yukiishizawa/published_papers/54144621 Kazuki Maeda Sota Koyama Kei Kawada Toshinobu Hayashi Toshihiko Yoshioka Tomoaki Ishida Hitoshi Fukuda I O Horikawa Fuka Aizawa Takahiro Niimura Kenta Yagi Mitsuhiro Goda Yuki Izawa-Ishizawa Shinji Abe Keisuke Ishizawa Fosnetupitant Versus Fosaprepitant for Delayed Vomiting Upon Irinotecan-Oxaliplatin Combination Chemotherapy for Pancreatic/Colorectal Cancer. BACKGROUND/AIM: Real-world comparative data on neurokinin-1 receptor antagonists are needed among patients receiving FOLFOXIRI or FOLFIRINOX. We aimed to evaluate the antiemetic effectiveness of fosnetupitant versus that of fosaprepitant in patients treated with FOLFOXIRI/FOLFIRINOX regimens for pancreatic/colorectal cancer. PATIENTS AND METHODS: This single-center retrospective study included patients treated from April 2018 to September 2024. Patients were matched 1:1 between treatment groups via propensity scores based on age, sex, alcohol history, prior treatment, and regimen dose, as appropriate. Antiemetic effectiveness was assessed as no vomiting/no nausea during days 1-7; safety outcomes were also evaluated. Inverse probability of treatment weighting (IPTW) was conducted to validate the robustness of the results. Between-group comparisons were performed using Fisher's exact tests for categorical variables and Mann-Whitney U-tests for continuous variables. RESULTS: After matching, 43 patient pairs in the pancreatic cancer cohort and 28 pairs in the colorectal cancer cohort were analyzed; the groups had generally comparable baseline characteristics. In the pancreatic cancer cohort, fosnetupitant was associated with higher no-vomiting rates during the long-delayed phase (100% vs. 81%, p=0.006) and overall period (95% vs. 74%, p=0.014) than fosaprepitant. No significant differences in effectiveness were observed in the colorectal cancer cohort. Injection site reactions were significantly less frequent with fosnetupitant in the colorectal cancer cohort (4% vs. 29%, p=0.025). These findings remained consistent in the IPTW sensitivity analysis. CONCLUSION: The effectiveness of fosnetupitant may vary according to cancer type, suggesting the need to tailor antiemetic strategies for patients receiving irinotecan-oxaliplatin combination chemotherapy. Anticancer research 46 6 3191 3203 20260600 10.21873/anticanres.18190 42203343 yukiishizawa/published_papers/54165254 薗田悠平相澤風花西橋彩香谷田奨太八木健太新村貴博堀川伊和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徳島医学会四国医学雑誌 2758-3279 81 5-6 246 247 20260400 yukiishizawa/published_papers/54165248 酒巻左奈子合田光寛堀川伊和新村貴博相澤風花八木健太川田敬石澤有紀石澤啓介 MATEを含む膜輸送体複合体の相互作用解析徳島医学会四国医学雑誌 2758-3279 81 5-6 252 252 20260400 yukiishizawa/published_papers/54054246 Shiho Ueta Takahiro Niimura Mitsuhiro Goda Tomoaki Ishida Naohiro Iwata Tatsuaki Takeda Kei Kawada Koji Miyata Fuka Aizawa Kenta Yagi Hirofumi Hamano Masayuki Chuma Yuki Izawa-Ishizawa Yoshito Zamami Keisuke Ishizawa Muscle Atrophy-Related Adverse Events of Antidiabetic Drug Classes: A Pharmacovigilance Analysis Using VigiBase Data. BACKGROUND: Diabetes mellitus-a chronic metabolic disorder associated with an increased risk of muscle atrophy-can significantly impact patients' quality of life and overall health outcomes. While antidiabetic medications are crucial for managing blood glucose levels, some have been linked to muscle-related adverse events, potentially exacerbating the already elevated risk of muscle deterioration in diabetic patients. However, a comprehensive analysis of muscle atrophy-related adverse events across different classes of antidiabetic drugs has been lacking. Therefore, this study investigates the profile of muscle atrophy-related adverse events across major antidiabetic drug classes using the World Health Organization's (WHO's) Individual Case Safety Reports database. METHODS: A pharmacovigilance analysis was conducted using data from VigiBase, the WHO's global reporting database, from 1968 to September 2025. The study examined adverse event signals related to muscle atrophy, sarcopenia, muscular weakness and motor function decline for nine classes of antidiabetic medications. Reporting odds ratios (RORs) were calculated to assess signal detection, and co-occurrence patterns of