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相澤風花

徳島大学

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リサーチマップ・
Jグローバル
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2025年8月1日更新

職名: 特任講師
電話: 0886158583
電子メール: f_aizawa@tokushima-u.ac.jp
学歴: 2009/4: 神戸学院大学薬学部薬学科 ( - 2015. 3.)
2015/4: 神戸学院大学大学院薬学研究科 ( - 2019. 3.) (博士後期課程)
学位: 博士 / 博士(薬学) (神戸学院大学) (2019年)
職歴・経歴: 2019/4: 徳島大学病院薬剤部薬剤師
2020/10: 徳島大学病院薬剤部特任助教
2025/4: 徳島大学病院総合臨床研究センター社会実装推進部門特任講師

専門分野・研究分野: ライフサイエンス (Life sciences) [薬理学 (Pharmacology)]
ライフサイエンス (Life sciences) [神経科学一般 (Neuroscience - general)]
ライフサイエンス (Life sciences) [医療薬学 (Clinical pharmacy)]

研究者総覧で最新データを確認する

2025年8月1日更新

専門分野・研究分野: ライフサイエンス (Life sciences) [薬理学 (Pharmacology)]
ライフサイエンス (Life sciences) [神経科学一般 (Neuroscience - general)]
ライフサイエンス (Life sciences) [医療薬学 (Clinical pharmacy)]
担当経験のある授業科目: 基礎化学/基礎化学概論 (共通教育)
指導経験: 研究者総覧に該当データはありませんでした。

研究者総覧で最新データを確認する

2025年8月1日更新

専門分野・研究分野: ライフサイエンス (Life sciences) [薬理学 (Pharmacology)]
ライフサイエンス (Life sciences) [神経科学一般 (Neuroscience - general)]
ライフサイエンス (Life sciences) [医療薬学 (Clinical pharmacy)]

研究テーマ: 研究者総覧に該当データはありませんでした。

著書

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論文

Fuka Aizawa, Kenta Yagi, Maki Sato, Takahiro Niimura, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa :
Influence of statin intervention on peripheral neuropathy in patients treated with anticancer drugs identified from the insurer database,
Journal of Pharmaceutical Health Care and Sciences, 11, 1, 2025.

(キーワード): Chemotherapy-induced peripheral neuropathy / HMG-CoA reductase inhibitor / Oxaliplatin / Paclitaxel / Supportive care
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/s40780-025-00428-3
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-105002872844

(DOI: 10.1186/s40780-025-00428-3, Elsevier: Scopus) Yuhei Sonoda, Fuka Aizawa, Nanami Tomochika, Kanaho Miyauchi, Ayaka Nishibashi, Shimon Takahashi, Hidetaka Kosako, Shota Tanida, Kenta Yagi, Takahiro Niimura, Mitsuhiro Goda, Kei Kawada, Yuki Izawa-Ishizawa and Keisuke Ishizawa :
Ursodeoxycholic acid alleviates multiple sclerosis via TGR5-dependent microglial regulation in mice,
European Journal of Pharmacology, 1003, 2025.

(キーワード): Bile acid / Experimental autoimmune encephalomyelitis / Inflammation / Multiple sclerosis / TGR5 / Ursodeoxycholic acid
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ejphar.2025.177941
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-105010642086

(DOI: 10.1016/j.ejphar.2025.177941, Elsevier: Scopus) Koji Miyata, Yuki Izawa-Ishizawa, Takahiro Niimura, Toshihiko Yoshioka, Mizusa Hyodo, Shuto Itokazu, Tatsumi Miyata, Fuka Aizawa, Kenta Yagi, Kei Kawada, Hirofumi Hamano, Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa :
Pharmacovigilance study for the identification of mogamulizumab-induced immune-related adverse events using a real-world database,
The Oncologist, 30, 7, 2025.

(キーワード): disproportionality analysis / irAEs / mogamulizumab / sézary syndrome / VigiBase
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/oncolo/oyaf201
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-105010922648

(DOI: 10.1093/oncolo/oyaf201, Elsevier: Scopus) Rie Ando-Matsuoka, Kei Kawada, Takahiro Niimura, Hitoshi Fukuda, Tomoaki Ishida, Toshihiko Yoshioka, Yu Kawanishi, Tomohito Kadota, Shinji Abe, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Tetsuya Ueba and Keisuke Ishizawa :
Risk factors for clazosentan-induced fluid retention in subarachnoid hemorrhage from the Japanese adverse event database,
Journal of Stroke & Cerebrovascular Diseases, 34, 6, 2025.

(キーワード): Cerebral vasospasm / Clazosentan / Fasudil / Subarachnoid hemorrhage
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jstrokecerebrovasdis.2025.108296
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-105001481060

(DOI: 10.1016/j.jstrokecerebrovasdis.2025.108296, Elsevier: Scopus) Ayaka Nitta, Mitsuhiro Goda, Takahiro Niimura, Toshiki Kajihara, Maki Sato, Masayuki Chuma, Kei Kawada, Kaito Tsujinaka, Koji Miyata, Yuki Kono, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa :
Rifampicin in combination treatments for methicillin-resistant staphylococcal prosthetic joint infections: Claims database evaluation using a cohort of 52,588 hip arthroplasty patients.,
International Journal of Clinical Pharmacology and Therapeutics, 2025.

(要約): Hip arthroplasty is a common surgical procedure effective for pain relief and maintaining walking function. Prosthetic joint infection (PJI) is a serious complication. Rifampicin combination therapy is widely used to treat PJIs caused by Staphylococcus aureus or coagulase-negative Staphylococcus, which are challenging to treat due to biofilm formation. However, its effectiveness is unclear. The effectiveness of anti-methicillin-resistant Staphylococcus aureus (MRSA) antibiotics combined with rifampicin is also unclear.This study assessed the effectiveness and safety of MRSA antibiotics combined with rifampicin for treating methicillin-resistant staphylococcal PJI using a Japanese clinical database.This retrospective analysis used the claims database to examine data on PJI after hip arthroplasty among patients aged 20 years or older who were treated with anti-MRSA antibiotics, with or without rifampicin, from 2014 to 2021. The primary outcome was defined as no revision arthroplasty, while the safety outcomes were renal dysfunction and hypersensitivity.Among 52,588 patients who underwent hip replacement or artificial head insertion surgeries, 53 were treated for PJI with anti-MRSA antibiotics and received debridement, antibiotics, and implant retention, with 33 without rifampicin and 20 with rifampicin. The incidence of revision arthroplasty did not differ significantly between the two groups (3 vs. 5 patients; log-rank test, p = 0.195). The incidence of adverse events was similar between the two groups.In this analysis, rifampicin combination therapy provided no additional benefit in treating methicillin-resistant PJI after hip replacement surgery. If used together, close monitoring for the occurrence of adverse effects is advised.
(徳島大学機関リポジトリ): ● Metadata: 2013220
(出版サイトへのリンク): ● Publication site (DOI): 10.5414/CP204740
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 40396698; ● Search Scopus @ Elsevier (PMID): 40396698; ● Search Scopus @ Elsevier (DOI): 10.5414/CP204740

(徳島大学機関リポジトリ: 2013220, DOI: 10.5414/CP204740, PubMed: 40396698) Yoshika Sakamoto, Takahiro Niimura, Mitsuhiro Goda, Nanami Tomochika, Wakana Murakawa, Fuka Aizawa, Kenta Yagi, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa :
Unravelling the cardioprotective effects of calcitriol in Sunitinib-induced toxicity: A comprehensive in silico and in vitro study,
Biomedicine & Pharmacotherapy, 188, 118137, 2025.

(要約): Sunitinib (SUN), a drug used to treat advanced renal cell carcinoma and other cancers, causes cardiotoxicity. This study aimed to identify a potential drug candidate to counteract SUN-induced cardiotoxicity. We analysed real-world data from adverse event report databases of existing clinically approved drugs to identify potential candidates. Through in silico analyses and in vitro experiments, the mechanisms of action were determined. The study identified calcitriol (CTL), an active form of vitamin D, as a promising candidate against SUN-induced cardiotoxicity. In H9c2 cells, SUN decreased cell viability significantly, whereas CTL mitigated this effect significantly. The SUN-treated group exhibited increased autophagy in H9c2 cells, which was reduced significantly in the CTL group. Bioinformatics analysis using Ingenuity Pathway Analysis revealed the mechanistic target of rapamycin (mTOR) as a common factor between autophagy and CTL. Notably, rapamycin, an mTOR inhibitor, nullified the effects of CTL on cell viability and autophagy. Furthermore, SUN treatment led to significant reductions in cardiomyocyte diameters and increases in their widths, changes that were inhibited by CTL. SUN also induced morphological changes in surviving H9c2 cells, causing them to adopt a rounded shape, whereas CTL improved their morphology to resemble the elongated shape of the control group. In conclusion, the findings of the present study suggest that CTL has the potential to prevent SUN-induced cardiomyocyte damage through autophagy, particularly via mTOR-mediated pathways. The findings indicate that CTL could serve as an effective prophylactic agent against SUN-induced cardiotoxicity, offering a promising avenue for further research and potential clinical applications.
(キーワード): Advanced renal cell carcinoma / Autophagy / Calcitriol / Cardiotoxicity / MTOR / Sunitinib
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.biopha.2025.118137
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 40373630; ● Summary page in Scopus @ Elsevier: 2-s2.0-105004893179

(DOI: 10.1016/j.biopha.2025.118137, PubMed: 40373630, Elsevier: Scopus) Kenta Yagi, Kajizono Makoto, Maruo Akinori, Shinmura Wataru, NItta Yuuki, Yoshioka Toshihiko, Masayuki Chuma, Ishida Shunsuke, Higashionna Tsukasa, Tanaka Hiroaki, Fuka Aizawa, Takahiro Niimura, Mitsuhiro Goda, Kei Kawada, Yuki Izawa-Ishizawa, Yoshito Zamami, Kosaka Shinji, Tasaki Yoshikazu and Keisuke Ishizawa :
Effective drug dosage rounding reduces healthcare expenses in the Japanese healthcare system,
Drugs & Therapy Perspectives, 2025.

(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s40267-025-01144-6
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-105000760714

(DOI: 10.1007/s40267-025-01144-6, Elsevier: Scopus) Yuki Kono, Takahiro Niimura, Mitsuhiro Goda, Shiho Ueta, Kei Kawada, Koji Miyata, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa :
Cardiovascular Toxicity Profile of Macrolides Investigated Using VigiBase Data: A Pharmacovigilance Study.,
Cardiovascular Toxicology, 25, 3, 498-506, 2025.

