Tokushima University / Educator and Researcher Directory --- Goda, Mitsuhiro

Personal Web Page

https://researchmap.jp/40585965 (researchmap)

https://orcid.org/0000-0001-5345-1479 (ORCID)

Field of Study

○	Life sciences [Pharmacology]

Subject of Study

Book / Paper

Book:

1.	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.
2.	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)

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.	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)
11.	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)
12.	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)
13.	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)
14.	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)
15.	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)
16.	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)
17.	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)
18.	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)
19.	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)
20.	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)
21.	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)
22.	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)
23.	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)
24.	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)
25.	Yasutaka Sato, Satoshi Sakaguchi, Kenshi Takechi, Masayuki Chuma, Kenta Yagi, Chikako Kane, Mitsuhiro Goda, Hirofumi Hamano, Yuki Aoe, Hiroshi Nokihara, Yoshiaki Kubo, Ichiro Hashimoto and Hiroaki Yanagawa : Trends in Investigator-Initiated Clinical Studies at a University Hospital after Enforcement of the 2018 Clinical Trials Act in Japan., Biological & Pharmaceutical Bulletin, Vol.45, No.3, 374-377, 2022. (Summary) In April 2018, the Clinical Trials Act pertaining to investigator-initiated clinical trials was passed in Japan. The purpose of this study was to investigate activity in investigator-initiated clinical studies before and after enforcement of the new Clinical Trials Act. This was done by analysing the records of the Ethics Committee of Tokushima University Hospital, which reviews studies based on the Japanese government's Ethical Guidelines for Medical and Health Research Involving Human Subjects prior to the Clinical Trials Act, and records of the Certified Review Board established at Tokushima University under the Clinical Trials Act in 2018. The number of new applications to these two review boards during fiscal years 2015-2017 (pre-Act) and fiscal years 2018 and 2019 (post-Act) were used as an indicator of activity in investigator-initiated clinical studies. The number of new applications to the Ethics Committee was 303, 261, 316, 303, and 249 in 2015, 2016, 2017, 2018, and 2019, respectively. The data show that the total number of new interventional studies decreased from 50.3 in average in 2015-2017 (pre-Act) to 42 in 2018 and 40 in 2019 (post-Act), respectively. These results suggest that fewer interventional studies were started following enforcement of the new Clinical Trials Act. To confirm this trend and identify contributing factors, further studies are required. In addition, possible way, such as broader contribution of clinical research coordinators, to promote clinical studies in the new Clinical Trials Act era should be examined. (Keyword) Clinical Trials as Topic / Hospitals, University / Humans / Japan (Tokushima University Institutional Repository) ● Metadata: 117363 (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b21-00753 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35228403 ● CiNii @ National Institute of Informatics (CRID): 1390854717424551552 ● Summary page in Scopus @ Elsevier: 2-s2.0-85125568858 (Tokushima University Institutional Repository: 117363, DOI: 10.1248/bpb.b21-00753, PubMed: 35228403, CiNii: 1390854717424551552, Elsevier: Scopus)
26.	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)
27.	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)
28.	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)
29.	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)
30.	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): 1520853834956336128 (Tokushima University Institutional Repository: 116038, CiNii: 1520853834956336128)
31.	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)
32.	Hirofumi Hamano, Yasumasa Ikeda, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Masayuki Chuma, Michiko Yamashita, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Izawa-Ishizawa Yuki, Licht Miyamoto, Ishizawa Keisuke, Hiromichi Fujino, Toshiaki Tamaki, Ken-ichi Aihara and Koichiro Tsuchiya : Diphenhydramine may be a preventive medicine against cisplatin-induced kidney toxicity, Kidney International, Vol.99, No.4, 885-889, 2021. (Summary) Cisplatin is widely used as an anti-tumor drug for the treatment of solid tumors. Unfortunately, it causes kidney toxicity as a critical side effect, limiting its use, given that no preventive drug against cisplatin-induced kidney toxicity is currently available. Here, based on a repositioning analysis of the Food and Drug Administration Adverse Events Reporting System, we found that a previously developed drug, diphenhydramine, may provide a novel treatment for cisplatin-induced kidney toxicity. To confirm this, the actual efficacy of diphenhydramine was evaluated in in vitro and in vivo experiments. Diphenhydramine inhibited cisplatin-induced cell death in kidney proximal tubular cells. Mice administered cisplatin developed kidney injury with significant dysfunction (mean plasma creatinine: 0.43 vs 0.15 mg/dl) and showed augmented