患者におけるUGT1A1 遺伝子多型とイリノテカンの投与量に関する検討, 第26回日本医療薬学会年会, Sep. 2016.
275.	Naoto Okada, 御牧夕紀子, 桑原絵美, Yoshihiro Matsudate, Shinji Abe, Chiemi Sato, Yoshiaki Kubo, Keisuke Ishizawa and Kazuyoshi Kawazoe : ニボルマブ投与による末梢血リンパ球比率の変化が副作用発現及び治療効果に与える影響, 第26回日本医療薬学会年会, Sep. 2016.
276.	濱野裕章, 中本亜樹, Naoto Okada, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : GEM + nabPTX 療法における高ビリルビン血症が副作用発現に与える影響, 第26回日本医療薬学会年会, Sep. 2016.
277.	中本亜樹, 濱野裕章, Naoto Okada, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : DPP-4 阻害薬服用患者における他のDPP-4 阻害薬への切り替えによるLDL-C 低下作用の検討, 第26回日本医療薬学会年会, Sep. 2016.
278.	桑原絵美, Naoto Okada, 高瀬友佳子, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 徳島大学病院におけるニボルマブの使用状況と今後の有害事象対策, 第26回日本医療薬学会年会, Sep. 2016.
279.	櫻田巧, Naoto Okada, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : ペメトレキセド投与後の皮疹出現は好中球減少症のリスク因子となる, 第26回日本医療薬学会年会, Sep. 2016.
280.	Yoshito Zamami, 今西正樹, Kenshi Takechi, 小山敏広, 大島礼子, 樋之津史郎, 狩野光伸 and Keisuke Ishizawa : 新規心肺蘇生薬の開発を目指したドラッグリポジショニング研究, 日本高血圧学会総会プログラム・抄録集, 437, Sep. 2016. (Keyword) 心肺蘇生法新薬開発医薬品の適応拡大
281.	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.
282.	Yoshito Zamami, Masaki Imanishi, Kenshi Takechi, 小山敏広, 大島礼子, 樋之津史郎, 狩野光伸 and Keisuke Ishizawa : 症例データベースを活用して新規心肺蘇生薬の開発を目指したドラッグリポジショニング研究, 第2回日本医薬品安全性学会学術大会( 岐阜), Jul. 2016.
283.	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.
284.	柴田高洋, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 外来診療棟を主としたMRSAの実態調査, 医療薬学フォーラム2016/第24回クリニカルファーマシーシンポジウム (大津), Jun. 2016.
285.	Yoshito Zamami, Masaki Imanishi, Kenshi Takechi, 小山敏広, 大島礼子, 今井徹, 樋之津史郎, 狩野光伸 and Keisuke Ishizawa : ドラッグリポジショニングを切り口とした新規心肺蘇生薬の探索研究-大規模医療情報を活用した検討-, 医療薬学フォーラム2016/第24回クリニカルファーマシーシンポジウム (大津 ), Jun. 2016.
286.	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.
287.	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.
288.	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.
289.	石田俊介, 坂本久美子, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 持参薬管理業務における周術期中止医薬品の管理ツール導入による効果, 第19回日本医薬品情報学会総会・学術大会 (町田市), Jun. 2016.
290.	Keisuke Ishizawa : 救急集中治療を変える!!薬学から重症患者の治療向上に寄与するエビデンスを創り発信する．, 日本薬学会第136年会シンポジウムS20オーガナイザー( 横浜), Mar. 2016.
291.	Yoshito Zamami, Masaki Imanishi, 小山敏広, 大島礼子, 樋之津史郎, 狩野光伸 and Keisuke Ishizawa : 心肺停止患者における社会復帰率の向上を志向したドラッグリポジショニング研究, 日本薬学会第136年会シンポジスト( 横浜 ), Mar. 2016.
292.	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.
293.	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.
294.	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.
295.	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.
296.	Yuya Horinouchi, 櫻田巧, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : ベバシズマブ投与患者における高血圧のリスクファクター, 日本薬学会第136年会( 横浜), Mar. 2016.
297.	小中健, 花房剛志, 田中恭平, Naoto Okada, Masaki Imanishi, Yoshito Zamami, Kazuyoshi Kawazoe and Keisuke Ishizawa : パクリタキセル誘発性神経障害に対する漢方製剤抽出物の影響, 日本薬学会第136 年会( 横浜), Mar. 2016.
298.	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.
299.	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.
300.	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.
301.	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.
302.	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.
303.	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.
304.	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.
305.	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.
306.	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.
307.	Naoto Okada, 花房剛志, Shinji Abe, Chiemi Sato, 中村敏己, Kazuhiko Teraoka, Keisuke Ishizawa and Kazuyoshi Kawazoe : 自家造血幹細胞移植併用大量化学療法における味覚障害の発現に関与する危険因子の探索, 日本薬学会第136年会, Mar. 2016.
308.	Keisuke Ishizawa : 「教授就任記念講演」サイエンスを基盤とする臨床薬剤業務の実践, 第252回徳島医学会学術集会(徳島), Feb. 2016.
309.	濱野裕章, 中本亜樹, 村上明希, 田中里奈, Naoto Okada, Kazuhiko Teraoka, 中村敏己 and Keisuke Ishizawa : アルカリ化剤はイリノテカンによる好中球減少症を予防する, 第252回徳島医学会学術集会(徳島), Feb. 2016.
310.	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.
311.	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.
312.	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.
313.	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.
314.	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.
315.	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.
316.	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.
317.	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.
318.	石田俊介, 伏谷秀治, 坂本久美子, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Keisuke Ishizawa : 管理ツールによる臨床検査値を指標とした副作用モニタリングの効率化, 第54回中国四国支部学術大会(高知), Nov. 2015.