(要約): Macrolides are associated with cardiovascular toxicity risk. However, data on their cardiovascular toxicity profiles beyond QT prolongation are limited, and differences in the profiles among various macrolide antibiotics remain unclear. We investigated the cardiovascular toxicity profiles of different macrolides using VigiBase, a global database of individual case-safety reports. Disproportionality analysis was performed using VigiBase, the WHO Pharmacovigilance database, from 1968 to December 2023. Associations between five macrolides (erythromycin, clarithromycin, azithromycin, josamycin, and roxithromycin) and adverse events (20 cardiovascular toxicities and diarrhea as a positive control) were predicted using the reporting odds ratio. Reported outcomes were evaluated for suggested drug-adverse event associations. Among the 36,129,107 reports analyzed, azithromycin was the most commonly used macrolide, followed by erythromycin, clarithromycin, roxithromycin, and josamycin. Diarrhea was frequently reported among users. Azithromycin use was associated with hypertension, cardiac valve disorders, supraventricular tachyarrhythmias, ventricular tachyarrhythmias, torsade de pointes/QT prolongation, cardiac conduction disorders, heart failure, and hemorrhage-related laboratory abnormalities. Erythromycin and clarithromycin use were also associated with cardiac valve disorders, ventricular tachyarrhythmias, torsade de pointes/QT prolongation, and cardiac conduction disorders. The rates of caused/prolonged hospitalization in azithromycin-related hypertension, heart failure, and bleeding-related laboratory abnormality were 46%, 45%, and 50%, respectively. Each of the macrolide antimicrobials was associated with various cardiovascular toxicities, including Cardiac valve disorder, shock, and QT prolongation. Notably, azithromycin was associated with an increased frequency of reported hypertension and heart failure, distinguishing it from the other drugs. These results highlight the importance of considering the cardiovascular toxicity profile of individual macrolide antibiotics when prescribing them.
(キーワード): Macrolides / Pharmacovigilance / Adverse Drug Reaction Reporting Systems
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12012-025-09970-w
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39971867; ● Search Scopus @ Elsevier (PMID): 39971867; ● Search Scopus @ Elsevier (DOI): 10.1007/s12012-025-09970-w

(DOI: 10.1007/s12012-025-09970-w, PubMed: 39971867) Hiroshi Bando, Mitsuhiro Goda, Masahito Nakataki, Keita Hirai, Yuki Nitta, Kei Kawada, Toshihiko Yoshioka, Masaya Kanda, Atsushi Ogawa, Chiaki Mukuta-Murakami, Kaito Tsujinaka, Koji Miyata, Kohei Kitagawa, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Masayuki Chuma, Takafumi Naito, Yoshikazu Tasaki, Shusuke Numata and Keisuke Ishizawa :
Flunitrazepam increases the risk of lamotrigine-induced cutaneous adverse reactions: Combined analysis of medical big data and clinical research,
Psychiatry and Clinical Neurosciences, 2025.

(キーワード): flunitrazepam / lamotrigine / medical big data / rash / UDP-glucuronosyltransferase
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/pcn.13866
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-105010849222

(DOI: 10.1111/pcn.13866, Elsevier: Scopus) Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Kenta Yagi, Mitsuhiro Goda, Hideki Nawa, Yuya Horinouchi, Toshimi Nakamura, Harumasa Hakuno, Kazuaki Shinomiya, 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, 10, 1, 61, 2024.

(要約): Understanding the roles and competencies of professions outside of one's specialty is essential for providing efficient healthcare. However, it is difficult for medical professionals to understand the roles and competencies of other related professions while performing their duties. This study examined the impact of clinical practice-based interprofessional education (IPE) on pharmacy students, who are future medical professionals. Sixty-eight pharmaceutical students undergoing clinical practice were divided into non-IPE or IPE groups, with the IPE group attending an educational program with medical students conducted by doctors, pharmacists, and teachers during the clinical practice period. The effect was evaluated through a group survey using self-administered questionnaires focusing on contributing to multidisciplinary team medicine based on the Readiness for Interprofessional Learning Scale. The survey included specific behavioral objectives (SBOs), the Readiness for Interpersonal Learning Scale (RIPLS), and Kikuchi's Scale of Social Skills (KiSS-18). Regardless of group, SBOs [non-IPE: 3.2, 95% CI (2.6-3.8), p < 0.001; IPE: 3.7, 95% CI (2.5-4.9), p < 0.001] and social skills [non-IPE: 4.0, 95% CI (2.5-6.1), p < 0.001; IPE: 6.7 95% CI (3.0-10.4), p < 0.001] showed improvement after the clinical practice. In RIPLS Factor 3, pharmacy students with IPE awareness scored significantly higher by 1.5 points [95% CI (0.2-2.8), p = 0.025] post-practice than those without IPE awareness. This study suggests that IPE for students during clinical practice could enhance their expertise in multidisciplinary medicine and facilitate the development of seamless team care in the future. This study was retrospectively registered and conducted in compliance with the "Ethical Guidelines for Medical Research Involving Human Subjects" and was approved by The Ethics Committee of Tokushima University Hospital (approval number: 3544).
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/s40780-024-00382-6
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39354644; ● Search Scopus @ Elsevier (PMID): 39354644; ● Search Scopus @ Elsevier (DOI): 10.1186/s40780-024-00382-6

(DOI: 10.1186/s40780-024-00382-6, PubMed: 39354644) 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, 180, 105863, 2024.

(要約): Some therapeutic agents have been found to have effects beyond their primary indications. Peripheral neuropathy, a common side effect of chemotherapy, remains inadequately treated. Identifying additional properties of existing medications could thus uncover novel therapeutic avenues. Previous studies have identified an additional effect of simvastatin in reducing neuropathy; however, the mechanism underlying this effect remains unclear. We investigated the novel effects of statins on chemotherapy-induced peripheral neuropathy in mice. Mice treated with oxaliplatin or paclitaxel did not show exacerbation or improvement in cold sensations upon acetone testing with statin administration. However, concurrent oral statin treatment mitigated the nociceptive response to mechanical stimuli induced by each anti-tumor agent. Co-administration of a glutathione S-transferase inhibitor, which modulates redox reactions, abolished the ameliorative effect of statins on mechanical nociceptive behavior. Additionally, the glutathione S-transferase inhibitor did not affect normal sensory perception or impair the anti-tumor effect of chemotherapy agents. A search for GST-associated molecules and pathways using artificial intelligence revealed that GST regulates inflammatory cytokines as a regulatory or causative gene. Our findings suggest that statins have class effects that ameliorate cytotoxic anti-cancer drug-induced mechanical allodynia via GST pathway activation.
(キーワード): Animals / Oxaliplatin / Paclitaxel / Peripheral Nervous System Diseases / Glutathione Transferase / Mice / Hydroxymethylglutaryl-CoA Reductase Inhibitors / Male / Antineoplastic Agents / Mice, Inbred C57BL
(徳島大学機関リポジトリ): ● Metadata: 2012457
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.neuint.2024.105863
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39307458; ● Search Scopus @ Elsevier (PMID): 39307458; ● Search Scopus @ Elsevier (DOI): 10.1016/j.neuint.2024.105863

(徳島大学機関リポジトリ: 2012457, DOI: 10.1016/j.neuint.2024.105863, PubMed: 39307458) Koji Miyata, Yuki Izawa-Ishizawa, Kaito Tsujinaka, Honoka Nishi, Syuto Itokazu, Tatsumi Miyata, Masateru Kondo, Toshihiko Yoshioka, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Maki Sato, Mizusa Hyodo, Hirofumi Hamano, Kei Kawada, Masayuki Chuma, Yoshito Zamami, Koichi Tsuneyama, Mitsuhiro Goda and Keisuke Ishizawa :
Unveiling the association between fluoroquinolones and aortic diseases using real-world database analysis and pharmacological experiments,
Biomedicine & Pharmacotherapy, 179, 117418, 2024.

(要約): Fluoroquinolones, which are widely used antibiotics, have been linked to aortic disease, which prompted an FDA warning in 2018. Recent reports have challenged the perception that fluoroquinolones pose a significant risk for vascular diseases. This study aimed to investigate whether fluoroquinolones increase the risk of aortic diseases by focusing on the onset of aortic dissection. Levofloxacin (LVFX), a fluoroquinolone, was studied in vitro using cultured vascular cells and in vivo using a mouse model prone to aortic dissection. Risk of adverse drug events was analyzed using VigiBase, a global safety database, and a retrospective cohort analysis was conducted using the JMDC Claims database. LVFX resulted in endothelial cell injury and increased matrix metalloproteinases in vitro. However, in vivo studies showed no significant effect on elastin degradation or aortic dissection incidence. The effect of LVFX on endothelial injury was altered during the onset of dissection, exacerbating injury before onset but inhibiting it afterward. Safety database analysis showed no significant risk signals for aortic dissection associated with fluoroquinolones, which was supported by findings in the receipt database. Inconsistencies were observed in the in vitro and in vivo actions of fluoroquinolones and differences in their effects on aortic dissection and aneurysms. Despite cytotoxicity, the risk of aortic dissection was not significantly increased in clinical scenarios. Based on our findings, concerns regarding aortic diseases do not justify discontinuation of fluoroquinolone use. Further studies are needed to elucidate the conflicting actions of fluoroquinolones, taking into account background pathophysiology such as infection and inflammation.
(キーワード): Aortic aneurysm / Aortic dissection / Endothelial cell injury / Fluoroquinolones / Real-world database
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.biopha.2024.117418
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39265233; ● Summary page in Scopus @ Elsevier: 2-s2.0-85203457086

(DOI: 10.1016/j.biopha.2024.117418, PubMed: 39265233, Elsevier: Scopus) Naoki Okamoto, Kenta Yagi, Sayaka Imawaka, Mayu Takaoka, Fuka Aizawa, Takahiro Niimura, Mitsuhiro Goda, Koji Miyata, Kei Kawada, Yuki Izawa-Ishizawa, Satoshi Sakaguchi and Keisuke Ishizawa :
Asciminib, A Novel Allosteric Inhibitor of BCR-ABL1, Shows Synergistic Effects When Used in Combination with Imatinib with or without Drug Resistance.,
Pharmacology Research & Perspectives, 12, 4, e1214, 2024.

(要約): In the treatment of chronic myeloid leukemia (CML), resistance to BCR-ABL inhibitors makes it difficult to continue treatment and is directly related to life expectancy. Therefore, asciminib was introduced to the market as a useful drug for overcoming drug resistance. While combining molecular targeted drugs is useful to avoid drug resistance, the new BCR-ABL inhibitor asciminib and conventional BCR-ABL inhibitors should be used as monotherapy in principle. Therefore, we investigated the synergistic effect and mechanism of the combination of asciminib and imatinib. We generated imatinib-resistant cells using the human CML cell line K562, examined the effects of imatinib and asciminib exposure on cell survival using the WST-8 assay, and comprehensively analyzed genetic variation related to drug resistance using RNA-seq and real-time PCR. A synergistic effect was observed when imatinib and asciminib were combined with or without imatinib resistance. Three genes, GRRP1, ESPN, and NOXA1, were extracted as the sites of action of asciminib. Asciminib in combination with BCR-ABL inhibitors may improve the therapeutic efficacy of conventional BCR-ABL inhibitors and prevent the development of resistance. Its dosage may be effective even at minimal doses that do not cause side effects. Further verification of this mechanism of action is needed. Additionally, cross-resistance between BCR-ABL inhibitors and asciminib may occur, which needs to be clarified through further validation as soon as possible.
(キーワード): Imatinib Mesylate / Humans / Fusion Proteins, bcr-abl / Drug Synergism / Drug Resistance, Neoplasm / K562 Cells / Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Protein Kinase Inhibitors / Cell Survival / Antineoplastic Combined Chemotherapy Protocols / Antineoplastic Agents / Niacinamide / Pyrazoles
(徳島大学機関リポジトリ): ● Metadata: 2007994
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/prp2.1214
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39031848; ● Search Scopus @ Elsevier (PMID): 39031848; ● Search Scopus @ Elsevier (DOI): 10.1002/prp2.1214

(徳島大学機関リポジトリ: 2007994, DOI: 10.1002/prp2.1214, PubMed: 39031848) 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, 11, 2024.