adverse events were analysed. RESULTS: Among 41 551 306 adverse event reports, 2 095 847 were related to antidiabetic medications. Safety signals for muscle atrophy were detected with sulfonylureas (ROR: 1.2, 95% CI: 1.01-1.43, p = 0.042), GLP-1 analogues (ROR: 1.2, 95% CI: 1.02-1.41, p = 0.031) and SGLT2 inhibitors (ROR: 1.5, 95% CI: 1.19-1.78, p < 0.001). SGLT2 inhibitors also showed a signal for sarcopenia (ROR: 6.2, 95% CI: 3.71-10.3, p < 0.001). Biguanides demonstrated signals for muscular weakness (ROR: 1.6, 95% CI: 1.54-1.71, p < 0.001) and motor function decline (ROR: 1.7, 95% CI: 1.41-2.13, p < 0.001). Thiazolidinediones, glinides, DPP-4 inhibitors and alpha-glucosidase inhibitors showed no safety signals for the examined adverse events. Additionally, co-occurrence analysis revealed frequent associations between muscle atrophy and nausea/vomiting, falls and decreased appetite across different drug classes. CONCLUSIONS: These findings indicate notable differences in the profiles of muscle atrophy-related adverse events among major classes of antidiabetic drugs, suggesting that drug selection may influence the risk of muscle function decline in patients. Clinicians should consider these safety profiles when prescribing antidiabetic therapies; however, causal relationships cannot be inferred solely from pharmacovigilance data. Further studies are warranted to establish causality between antidiabetic drug use and muscle-related adverse events and to elucidate the underlying mechanisms. Journal of cachexia, sarcopenia and muscle 17 2 e70251 null 20260400 10.1002/jcsm.70251 41980862 yukiishizawa/published_papers/52813547 Yuki Kono Takahiro Niimura Yumiko Hosaka Koji Yahara Aki Hirabayashi Toshiki Kajihara Mitsuhiro Goda Koji Miyata Kei Kawada Fuka Aizawa Kenta Yagi Yuki Izumi Yuki Izawa-Ishizawa Keisuke Ishizawa Impact of antimicrobial stewardship interventions in pediatric populations on antimicrobial resistance: analysis of national claim and antimicrobial resistance surveillance data in Japan. BACKGROUND: Excessive antibiotic use contributes to the emergence of antimicrobial resistance (AMR). The Japanese government implemented an antimicrobial stewardship incentive program for the pediatric population in 2018. However, its effect on prescription patterns and the AMR rates remains unclear. OBJECTIVES: To investigate the impact of the implementation of the antimicrobial stewardship incentive program on AMR rates through changes in antimicrobial prescribing patterns. METHODS: We retrospectively analyzed prescription patterns using data from a nationwide claims database and extracted pediatric patient data from healthcare facilities with ≥20 beds from January 2014 to July 2021. The antibiotic prescription amounts were calculated per 1,000 patient-days. The AMR rates of urinary E. coli were analyzed using data from the comprehensive national AMR surveillance database. Changes were evaluated using interrupted time-series analysis. RESULTS: After the intervention, antibiotic prescription patterns in 8,292 healthcare facilities of both broad- and narrow-spectrum antimicrobials, but not of first-generation cephalosporin, showed a decreasing trend. Prescriptions of fluoroquinolone and broad-spectrum penicillin prescriptions changed from increasing to decreasing trends, whereas those of third-generation cephalosporins continued to decline. The AMR patterns of urinary E. coli to both broad- and narrow-spectrum antibiotics showed decreasing trends in over 800 healthcare facilities. CONCLUSIONS: After the introduction of the antimicrobial stewardship incentive program, prescriptions for broad-spectrum antibiotics and a part of narrow-spectrum antibiotics declined and the AMR rates of urinary E. coli to both broad- and narrow-spectrum antibiotics decreased. These findings suggest the effectiveness of policy-driven interventions for containing AMR in the pediatric population. The Journal of hospital infection null null 20260112 10.1016/j.jhin.2025.12.010 41534744 yukiishizawa/published_papers/54165222 Kazuki Maeda Kei Kawada Toshinobu Hayashi Sota Koyama Tomoaki Ishida Toshihiko Yoshioka Hitoshi Fukuda Io Horikawa Fuka Aizawa Takahiro Niimura Kenta Yagi Mitsuhiro Goda