319.	柴田高洋, Naoto Okada, 伏谷秀治, Hirofumi Shibata, Kazuyoshi Kawazoe and Keisuke Ishizawa : 実態調査からみる来院者が院内MRSAの伝播に及ぼす影響, 第54回中国四国支部学術大会(高知), Nov. 2015.
320.	花房剛志, Naoto Okada, 生田賢治, 小中健, Kazuyoshi Kawazoe, 中村敏己, Kazuhiko Teraoka, Masahiro Abe and Keisuke Ishizawa : 自家末梢血幹細胞移植併用大量化学療法施行時の味覚障害に対するクライオセラピーの有用性, 第54回中国四国支部学術大会(高知), Nov. 2015.
321.	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.
322.	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.
323.	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.
324.	柴田高洋, Naoto Okada, 伏谷秀治, Hirofumi Shibata, Kazuyoshi Kawazoe and Keisuke Ishizawa : 院内MRSA分布へ来院者が及ぼす影響, 第25回日本医療薬学会年会, Nov. 2015.
325.	西迫寛隆, 中川博之, Momoyo Azuma, Naoto Okada, 上村卓広, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Keisuke Ishizawa : 当院におけるカンジダ血症治療に対するガイドライン遵守率向上への取り組み, 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.
326.	濱野裕章, 中本亜樹, 村上明希, 田中里奈, Naoto Okada, Kazuhiko Teraoka, 中村敏己 and Keisuke Ishizawa : イリノテカンによる好中球減少症に対するアルカリ化剤の効果, 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.
327.	辻弥生, Youichi Sato, Kazuyoshi Kawazoe, Aiko Yamauchi and Keisuke Ishizawa : NSAIDsの種類及び服薬期間，頻度と発癌リスクに関するメタ解析, 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.
328.	柴田高洋, Naoto Okada, 伏谷秀治, Hirofumi Shibata, Kazuyoshi Kawazoe and Keisuke Ishizawa : 実態調査からみる来院者が院内MRSAの伝播に及ぼす影響, 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.
329.	花房剛志, Naoto Okada, 生田賢治, 小中健, Kazuyoshi Kawazoe, 中村敏己, Kazuhiko Teraoka, Masahiro Abe and Keisuke Ishizawa : 自家末梢血幹細胞移植併用大量化学療法施行時の味覚障害に対するクライオセラピーの有用性, 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.
330.	Naoto Okada, 伏谷秀治, Momoyo Azuma, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Keisuke Ishizawa : 抗MRSA薬を用いた治療に対する薬剤師介入の有用性:プロトコルに基づく薬物治療管理と多職種介入による臨床効果及び医療経済効果, 第25回日本医療薬学会年会, Nov. 2015.
331.	Naoto Okada, Shinji Abe, Chiemi Sato, Mami Azuma, Kazuyoshi Kawazoe, Akira Otaka and Keisuke Ishizawa : 徳島大学病院における模擬体験型学習を用いた実務実習の評価, 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.
332.	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.
333.	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.
334.	Naoto Okada, Kazuyoshi Kawazoe and Keisuke Ishizawa : 考える力の醸成を目指した実務実習の実践, 医療療薬学フォーラム2015/第23回クリニカルファーマシーシンポジウム, Jul. 2015.
335.	石田俊介, 伏谷秀治, 前田和輝, 渡邉美穂, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Keisuke Ishizawa : 当院薬剤部における管理ツール作成による副作用情報収集の効率化, 第18回日本医薬品情報学会(岡山), Jun. 2015.
336.	桐野靖, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Keisuke Ishizawa : 精神科病棟における炭酸リチウムの適正使用状況の推移, 第18回日本医薬品情報学会(岡山), Jun. 2015.
337.	Naoto Okada, 下岡幸恵, Momoyo Azuma and Keisuke Ishizawa : プロトコルに基づく薬物治療管理が医師の診療行動へ与える影響, 第63回日本化学療法学会総会, Jun. 2015.
338.	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.
339.	Naoto Okada, 伏谷秀治, Momoyo Azuma, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe, Hiroyoshi Watanabe, Masahiro Abe and Keisuke Ishizawa : 病棟薬剤によるプロトコルに基づく薬物治療管理の実践∼抗MRSA薬の適正使用に対する効果∼, 日本薬学会第135年会, Mar. 2015.
340.	西迫寛隆, 中川博之, Momoyo Azuma, 下岡幸恵, 伏谷秀治, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Keisuke Ishizawa : 徳島大学病院における真菌感染BUNDLEの活用について, 日本薬学会第135年会, Mar. 2015.
341.	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.
342.	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.
343.	Shinya Kobayashi, Kohta Moriyama, Misa Matsuda, Naoto Okada, 福壽由法, 富加見正樹, 森本俊司, Kazuyoshi Kawazoe and Keisuke Ishizawa : キクイモ(Helianthus tuberosus)の肝臓における脂肪蓄積抑制効果の検討, 日本薬学会第135年会, Mar. 2015.
344.	Naoto Okada, 伏谷秀治, Momoyo Azuma, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe, Hiroyoshi Watanabe, Masahiro Abe and Keisuke Ishizawa : 病棟薬剤によるプロトコルに基づく薬物治療管理の実践∼抗MRSA薬の適正使用に対する効果, 日本薬学会第135年会(神戸), Mar. 2015.
345.	Keiji Ogura, Hiroko Hirakawa, Takuya Morisaki, Jun Yamamoto, Koji Ebisuno, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya, Akira Shigenaga and Akira Otaka : 低酸素環境応答型アミノ酸の開発研究, 日本薬学会第135年会, Mar. 2015.
346.	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.
347.	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.
348.	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.
349.	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.
350.	今西正樹, 井口道代, 冨田紀子, ツナピパナギオタ, 松永慎司, Keisuke Ishizawa, Toshiaki Tamaki and Shuhei Tomita : 血管リモデリングにおける平滑筋由来hypoxia-inducible factor-1αの役割, 第88回日本薬理学会年会(愛知), Mar. 2015.