(要約): = 0.246, respectively). These results suggest that beta blockers may differ in their all-cause mortality benefits according to age.
(徳島大学機関リポジトリ): ● Metadata: 2012787
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fcvm.2024.1377228
(文献検索サイトへのリンク): ● 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

(徳島大学機関リポジトリ: 2012787, DOI: 10.3389/fcvm.2024.1377228, PubMed: 38883984) 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, 15, 2024.

(要約): 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.
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fphar.2024.1302055
(文献検索サイトへのリンク): ● 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) 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, 62, 2, 69-76, 2024.

(要約): A total of 353 patients were included, of which 61 were included in the ILD group. The median time to onset of ILD after ICI administration was 3 months. Multivariate logistic regression analysis revealed that pre-treatment with EGFR-TKI was not associated with ICI-associated ILD (odds ratio: 0.26, 95% confidence interval: 0.033 - 2.01).
(キーワード): Humans / Lung Neoplasms / Immune Checkpoint Inhibitors / Carcinoma, Non-Small-Cell Lung / Retrospective Studies / Japan / Lung Diseases, Interstitial / ErbB Receptors / Protein Kinase Inhibitors
(出版サイトへのリンク): ● Publication site (DOI): 10.5414/CP204491
(文献検索サイトへのリンク): ● 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) Koji Miyata, Yuki Izawa-Ishizawa, Takahiro Niimura, Hirofumi Hamano, Fuka Aizawa, Kenta Yagi, Kei Kawada, Yoshito Zamami, Mitsuhiro Goda and Keisuke Ishizawa :
The Association between PDE5 Inhibitors and Aneurysm/Arterial Dissection: A Pharmacovigilance Study Using WHO Safety Database,
The Journal of Medical Investigation : JMI, 71, 1-2, 134-140, 2024.

(要約): Aneurysm and arterial dissection have been reported as adverse drug events, associated with angiogenesis inhibitors and fluoroquinolones. Specifically, several cases of severe arterial disease following cGMP-specific phosphodiesterase type 5 (PDE5) inhibitors usage have recently been reported. It is necessary to ascertain the risks of serious adverse events caused by PDE5 inhibitors. We aimed to evaluate the association of aneurysm and artery dissection with PDE5 inhibitors using VigiBase, which is a World Health Organization database of spontaneously reported adverse events, for explorative hypothesis-generating analysis. We performed disproportionality analysis using a dataset from inception in 1967 to December 2022 and calculated reporting odds ratios (ROR) between PDE5 inhibitors and arterial diseases. We extracted 195,839 reports on PDE5 inhibitors with 254 reports of arterial disease as adverse events from VigiBase. Disproportionality analysis showed disproportional signals for PDE5 inhibitors (ROR, 2.30;95% confidence intervals, 2.04-2.61);disproportional signals were detected in analyses restricting the lesion site to the aorta or cerebral arteries. From stratified analysis, disproportional signals were noted in females, as well as males, generally recognized as a risk factor for artery diseases. This real-world data analysis suggests that PDE5 inhibitors may play a role in the development of lethal arterial disease. J. Med. Invest. 71 : 134-140, February, 2024.
(キーワード): Adverse event / Aneurysm / Arterial dissection / PDE5 inhibitors / Pharmacovigilance
(出版サイトへのリンク): ● Publication site (DOI): 10.2152/jmi.71.134
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38735709; ● Summary page in Scopus @ Elsevier: 2-s2.0-85192870665

(DOI: 10.2152/jmi.71.134, PubMed: 38735709, Elsevier: Scopus) 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, 16, 11, 2369-2381, 2023.

(要約): 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.
(キーワード): Mice / Animals / Humans / Cisplatin / Valproic Acid / Prospective Studies / Acute Kidney Injury / Kidney / Apoptosis / Mice, Inbred C57BL
(徳島大学機関リポジトリ): ● Metadata: 2011485
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/cts.13638
(文献検索サイトへのリンク): ● 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

(徳島大学機関リポジトリ: 2011485, DOI: 10.1111/cts.13638, PubMed: 37700528) 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, 167, 2023.

(要約): 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.
(徳島大学機関リポジトリ): ● Metadata: 2012024
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.biopha.2023.115504
(文献検索サイトへのリンク): ● 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

(徳島大学機関リポジトリ: 2012024, DOI: 10.1016/j.biopha.2023.115504, PubMed: 37722188) 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.

(要約): 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.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s40264-023-01300-9
(文献検索サイトへのリンク): ● 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) 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.

(要約): 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.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10238-023-01008-1
(文献検索サイトへのリンク): ● 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) Takahiro Niimura, Mitsuhiro Goda, Koji Miyata, Jun Matsumoto, Toshihiko Yoshioka, Hirofumi Hamano, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Yoshito Zamami and Keisuke Ishizawa :
Evaluation of cardiovascular toxicity of the atezolizumab and bevacizumab combination,
Frontiers in Drug Safety and Regulation, 3, 2023.

(キーワード): adverse event / atezolizumab / bevacizumab / cardiovascular toxicity / thromboembolism
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fdsfr.2023.1213771
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85204179640

(DOI: 10.3389/fdsfr.2023.1213771, Elsevier: Scopus) 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, 63, 4, 473-479, 2022.

(要約): 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.
(キーワード): Male / United States / Humans / Female / Aged / Immune Checkpoint Inhibitors / United States Food and Drug Administration / Myocarditis / Myasthenia Gravis / Myositis
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/jcph.2187
(文献検索サイトへのリンク): ● 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) 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, 84, 1, 75-83, 2022.

(要約): 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.
(キーワード): Humans / Proton Pump Inhibitors / Endothelial Growth Factors / Molecular Docking Simulation / Peptic Ulcer / Pyrroles / Neoplasms
(徳島大学機関リポジトリ): ● Metadata: 2011046
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/ddr.22013
(文献検索サイトへのリンク): ● 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

(徳島大学機関リポジトリ: 2011046, DOI: 10.1002/ddr.22013, PubMed: 36484282) 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, 27, 7, e554-e560, 2022.

(要約): This single-arm, phase II study recruited patients with non-squamous non-small cell lung cancer and malignant pleural mesothelioma scheduled to receive chemotherapy including pemetrexed. Patients received 2 mg of dexamethasone daily from days 2 to 6 after chemotherapy with pemetrexed. The primary endpoint was the 3-week incidence of rash eruptions.
(キーワード): Adrenal Cortex Hormones / Carcinoma, Non-Small-Cell Lung / Cisplatin / Dexamethasone / Exanthema / Humans / Lung Neoplasms / Mesothelioma, Malignant / Pemetrexed
(徳島大学機関リポジトリ): ● Metadata: 2010208
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/oncolo/oyab077
(文献検索サイトへのリンク): ● 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

(徳島大学機関リポジトリ: 2010208, DOI: 10.1093/oncolo/oyab077, PubMed: 35325241) 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, 928, 175083, 2022.

(要約): The Gene Expression Omnibus (GEO), Library of Integrated Network-based Cellular Signatures (LINCS), and Food and Drug Administration Adverse Events Reporting System (FAERS) databases were used to extract candidate prophylactic drugs. Mouse models of doxorubicin-induced cardiac events were generated by intraperitoneal administration of 20 mg/kg of doxorubicin on Day 1 and oral administration of prophylactic candidate drugs for 6 consecutive days beginning the day before doxorubicin administration. On Day 6, mouse hearts were extracted and examined for mRNA expression of apoptosis-related genes.
(キーワード): Animals / アポトーシス (apoptosis) / Cardiotoxicity / データ解析 (data analysis) / Doxorubicin / Mice / Myocytes, Cardiac / Pharmaceutical Preparations / RNA, Messenger / Sirolimus
(徳島大学機関リポジトリ): ● Metadata: 2010188
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ejphar.2022.175083
(文献検索サイトへのリンク): ● 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

(徳島大学機関リポジトリ: 2010188, DOI: 10.1016/j.ejphar.2022.175083, PubMed: 35659512) 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, 15, 7, 1664-1675, 2022.

(要約): 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.
(キーワード): Acute Kidney Injury / Animals / Cisplatin / データ解析 (data analysis) / Fenofibrate / 腎疾患 (kidney disease) / Mice / Prospective Studies
(徳島大学機関リポジトリ): ● Metadata: 2010189
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/cts.13282
(文献検索サイトへのリンク): ● 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

(徳島大学機関リポジトリ: 2010189, DOI: 10.1111/cts.13282, PubMed: 35445533) 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, 27, 10371-10386, 2022.

(要約): The online version contains supplementary material available at 10.1007/s10639-022-11032-5.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10639-022-11032-5
(文献検索サイトへのリンク): ● 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) 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, 148, 2022.

(要約): 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.
(キーワード): 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
(徳島大学機関リポジトリ): ● Metadata: 2010230
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.biopha.2022.112744
(文献検索サイトへのリンク): ● 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

(徳島大学機関リポジトリ: 2010230, DOI: 10.1016/j.biopha.2022.112744, PubMed: 35240525) 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, 43, 11, 1910-1920.e3, 2021.

(要約): The prevalences of VIN were 29.5% (18/61) and 7.1% (3/42) in the VT and VC groups, respectively. Multivariate logistic regression analysis of data from all patients revealed concurrent use of tazobactam/piperacillin (odds ratio [OR] = 4.59; P = 0.039) and AUC increase (OR = 1.01; P < 0.01) as risk factors for VIN, but only concurrent use of tazobactam/piperacillin was identified as a risk factor in patients with an AUC of <600 μg · h/mL, the guideline-recommended value (OR = 9.52; P = 0.041). Moreover, the vancomycin exposure-toxicity curve showed that in the guideline-recommended AUC range, VIN probability was consistently higher and the slope of VIN probability was greater in the VT group than in the VC group.
(キーワード): Acute Kidney Injury / Anti-Bacterial Agents / Bayes Theorem / Cefepime / Drug Therapy, Combination / Humans / Penicillanic Acid / Piperacillin / Piperacillin, Tazobactam Drug Combination / Prevalence / Retrospective Studies / Vancomycin
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.clinthera.2021.09.007
(文献検索サイトへのリンク): ● 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) 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.

(要約): 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.
(徳島大学機関リポジトリ): ● Metadata: 2008943
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/cts.13045
(文献検索サイトへのリンク): ● 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

(徳島大学機関リポジトリ: 2008943, DOI: 10.1111/cts.13045, PubMed: 33982438) 石澤有紀, 合田光寛, 相澤風花, 座間味義人, 濱野裕章, 八木健太, 池田康将, 石澤啓介, 玉置俊晃 :
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,
四国医学雑誌, 77, 1,2, 57-62, 2021年.