Yuki Izawa-Ishizawa Keisuke Ishizawa Comparative Efficacy of Fosnetupitant and Fosaprepitant for Delayed Vomiting in Patients Receiving Irinotecan-Oxaliplatin Combination Chemotherapy: A Retrospective Propensity Score-Matched Study. PURPOSE: Appropriate prevention of chemotherapy-induced nausea and vomiting (CINV) is essential for improving patients' quality of life; however, no studies have compared neurokinin-1 receptor antagonists in regimens combining oxaliplatin and irinotecan. We aimed to compare the antiemetic efficacy of fosnetupitant and fosaprepitant in patients receiving FOLFIRINOX or FOLFOXIRI regimens. PATIENTS AND METHODS: We reviewed records of patients receiving FOLFIRINOX or FOLFOXIRI between April 1, 2018 and September 30, 2024 at Tokushima University Hospital. Eligible patients completed the first chemotherapy cycle, received standard triple antiemetic prophylaxis, and had complete nursing-recorded CINV follow-up data for days 1-7. Patients were matched 1:1 using propensity scores for age, sex, alcohol consumption history, prior treatment, regimen, and chemotherapy doses. The primary objective was to compare the incidence of vomiting during the long-delayed phase (days 6-7) between the fosnetupitant and fosaprepitant groups. The no-vomiting and no-nausea rates were compared using Fisher's exact test, and the time to first vomiting using the Log rank test. RESULTS: After matching, data from 68 balanced patient pairs were analyzed. The fosnetupitant group had higher no-vomiting rates in the long-delayed phase (100% vs. 91.2%, p=0.028) and overall period (95.6% vs. 83.8%, p=0.045), compared with the fosaprepitant group. No significant intergroup difference was observed in the overall no-nausea rate (26.5% vs. 32.3%, p=0.573). With fosnetupitant, the time to first vomiting was longer (3/68 vs. 11/68, hazard ratio: 0.20, p=0.045), injection site reactions were fewer (0.0% vs. 19.1%, p<0.001), and constipation and hiccup incidences were fewer (p>0.05). CONCLUSION: Despite the retrospective design, possible calendar-time confounding, and limited number of events, our results suggest that fosnetupitant offers better control of long-delayed and overall vomiting and a favorable safety profile, compared with fosaprepitant, in patients receiving FOLFIRINOX/FOLFOXIRI regimens. Cancer management and research 18 579955 579955 20260000 10.2147/CMAR.S579955 42273006 yukiishizawa/published_papers/52488971 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 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. BACKGROUND: 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. OBJECTIVE: This study assessed the effectiveness and safety of MRSA antibiotics combined with rifampicin for treating methicillin-resistant staphylococcal PJI using a Japanese clinical database. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: 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. International journal of clinical pharmacology and therapeutics 63 8 362 371 20250800 10.5414/CP204740 40396698 yukiishizawa/published_papers/52624342 Kazuya Sato Kei Kawada Tomoaki Ishida Toru Kubo Miyata Koji Fuka Aizawa Kenta Yagi Yuki Izawa-Ishizawa Takahiro Niimura Mitsuhiro Goda Keisuke Ishizawa Trends in the use of sodium-glucose cotransporter-2 inhibitors and characteristics of adverse event reporting in patients with heart failure in Japan: reports from the medical administration database and the adverse event reporting database. BACKGROUND: Heart failure (HF) is a global health issue with a high prevalence in aging populations. Sodium-glucose cotransporter-2 (SGLT2) inhibitors reduce HF-related hospitalizations and mortality; however, their adverse drug events (ADEs) require further evaluation. RESEARCH DESIGN AND METHODS: Using the Japan Medical Data Center and Japanese Adverse Drug Event Report (JADER) databases, we analyzed prescribing trends and ADE risk factors. Multivariate logistic regression assessed associations between patient characteristics and ADEs, adjusting for age, sex, medication use, and comorbidities. Decision tree analyses stratified ADE risks. RESULTS: SGLT2 inhibitor prescriptions increased from 1.63% (2018) to 9.08% (2022), with a notable rise in 2021. JADER