oxidative stress, increased apoptosis, elevated inflammatory cytokines, and MAPKs activation. However, most of these symptoms were suppressed by treatment with diphenhydramine. Furthermore, the concentration of cisplatin in the kidney was significantly attenuated in diphenhydramine-treated mice (mean platinum content: 70.0 vs 53.4 μg/g dry kidney weight). Importantly, diphenhydramine did not influence or interfere with the anti-tumor effect of cisplatin in any of the in vitro or in vivo experiments. In a selected cohort of 98 1:1 matched patients from a retrospective database of 1467 patients showed that patients with malignant cancer who had used diphenhydramine before cisplatin treatment exhibited significantly less acute kidney injury compared to ones who did not (6.1 % vs 22.4 %, respectively). Thus, diphenhydramine demonstrated efficacy as a novel preventive medicine against cisplatin-induced kidney toxicity. (Tokushima University Institutional Repository) ● Metadata: 115399 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.kint.2020.10.041 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33307103 ● Search Scopus @ Elsevier (PMID): 33307103 ● Search Scopus @ Elsevier (DOI): 10.1016/j.kint.2020.10.041 (Tokushima University Institutional Repository: 115399, DOI: 10.1016/j.kint.2020.10.041, PubMed: 33307103)
33.	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)
34.	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)
35.	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)
36.	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)
37.	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)
38.	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)
39.	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)
40.	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)
41.	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)
42.	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)
43.	Hiromu Kawasaki, Mitsuhiro Goda, Satoko Fukuhara, Narumi Hashikawa-Hobara, Yoshito Zamami and Shingo Takatori : Nerve growth factor (NGF) has an anti-tumor effects through perivascular innervation of neovessels in HT1080 fibrosarcoma and HepG2 hepatitis tumor in nude mice., Journal of Pharmacological Sciences, 2019. (Summary) This study investigated whether NGF prevents tumor growth by promoting neuronal regulation of tumor blood flow. HT1080 fibrosarcoma cells or HepG2 hepatitis cells were subcutaneously implanted into nude mice. On Day 21 after the implantation of tumor cells, human NGF (40 or 80 ng/h for 14 days) was administered using a micro-osmotic pump. Growth rates of both tumors were significantly inhibited by the treatment of NGF, and the survival rate was also extended. Significant suppression of HT1080 tumor growth lasted after withdrawing NGF. NGF markedly increased the density of α-smooth muscle actin (α-SMA)-immunoreactive (ir) cells without changing neovessel density in HT1080 tumor tissues. Double immunostaining demonstrated protein gene product (PGP) 9.5-ir nerves around α-SMA-ir cells were found in HT1080 tumor tissue treated with NGF. The blood flow in HepG2 tumors treated with saline was significantly higher than in the non-tumor control area, but the tumor blood flow was markedly reduced by NGF treatment. In in vitro studies, NGF significantly accelerated migration of aortic smooth muscle cells but not endothelial cells, whereas NGF had no cytotoxic action on both cells. NGF inhibits tumor growth via indirect action, probably through innervation and maturation of tumor neovasculature, which regulates blood flow into tumor tissues. (Tokushima University Institutional Repository) ● Metadata: 114596 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2019.02.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31178329 ● Summary page in Scopus @ Elsevier: 2-s2.0-85066808434 (Tokushima University Institutional Repository: 114596, DOI: 10.1016/j.jphs.2019.02.011, PubMed: 31178329, Elsevier: Scopus)
44.	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)
45.	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)
46.	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)
47.	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)
48.	Mitsuhiro Goda, Shingo Takatori, Saori Atagi, Narumi Hashikawa-Hobara and Hiromu Kawasaki : Nerve growth factor facilitates perivascular innervation in neovasculatures of mice., Journal of Pharmacological Sciences, Vol.131, No.4, 251-258, 2016. (Summary) It is well known that blood vessels including arterioles have a perivascular innervation. It is also widely accepted that perivascular nerves maintain vascular tone and regulate blood flow. Although there are currently prevailing opinions, unified views on the innervation of microcirculation in any organs have not been established. The present study was designed to investigate whether there are perivascular nerves innervated in microvessels and neovessels. Furthermore, we examined whether nerve growth factor (NGF) can exert a promotional effect on perivascular nerve innervation in neovessels of Matrigel plugs. A Matrigel was subcutaneously implanted in mouse. The presence of perivascular nerves in Matrigel on Day 7-21 after the implantation was immunohistochemically studied. NGF or saline was subcutaneously administered by an osmotic mini-pump for a period of 3-14 days. The immunostaining of neovasculatures in Matrigel showed the presence of perivascular nerves on Day 21 after Matrigel injection. Perivascular nerve innervation of neovessels within Matrigel implanted in NGF-treated mice was observed in Day 17 after Matrigel implantation. However, NGF treatment did not increase numbers of neovessels in Matrigel. These results suggest that perivascular nerves innervate neovessels as neovasculatures mature and that NGF accelerates the innervation of perivascular nerves in neovessels. (Keyword) Angiogenesis Inducing Agents / Animals / collagen / Drug Combinations / Laminin / Male / Mice / Microvessels / Neovascularization, Physiologic / Nerve Growth Factor / Neurogenesis / Proteoglycans (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2016.07.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27493098 ● Search Scopus @ Elsevier (PMID): 27493098 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2016.07.002 (DOI: 10.1016/j.jphs.2016.07.002, PubMed: 27493098)