(要約): 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.
(キーワード): aortic dissection / endothelial dysfunction / statin / ポリフェノール (polyphenol) / large medical databases
(徳島大学機関リポジトリ): ● Metadata: 2008973
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050585658873174784

(徳島大学機関リポジトリ: 2008973, CiNii: 1050585658873174784) Naoto Okada, Noriko Fujiwara, Momoyo Azuma, Kaito Tsujinaka, Masayuki Chuma, Kenta Yagi, Hirofumi Hamano, Fuka Aizawa, Mitsuhiro Goda, Yasushi Kirino, Toshimi Nakamura, Yoshito Zamami, Ichiro Hashimoto and Keisuke Ishizawa :
Assessment of adherence to post-exposure prophylaxis with oseltamivir in healthcare workers: A retrospective questionnaire-based study,
Biological & Pharmaceutical Bulletin, 44, 6, 869-874, 2021.

(要約): Post-exposure prophylaxis (PEP) for healthcare workers is one of the effective strategies for preventing nosocomial outbreaks of influenza. However, PEP adherence in healthcare workers is rarely analysed, and no strategies have been established to improve adherence to PEP for healthcare workers. We aimed to retrospectively analyse adherence to PEP and the factors associated with non-adherence in healthcare workers. A survey of 221 healthcare workers who were eligible for PEP at Tokushima University Hospital in the 2016/2017 season was conducted. Once-daily oseltamivir (75 mg for 10 d) was used as the PEP regimen. Of the 221 healthcare workers, 175 received PEP and were surveyed for adherence using a questionnaire. Of the 130 healthcare workers who responded to the questionnaire, 121 (93.1%) had been vaccinated. In this survey, 82 healthcare workers (63.1%) did not fully complete PEP. Multiple logistic regression analysis revealed that physicians (odds ratio: 4.62, 95% confidence interval [CI]: 2.08-10.25) and non-vaccination (odds ratio: 9.60, 95% CI: 1.12-82.25) were the factors for non-adherence to PEP. Of the 47 healthcare workers who responded to the item regarding reasons for non-adherence, 36 (76.6%) reported forgetting to take oseltamivir or discontinuing it due to a misguided self-decision that continuation of PEP was unnecessary, and 5 (10.6%) reported discontinuing treatment due to adverse effects. In conclusion, healthcare workers, particularly physicians, had low PEP adherence owing to forgetting or stopping to take oseltamivir due to a misguided self-decision. To obtain the maximum preventive effect of PEP, medication education should be provided to endorse PEP compliance.
(キーワード): Adherence / Healthcare worker / Influenza / Oseltamivir / Post-exposure prophylaxis
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b21-00165
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34078819; ● Summary page in Scopus @ Elsevier: 2-s2.0-85107184561

(DOI: 10.1248/bpb.b21-00165, PubMed: 34078819, Elsevier: Scopus) Fuka Aizawa, Shumpei Sato, Fumiyoshi Yamazaki, Ikuko Yao, Takuya Yamashita, Kazuo Nakamoto, Fumiyo Kasuya, Mitsutoshi Setou and Shogo Tokuyama :
N-3 fatty acids modulate repeated stress-evoked pain chronicity,
Brain Research, 1714, 218-226, 2019.

(要約): N-3 fatty acids, including docosahexaenoic acid (DHA), have a beneficial effect in both pain and psychiatric disorders. In fact, we previously reported that stress-induced pain prolongation might be mediated through the suppression of the G-protein coupled-receptor 40/free fatty acid receptor 1 (GPR40/FFAR1), which is activated by DHA and long-chain fatty acids. However, the involvement of GPR40/FFAR1 ligands in the development of stress-induced chronic pain has not yet been described. In this study, we investigated the role of DHA in stress-evoked pain chronicity using diet-induced n-3 fatty acid deficient mice. The n-3 fatty acid deficient mice showed exacerbation of anxiety-like behavior after repeated exposure to social defeat stress. The intact n-3 fatty acid deficient mice showed a decrease in paw threshold values. On the other hand, paw withdrawal thresholds of defeated but not non-stressed, n-3 fatty acid deficient mice continued until day 49 after paw surgery. We evaluated changes in phosphatidylcholine composition in the brains of repeat stress-evoked chronic pain model mice which were not on n-3 fatty acid deficiency diets. On day 7 after paw surgery, phosphatidylcholines with DHA and other long-chain fatty acids were found to have decreased in the brains of stressed mice. Moreover, stress-induced persistent mechanical allodynia was improved by oral DHA supplementation. These results indicated that chronic stress may directly affect brain lipid composition; the related changes could be involved in chronic pain development. Our findings suggested that n-3 fatty acids, particularly DHA, are useful as a potential therapeutic target for stress-evoked chronic pain.
(キーワード): DHA / n-3 deficient / Phospholipid / Stress-induced pain
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.brainres.2019.03.001
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30831087; ● Summary page in Scopus @ Elsevier: 2-s2.0-85062630014

(DOI: 10.1016/j.brainres.2019.03.001, PubMed: 30831087, Elsevier: Scopus) Fuka Aizawa, Kazuo Nakamoto and Shogo Tokuyama :
The involvement of free fatty acid-GPR40/FFAR1 signaling in chronic social defeat stress-induced pain prolongation in C57BL/6J male mice,
Psychopharmacology, 235, 8, 2335-2347, 2018.

(要約): Depression and anxiety can cause the development of chronic pain. However, the mechanism of chronic pain induced by emotional dysfunction is still unknown. Previously, we demonstrated that the G protein-coupled receptor 40/free fatty acid receptor 1 (GPR40/FFAR1) signaling in the brain is related to regulation of both pain and emotion. In the present study, we proved that the role of GPR40/FFAR1 signaling in the development of chronic pain is induced by emotional dysfunction. Repeated social defeat (SD)-stressed mice showed the impairment of social interaction and anxiety behavior. These mice also caused pain prolongation after paw-incision comparison with non-SD mice. This pain prolongation was markedly continued by infusion of the GPR40/FFAR1 antagonist, GW1100 during SD stress but not non-SD stress. Although, infusion of the GW1100 during SD stress did not cause deterioration of the emotional behavior. Furthermore, GW1100-treated SD-mice showed strong tendency of emotional dysfunction after paw incision. Our findings indicate that the dysfunction of fatty acids-GPR40/FFAR1 signaling in the brain underlying stress condition might be related to the development of chronic pain.
(キーワード): Chronic pain / Emotional dysfunction / Free fatty acid / GPR40/FFAR1
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00213-018-4930-8
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29931581; ● Summary page in Scopus @ Elsevier: 2-s2.0-85048782556

(DOI: 10.1007/s00213-018-4930-8, PubMed: 29931581, Elsevier: Scopus) Kazuo Nakamoto, Fuka Aizawa, Kei Miyagi, Takuya Yamashita, Mitsumasa Mankura, Yutaka Koyama, Fumiyo Kasuya, Akira Hirasawa, Takashi Kurihara, Atsuro Miyata and Shogo Tokuyama :
Dysfunctional GPR40/FFAR1 signaling exacerbates pain behavior in mice,
PLoS ONE, 12, 7, e0180610, 2017.

(要約): We previously showed that activation of G protein-coupled receptor 40/free fatty acid receptor 1 (GPR40/FFAR1) signaling modulates descending inhibition of pain. In this study, we investigated the involvement of fatty acid-GPR40/FFAR1 signaling in the transition from acute to chronic pain. We used GPR40/FFAR1-knockout (GPR40KO) mice and wild-type (WT) mice. A plantar incision was performed, and mechanical allodynia and thermal hyperalgesia were evaluated with a von Frey filament test and plantar test, respectively. Immunohistochemistry was used to localize GPR40/FFAR1, and the levels of free fatty acids in the hypothalamus were analyzed with liquid chromatography-tandem mass spectrometry. The repeated administration of GW1100, a GPR40/FFAR1 antagonist, exacerbated the incision-induced mechanical allodynia and significantly increased the levels of phosphorylated extracellular signal-regulated kinase in the spinal cord after low-threshold touch stimulation in the mice compared to vehicle-treated mice. The levels of long-chain free fatty acids, such as docosahexaenoic acid, oleic acid, and palmitate, which are GPR40/FFAR1 agonists, were significantly increased in the hypothalamus two days after the surgery compared to levels in the sham group. Furthermore, the incision-induced mechanical allodynia was exacerbated in the GPR40KO mice compared to the WT mice, while the response in the plantar test was not changed. These findings suggested that dysfunction of the GPR40/FFAR1 signaling pathway altered the endogenous pain control system and that this dysfunction might be associated with the development of chronic pain.
(キーワード): Animals / Behavior, Animal / Benzoates / Docosahexaenoic Acids / Hyperalgesia / Hypothalamus / Mice / Mice, Knockout / Oleic Acid / Pain Measurement / Palmitic Acid / Phosphorylation / Pyrimidines / Receptors, G-Protein-Coupled / Signal Transduction
(出版サイトへのリンク): ● Publication site (DOI): 10.1371/journal.pone.0180610
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28723961; ● Summary page in Scopus @ Elsevier: 2-s2.0-85030440993

(DOI: 10.1371/journal.pone.0180610, PubMed: 28723961, Elsevier: Scopus) Kazuo Nakamoto, Fuka Aizawa, Megumi Kinoshita, Yutaka Koyama and Shogo Tokuyama :
Astrocyte activation in locus coeruleus is involved in neuropathic pain exacerbation mediated by maternal separation and social isolation stress,
Frontiers in Pharmacology, 8, JUN, 2017.

(キーワード): Astrocyte / Early life stress / Glia / Locus coeruleus / Maternal separation and social isolation stress
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fphar.2017.00401
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85021627936

(DOI: 10.3389/fphar.2017.00401, Elsevier: Scopus) Fuka Aizawa, Yoshihiro Ogaki, Natsuki Kyoya, Takashi Nishinaka, Kazuo Nakamoto, Takashi Kurihara, Akira Hirasawa, Atsuro Miyata and Shogo Tokuyama :
The Deletion of GPR40/FFAR1 Signaling Damages Maternal Care and Emotional Function in Female Mice,
Biological & Pharmaceutical Bulletin, 40, 8, 1255-1259, 2017.

(要約): The free fatty acid receptor 1 (GPR40/FFAR1) is activated by polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acids (DHA). This receptor has been the focus of many studies regarding physiological functions of the central nervous system. PUFAs are essential for neuronal development and maintenance of neuronal function; thus, the decrease of PUFAs in the brain is closely related to the induction of psychiatric diseases associated with emotional disorder, such as anxiety, depression, and schizophrenia. However, details of the mechanisms remain unclear. In this study, we investigated changes of maternal and/or emotional behavior caused by a deficiency of GPR40/FFAR1 signaling. GPR40/FFAR1 deficient (FFAR1^-/-) female mice exhibited impaired maternal care such as retrieving behaviors and an increased rate of neglect and infanticide when compared to wild type (WT) female mice. Furthermore, FFAR1^-/- female mice showed increased time spent in the open arms in an elevated plus maze test, reduction of locomotor activity and social interaction behavior, and decreased sucrose intake, when compared to WT female mice. In conclusion, these findings suggest that PUFAs-GPR40/FFAR1 signaling might function, at least in part, as a regulatory factor of emotional and maternal behavior in mice.
(キーワード): Emotional damage / Free fatty acid receptor 1 / Maternal behavior / Polyunsaturated fatty acid
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b17-00082
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28769007; ● Summary page in Scopus @ Elsevier: 2-s2.0-85026754757

(DOI: 10.1248/bpb.b17-00082, PubMed: 28769007, Elsevier: Scopus) Fuka Aizawa, Takashi Nishinaka, Takuya Yamashita, Kazuo Nakamoto, Takashi Kurihara, Akira Hirasawa, Fumiyo Kasuya, Atsuro Miyata and Shogo Tokuyama :
GPR40/FFAR1 deficient mice increase noradrenaline levels in the brain and exhibit abnormal behavior,
Journal of Pharmacological Sciences, 132, 4, 249-254, 2016.