analysis showed an increasing number of ADE reports, primarily dehydration, urinary tract infections, and renal impairment. Decision tree analyses identified risk factors: dehydration (age ≥80 years, tolvaptan use), urinary tract infection (female sex, renal dysfunction), and renal impairment (angiotensin receptor-neprilysin inhibitor use, history of renal dysfunction). CONCLUSIONS: Personalized risk assessment and monitoring are crucial for optimizing SGLT2 inhibitor therapy, particularly in older patients with HF and renal impairment. Expert opinion on drug safety 1 11 20250731 10.1080/14740338.2025.2539543 40711847 yukiishizawa/published_papers/52624340 Mizusa Hyodo Kei Kawada Tomoaki Ishida Yuki Izawa-Ishizawa Ryoko Matoba Rina Okamoto Kohei Jobu Io Horikawa Fuka Aizawa Kenta Yagi Takahiro Niimura Yayoi Kawano Shinji Abe Yukihiro Hamada Mitsuhiro Goda Keisuke Ishizawa Atractylodes lancea (Thunb.) DC. [Asteraceae] Rhizome-Derived Exosome-like Nanoparticles Suppress Lipopolysaccharide-Induced Inflammation by Reducing Toll-like Receptor 4 Expression in BV-2 Murine Microglial Cells. Background/Objectives:Atractylodes lancea (Thunb.) DC. [Asteraceae] (ALR)-derived exosome-like nanoparticles (ALR-ELNs) exhibit anti-neuroinflammatory effects in microglial cells. However, the associated mechanisms and pathways are unknown. We aimed to characterize the effects of ALR-ELNs on inflammatory responses of BV-2 microglial cells to lipopolysaccharide (LPS) using RNA sequencing. Methods: ALR-ELNs were fractionated from ALR. BV-2 microglial murine cells were stimulated with LPS after treatment with ALR-ELNs. RNA sequencing was performed to analyze variations in mRNA levels. Ingenuity pathway analysis (IPA) was performed to investigate the mechanism of action of ALR-ELNs. mRNA expression was assessed using real-time quantitative polymerase chain reaction (qPCR). Results: The expression of 651 genes was downregulated, whereas that of 1204 genes was upregulated in LPS-stimulated BV2 cells pretreated with ALR-ELNs. The IPA showed that the effects of ALR-ELNs on inflammation took place through pathogen-influenced signaling. Network analysis via IPA showed that the Toll-like receptor (TLR) is involved in the suppression of inflammation by ALR-ELNs. The qPCR analysis showed that pretreatment with ALR-ELNs significantly reduced TLR4 mRNA expression. Conclusions: ALR-ELNs suppress the release of inflammatory mediators by downregulating TLR4 expression, which is a novel mechanism by which ALR-ELNs act on microglia. Identifying active ingredients in ALR-ELNs that downregulate TLR4 expression can advance the development of therapeutic drugs for neuroinflammatory diseases. Pharmaceuticals (Basel, Switzerland) 18 8 null null 20250724 10.3390/ph18081099 40872491 yukiishizawa/published_papers/52476824 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 Keisuke Ishizawa Pharmacovigilance study for the identification of mogamulizumab-induced immune-related adverse events using a real-world database. BACKGROUND: Mogamulizumab is a humanized anti-CCR4 monoclonal antibody used for relapsed/refractory adult T-cell leukemia, cutaneous T-cell lymphoma, and/or Sézary syndrome. Reports of immune-related adverse events (irAEs) in these patients are increasing, and the association between irAEs and mogamulizumab remains to be elucidated. This study aimed to evaluate the association between mogamulizumab and immune-related adverse events (irAEs), as well as to characterize the irAEs associated with mogamulizumab using data from a large-scale spontaneous reporting system. METHODS: We performed an exploratory hypothesis-generating analysis of patients from 1967 to September 2023 using VigiBase, a World Health Organization spontaneous adverse event reporting system database. We performed a disproportionality analysis and determined the reporting odds ratios and information components between the drugs of interest and each irAE. RESULTS: Mogamulizumab was associated with some irAEs, including myocarditis, severe cutaneous adverse reactions, hepatitis, and myositis. Mogamulizumab exhibited significantly higher reporting rates of these 4 irAEs compared to the anticancer agents other than mogamulizumab. Conversely, the