351.	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.
352.	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.
353.	野田和克, Momoyo Azuma, 西迫寛隆, 伏谷秀治, 佐藤雅美, 畑美智子, Keisuke Ishizawa and Yasuhiko Nishioka : 真菌感染BUNDLEの徳島大学病院での活用について, 第250回徳島医学会学術集会, Feb. 2015.
354.	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.
355.	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.
356.	Ken Konaka, 櫻田巧, Takahiro Shibata, Naoto Okada, 西迫寛隆, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Keisuke Ishizawa : 大腸がんにおけるEGFR抗体薬による低マグネシウム血症の発現状況および発現因子に関する検討, 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講演要旨集, 297, Nov. 2014.
357.	鈴木杏奈, 田中里奈, Ken Konaka, Naoto Okada, 上村卓広, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Keisuke Ishizawa : 放射線併用化学療法(シスプラチン)における腎障害の危険因子の探索, 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講演要旨集, 296, Nov. 2014.
358.	坂東佐奈子, 櫻田巧, 泉侑希, Ken Konaka, Naoto Okada, Kazuhiko Teraoka, 中村敏己, Kazuyoshi Kawazoe and Keisuke Ishizawa : 胸膜癒着術におけるユニタルクとビシバニールの副作用の比較, 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講演要旨集, 296, Nov. 2014.
359.	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.
360.	坂東左奈子, 櫻田巧, 泉侑希, 小中健, Naoto Okada, Kazuhiko Teraoka, 中村敏己, Kazuyoshi Kawazoe and Keisuke Ishizawa : 胸膜癒着術におけるユニタルクとピシバニールの副作用の比較, 第53回中国四国支部学術大会(広島), Nov. 2014.
361.	櫻田巧, Souji Kakiuchi, Yuya Horinouchi, 西迫寛隆, Naoto Okada, Kazuhiko Teraoka, 中村敏己, Kazuyoshi Kawazoe, Yasuhiko Nishioka and Keisuke Ishizawa : ペメトレキセドによる発疹に関与する因子の同定とステロイド追加投与の有効性の検討, 第53回中国四国支部学術大会(広島), Nov. 2014.
362.	山根萌, Licht Miyamoto, 冨田洋輔, 竹之熊和也, 川崎彩, 山岡朋美, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : ヒト腎糸球体内皮細胞における亜硝酸塩によるAMPK-eNOS活性化経路の検討, 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.
363.	川崎彩, Licht Miyamoto, 山岡朋美, 山根萌, Keisuke Ishizawa and Koichiro Tsuchiya : 交感神経系刺激による肝臓の糖代謝および脂質代謝の制御におけるAMPKの意義, 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.
364.	山岡朋美, Licht Miyamoto, 川崎彩, 山根萌, 高橋梨恵, Keisuke Ishizawa, Rin Miyajima, Akira Shigenaga, Akira Otaka and Koichiro Tsuchiya : Leptinによる骨格筋培養細胞での代謝制御作用におけるSIRT1の役割, 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.
365.	Kohta Moriyama, Kohsuke Miyataka, Shinya Kobayashi, Misa Matsuda, Naoto Okada, Kazuyoshi Kawazoe and Keisuke Ishizawa : 高脂肪食負荷ラットを用いたキクイモの新規機能性探索研究, 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講演要旨集, 157, Nov. 2014.
366.	Aki Murakami, Yayoi Tsuji, Misa Matsuda, Naoto Okada, Kazuyoshi Kawazoe and Keisuke Ishizawa : ヒト腸管上皮細胞において枳実，陳皮抽出物がP糖タンパク質を介した薬物の排出に与える影響, 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講演要旨集, 156, Nov. 2014.
367.	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.
368.	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.
369.	山根萌, Licht Miyamoto, 冨田洋輔, 竹之熊和也, 川崎彩, 山岡朋美, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 亜硝酸塩による AMPK-eNOS 経路活性化, 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.
370.	柴田高洋, Naoto Okada, 伏谷秀治, Hirofumi Shibata, Kazuyoshi Kawazoe and Keisuke Ishizawa : PCR を用いた病院内のMRSA の動向調査, 第53回中国四国支部学術大会(広島), Nov. 2014.
371.	鈴木杏奈, 田中里奈, 小中健, Naoto Okada, 上村卓広, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Keisuke Ishizawa : 放射線併用化学療法(シスプラチン)における腎障害の危険因子の探索, Nov. 2014.
372.	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.
373.	山根萌, Licht Miyamoto, 冨田洋輔, 竹之熊和也, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : ヒト腎糸球体内皮細胞におけるAMPK-eNOS経路の活性化, 第126回日本薬理学会近畿部会, Oct. 2014.
374.	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.
375.	Licht Miyamoto, 渡辺勝志, 土橋有希, 山根萌, 田岡千明, 松下剛史, 笠原真一郎, 神谷昌樹, Keisuke Ishizawa, Shinji Abe, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖オリゴグリセロールを用いた難水溶性化合物の物性，薬物動態，薬効の改善, 次世代を担う創薬・医療薬理シンポジウム2014, Aug. 2014.
376.	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.
377.	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.
378.	山根萌, Licht Miyamoto, 冨田洋輔, 竹之熊和也, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 亜硝酸塩による AMPK-eNOS 経路活性化, 次世代を担う創薬・医療薬理シンポジウム 2014, Aug. 2014.
379.	山根萌, Licht Miyamoto, 冨田洋輔, 竹之熊和也, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 亜硝酸塩によるAMPK-eNOS経路活性化, 生体機能と創薬シンポジウム 2014, Aug. 2014.
380.	矢野友章, Licht Miyamoto, 竹之熊和也, 福田恵介, 津田勝範, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 食事による血中NOレベル変動の検討, 第249回徳島医学会, Jul. 2014.