(要約): The free fatty acid receptor 1 (GPR40/FFAR1) is a G protein-coupled receptor, which is activated by long chain fatty acids. We have previously demonstrated that activation of brain GPR40/FFAR1 exerts an antinociceptive effect that is mediated by the modulation of the descending pain control system. However, it is unclear whether brain GPR40/FFAR1 contributes to emotional function. In this study, we investigated the involvement of GPR40/FFAR1 in emotional behavior using GPR40/FFAR1 deficient (knockout, KO) mice. The emotional behavior in wild and KO male mice was evaluated at 9-10 weeks of age by the elevated plus-maze test, open field test, social interaction test, and sucrose preference test. Brain monoamines levels were measured using LC-MS/MS. The elevated plus-maze test and open field tests revealed that the KO mice reduced anxiety-like behavior. There were no differences in locomotor activity or social behavior between the wild and KO mice. In the sucrose preference test, the KO mice showed reduction in sucrose preference and intake. The level of noradrenaline was higher in the hippocampus, medulla oblongata, hypothalamus and midbrain of KO mice. Therefore, these results suggest that brain GPR40/FFAR1 is associated with anxiety- and depression-related behavior regulated by the increment of noradrenaline in the brain.
(キーワード): Anxiety / Free fatty acid / GPR40/FFAR1 / Noradrenaline / Sucrose preference
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jphs.2016.09.007
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27979701; ● Summary page in Scopus @ Elsevier: 2-s2.0-85006802549

(DOI: 10.1016/j.jphs.2016.09.007, PubMed: 27979701, Elsevier: Scopus) Fuka Aizawa, Takashi Nishinaka, Takuya Yamashita, Kazuo Nakamoto, Yutaka Koyama, Fumiyo Kasuya and Shogo Tokuyama :
Astrocytes release polyunsaturated fatty acids by lipopolysaccharide stimuli,
Biological & Pharmaceutical Bulletin, 39, 7, 1100-1106, 2016.

(要約): We previously reported that levels of long-chain fatty acids (FAs) including docosahexaenoic acids (DHA) increase in the hypothalamus of inflammatory pain model mice. However, the precise mechanisms underlying the increment of free fatty acids (FFAs) in the brain during inflammation remains unknown. In this study, we characterized FFAs released by inflammatory stimulation in rat primary cultured astrocytes, and tested the involvement of phospholipase A2 (PLA2) on these mechanisms. Lipopolysaccharide (LPS) stimulation significantly increased the levels of several FAs in the astrocytes. Under these conditions, mRNA expression of cytosolic PLA2 (cPLA2) and calcium-independent PLA2 (iPLA2) in LPS-treated group increased compared with the control group. Furthermore, in the culture media, the levels of DHA and arachidonic acid (ARA) significantly increased by LPS stimuli compared with those of a vehicle-treated control group whereas the levels of saturated FAs (SFAs), namely palmitic acid (PAM) and stearic acid (STA), did not change. In summary, our findings suggest that astrocytes specifically release DHA and ARA by inflammatory conditions. Therefore astrocytes might function as a regulatory factor of DHA and ARA in the brain.
(キーワード): Astrocyte / Docosahexaenoic acid (DHA) / Free fatty acid (FFA) / Inflammation / Phospholipase A2 (PLA2)
(出版サイトへのリンク): ● Publication site (DOI): 10.1248/bpb.b15-01037
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27374285; ● Summary page in Scopus @ Elsevier: 2-s2.0-84978177146

(DOI: 10.1248/bpb.b15-01037, PubMed: 27374285, Elsevier: Scopus) Kazuo Nakamoto, Fuka Aizawa, Takashi Nishinaka and Shogo Tokuyama :
Regulation of prohormone convertase 2 protein expression via GPR40/FFA1 in the hypothalamus,
European Journal of Pharmacology, 762, 459-463, 2015.

(要約): Previous studies have shown that the administration of docosahexaenoic acid (DHA) or GW9508, a GPR40/FFA1 (free fatty acid receptor) agonist, facilitates β-endorphin release in the arcuate nucleus of the hypothalamus in mice. However, the mechanisms mediating β-endorphin release induced by GPR40/FFA1 agonists remain unknown. In this study, we focused on the changes in expression of hypothalamic prohormone convertase (PC) 2, which is a calcium-dependent subtilisin-related proteolytic enzyme. The intracerebroventricular injection of DHA or GW9508 significantly increased PC2 protein expression in the hypothalamus. This increase in PC2 expression was inhibited by pretreatment with GW1100, a GPR40/FFA1 antagonist. Furthermore, PC2 protein expression gradually increased over time after complete Freund's adjuvant. These increase in PC2 expression were inhibited by pretreatment with GW1100. However, GW1100 by itself had no effect on PC2 levels. Taken together, our findings suggest that activation of the hypothalamic GPR40/FFA1 signaling pathway may regulate β-endorphin release via PC2, and regulate the endogenous pain control system.
(キーワード): Antinociception / GPR40/FFA1 / PC2 / β-endorphin
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ejphar.2015.06.013
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26071852; ● Summary page in Scopus @ Elsevier: 2-s2.0-84933036958

(DOI: 10.1016/j.ejphar.2015.06.013, PubMed: 26071852, Elsevier: Scopus) K. Nakamoto, T. Nishinaka, N. Sato, Fuka Aizawa, T. Yamashita, M. Mankura, Y. Koyama, F. Kasuya and S. Tokuyama :
The activation of supraspinal GPR40/FFA1 receptor signalling regulates the descending pain control system,
British Journal of Pharmacology, 172, 5, 1250-1262, 2015.

(要約): The ω-3 polyunsaturated fatty acids exert antinociceptive effects in inflammatory and neuropathic pain; however, the underlying mechanisms remain unclear. Docosahexaenoic acid-induced antinociception may be mediated by the orphan GPR40, now identified as the free fatty acid receptor 1 (FFA1 receptor). Here, we examined the involvement of supraspinal FFA1 receptor signalling in the regulation of inhibitory pain control systems consisting of serotonergic and noradrenergic neurons. Formalin-induced pain behaviours were measured in mice. Antinociception induced by FFA1 receptor agonists was examined by intrathecal injections of a catecholaminergic toxin, 5-HT lowering drug or these antagonists. The expression of FFA1 receptor protein and c-Fos was estimated by immunohistochemistry, and the levels of noradrenaline and 5-HT in the spinal cord were measured by LC-MS/MS. FFA1 receptors colocalized with NeuN (a neuron marker) in the medulla oblongata and with tryptophan hydroxylase (TPH; a serotonergic neuron marker) and dopamine β-hydroxylase (DBH; a noradrenergic neuron marker). A single i.c.v. injection of GW9508, a FFA1 receptor agonist, increased the number of c-Fos-positive cells and the number of neurons double-labelled for c-Fos and TPH and/or DBH. It decreased formalin-induced pain behaviour. This effect was inhibited by pretreatment with 6-hydroxydopamine, DL-p-chlorophenylalanine, yohimbine or WAY100635. Furthermore, GW9508 facilitated the release of noradrenaline and 5-HT in the spinal cord. In addition, GW1100, a FFA1 receptor antagonist, significantly increased formalin-induced pain-related behaviour. Activation of the FFA1 receptor signalling pathway may play an important role in the regulation of the descending pain control system.
(キーワード): Animals / Fenclonine / Formaldehyde / Male / Methylamines / Mice / Mice, Inbred Strains / Pain / Pain Measurement / Propionates / Receptors, G-Protein-Coupled / Signal Transduction
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/bph.13003
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25362997; ● Summary page in Scopus @ Elsevier: 2-s2.0-84922806191

(DOI: 10.1111/bph.13003, PubMed: 25362997, Elsevier: Scopus) Shinichi Harada, Yuka Haruna, Fuka Aizawa, Wataru Matsuura, Kazuo Nakamoto, Takuya Yamashita, Fumiyo Kasuya and Shogo Tokuyama :
Involvement of GPR40, a long-chain free fatty acid receptor, in the production of central post-stroke pain after global cerebral ischemia,
European Journal of Pharmacology, 744, 115-123, 2014.

(要約): Central post-stroke pain (CPSP), one of the complications of cerebral ischemia and neuropathic pain syndrome, is associated with specific somatosensory abnormalities. Although CPSP is a serious problem, detailed underlying mechanisms and standard treatments for CPSP are not well established. In this study, we assessed the role of GPR40, a long-chain fatty acid receptor, showing anti-nociceptive effects, in CPSP. We also examined the role of astrocytes in CPSP due to their effects in mediating the release of polyunsaturated fatty acids, which act as potential GPR40 ligands. The aim of this study was to determine the interactions between CPSP and astrocyte/GPR40 signaling. Male ddY mice were subjected to 30 min of bilateral carotid artery occlusion (BCAO). The development of hind paw mechanical hyperalgesia was measured after BCAO using the von Frey test. Neuronal damage was estimated by histological analysis on day 3 after BCAO. The thresholds for hind paw mechanical hyperalgesia were significantly decreased on days 1-28 after BCAO when compared with those of pre-BCAO assessments. BCAO-induced mechanical hyperalgesia was significantly decreased by intracerebroventricular injection of docosahexaenoic acid or GW9508, a GPR40 agonist; furthermore, these effects were reversed by GW1100, a GPR40 antagonist. The expression levels of glial fibrillary acidic protein, an astrocytic marker, and some free fatty acids were significantly decreased 5h after BCAO, although no effects of BCAO were noted on hypothalamic GPR40 protein expression. Our data show that BCAO-induced mechanical hyperalgesia is possible to be regulated by astrocyte activation and stimulation of GPR40 signaling.
(キーワード): Astrocyte / Central post-stroke pain (CPSP) / Docosahexaenoic acid (DHA) / Global ischemia (BCAO) / GPR40
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ejphar.2014.09.036
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25281202; ● Summary page in Scopus @ Elsevier: 2-s2.0-84918806496

(DOI: 10.1016/j.ejphar.2014.09.036, PubMed: 25281202, Elsevier: Scopus)

MISC

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, 130, 4, 553-556, 2022.

(キーワード): Adrenergic beta-Antagonists / Atenolol / Drug-Related Side Effects and Adverse Reactions / Female / Humans / Hypertension / Japan / Male / Renal Insufficiency, Chronic
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/bcpt.13717
(文献検索サイトへのリンク): ● 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)

総説・解説

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, 12, 752174, Nov. 2021.