reporting rate of other irAEs, including endocrine autoimmune diseases induced by immune checkpoint inhibitors, was not significant in patients who received mogamulizumab. CONCLUSIONS: Mogamulizumab is associated with irAEs, including myocarditis, severe cutaneous adverse reactions, hepatitis, and myositis. The oncologist 30 7 null null 20250704 10.1093/oncolo/oyaf201 40637043 yukiishizawa/published_papers/52495788 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 Keisuke Ishizawa Ursodeoxycholic acid alleviates multiple sclerosis via TGR5-dependent microglial regulation in mice Elsevier BV European Journal of Pharmacology 0014-2999 177941 177941 20250700 10.1016/j.ejphar.2025.177941 yukiishizawa/published_papers/52435326 Yoshika Sakamoto Takahiro Niimura Mitsuhiro Goda Nanami Tomochika Wakana Murakawa Fuka Aizawa Kenta Yagi Hirofumi Hamano Yuki Izawa-Ishizawa Yoshito Zamami Keisuke Ishizawa Unravelling the cardioprotective effects of calcitriol in Sunitinib-induced toxicity: A comprehensive in silico and in vitro study. 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. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 188 118137 118137 20250700 10.1016/j.biopha.2025.118137 40373630 yukiishizawa/published_papers/52813568 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徳島医学会四国医学雑誌 2758-3279 81 1-2 83 83 20250600 yukiishizawa/published_papers/49948703 Fuka Aizawa Kenta Yagi Maki Sato Takahiro Niimura Mitsuhiro Goda Yuki Izawa-Ishizawa Keisuke Ishizawa Influence of statin intervention on peripheral neuropathy in patients treated with anticancer drugs identified from the insurer database. BACKGROUND: Statins, hydroxymethylglutaryl-CoA reductase inhibitors, possess neuroprotective properties. Given the potential neuroprotective properties of statins and their prevalent use in clinical settings, we aimed to investigate their impact on chemotherapy-induced peripheral neuropathy (CIPN) in Japan by assessing both their safety and efficacy in this context. METHODS: We conducted a retrospective observational study using the Japan Medical Data Centre database, which includes data from 2005 to 2021. We included patients who underwent anticancer therapy and were categorized into non-statin (10,920) and statin (1,537) groups. These groups were matched using a propensity score, resulting in 2,548 non-statin and 1,274 statin users. The primary endpoints were the incidence of CIPN post-first prescription of each anticancer drug and overall survival. RESULTS: Treatment with statins did not increase the incidence of CIPN (non-statin 27.2% vs. statin 28.4%, P = 0.443). Nevertheless, the incidence of CIPN was significantly high among women (non-statin 28.0% vs. statin 33.2%, P = 0.025). Overall survival was not impacted by statin use (hazard ratio 0.98, 95%CI: 0.83-1.16, P = 0.8846). Among men treated with paclitaxel, we observed an improvement in overall survival (hazard ratio: 0.72; 95% CI: 0.56-0.92; P = 0.0110). CONCLUSIONS: The use of statins in patients with cancer was not associated with CIPN incidence. However, in men receiving paclitaxel treatment, statins may be linked to improved overall survival. Further studies are necessary to clarify the factors influencing prognosis and CIPN severity. Journal of pharmaceutical health care and sciences 11 1 27 27 20250407 10.1186/s40780-025-00428-3 40197323 yukiishizawa/published_papers/49948709 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 Keisuke Ishizawa Risk factors for clazosentan-induced fluid retention in subarachnoid hemorrhage from the Japanese adverse event database. BACKGROUND: Clazosentan, a selective endothelin receptor antagonist, is used to prevent cerebral vasospasm. We investigated patient characteristics and concomitant medications associated with an increased risk of clazosentan-induced fluid retention, the risk factors of which remain unknown. METHODS: We retrospectively reviewed cases of clazosentan-induced adverse drug reactions from the Japanese Adverse Drug Event Report (JADER) database, published by the Pharmaceuticals and Medical Devices Agency. We investigated the time course of fluid retention onset following clazosentan administration before analyzing whether specific