49.	Ayako Yokomizo, Shingo Takatori, Narumi Hashikawa-Hobara, Mitsuhiro Goda and Hiromu Kawasaki : Characterization of Perivascular Nerve Distribution in Rat Mesenteric Small Arteries., Biological & Pharmaceutical Bulletin, Vol.38, No.11, 1757-1764, 2015. (Summary) The distribution pattern of perivascular nerves in some branches of rat mesenteric arteries was studied. Mesenteric arteries isolated from 8-week-old Wistar rats were divided into the 1st-, 2nd-, and 3rd-order branches. The distribution of perivascular nerves in each branch was immunohistochemically evaluated using antibodies against neuropeptide Y (NPY), tyrosine hydroxylase (TH), calcitonin gene-related peptide (CGRP), substance P (SP), and neuronal nitric oxide synthase (nNOS). The density of NPY-, TH-, CGRP-, and SP-like immunoreactive (LI) nerves in the 2nd and 3rd branches was significantly greater than that in the 1st branch, and a negative relationship was found between nerve density and arterial diameter, except for TH-LI nerves. The density of NPY- and TH-LI nerves in all branches, which was similar, was greater than that of CGRP- (except for NPY-LI nerves in the 1st branch), SP-, or nNOS-LI nerves. Double immunostaining revealed that TH-LI nerves made contact with nNOS-LI, CGRP-LI, and SP-LI nerves and that CGRP-LI nerves made contact with TH-, NPY-, or nNOS-LI nerves, while TH-LI and CGRP-LI nerves nearly merged with NPY-LI and SP-LI nerves, respectively. These results suggest that the each branch of mesenteric arteries is densely innervated by vasoconstrictor nerves containing NPY, TH, and vasodilator CGRP nerves. They also suggest that the intense density of perivascular nerves in the 2nd and 3rd branches may contribute to maintaining vascular tone. (Keyword) Animals / Calcitonin Gene-Related Peptide / Mesenteric Arteries / Mesentery / Microcirculation / Microvessels / Nerve Fibers / Neuropeptide Y / Neuropeptides / Nitric Oxide Synthase Type I / Rats, Wistar / Substance P / Sympathetic Nervous System / Tyrosine 3-Monooxygenase / Vasoconstriction / Vasodilation (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b15-00461 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26521827 ● Search Scopus @ Elsevier (PMID): 26521827 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b15-00461 (DOI: 10.1248/bpb.b15-00461, PubMed: 26521827)
50.	Yoko Sone, Eiko Ochi, Akiko Matsuyama, Satoko Fukuhara, Mitsuhiro Goda, Shingo Takatori and Hiromu Kawasaki : [Influence of nerve growth factor (NGF) on distribution of perivascular nerves in tumor neovasculatures of mouse corneal]., Journal of the Pharmaceutical Society of Japan, Vol.132, No.2, 157-160, 2012. (Summary) Angiogenesis, or new blood vessel formation, is critical for the growth and spread of tumors. The vascular tone and tissue blood flow are maintained and regulated by perivascular nerves. However, many studies have reported that tumor neovascular vessels have no innervation of perivascular nerves. We have shown that nerve growth factor (NGF) facilitated perivascular innervation and suppressed the tumor growth. From these results, we hypothesized that the neuronal regulation of blood flow toward tumors via perivascular nerves may lead suppression of the tumor growth. Therefore, the aim of this study is to investigate effect of NGF on distribution of perivascular nerves and neovessel form in tumor tissues, which were generated by mouse corneal micropocket method. A gel, which contained DU145 prostate carcinoma cells, was implanted into the mouse corneal. NGF or saline was subcutaneously administered using an osmotic mini-pump. After 1 week, the distribution of perivascular nerves in mouse corneal were immunohistochemically studied. Also, the density of neovessels (immunocytochemically stained CD31) and smooth muscles (α-smooth muscle actin; SMA) in tumor tissues was quantified by the computer-assisted image processing. Four days after implantation of tumor cells in mouse corneal, many neovessels generated from corneal limbal vessels were observed in tumor tissues. Treatment of mouse with NGF resulted in innervation of perivascular nerves around tumor neovessels, but not observed in saline-treated group. NGF treatment increased SMA-, but not CD31-, immunopositive cells. These results suggest that NGF may facilitate innervations of perivascular nerve to regulate the blood flow in tumor neovessels. (Keyword) Actins / Animals / cornea / Corneal Diseases / Eye Neoplasms / Humans / Male / Mice / Mice, Inbred BALB C / Neoplasm Transplantation / Neovascularization, Pathologic / Nerve Growth Factor / Platelet Endothelial Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.132.157 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22293692 ● Search Scopus @ Elsevier (PMID): 22293692 ● Search Scopus @ Elsevier (DOI): 10.1248/yakushi.132.157 (DOI: 10.1248/yakushi.132.157, PubMed: 22293692)