(徳島大学機関リポジトリ): ● Metadata: 2009778
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fphar.2021.752174
(文献検索サイトへのリンク): ● Search Scopus @ Elsevier (DOI): 10.3389/fphar.2021.752174

(徳島大学機関リポジトリ: 2009778, DOI: 10.3389/fphar.2021.752174) 相澤風花, K. Nakamoto, A. Hirasawa, T. Kurihara, A. Miyata, S. Tokuyama :
JSNP excellent presentation award for CINP2016: GPR40/FFAR1,
Japanese Journal of Neuropsychopharmacology, 37, 3, 87-88, 2017年6月.

(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85029325098

(Elsevier: Scopus) K. Nakamoto, Fuka Aizawa, T. Yamashita, M. Mankura, Y. Koyama, F. Kasuya, A. Hirasawa, T. Kurihara, A. Miyata and S. Tokuyama :
JSNP Excellent presentation award for CINP2016:; GPR40/FFAR1,
Japanese Journal of Neuropsychopharmacology, 37, 3, 89-90, Jun. 2017.

(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85029330132

(Elsevier: Scopus)

講演・発表

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. Kanda Masaya, Mitsuhiro Goda, Kei Kawada, Bando Takashi, Ishida Shunsuke, Itokazu Shuto, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa and Keisuke Ishizawa :
Development of a strategy to prevent cisplatin-induced kidney injury by targeting MATE-type transporters,
ISSX/JSSX 2024 Meeting, ホノルル, Sep. 2024. Mitsuhiro Goda, Kanda Masaya, Kei Kawada, Ogawa Atsushi, Hyodo Mizusa, Kenta Yagi, Fuka Aizawa, Takahiro Niimura, Yuki Izawa-Ishizawa and Keisuke Ishizawa :
MATE are bound to a multiprotein complex containing NHE3, and it's causing functional interactions,
ISSX/JSSX 2024 Meeting, Sep. 2024. 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. 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. 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. 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. 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. 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. 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. 相澤風花, 西橋彩香, 薗田悠平, 谷田奨太, 八木健太, 新村貴博, 山﨑博輝, 合田光寛, 川田敬, 石澤有紀, 石澤啓介 :
胆汁酸- 胆汁酸受容体TGR5 シグナルによる多発性硬化症改善機構の解明,
医療薬学フォーラム2025 / 第33回クリニカルファーマシーシンポジウム, 2025年6月. 八木健太, 新村貴博, 相澤風花, 川田敬, 合田光寛, 石澤有紀, 矢野貴久, 石澤啓介 :
臨床・基礎研究を加速するデータベース解析の活用,
医療薬学フォーラム2025 / 第33回クリニカルファーマシーシンポジウム, 2025年6月. 佐川真琳, 八木健太, 髙岡麻佑, 相澤風花, 合田光寛, 新村貴博, 川田敬, 石澤有紀, 櫻田巧 (名), 石澤啓介 :
造血幹細胞移植前処置薬の薬効を増強する薬剤の探索,
第22回日本臨床腫瘍学会学術集会, 2025年3月. Fuka Aizawa, Okabayashi Ami, Takahiro Niimura, Takeuchi Karin, Kenta Yagi, Yoshito Zamami, Mitsuhiro Goda, Kei Kawada, Yuki Izawa-Ishizawa and Keisuke Ishizawa :
HMG-CoA reductase inhibitors alleviate different types of chemotherapy induced-peripheral neuropathy via activation of GST.,
APPW2025, Mar. 2025. 薗田悠平, 相澤風花, 西橋彩香, 八木健太, 新村貴博, 合田光寛, 川田敬, 石澤有紀, 石澤啓介 :
胆汁酸製剤による多発性硬化症抑制効果の検討,
第270回徳島医学会学術集会, 2025年2月. 八木健太, 高岡麻佑, 佐川真琳, 相澤風花, 新村貴博, 合田光寛, 川田敬, 石澤有紀, 石澤啓介 :
造血幹細胞移植前処置薬とシナジー効果を示す薬剤の探索とそのメカニズムの解明,
第45回日本臨床薬理学会学術集会, 2024年12月. 相澤風花, 薗田悠平, 西橋彩香, 高橋志門, 八木健太, 新村貴博, 合田光寛, 川田敬, 石澤有紀, 石澤啓介 :
胆汁酸製剤がもたらす多発性硬化症抑制作用とメカニズムの検討,
第45回日本臨床薬理学会学術集会, 2024年12月. 岡林亜美, 相澤風花, 武内香凜, 合田光寛, 八木健太, 新村貴博, 石澤有紀, 川田敬, 石澤啓介 :
パクリタキセル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機序の検討,
第63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, 2024年11月. 糸数柊人, 石澤有紀, 宮田辰巳, 福岡媛乃, 兵藤瑞紗, 山尾珠美, 相澤風花, 新村貴博, 八木健太, 川田敬, 合田光寛, 石澤啓介 :
血管内皮細胞内ERK5が大動脈疾患発症に及ぼす影響の検討,
第63 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, 2024年11月. 石田朋奈, 合田光寛, 神田将哉, 加納菜々, 吉岡俊彦, 川田敬, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 石澤啓介 :
MATE型輸送体を標的とするシスプラチン誘発腎障害予防薬の開発,
第63 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, 2024年11月. 高岡麻佑, 八木健太, 合田光寛, 相澤風花, 新村貴博, 川田敬, 石澤有紀, 石澤啓介 :
造血幹細胞移植前処置薬の薬効を増強させる併用薬剤の作用メカニズムの解明,
第63 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, 2024年11月. 川田敬, 山本高成, 佐藤智恵美, 小川敦, 相澤風花, 八木健太, 石澤有紀, 新村貴博, 阿部真治, 合田光寛, 石澤啓介 :
国立大学での学部教育の実情と学生のキャリアアップ支援,
第34回日本医療薬学年会, 2024年11月. 神田将哉, 合田光寛, 石田朋奈, 石田俊介, 櫻田巧, 坂東貴司, 川田敬, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 桐野靖, 石澤啓介 :
シスプラチン誘発腎障害予防薬としてのSGLT2阻害薬の作用機序解明,
第34回日本医療薬学年会, 2024年11月. 河野祐輝, 新村貴博, 佐藤智恵美, 合田光寛, 川田敬, 八木健太, 相澤風花, 石澤有紀, 石澤啓介 :
小児抗菌薬適正使用加算が抗菌薬処方動向に与える影響の検討,
第34回日本医療薬学年会, 2024年11月. 相澤風花, 薗田悠平, 西橋彩香, 高橋志門 (名), 八木健太, 新村貴博, 合田光寛, 川田敬, 石澤有紀, 石澤啓介 :
胆汁酸シグナル制御による多発性硬化症抑制機序の解明,
第63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, 2024年11月. 石田朋奈, 合田光寛, 神田将哉, 加納菜々, 吉岡俊彦, 川田敬, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 石澤啓介 :
シスプラチン誘発腎障害に対するSGLT2阻害薬の有効性の検証,
次世代を担う若手のための創薬・医療薬理シンポジウム2024, 2024年9月. 髙岡麻佑, 八木健太, 合田光寛, 相澤風花, 新村貴博, 川田敬, 石澤有紀, 石澤啓介 :
造血幹細胞移植治療成績向上を目指した移植前処置薬の作用増強薬の探索,
次世代を担う若手のための創薬・医療薬理シンポジウム2024, 2024年9月. 神田将哉, 合田光寛, 石田朋奈, 石田俊介, 櫻田巧, 坂東貴司, 川田敬, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 石澤啓介 :
シスプラチン誘発腎臓障害の原因にアプローチする新たな予防戦略の開発,
第145回日本薬理学会近畿部会, 2024年7月. 川田敬, 石田智滉, 福田仁, 久保亨, 濵田知幸, 相澤風花, 八木健太, 石澤有紀, 新村貴博, 阿部真治, 合田光寛, 北岡裕章, 石澤啓介 :
高齢心不全患者における長期入院の危険因子の検討,
第8回日本臨床薬理学会中国・四国地方会, 2024年7月. 八木健太, 今若清香, 髙岡麻佑, 岡本尚大, 相澤風花, 新村貴博, 合田光寛, 川田敬, 石澤有紀, 石澤啓介 :
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, 2024年3月. 石澤有紀, 宮田晃志, 辻中海斗, 糸数柊人, 宮田辰巳, 近藤正輝, 新村貴博, 吉岡俊彦, 相澤風花, 八木健太, 川田敬, 合田光寛, 石澤啓介 :
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, 2024年3月. 宮田辰巳, 石澤有紀, 宮田晃志, 糸数柊人, 辻中海斗, 福岡媛乃, 相澤風花, 新村貴博, 八木健太, 川田敬, 合田光寛, 石澤啓介 :
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, 2024年3月. 糸数柊人, 石澤有紀, 宮田晃志, 宮田辰巳, 近藤正輝, 相澤風花, 新村貴博, 八木健太, 川田敬, 合田光寛, 石澤啓介 :
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, 2024年3月. 宮田晃志, 石澤有紀, 西穂香, 糸数柊人, 宮田辰巳, 辻中海斗, 近藤正輝, 新村貴博, 相澤風花, 八木健太, 川田敬, 合田光寛, 石澤啓介 :
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, 2023年12月. 川田敬, 石田智滉, 福田仁, 兵頭勇己, 浜田知幸, 久保亨, 相澤風花, 八木健太, 石澤有紀, 新村貴博, 合田光寛, 石澤啓介 :
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, 2023年12月. 杉本祐悟, 合田光寛, 石田朋奈, 加納菜々, 神田将哉, 吉岡俊彦, 相澤風花, 新村貴博, 八木健太, 川田敬, 石澤有紀, 石澤啓介 :
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, 2023年10月. 八木健太, 新村貴博, 坂口暁, 相澤風花, 川田敬, 合田光寛, 石澤有紀, 石澤啓介 :
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, 2023年10月. 神農麻里奈, 小川敦, 鈴木加奈, 萱野純史, 神田将哉, 辻中海斗, 坂東貴司, 新田綾香, 椋田千晶, 相澤風花, 川田敬, 櫻田巧, 桐野靖, 合田光寛, 石澤啓介 :
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, 2023年10月. 川田敬, 石田智滉, 相澤風花, 八木健太, 石澤有紀, 新村貴博, 阿部真治, 合田光寛, 石澤啓介 :
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, 2023年8月. 吉岡俊彦, 合田光寛, 石田朋奈, 杉本祐悟, 神田将哉, 櫻田巧, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 石澤啓介 :
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, 2023年8月. 杉本祐悟, 合田光寛, 石田朋奈, 加納菜々, 神田将哉, 吉岡俊彦, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 石澤啓介 :
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, 2023年8月. 友近七海, 相澤風花, 薗田悠平, 西橋彩香, 宮内奏穂, 合田光寛, 八木健太, 新村貴博, 石澤有紀, 朝田瑞穂, 植沢芳広, 石澤啓介 :
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, 2023年8月. 西穂香, 相澤風花, 石澤有紀, 辻中海斗, 宮田晃志, 吉岡俊彦, 近藤正輝, 糸数柊人, 宮田辰巳, 新村貴博, 相澤風花, 八木健太, 座間味義人, 合田光寛, 石澤啓介 :
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, 2023年8月. 森山大嗣, 相澤風花, 岡林亜美, 合田光寛, 八木健太, 新村貴博, 石澤有紀, 石澤啓介 :
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, 2023年8月. 内田和志, 運天拡人, 濱野裕章, 新村貴博, 合田光寛, 八木健太, 相澤風花, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2023年8月. 新村貴博, 宮田晃志, 八木健太, 相澤風花, 濱野裕章, 石澤有紀, 合田光寛, 座間味義人, 石澤啓介 :
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, 2023年8月. 吉岡俊彦, 合田光寛, 杉本祐悟, 石田朋奈, 神田将哉, 櫻田巧, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 石澤啓介 :
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, 2023年8月. 坂東寛, 合田光寛, 新村貴博, 新田侑生, 中馬真幸, 北川航平, 相澤風花, 八木健太, 石澤有紀, 櫻田巧, 石澤啓介 :
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, 2023年8月. 吉岡俊彦, 合田光寛, 神田将哉, 杉本祐悟, 石澤有紀, 八木健太, 相澤風花, 宮田晃志, 新村貴博, 櫻田巧, 桐野靖, 石澤啓介 :
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, 2023年8月. 神田将哉, 合田光寛, 吉岡俊彦, 杉本祐悟, 櫻田巧, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 石澤啓介 :
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, 2023年8月. 相澤風花, 岡林亜美, 森山大嗣, 八木健太, 合田光寛, 新村貴博, 石澤有紀, 石澤啓介 :
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, 2023年8月. 相澤風花, 岡林亜美, 森山大嗣, 八木健太, 高橋志門, 新村貴博, 合田光寛, 石澤有紀, 石澤啓介 :
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, 2023年7月. 川田敬, 石田智滉, 常風興平, 森沢惇平, 相澤風花, 八木健太, 石澤有紀, 新村貴博, 阿部真治, 合田光寛, 石澤啓介 :
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, 2023年6月. 岡本尚大, 八木健太, 今若清香, 髙岡麻佑, 國木悠理香, 石澤有紀, 相澤風花, 新村貴博, 合田光寛, 石澤啓介 :
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, 2023年6月. 阪本淑華, 友近七海, 新村貴博, 合田光寛, 相澤風花, 八木健太, 濱野裕章, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2023年6月. 運天拡人, 内田和志, 濱野裕章, 新村貴博, 合田光寛, 八木健太, 相澤風花, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2023年6月. 八木健太, 髙岡麻佑, 吉武愛哉, 丸尾陽成, 安藤里英, 相澤風花, 新村貴博, 石澤有紀, 濱野裕章, 合田光寛, 座間味義人, 石澤啓介 :
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, 2023年3月. 相澤風花, 岡林亜美, 森山大嗣, 八木健太, 合田光寛, 新田綾香, 新村貴博, 石澤有紀, 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, 2023年3月. 合田光寛, 糸林小友理, 神田将哉, 吉岡俊彦, 杉本祐悟, 石田朋奈, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 櫻田巧, 桐野靖, 石澤啓介 :
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, 2023年3月. 新村貴博, 運天拡人, 濱野裕章, 内田和志, 友近七海, 宮田晃志, 合田光寛, 八木健太, 相澤風花, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2023年3月. 宮田晃志, 石澤有紀, 濱野裕章, 新村貴博, 相澤風花, 八木健太, 座間味義人, 合田光寛, 石澤啓介 :
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, 2023年3月. 相澤風花, 八木健太, 新村貴博, 合田光寛, 座間味義人, 石澤有紀, 石澤啓介 :
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, 2023年1月. 新村貴博, 運天拡人, 濱野裕章, 内田和志, 宮田晃志, 合田光寛, 八木健太, 相澤風花, 石澤有紀, 座間味義人, 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, 2023年1月. 八木健太, 相澤風花, 新村貴博, 石澤有紀, 濱野裕章, 合田光寛, 座間味義人, 石澤啓介 :
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, 2023年1月. 合田光寛, 神田将哉, 吉岡俊彦, 相澤風花, 櫻田巧, 小川敦, 新村貴博, 八木健太, 石澤有紀, 石澤啓介 :
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, 2022年11月. 合田光寛, 相澤風花, 八木健太, 新村貴博, 櫻田巧, 小川敦, 石澤有紀, 座間味義人, 石澤啓介 :
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), 2022年11月. 岡田直人, 中村信元, 清水太郎, 安藤英紀, 相澤風花, 新村貴博, 八木健太, 合田光寛, 石田竜弘, 石澤啓介 :
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, 2022年9月. 岡田直人, 中村信元, 清水太郎, 安藤英紀, 相澤風花, 新村貴博, 八木健太, 合田光寛, 石田竜弘, 石澤啓介 :
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, 2022年9月. 八木健太, 丸尾陽成, 石田俊介, 鍛治園誠, 相澤風花, 宮田晃志, 新村貴博, 石澤有紀, 濱野裕章, 合田光寛, 座間味義人, 石澤啓介 :
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, 2022年9月. 山川裕介, 八木健太, 吉岡俊彦, 佐藤真希, 丸尾陽成, 宮田晃志, 相澤風花, 國木悠理香, 新村貴博, 坂口暁, 石澤有紀, 合田光寛, 座間味義人, 石澤啓介 :
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, 2022年9月. 合田光寛, 神田将哉, 吉岡俊彦, 新村貴博, 櫻田巧, 小川敦, 相澤風花, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年9月. 相澤風花, 岡林亜美, 森山大嗣, 薗田悠平, 高橋志門, 新村貴博, 合田光寛, 座間味義人, 吉岡俊彦, 八木健太, 石澤有紀, 石澤啓介 :
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, 2022年9月. 相澤風花, 岡林亜美, 森山大嗣, 薗田悠平, 高橋志門, 新田綾香, 合田光寛, 八木健太, 新村貴博, 座間味義人, 石澤有紀, 石澤啓介 :
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, 2022年8月. 神田将哉, 合田光寛, 吉岡俊彦, 小川敦, 石田俊介, 新村貴博, 相澤風花, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年8月. 坂東貴司, 中馬真幸, 合田光寛, 谷友歩, 國木悠理香, 小川敦, 櫻田巧, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年8月. 宮田晃志, 石澤有紀, 辻中海斗, 大峯航平, 西穂香, 糸数柊人, 新村貴博, 近藤正輝, 相澤風花, 濱野裕章, 八木健太, 座間味義人, 合田光寛, 石澤啓介 :
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, 2022年8月. 糸林小友理, 合田光寛, 杉本祐悟, 石田朋奈, 神田将哉, 吉岡俊彦, 小川敦, 櫻田巧, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年8月. 國木悠理香, 八木健太, 髙岡麻佑, 岡本尚大, 濱野裕章, 相澤風花, 新村貴博, 合田光寛, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年8月. 吉岡俊彦, 合田光寛, 糸林小友理, 杉本祐悟, 石田朋奈, 神田将哉, 小川敦, 櫻田巧, 相澤風花, 新村貴博, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年8月. 宮田晃志, 石澤有紀, 辻中海斗, 大峯航平, 西穂香, 糸数柊人, 新村貴博, 近藤正輝, 相澤風花, 濱野裕章, 八木健太, 座間味義人, 合田光寛, 石澤啓介 :
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, 2022年8月. 合田光寛, 神田将哉, 吉岡俊彦, 吉田愛美, 糸林小友理, 新村貴博, 櫻田巧, 小川敦, 岡田直人, 相澤風花, 八木健太, 濱野裕章, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年7月. 糸林小友理, 合田光寛, 吉田愛美, 杉本祐悟, 神田将哉, 吉岡俊彦, 櫻田巧, 相澤風花, 濱野裕章, 岡田直人, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年7月. 八木健太, 高岡麻佑, 丸尾陽成, 相澤風花, 新村貴博, 石澤有紀, 濱野裕章, 合田光寛, 座間味義人, 石澤啓介 :
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, 2022年7月. 阪本淑華, 友近七海, 新村貴博, 合田光寛, 相澤風花, 八木健太, 西内栞, 生田賢治, 濱野裕章, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年7月. 大峯航平, 近藤正輝, 合田光寛, 西穂香, 宮田晃志, 辻中海斗, 濱野裕章, 相澤風花, 八木健太, 座間味義人, 石澤啓介, 石澤有紀 :
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, 2022年7月. 國木悠理香, 八木健太, 高岡麻佑, 岡本尚大, 濱野裕章, 合田光寛, 新村貴博, 相澤風花, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年7月. 宮田晃志, 石澤有紀, 近藤正輝, 辻中海斗, 大峯航平, 西穂香, 糸数柊人, 新村貴博, 相澤風花, 濱野裕章, 八木健太, 座間味義人, 合田光寛, 石澤啓介 :
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, 2022年7月. 運天拡人, 濱野裕章, 新村貴博, 内田和志, 友近七海, 宮田晃志, 石田俊介, 合田光寛, 八木健太, 相澤風花, 座間味義人, 石澤啓介 :
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, 2022年7月. 安藤里英, 八木健太, 岡本尚大, 髙岡麻佑, 相澤風花, 濱野裕章, 石澤有紀, 合田光寛, 座間味義人, 石澤啓介 :
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, 2022年3月. 糸林小友理, 合田光寛, 吉田愛美, 杉本祐悟, 神田将哉, 吉岡俊彦, 櫻田巧, 相澤風花, 濱野裕章, 岡田直人, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年3月.