patient characteristics and concomitant medications were associated with an increased risk of clazosentan-induced fluid retention. RESULTS: Among 241 cases of clazosentan use identified, fluid retention occurred in 114 (47.3 %). The median time interval from clazosentan initiation to onset of fluid retention was 3 days, and 88.7 % of fluid retention cases were reported within 1 week of initiation. Patients with fluid retention were older than those without; patients >70 years old accounted for 63.16 % of the cohort with fluid retention vs 44.1 % of the cohort without fluid retention. Fluid retention occurred more frequently in patients with concomitant use of fasudil hydrochloride, a conventional vasospasm drug in Japan, than in those without. Multivariate logistic regression analysis revealed that older age (>70 years) and concomitant use of fasudil hydrochloride remained independent risk factors for fluid retention. CONCLUSIONS: Clazosentan-induced fluid retention occurred more frequently in older adult patients. Clazosentan combined with fasudil hydrochloride increased the incidence of fluid retention. These findings can guide pharmacological treatment of cerebral vasospasm in patients with subarachnoid hemorrhage. Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association 34 6 108296 108296 20250402 10.1016/j.jstrokecerebrovasdis.2025.108296 40179823 yukiishizawa/published_papers/54003349 Kenta Yagi Makoto Kajizono Akinori Maruo Wataru Shinmura Yuuki Nitta Toshihiko Yoshioka Masayuki Chuma Shunsuke Ishida Tsukasa Higashionna Hiroaki Tanaka Fuka Aizawa Takahiro Niimura Mitsuhiro Goda Kei Kawada Yuki Izawa-Ishizawa Yoshito Zamami Shinji Kosaka Yoshikazu Tasaki Keisuke Ishizawa Effective drug dosage rounding reduces healthcare expenses in the Japanese healthcare system Springer Science and Business Media LLC Drugs & Therapy Perspectives 1179-1977 41 4 160 167 20250324 10.1007/s40267-025-01144-6 yukiishizawa/published_papers/49258079 Yuki Kono Takahiro Niimura Mitsuhiro Goda Shiho Ueta Kei Kawada Koji Miyata Fuka Aizawa Kenta Yagi Yuki Izawa-Ishizawa Keisuke Ishizawa Cardiovascular Toxicity Profile of Macrolides Investigated Using VigiBase Data: A Pharmacovigilance Study. 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. Cardiovascular toxicology null null 20250219 10.1007/s12012-025-09970-w 39971867 yukiishizawa/published_papers/52813575 新田綾香合田光寛新村貴博佐藤真希川田敬辻中海斗宮田晃志河野祐輝相澤風花石澤啓介石澤有紀八木健太中馬真幸股関節形成術の術後感染症における抗MRSA薬とリファンピシン併用の実臨床成績診療報酬データベースを用いたレトロスペクティブ解析徳島医学会四国医学雑誌 2758-3279 80 5-6 257 258 20250200 yukiishizawa/published_papers/52400938 Masayuki Chuma Mitsuhiro Goda Hirofumi Hamano Takahiro Niimura Kenshi Takechi Kenta Yagi Yuki Izawa-Ishizawa Yoshito Zamami Keisuke Ishizawa Yoshikazu Tasaki [Promotion of the appropriate use of antimicrobial agents by utilizing medical big data]. The global surge in antimicrobial resistance (AMR) highlights the critical need for the development of innovative therapies and the appropriate use of antimicrobial agents. Our research focused on preventing, managing, and mitigating the adverse effects of treatments for infection with methicillin-resistant Staphylococcus aureus. In this review, we present our investigations utilizing medical big data. The first study aimed to elucidate the relationship between renal outcome and survival following the onset of vancomycin-associated nephrotoxicity (VAN). An initial analysis using the US Food and Drug Administration Adverse Events Reporting System (FAERS) database revealed elevated mortality rates among patients with VAN compared with those without VAN, forming the basis for further investigation. A subsequent, more rigorous, retrospective analysis using electronic medical records confirmed that poor survival outcomes were significantly associated with non-recovery from VAN, particularly when progression to acute kidney injury of stage ≥2 occurred. Therefore, preventing progression to severe VAN is critical for enhancing survival outcomes. The second study investigated the relationship between statin use and daptomycin-related musculoskeletal adverse events. By employing a mixed-method approach combining meta-analysis with disproportionality analysis of the FAERS data, a significant