381.	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.
382.	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.
383.	Licht Miyamoto, 渡邊勝志, 田岡千秋, 土橋有希, 松下剛史, Keisuke Ishizawa, Shinji Abe, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖オリゴグリセロール修飾による疎水性化合物の物性，薬物動態および薬効の改善, 日本薬学会第134年会, Mar. 2014.
384.	土橋有希, Shinji Abe, Licht Miyamoto, 松下剛史, 片桐彩人, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : 新規水溶性Paclitaxelの肺癌に対する抗腫瘍効果の検討, 日本薬学会第134年会, Mar. 2014.
385.	智子中西, Keisuke Ishizawa, Shinji Abe, Mari Nakase, Hirofumi Shibata, Chiemi Sato, Naokatu Arakaki, Youichi Sato, Naoshi Yamazaki, Jiro Kasahara, Mami Azuma, Tetsuo Yamazaki, Aiko Yamauchi, Yoshiharu Takiguchi and Koichiro Tsuchiya : Study of the method for development of case-problem solving abilities through advanced practice and the results that have been achieved, 日本薬学会第134年会, Mar. 2014.
386.	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.
387.	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.
388.	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.
389.	Licht Miyamoto, Megumi Yamane, Yohsuke Tomida, Kazuya Takenokuma, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 亜硝酸塩による腎保護作用および糖脂質代謝改善作用におけるAMPKの意義, 第87回日本薬理学会年会, Mar. 2014.
390.	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.
391.	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.
392.	Keisuke Ishizawa : 生活習慣病と薬物療法の基礎知識, 栄養改善指導支援事業地域活動実践栄養士研修会, Feb. 2014.
393.	山脇早穂, 佐藤佑太, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuichi Hamano : リチウム定量にあたえる共存物質の影響, 第37回徳島県医学検査学会, Dec. 2013.
394.	佐藤佑太, 山脇早穂, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuichi Hamano : セスキテルペンラクトン誘導体の鉄依存ラジカル生成過程の解明, 第37回徳島県医学検査学会, Dec. 2013.
395.	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.
396.	Keisuke Ishizawa : 生活習慣病∼その主な薬剤と栄養管理∼, 徳島県栄養士会スキルアップ&有床診療所研修会, Dec. 2013.
397.	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.
398.	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.
399.	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.
400.	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.
401.	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.
402.	智子中西, Keisuke Ishizawa, Shinji Abe, Mari Nakase, Hirofumi Shibata, Chiemi Sato, Naokatu Arakaki, Youichi Sato, Naoshi Yamazaki, Jiro Kasahara, Mami Azuma, Tetsuo Yamazaki, Aiko Yamauchi, Yoshiharu Takiguchi and Koichiro Tsuchiya : Study of the method for development of case-problem solving abilities through advanced practice and the results that have been achieved, 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.
403.	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.
404.	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.
405.	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.
406.	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.
407.	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.
408.	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.
409.	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.
410.	Licht Miyamoto, Masashi Watanabe, 河野舞, Yohsuke Tomida, Tsuyoshi Matsushita, 服部初彦, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖オリゴグリセロール修飾によるフェノフィブラートの物性および薬物動態，薬効の改善, 日本若学会第133年会, Mar. 2013.
411.	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.
412.	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.
413.	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.
414.	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.
415.	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.
416.	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.
417.	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.
418.	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.
419.	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.
420.	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.
421.	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.
422.	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.
423.	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.
424.	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.
425.	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.
426.	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.
427.	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.
428.	Akira Shigenaga, Keiji Ogura, Hiroko Hirakawa, Jun Yamamoto, Koji Ebisuno, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Akira Otaka : Design and synthesis of hypoxia-responsive amino acid which causes peptide bond cleavage in hypoxic cells, 第49回ペプチド討論会, Nov. 2012.
429.	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.
430.	Keisuke Ishizawa : 循環器疾患における酸化ストレス制御を基盤とする創薬研究, 次世代を担う創薬・医療薬理シンポジウム2012, Sep. 2012.
431.	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.
432.	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.
433.	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.
434.	渡邊勝志, Licht Miyamoto, 冨田洋輔, 河野舞, 田岡千明, 松下剛史, 神谷昌樹, 服部初彦, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖グリセロールオリゴマーによるフェノフィブラートの物性および薬物動態の改善, 生体機能と創薬シンポジウム2012, Aug. 2012.
435.	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.
436.	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.
437.	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.
438.	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.
439.	Licht Miyamoto, 河野舞, 中川剛夫, 服部初彦, 吉富康亮, Keisuke Ishizawa, Yoshiyuki Yoshimura, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖グリセロール修飾による新規水溶性プロブコール誘導体の開発と耐糖能改善作用のメカニズム, 第55回日本糖尿病学会年次学術集会, May 2012.
440.	Yoshiki Kashiwada, JIN Meina, 柴山恵美子, 和田悠, Keisuke Ishizawa, Licht Miyamoto, Koichiro Tsuchiya and 井端和郎 : スダチ(Citrus sudachi)果皮の有効利用に関する研究 (5) ―3-O-Feruloyl aldaric acid 1,4-lactone methyl esterの立体構造について―, 日本薬学会第132年会, No.2, 189, Mar. 2012.
441.	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.
442.	Shuichi Hamano, Yoko Kagawa, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : セスキテルペンラクトン誘導体の鉄依存ラジカル生成機構の検討, 日本薬学会大132年会, Mar. 2012.
443.	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.
444.	Licht Miyamoto, 河野舞, 中川剛夫, 服部初彦, 吉富康亮, Keisuke Ishizawa, Yoshiyuki Yoshimura, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖グリセロール修飾による新規水溶性プロブコール誘導体の開発と耐糖能改善作用のメカニズム, 日本薬学会年会, Mar. 2012.