(キーワード): データ解析 (data analysis) / 腎疾患 (kidney disease)

相澤風花, 梶本春奈, 森山大嗣, 岡林亜美, 合田光寛, 濱野裕章, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年3月.

(キーワード): データ解析 (data analysis)

吉岡俊彦, 合田光寛, 神田将哉, 吉田愛美, 糸林小友理, 杉本祐悟, 石澤有紀, 八木健太, 相澤風花, 濱野裕章, 岡田直人, 座間味義人, 石澤啓介 :
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, 2022年3月.

(キーワード): データ解析 (data analysis) / 腎疾患 (kidney disease)

宮田晃志, 石澤有紀, 近藤正輝, 辻中海斗, 大峯航平, 西穂香, 相澤風花, 濱野裕章, 座間味義人, 合田光寛, 石澤啓介 :
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, 2022年3月. 阪本淑華, 友近七海, 濱野裕章, 合田光寛, 新村貴博, 相澤風花, 八木健太, 仲村明人, 西内栞, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年3月. 國木悠理香, 八木健太, 吉田莉奈, 岡本尚大, 安藤里英, 山川裕介, 濱野裕章, 合田光寛, 新村貴博, 相澤風花, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年3月. 合田光寛, 神田将哉, 吉岡俊彦, 新村貴博, 櫻田巧, 小川敦, 岡田直人, 相澤風花, 八木健太, 濱野裕章, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2022年3月.

(キーワード): データ解析 (data analysis)

西内栞, 斎藤広海, 新村貴博, 座間味義人, 合田光寛, 八木健太, 相澤風花, 濱野裕章, 石澤有紀, 石澤啓介 :
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, 2021年12月. 安藤里英, 八木健太, 岡本尚大, 相澤風花, 濱野裕章, 石澤有紀, 合田光寛, 座間味義人, 石澤啓介 :
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, 2021年11月. 吉田愛美, 合田光寛, 杉本祐悟, 八木田ひかり, 神田将哉, 吉岡俊彦, 櫻田巧, 相澤風花, 濱野裕章, 岡田直人, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2021年11月.