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)

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)

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.	Mitsuhiro Goda, Kanda Masaya, Yoshioka Toshihiko, Miyata Koji, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Sakurada Takumi and Yuki Izawa-Ishizawa : Discovery of preventive drugs for cisplatin-induced acute kidney injury., 19th World Congress of Basic & Clinical Pharmacology (WCP2023), Glasgow, Jul. 2023.
10.	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.
11.	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.
12.	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.
13.	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.
14.	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.

Proceeding of Domestic Conference:

1.	Kenta Yagi, Sayaka Imawaka, Mayu Takaoka, Naoki Okamoto, Fuka Aizawa, Takahiro Niimura, Mitsuhiro Goda, Kei Kawada, Yuki Izawa-Ishizawa and Keisuke Ishizawa : Bcr-Abl 阻害剤に対する慢性骨髄性白血病細胞の耐性獲得メカニズムの探索, 第144回日本薬理学会近畿部会, Mar. 2024.
2.	Yuki Izawa-Ishizawa, Koji Miyata, Kaito Tsujinaka, Shuto Itokazu, Tatsumi Miyata, Masateru Kondoh, Takahiro Niimura, Toshihiko Yoshioka, Fuka Aizawa, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : フルオロキノロン系抗菌薬による大動脈疾患リスクに関する2つの矛盾, 第144回日本薬理学会近畿部会, Mar. 2024.
3.	Fuka Aizawa, Ami Okabayashi, Daishi Moriyama, Kenta Yagi, Takahiro Niimura, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Kei Kawada and Keisuke Ishizawa : HMG-CoA還元酵素阻害剤はGST を介して抗がん剤誘発性機械的刺激応答閾値低下を改善する, 第144回日本薬理学会近畿部会, Mar. 2024.
4.	Tatsumi Miyata, Yuki Izawa-Ishizawa, Koji Miyata, Shuto Itokazu, Kaito Tsujinaka, Himeno Fukuoka, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : レボフロキサシンの血管炎症への影響, 第268回徳島医学会, Mar. 2024.
5.	Shuto Itokazu, Yuki Izawa-Ishizawa, Koji Miyata, Tatsumi Miyata, Masateru Kondoh, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : 杜仲葉エキスによる大動脈疾患発症抑制効果の検討, 第268回徳島医学会, Mar. 2024.
6.	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.
7.	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.
8.	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.
9.	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.
10.	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.
11.	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.
12.	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.
13.	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.
14.	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.
15.	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.
16.	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.
17.	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.
18.	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.
19.	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.
20.	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.
21.	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.
22.	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.
23.	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.
24.	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.
25.	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.
26.	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.
27.	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.
28.	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.
29.	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.
30.	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.
31.	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.
32.	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.
33.	Fuka Aizawa, 岡林亜美, Daishi Moriyama, Kenta Yagi, Mitsuhiro Goda, NITTA Ayaka, Takahiro Niimura, 石澤有紀 and 石澤啓介 : 抗がん剤誘発性末梢神経障害克服に向けたスタチン系薬剤による有効性検討, 日本薬学会第143年会, Mar. 2023.
34.	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.
35.	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.
36.	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.
37.	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.
38.	Takahiro Niimura, Hiroto Unten, Hirofumi Hamano, Kazushi Uchida, MIYATA Koji, Mitsuhiro Goda, Kenta Yagi, Fuka Aizawa, Yuki Izawa-Ishizawa, Yoshito Zamami and 石澤啓介 : PD-1ノックアウトマウスを用いた免疫チェックポイント阻害剤関連心筋炎の新規病態モデル開発, 第32回日本循環薬理学会, Jan. 2023.
39.	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.
40.	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.
41.	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.
42.	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.
43.	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.
44.	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.
45.	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.
46.	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.
47.	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.
48.	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.
49.	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.
50.	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.
51.	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.
52.	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.
53.	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.
54.	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.
55.	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.
56.	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.
57.	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.
58.	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.
59.	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.
60.	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.
61.	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.
62.	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.
63.	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.
64.	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.
65.	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.
66.	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.
67.	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.
68.	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.
69.	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
70.	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
71.	Toshihiko Yoshioka, Mitsuhiro Goda, Masaya Kanda, Ami Yoshida, Sayuri Itobayashi, Yugo Sugimoto, Yuki Izawa-Ishizawa, Kenta Yagi, Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Yoshito Zamami and Keisuke Ishizawa : シスプラチン誘発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
72.	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.
73.	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.
74.	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.
75.	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
76.	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.
77.	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
78.	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.
79.	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
80.	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.
81.	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.
82.	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