445.	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.
446.	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.
447.	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.
448.	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.
449.	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.
450.	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.
451.	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.
452.	Licht Miyamoto, 河野舞, 中川剛夫, 服部初彦, 吉富康亮, Keisuke Ishizawa, Yoshiyuki Yoshimura, Hisao Nemoto and Koichiro Tsuchiya : 水溶性プロブコール誘導体による新たなメカニズムを介した耐糖能およびインスリン感受性の改善, 第244回徳島医学会学集会, Feb. 2012.
453.	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.
454.	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.
455.	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.
456.	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.
457.	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.
458.	Jumpei Taniguchi, Keisuke Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi, Toshiaki Tamaki and Shuhei Tomita : 血管平滑筋細胞のhypoxia-inducible factor-1αはangiotensinⅡ誘発血管リモデリングの形成に関与する, 第50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. 2011.
459.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Jumpei Taniguchi, Shoko Fujii, Asami Nuno, Yuta Suzuki, Licht Miyamoto, Yoshitaka Kihira, Koichiro Tsuchiya, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : マウス血管リモデリングに対するnitrosonifedipineの抑制効果, 第50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. 2011.
460.	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.
461.	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.
462.	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.
463.	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.
464.	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.
465.	Jumpei Taniguchi, Keisuke Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, 久次米敏秀, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi, Toshiaki Tamaki and Shuhei Tomita : 動脈硬化におけるhypoxia-inducible factor-1αの新規治療標的分子としての可能性, 医療薬学フォーラム2011/第19回クリニカルファーマシーシンポジウム, Jul. 2011.
466.	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.
467.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : ヒト腎糸球体血管内皮細胞において細胞内遊離鉄はangiotensin ⅡによるICAM-1の発現を増強する, 第54回日本腎臓学会学術集会, Jun. 2011.
468.	Yasumasa Ikeda, 田島壮一郎, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄除去薬による糖尿病の病態改善効果の検討, 第84回日本内分泌学会学術集会, Apr. 2011.
469.	Yasumasa Ikeda, Soichiro Tajima, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Iron elimination ameliorated glucose tolerance through suppression of oxidative stress and inflammation on fat in diabetic mice, 第75回日本循環器学会総会・学術集会, Mar. 2011.
470.	Yasumasa Ikeda, Ken-ichi Aihara, Masashi Akaike, Sumiko Yoshida, Takashi Iwase, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Masataka Sata, Toshio Matsumoto and Toshiaki Tamaki : Heparin cofactor II enhances vascular endothelial cells function and angiogenesis, 第75回日本循環器学会総会・学術集会, Mar. 2011.
471.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Soichiro Tajima, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : The alternation of iron transport-related genes in high fat diet-induced obese and diabetic mice, 第84回日本薬理学会年会, Mar. 2011.
472.	Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : bFGF and insulin differentially regulate hypoxia-inducible factor-1 alpha in adipocytes, 第84回日本薬理学会年会, Mar. 2011.
473.	Yayoi Fukuhara, Shuhei Tomita, Masahisa Urata, Yoshitaka Kihira, Mitsuru Takaku, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Role of HIF-1b in endothelial cells in monocrotaline-induced pulmonary hypertension, 第84回日本薬理学会年会, Mar. 2011.
474.	Yasumasa Ikeda, Soichiro Tajima, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine, an iron chelator, promotes revascularization via endothelial cells activation, 第84回日本薬理学会年会, Mar. 2011.
475.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Erika Tominaga, Junpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine, a photodegrative metabolite of nifedipine, improves angiotensin -induced vascular remodeling, 第84回日本薬理学会年会, Mar. 2011.
476.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Angiotensin -induced vascular remodeling is surpressed in smooth muscle cell-specific hypoxia-inducible factor-1a deficient mice, 第84回日本薬理学会年会, Mar. 2011.
477.	Masaki Imanishi, Keisuke Ishizawa, Takumi Sakurada, 富永えりか, Yuya Horinouchi, Jumpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineによる血管リモデリング抑制効果の検討, 日本薬学会第131回年会, Mar. 2011.
478.	Yuya Horinouchi, Koichiro Tsuchiya, 田島壮一郎, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : Nitrosonifedipine の細胞保護効果に関する検討, 日本薬学会第131年会, Mar. 2011.
479.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensinⅡ誘発血管リモデリングにおけるhypoxia-inducible factor-1αの役割, 第40回日本心脈管作動物質学会, Feb. 2011.
480.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 鉄除去は脂肪肥大を抑制して糖尿病を改善する, 第40回日本心脈管作動物質学会, Feb. 2011.
481.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Yuya Horinouchi, 富永えりか, Jumpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : AngiotensinⅡ誘発血管リモデリングに対するニトロソニフェジピンの抑制作用, 第40回日本心脈管作動物質学会, Feb. 2011.
482.	Yasumasa Ikeda, 田島壮一郎, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : マウス下肢虚血モデルにおいて鉄キレート剤Deferoxamineは酸化ストレスとアポトーシスを抑制する, 第40回日本心脈管作動物質学会, Feb. 2011.
483.	Noriko Yamano, Yasumasa Ikeda, 田島壮一郎, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 高脂肪食負荷肥満マウスにおける鉄吸収動態の検討, 第40回日本心脈管作動物質学会, Feb. 2011.
484.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 鉄除去は脂肪肥大を抑制して糖尿病を改善する, 第40回日本心脈管作動物質学会, Feb. 2011.
485.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Yuya Horinouchi, 富永えりか, Jumpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : AngiotensinⅡ誘発血管リモデリングに対するニトロソニフェジピンの抑制作用, 第40回日本心脈管作動物質学会, Feb. 2011.
486.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensinⅡ誘発血管リモデリングにおけるhypoxia-inducible factor-1αの役割, 第40回日本心脈管作動物質学会, Feb. 2011.