association between statin therapy and daptomycin-related rhabdomyolysis was identified. This highlights the importance of cautious statin and daptomycin use, with careful consideration of potential safety risks. Each medical big-data database possesses unique characteristics that require careful consideration during analysis. The accurate interpretation of medical big data, coupled with its integration with complementary methodologies, will produce more robust and reliable research outcomes across diverse fields. Nihon yakurigaku zasshi. Folia pharmacologica Japonica 160 3 178 183 20250000 10.1254/fpj.24081 40307046 yukiishizawa/published_papers/47952731 Fuka Aizawa Haruna Kajimoto Ami Okabayashi Daishi Moriyama Kenta Yagi Shimon Takahashi Yuhei Sonoda Takahiro Shibata Mitsuhiro Goda Takahiro Niimura Yuki Izawa-Ishizawa Hirofumi Hamano Kei Kawada Yoshito Zamami Keisuke Ishizawa Statins ameliorate oxaliplatin- and paclitaxel-induced peripheral neuropathy via glutathione-S-transferase. 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. Neurochemistry international 105863 105863 20240920 10.1016/j.neuint.2024.105863 39307458 yukiishizawa/published_papers/47866983 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 Keisuke Ishizawa Unveiling the association between fluoroquinolones and aortic diseases using real-world database analysis and pharmacological experiments. 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. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 179 117418 117418 20240911 10.1016/j.biopha.2024.117418 39265233 yukiishizawa/published_papers/47422447 Naoki Okamoto Kenta Yagi Sayaka Imawaka Mayu Takaoka Fuka Aizawa Takahiro Niimura Mitsuhiro Goda Koji Miyata Kei Kawada Yuki Izawa-Ishizawa Satoshi Sakaguchi Keisuke Ishizawa Asciminib, a novel allosteric inhibitor of BCR-ABL1, shows synergistic effects when used in combination with imatinib with or without drug resistance. 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. Pharmacology research & perspectives 12 4 e1214 null 20240800 10.1002/prp2.1214 39031848 yukiishizawa/published_papers/46680337 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 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 Introduction Guideline-directed medical therapy with renin-angiotensin system (RAS) inhibitors and beta-blockers has improved the survival of patients with heart failure (HF) and reduced left ventricular ejection fraction (HFrEF). However, it is unclear whether RAS inhibitors and beta-blockers can be administered to older patients with HF. Therefore, this study aimed to investigate the effects of beta-blockers and RAS inhibitors on the prognosis of older patients with HFrEF. Methods Demographic, clinical, and pharmacological data from 1,061 patients with acute decompensated HF, enrolled in the Kochi Registry of Subjects with Acute Decompensated Heart Failure (Kochi YOSACOI study), were analyzed to assess their impact on mortality. Additionally, a machine learning approach was applied to complement the conventional statistical model for analysis. Patients with HFrEF (n = 314) were divided into the all-cause mortality within 2 years group (n = 80) and the survivor group (n = 234). Results Overall, 41.1% (129/314) of the patients were aged ≥80, and 25.5% (80/314) experienced all-cause mortality within 2 years. Furthermore, 57.6% (181/314) and 79.0% (248/314) were prescribed RAS inhibitors and beta-blockers, respectively. Our analysis showed that RAS inhibitor use was associated with reduced all-cause mortality and cardiac death in patients with HFrEF of all ages (P &lt; 0.001), and beta-blocker use had an interaction with age. Machine learning revealed that the use of beta-blockers altered the risk of mortality, with a threshold of approximately 80 years of age. Beta-blocker use was associated with lower all-cause mortality and cardiac death in patients with HFrEF aged &lt;80 years (P &lt; 0.001) but not in those aged ≥80 years (P = 0.319 and P = 0.246, respectively). These results suggest that beta blockers may differ in their all-cause mortality benefits according to age. Conclusions RAS inhibitors prevented all-cause mortality and cardiac death at all ages, whereas beta-blockers