83.	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
84.	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
85.	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
86.	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
87.	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.
88.	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.
89.	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.
90.	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.
91.	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
92.	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.
93.	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
94.	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
95.	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
96.	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
97.	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
98.	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.
99.	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
100.	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
101.	Yasumasa Ikeda, Hirofumi Hamano, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Masayuki Chuma, Yoshito Zamami, Licht Miyamoto, 石澤啓介, Hiromichi Fujino, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Identification of a candidate drug for the prevention of cisplatin-induced nephrotoxicity by a database analysis -basic research-clinical study, 第94回日本薬理学会年会, Mar. 2021.
102.	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.
103.	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.
104.	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
105.	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
106.	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.
107.	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.
108.	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.
109.	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.
110.	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
111.	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.
112.	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.
113.	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.
114.	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.
115.	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.
116.	Yasumasa Ikeda, Hirofumi Hamano, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, 石澤啓介, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン起因性腎障害を予防する既存薬の同定, 第63回日本腎臓学会学術総会, Aug. 2020.
117.	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.
118.	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
119.	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.
120.	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.
121.	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.
122.	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.
123.	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.
124.	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.
125.	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.
126.	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.
127.	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.
128.	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.
129.	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.
130.	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.
131.	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.
132.	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.
133.	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.
134.	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.
135.	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.
136.	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.
137.	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.
138.	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.
139.	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.
140.	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.
141.	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.
142.	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.
143.	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.
144.	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.
145.	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.
146.	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.
147.	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.
148.	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.
149.	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.
150.	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.
151.	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.
152.	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.
153.	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.
154.	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.
155.	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.
156.	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.
157.	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.
158.	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.
159.	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.
160.	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.
161.	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.
162.	生藤来希, Masaki Imanishi, 山川祐介, Keijo Fukushima, 前川晃子, Yuya Horinouchi, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino and Koichiro Tsuchiya : 大腸がん増大におけるがん関連線維芽細胞由来ERKSの役割, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
163.	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.

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

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 )
Gendered innovation in cancer chemotherapy - real world data driven pharmacological research (Project/Area Number: 22K06863 )
Elucidation of the relationship between infectious diseases and aortic diseases by big data analysis and in vivo experiments (Project/Area Number: 21H02646 )
Development of an Evaluation System for Synergistic Effects and Pharmacological Verification (Project/Area Number: 20H05799 )
Establishment of optimal supportive care for prevention of drug-induced kidney injury using medical big data (Project/Area Number: 20K07132 )
Elucidation of the role of ERK5 and the mechanism of epithelial-mesenchymal transition for cancer metastasis control (Project/Area Number: 19K07321 )
Development of a treatment for post-cardiopulmonary resuscitation encephalopathy utilizing existing approved drugs using large-scale medical claims database (Project/Area Number: 18K06785 )
Elucidation of pathophysiology of aortic dissection and development of the preventive strategies by medical big data and novel model mice (Project/Area Number: 18K06686 )
Physiological analysis of MATE transporters as testosterone transporter (Project/Area Number: 17K18262 )
The antitumor effects of nerve growth factor on human cancer cells (Project/Area Number: 22800045 )
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Associate Professor : Goda, Mitsuhiro

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