(キーワード): 腎疾患 (kidney disease) / データ解析 (data analysis)

大峯航平, 近藤正輝, 合田光寛, 西穂香, 宮田晃志, 辻中海斗, 濱野裕章, 相澤風花, 八木健太, 座間味義人, 石澤啓介, 石澤有紀 :
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, 2021年11月. 岡田直人, 中本亜樹, 泉侑希, 中馬真幸, 合田光寛, 八木健太, 相澤風花, 濱野裕章, 座間味義人, 東桃代, 石澤啓介 :
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, 2021年11月. 吉岡俊彦, 合田光寛, 神田将哉, 吉田愛美, 糸林小友理, 杉本祐悟, 石澤有紀, 八木健太, 相澤風花, 濱野裕章, 岡田直人, 座間味義人, 石澤啓介 :
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, 2021年10月.

(キーワード): 腎疾患 (kidney disease) / データ解析 (data analysis)

吉田愛美, 合田光寛, 杉本祐悟, 八木田ひかり, 神田将哉, 吉岡俊彦, 櫻田巧, 石澤有紀, 相澤風花, 濱野裕章, 岡田直人, 八木健太, 座間味義人, 石澤啓介 :
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, 2021年10月.

(キーワード): データ解析 (data analysis) / 腎疾患 (kidney disease)

谷友歩, 中馬真幸, 合田光寛, 坂東貴司, 近藤正輝, 國木悠理香, 濱野裕章, 新村貴博, 岡田直人, 相澤風花, 八木健太, 石澤啓介 :
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, 2021年10月.

(キーワード): データ解析 (data analysis)

梶本春奈, 森山大嗣, 相澤風花, 新村貴博, 座間味義人, 合田光寛, 八木健太, 濱野裕章, 石澤有紀, 石澤啓介 :
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, 2021年10月.

(キーワード): データ解析 (data analysis)

高橋志門, 武智研志, 定作奈津美, 濱野裕章, 相澤風花, 八木健太, 合田光寛, 石澤有紀, 石澤啓介 :
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, 2021年10月.

(キーワード): データ解析 (data analysis)

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. 辻中海斗, 岡田直人, 藤原範子, 合田光寛, 八木健太, 相澤風花, 濱野裕章, 櫻田巧, 桐野靖, 座間味義人, 東桃代, 石澤啓介 :
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, 2021年10月. 岡田直人, 中本亜樹, 泉侑希, 中馬真幸, 合田光寛, 八木健太, 相澤風花, 濱野裕章, 座間味義人, 東桃代, 石澤啓介 :
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, 2021年10月. 相澤風花, 梶本春奈, 森山大嗣, 新村貴博, 合田光寛, 新田綾香, 高橋志門, 濱野裕章, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2021年10月.

(キーワード): データ解析 (data analysis)

座間味義人, 新村貴博, 濱野裕章, 合田光寛, 相澤風花, 八木健太, 石澤有紀, 石澤啓介 :
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, 2021年10月.

(キーワード): データ解析 (data analysis)

濱野裕章, 座間味義人, 合田光寛, 相澤風花, 八木健太, 石澤啓介 :
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, 2021年10月.

(キーワード): データ解析 (data analysis)

中馬真幸, 中本亜樹, 坂東貴司, 新村貴博, 岡田直人, 相澤風花, 濱野裕章, 八木健太, 合田光寛, 座間味義人, 石澤啓介, 田崎嘉一 :
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, 2021年10月.

(キーワード): データ解析 (data analysis)

神田将哉, 合田光寛, 吉岡俊彦, 吉田愛美, 新村貴博, 櫻田巧, 小川敦, 岡田直人, 相澤風花, 座間味義人, 八木健太, 濱野裕章, 石澤有紀, 石澤啓介 :
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, 2021年10月.

(キーワード): データ解析 (data analysis) / 腎疾患 (kidney disease)

合田光寛, 神田将哉, 吉岡俊彦, 吉田愛美, 新村貴博, 櫻田巧, 小川敦, 岡田直人, 相澤風花, 八木健太, 濱野裕章, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2021年10月.

(キーワード): データ解析 (data analysis) / 腎疾患 (kidney disease)

辻中海斗, 石澤有紀, 新村貴博, 吉岡俊彦, 合田光寛, 近藤正輝, 大峯航平, 西穂香, 宮田晃志, 濱野裕章, 相澤風花, 八木健太, 座間味義人, 石澤啓介 :
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, 2021年7月. 梶本春奈, 森山大嗣, 相澤風花, 新村貴博, 座間味義人, 合田光寛, 八木健太, 濱野裕章, 石澤有紀, 石澤啓介 :
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, 2021年6月.

(キーワード): データ解析 (data analysis) / 腎疾患 (kidney disease)

谷友歩, 中馬真幸, 合田光寛, 坂東貴司, 近藤正輝, 國木悠理香, 濱野裕章, 新村貴博, 岡田直人, 相澤風花, 八木健太, 石澤有紀, 座間味義人, 石澤啓介 :
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, 2021年6月.

(キーワード): データ解析 (data analysis) / 腎疾患 (kidney disease)

相澤風花, 座間味義人, 新村貴博, 川尻雄大, 合田光寛, 八木健太, 石澤有紀, 石澤啓介 :
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, 2021年3月. 新村貴博, 座間味義人, 川尻雄大, 合田光寛, 相澤風花, 八木健太, 石澤有紀, 石澤啓介 :
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, 2021年3月.

(キーワード): データ解析 (data analysis)

相澤風花, 座間味義人, 濱野裕章, 岡田直人, 林明希, 八木健太, 合田光寛, 桐野靖, 中村敏己, 石澤啓介 :
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, 2021年3月. 相澤風花, 梶本春奈, 森山大嗣, 新村貴博, 座間味義人, 濱野裕章, 合田光寛, 八木健太, 石澤有紀, 石澤啓介 :
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, 2021年3月. 合田光寛, 座間味義人, 新村貴博, 萱野純史, 濱野裕章, 岡田直人, 相澤風花, 八木健太, 石澤有紀, 桐野靖, 中村敏己, 石澤啓介 :
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, 2021年3月. 阪本淑華, 座間味義人, 新村貴博, 相澤風花, 八木健太, 合田光寛, 石澤有紀, 石澤啓介 :
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, 2021年3月.

(キーワード): データ解析 (data analysis)

相澤風花, 合田光寛, 神田将哉, 吉岡俊彦, 吉田愛美, 新村貴博, 八木健太, 濱野裕章, 岡田直人, 座間味義人, 石澤有紀, 石澤啓介 :
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, 2020年11月.

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補助金・競争的資金: 抗VEGF療法の治療効果向上を目指した最適な支持療法薬の解明 (研究課題/領域番号: 24K09959 )
デジタルサイエンスを応用した抗がん剤関連性末梢神経障害治療薬の創出 (研究課題/領域番号: 24K09832 )
リアルワールドデータを活用した薬剤性腎障害に対する新規予防戦略の開発 (研究課題/領域番号: 23K06234 )
MDB活用による抗がん剤誘発性末梢神経障害予防薬の確立 (研究課題/領域番号: 22K15292 )
性差を考慮したがん化学療法の確立―リアルワールドデータ駆動型薬理学研究 (研究課題/領域番号: 22K06863 )
データマイニングと疾患モデルによる感染症と大動脈疾患の包括的な連関解明 (研究課題/領域番号: 21H02646 )
シナジー効果の評価系構築と薬理的検証 (研究課題/領域番号: 20H05799 )
リアルワールドデータの応用による新規化学療法誘発末梢神経障害予防法の確立 (研究課題/領域番号: 20K16007 )
研究者番号（80848367）による検索

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2025年8月1日更新

専門分野・研究分野: ライフサイエンス (Life sciences) [薬理学 (Pharmacology)]
ライフサイエンス (Life sciences) [神経科学一般 (Neuroscience - general)]
ライフサイエンス (Life sciences) [医療薬学 (Clinical pharmacy)]
所属学会・所属協会: 日本薬学会
日本医療薬学会
日本薬理学会
日本臨床薬理学会
委員歴・役員歴: 日本薬学会 (薬理系薬学部会若手世話人 [2024年4月])
日本薬理学会 (次世代の会若手世話人 [2025年4月])
受賞: 2021年10月, Postdoctoral Award (日本医療薬学会)
2023年12月, 第44回日本臨床薬理学会学術総会優秀発表賞 (日本臨床薬理学会)
2023年, 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優秀ポスター賞 (日本薬学会)
2024年10月, 30th Congress of the Federation of Asian Pharmaceutical Associations; FAPA2024 (FAPA)
2025年3月, APPW2025 Young Investigator Award (APPW)
2025年, 日本薬学会薬理系薬学部会奨励賞 (日本薬学会)
2025年, 医療薬学フォーラム2025 第33回クリニカルファーマシーシンポジウム優秀ポスター賞 (日本薬学会)
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2025年8月3日更新

2025年8月2日更新

Ｊグローバル

Jグローバル最終確認日: 2025/8/2 01:40
氏名（漢字）: 相澤風花
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氏名（英字）: Aizawa Fuka
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researchmap最終確認日: 2025/8/3 01:50
氏名（漢字）: 相澤風花
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氏名（英字）: Aizawa Fuka
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登録日時: 2019/4/1 19:15
更新日時: 2025/7/16 16:19
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学位: 博士（薬学）
学位授与機関: 神戸学院大学
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2025年8月2日更新

研究者番号: 80848367

所属（現在）: 2025/4/1 : 徳島大学, 病院, 特任講師

所属（過去の研究課題 情報に基づく）*注記: 2020/4/1 – 2024/4/1 : 徳島大学, 病院, 特任助教

審査区分/研究分野

研究代表者

小区分47040:薬理学関連

研究代表者以外

学術変革領域研究区分(Ⅳ)
小区分47060:医療薬学関連
小区分48030:薬理学関連

キーワード

研究代表者

抗がん剤誘発性末梢神経障害 / オキサリプラチン / HMG-CoA還元酵素阻害剤 / 行動薬理 / 酸化ストレス / 末梢神経障害 / 化学療法 / 医療ビッグデータ / HMG~CoA還元酵素阻害剤 / 抗がん剤支持療法 / glutathione transferase / 医療データ / AI創薬 / パクリタキセル / データベース解析 / 疼痛 / 感覚異常 / 抗悪性腫瘍剤 / データサイエンス / ドラッグリポジショニング

研究代表者以外

薬剤シナジー効果 / 遺伝子発現データベース / オミックスデータベース / 病態モデル解析 / 遺伝子発言データベース / 大動脈解離 / 大動脈瘤 / 医療ビッグデータ / 感染症 / 抗菌薬 / リアルワールドデータベース / 薬物有害事象 / がん化学療法 / 性差医学 / 大動脈疾患 / 性差医療 / リアルワールドデータ / 有害事象 / 抗VEGF薬 / 支持療法薬 / プロトンポンプ阻害剤 / 薬剤性腎障害 / 医療ビッグデータ解析 / ドラッグリポジショニング

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相澤風花