487.	Yasumasa Ikeda, 田島壮一郎, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine, an iron chelator, enhances angiogenesis through Akt-eNOS-dependent pathway in endothelial cells, 第18回日本血管生物医学会学術集会, Dec. 2010.
488.	Yuuko Imamura, Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : HIF-2/ARNT control hair differentiation by up-regulating p21Waf1/Cip1, 第33回日本分子生物学会年会, Dec. 2010.
489.	Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 脂肪細胞における塩基性繊維芽細胞増殖因子による低酸素誘導因子誘導とそれを介した糖輸送担体発現誘導, 第118回日本薬理学会近畿部会, Nov. 2010. (Keyword) 第118回日本薬理学会近畿部会
490.	Keisuke Ishizawa, 中西智子, Hirofumi Shibata, Shinji Abe, Mayumi Sugimura, Chieko Okumura, Yoshiyuki Yoshimura, Youichi Sato, Naokatu Arakaki, Kazuyoshi Kawazoe, Mami Azuma, Koichiro Tsuchiya, Aiko Yamauchi, Tetsuo Yamazaki and Kazuo Minakuchi : 徳島大学における薬学部・薬剤部連携による病院実務実習の実践, 第20回日本医療薬学会年会, Nov. 2010.
491.	富永えりか, Keisuke Ishizawa, Masaki Imanishi, 櫻田巧, 谷口順平, 藤井聖子, Yuya Horinouchi, Yoshitaka Kihira, Shinji Abe, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Toshiaki Tamaki and Kazuo Minakuchi : アンジオテンシンII による血管リモデリングに対するニトロソニフェジピンの影響, 第49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. 2010.
492.	Keisuke Ishizawa : 腎・心血管障害における細胞内分子機構解明とその治療法の開発, 第49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. 2010.
493.	田島壮一郎, Yasumasa Ikeda, Yuya Horinouchi, Yoshitaka Kihira, Shuhei Tomita, Noriko Yamano, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄キレート剤 deferoxamine は内皮細胞活性化により血管新生を促進する, 第20回日本循環薬理学会, Nov. 2010.
494.	Koichiro Tsuchiya, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita and Toshiaki Tamaki : 亜硝酸塩由来血中NO動態に与える経口鉄の影響, 第22回腎とフリーラジカル研究会, Oct. 2010.
495.	Masaki Imanishi, Keisuke Ishizawa, 富永えりか, 櫻田巧, Yuya Horinouchi, 谷口順平, 藤井聖子, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II による血管平滑筋細胞の遊走および増殖に対するnifedipine代謝物の抑制作用とそのメカニズム, 第33回日本高血圧学会, Oct. 2010.
496.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 2型糖尿病モデルマウスに対する鉄キレート剤による糖尿病改善効果の検討, 第34回日本鉄バイオサイエンス学会学術集会, Sep. 2010.
497.	藤井聖子, Keisuke Ishizawa, Masaki Imanishi, 富永えりか, 桜田巧, 谷口順平, Yuya Horinouchi, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Toshiaki Tamaki and Koichiro Tsuchiya : AngiotensinⅡ誘発血管リモデリングに対するnitrosonifedipineの抑制効果, 次世代を担う創薬・医療薬理シンポジウム2010, Sep. 2010.
498.	Shuhei Tomita, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 動脈硬化に伴う血管リモデリングに対してT細胞のHIF-1 は抑制的に機能する．, 第31回日本炎症再生医学会, Aug. 2010.
499.	Masaki Imanishi, Keisuke Ishizawa, 富永えりか, Yuya Horinouchi, 谷口順平, 藤井聖子, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nifedipine代謝物によるangiotensin II 誘発血管平滑筋細胞遊走及び増殖に対する抑制作用, 第117回日本薬理学会近畿部会, Jul. 2010.
500.	Keisuke Ishizawa, Masaki Imanishi, Erika Tminaga, Yuya Horinouchi, Takumi Sakurada, Zyunpei Taniguchi, Seiko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Toshiaki Tamaki and Koichiro Tsuchiya : Nifedipine代謝物はangiotensinⅡによる血管平滑筋細胞遊走および増殖を抑制する, 第63回日本酸化ストレス学会, Jun. 2010.
501.	Yasumasa Ikeda, Koichiro Tsuchiya, 田島壮一郎, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Yoshihisa Takaishi and Toshiaki Tamaki : The effect of SUDACHI peel, a specialty of Tokushima, as anti-metabolic syndrome, 第83回日本薬理学会年会シンポジウム「肥満の栄養ゲノミクスと薬理ゲノミクス」, Mar. 2010.
502.	Keisuke Ishizawa, Masanori Yoshizumi, Dortsuren Naruantungalag, 今村優子, Yasumasa Ikeda, Junji Terao, Koichiro Tsuchiya and Toshiaki Tamaki : ケルセチンの生体内代謝と動脈硬化予防効果, 第83回日本薬理学会年会シンポジウム「健康食品の薬理学」, Mar. 2010.
503.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, 櫻田巧, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : KK-Ay マウスにおける鉄キレート剤Deferoxamineによる糖尿病病態改善効果の検討, 第83回日本薬理学会, Mar. 2010.
504.	Yayoi Fukuhara, Shuhei Tomita, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Masanori Yoshizumi and Toshiaki Tamaki : T細胞のHIF-1aは，動脈硬化に伴う血管リモデリングを抑制的に制御する, 第39回日本心脈管作動物質学会, Feb. 2010.
505.	Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita and Toshiaki Tamaki : 鉄キレート剤 Deferoxamine の血管新生左葉―マウス下肢虚血モデルにおける検討―, 第39回日本心脈管作動物質学会, Feb. 2010.
506.	Keisuke Ishizawa, Kazuyoshi Kawazoe, Mami Azuma, Koichiro Tsuchiya, Aiko Yamauchi, Tetsuo Yamazaki, Kazuo Minakuchi, 智子中西, Hirofumi Shibata, Shinji Abe, Mayumi Sugimura, Chieko Okumura, Yoshiyuki Yoshimura, Youichi Sato and Naokatu Arakaki : P1-571 徳島大学における薬学部・薬剤部連携による病院実務実習の実践(一般演題ポスター発表,薬学教育(実務実習),臨床から学び臨床へと還元する医療薬学), The Annual Meeting of Japanese Society of Pharmaceutical Health Care and Sciences, Vol.20, No.0, 382, 2010. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390845713041900800 (CiNii: 1390845713041900800)
507.	富永えりか, Keisuke Ishizawa, 櫻田巧, 今西正樹, 谷口順平, Kazuyoshi Kawazoe, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : Angiotensin IIによる血管平滑筋細胞遊走に対するnifedipine代謝物の影響, 第30回日本臨床薬理学会年会, Dec. 2009.
508.	富永えりか, Keisuke Ishizawa, 櫻田巧, 今西正樹, 谷口順平, 山﨑有希子, Yoshitaka Kihira, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : ニフェジピン代謝物はアンジオテンシンⅡ誘発血管平滑筋細胞遊走を抑制する, 第48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. 2009.
509.	山﨑有希子, Keisuke Ishizawa, 富永えりか, 谷口順平, 櫻田巧, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Toshiaki Tamaki and Kazuo Minakuchi : アンジオテンシンⅡによる血管平滑筋細胞遊走・増殖における細胞内鉄の関与, 第48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. 2009.
510.	福原弥生, Shuhei Tomita, 浦田将久, Yoshitaka Kihira, 池田康将, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : モノクロタリン誘導肺高血圧症モデルマウスにおける血管内皮細胞の低酸素応答因子(HIF-1b)の役割, 第116回日本薬理学会近畿部会, Jun. 2009.
511.	Yoshitaka Kihira, 御園生裕明, Keisuke Ishizawa, 池田康将, Shuhei Tomita and Toshiaki Tamaki : 電位依存性Kチャネル Kv2.1とKv2.2の相互作用, 第115回日本薬理学会近畿部会, Jun. 2009.
512.	田島壮一郎, Koichiro Tsuchiya, 濱本磨以, Yuya Horinouchi, Shuhei Tomita, Keisuke Ishizawa, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : Angiotensin IIによるヒト腎糸球体血管内皮細胞(HGEC)内における鉄動態の検討, 日本薬学会129年会, Mar. 2009.
513.	廣永有沙, Keisuke Ishizawa, 山崎有希子, 野瀬文乃, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : オルメサルタンはPDGF誘導メサンギウム細胞遊走をAT1受容体非依存的に抑制する, 第47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, 189, Nov. 2008.
514.	田岡千明, Koichiro Tsuchiya, 神谷昌樹, Hisao Nemoto, Keisuke Ishizawa, Kunihisa Yamaguchi, Yoshiharu Takiguchi and Toshiaki Tamaki : 水溶性Fenofibrate製剤の作成と中性脂肪低下作用の検討, 第111回日本薬理学会近畿部会, 81, Jun. 2007.
515.	松村敏彦, 宮本由加里, 黒川ふみ, Shinji Abe, 榊原啓之, Keisuke Ishizawa, Koichiro Tsuchiya, 清水寛, Junji Terao, Toshiaki Tamaki, Kazuyoshi Kawazoe and Kazuo Minakuchi : ラット強制水泳試験における漢方薬の抗うつ作用の検討, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 125, Oct. 2006.
516.	平広範, Keisuke Ishizawa, 廣永有沙, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : 血管内皮細胞障害におけるアンジオテンシンII受容体拮抗薬の保護効果, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 102, Oct. 2006.
517.	南有紀, 塩田直青子, Toshitaka Ikehara, 庄野正行, Keisuke Ishizawa, Kazuo Yoshizaki, Yohsuke Kinouchi, Shinji Abe, Hitoshi Houchi, Kazuyoshi Kawazoe and Kazuo Minakuchi : ウシ副腎髄質細胞の容積変化に及ぼす変動磁界の影響, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 76, Oct. 2006.
518.	Kazuyoshi Kawazoe, 松村敏彦, 黒川ふみ, 榊原啓之, Keisuke Ishizawa, Koichiro Tsuchiya, 清水寛, Junji Terao, Toshiaki Tamaki and Kazuo Minakuchi : ラット強制水泳試験による漢方薬の抗うつ作用評価, 第109回日本薬理学会近畿部会, 30, Jun. 2006.
519.	安田裕美, Miwa Bando, Eiji Hosoi, 井上めぐみ, 白潟朋美, Keisuke Ishizawa, Kazuyoshi Kawazoe, Kazuo Minakuchi and 芳地一 : ヒト活性化血小板における抗血小板薬の効果, 第29回徳島県医学検査学会抄録集, 27, Dec. 2005.
520.	西迫寛隆, Keisuke Ishizawa, 溝口徹也, 桐野靖, Shinji Abe, Kazuyoshi Kawazoe and Kazuo Minakuchi : 結核病棟薬剤管理指導におけるワークシートの活用とNSTとの連携, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 190, Nov. 2005.
521.	富永樹, 黒川ふみ, Keisuke Ishizawa, 鳥井真由美, 大山真由美, 胡田順子, 濱野修一, Kazuyoshi Kawazoe, Hitoshi Houchi and Kazuo Minakuchi : アスピリンと非ステロイド性消炎鎮痛薬のヒト血小板凝集能へ及ぼす併用効果, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 136, Nov. 2005.
522.	三木智重子, Keisuke Ishizawa, 松村敏彦, 木宿昌俊, Kazuyoshi Kawazoe and Kazuo Minakuchi : アルドステロンはBig MAP kinase 1 (BMK1)活性化を介してラット平滑筋細胞を増殖させる, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 115, Nov. 2005.
523.	Hiromi Sasaki, 南有紀, Toshitaka Ikehara, 細川敬子, Hisao Yamaguchi, Kazuo Yoshizaki, Yohsuke Kinouchi, Keisuke Ishizawa, Kazuyoshi Kawazoe, Hitoshi Houchi and Kazuo Minakuchi : 牛副腎髄質由来細胞内の一過性Ca²⁺増加機構に対する磁界の影響, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 126, Nov. 2005.
524.	井上めぐみ, 白潟朋美, Keisuke Ishizawa, Kazuyoshi Kawazoe, 安田裕美, 板東美和, Eiji Hosoi, Hitoshi Houchi and Kazuo Minakuchi : 抗血小板薬におけるヒト血小板内Ca²⁺濃度の変動と凝集の抑制, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 124, Nov. 2005.
525.	杉本理香, Keisuke Ishizawa, 平広範, 勝部紗和子, 桐野靖, Kazuyoshi Kawazoe and Kazuo Minakuchi : ラットメサンギウム細胞の遊走および増殖に対するアディポネクチンの作用とそのメカニズム, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 124, 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.	津田勝範, Licht Miyamoto, 森本悠里, Shuichi Hamano, Keisuke Ishizawa, 木平考高, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 鉄過剰ストレスに対するニトロソニフェジピン(NO-NIF)の抗酸化メカニズム検討, 徳島医学会, Aug. 2015.
4.	Keisuke Ishizawa : 酸化ストレス制御で循環器疾患と戦う, 薬学部だより, Vol.13, 4, Jan. 2014.
5.	Keisuke Ishizawa : 「縁」と「和」が生むvirtuous cycle, Folia Pharmacologica Japonica, Vol.141, No.3, 179, Mar. 2013.
6.	Keisuke Ishizawa : 酸化ストレスと生活習慣病(4) 脂質異常症, 県薬だより-情報とくしま-, Vol.73, 23-25, Sep. 2012.
7.	Keisuke Ishizawa : 酸化ストレスと生活習慣病(3) 糖尿病, 県薬だより-情報とくしま-, Vol.72, 12-14, Jun. 2012.
8.	Keisuke Ishizawa : 酸化ストレスと生活習慣病(2) 高血圧, 県薬だより-情報とくしま-, Vol.71, 36-38, Mar. 2012.
9.	Keisuke Ishizawa : 酸化ストレスと生活習慣病(1) 酸化ストレスの基礎, 県薬だより-情報とくしま-, Vol.70, 20-22, Dec. 2011.
10.	Keisuke Ishizawa : 服薬指導ケーススタディー HPNの支援, Clinical Pharmacist, Vol.56, 6-7, Jun. 2006.
11.	Kazuo Minakuchi and Keisuke Ishizawa : Interview 薬剤業務の周辺, カレントファーマシー, Vol.22, 5-6, Dec. 2004.
12.	Kazuo Minakuchi and Keisuke Ishizawa : 適切な栄養療法をサポートする NSTにおける薬剤師の役割, GSKファーマシストジャーナル, Vol.7, 4-6, Nov. 2004.
13.	Keisuke Ishizawa : 栄養サポートチーム(NST)における薬剤師の役割, 徳島県病薬会誌, Vol.73, 25-26, 2004.

Report:

1.	Keisuke Ishizawa : 米国における臨床薬剤師教育制度および卒後教育制度の研究, 厚生労働科学研究費補助金医薬品・医療機器等レギュラトリーサイエンス総合研究推進事業, 809-828, Mar. 2005.
2.	Masanori Yoshizumi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : インスリン抵抗性に対するロサルタンおよびロサルタンと運動の併用による効果-モデルラットを用いたin vivoでの検討-, 第17回健康医科学研究助成論文集, No.17, 124-134, Tokyo, Mar. 2002.

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

抗VEGF療法の治療効果向上を目指した最適な支持療法薬の解明 (Project/Area Number: 24K09959 )
大規模医療情報とオミクスデータを活用した新たな薬剤性間質性肺疾患予防薬の開発 (Project/Area Number: 24K09927 )
デジタルサイエンスを応用した抗がん剤関連性末梢神経障害治療薬の創出 (Project/Area Number: 24K09832 )
リアルワールドデータを活用した薬剤性腎障害に対する新規予防戦略の開発 (Project/Area Number: 23K06234 )
リアルワールドデータの統合解析で拓くがん免疫薬物療法の致死的有害事象回避法の構築 (Project/Area Number: 22K06724 )
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 pathophysiology of aortic dissection and development of the preventive strategies by medical big data and novel model mice (Project/Area Number: 18K06686 )
Development of novel aortic dissection model based on vascular endothelial dysfunction and elucidation of pathophysiological mechanisms (Project/Area Number: 15K07967 )
The effects of renin-angiotensin system control by HIF-1alpha in arteriosclerosis formation (Project/Area Number: 25860063 )
Activation mechanisms of AMPK by nitrite (Project/Area Number: 25460332 )
Functional analysis and pathological roles of HIF-1α in vascular remodeling (Project/Area Number: 23790298 )
The renal protective effects of nitrite salts in diabetic nephropathy model rats. (Project/Area Number: 22590241 )
CharaGterization of the evoked inflammation via hypoxic response in endothelial cells (Project/Area Number: 19590281 )
Effects of radio-frequency electromagnetic field on physiological functions of nerve cells (Project/Area Number: 19510032 )
Physiological and pathophysiological role of nitrite-derived nitric oxide formation (Project/Area Number: 17390066 )
Search by Researcher Number (60398013)

Professor : Ishizawa, Keisuke

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