had different effects depending on the patient's age. This study suggested that the choice of beta-blockers and RAS inhibitors is more important in older patients with HFrEF than in younger patients with the same condition. Frontiers Media SA Frontiers in Cardiovascular Medicine 2297-055X 11 null null 20240531 10.3389/fcvm.2024.1377228 yukiishizawa/published_papers/54165269 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 (一社)日本臨床薬理学会日本臨床薬理学会学術総会抄録集 2436-5580 45 np331 np332 20240000 yukiishizawa/published_papers/54165264 新村貴博植田詩穂村川和奏奈阿部菜摘八木健太相澤風花合田光寛石澤有紀石澤啓介糖尿病治療薬に関連した筋萎縮に関する検討 (一社)日本臨床薬理学会日本臨床薬理学会学術総会抄録集 2436-5580 45 np500 np500 20240000 yukiishizawa/published_papers/54165259 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 (一社)日本臨床薬理学会日本臨床薬理学会学術総会抄録集 2436-5580 45 np505 np506 20240000 yukiishizawa/published_papers/46486447 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 Keisuke Ishizawa Atractylodes lancea (Thunb.) DC. [Asteraceae] rhizome-derived exosome-like nanoparticles suppress lipopolysaccharide-induced inflammation in murine microglial cells. BACKGROUND: Exosome-like nanoparticles (ELNs) mediate interspecies intercellular communications and modulate gene expression. HYPOTHESIS/PURPOSE: 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. METHODS: 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 in vitro, 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. RESULTS: 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 Il1b, Il6, iNos, ccl2, and cxcl10 in BV-2 cells, which increased upon LPS exposure, were significantly reduced following ALR-ELN treatment. Moreover, the mRNA levels of heme oxygenase 1, Irf7, ccl12, and Irg1 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. CONCLUSION: 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. Frontiers in pharmacology 15 1302055 1302055 20240000 10.3389/fphar.2024.1302055 38738173 yukiishizawa/published_papers/46485652 Hirofumi Hamano Yoshito Zamami Soichiro Ushio Takahiro Niimura Mitsuhiro Goda Yuki Izawa-Ishizawa Keisuke Ishizawa [Development of Preventive Methods for Drug-induced Cardiotoxicity Using a Large-scale Medical Information Database]. Cancer therapies have evolved considerably thereby substantially improving the survival of patients with cancer. However, cardiotoxicity, such as myocarditis and heart failure, induced by anticancer drugs, including immune checkpoint inhibitor(ICI)s and doxorubicin, present serious challenges. Numerous observations have indicated increased risks of cardiotoxicity- and cancer-related mortality in patients with drug-induced cardiotoxicity. Therefore, the prevention and management of drug-induced cardiotoxicity should be prioritized to enable sustainable long-term treatment while preserving patients' quality of life. Recently, medical research has been primarily focused on elucidation of therapeutic benefits and adverse events using medical big data, including worldwide databases of adverse events. The aim of the present study was to establish prevention strategies for drug-induced cardiotoxicity and advance data analytics. A data-driven approach was adopted to comprehensively analyze patient data and drug-induced cardiotoxicity. These data analytics revealed numerous risk factors, leading to the development of drugs that mitigate these factors. Furthermore, many unknown adverse events with molecularly targeted drugs were brought to light. Consequently, the importance of managing adverse events, guided by insights from data science, is predicted to increase. In this symposium review, we introduce our research exemplifying pharmaceutical studies utilizing medical big data. In particular, we discuss in detail the risk factors associated with myocarditis induced by immune checkpoint inhibitors along with prophylactic agents to mitigate doxorubicin-induced cardiotoxicity. Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan 144 3 257 264 20240000 10.1248/yakushi.23-00164-2 38432934 yukiishizawa/published_papers/46485646 Koji Miyata Yuki Izawa-Ishizawa Takahiro Niimura Hirofumi Hamano Fuka Aizawa Kenta Yagi Kei Kawada Yoshito Zamami Mitsuhiro Goda Keisuke Ishizawa The Association between PDE5 Inhibitors and Aneurysm/Arterial Dissection:A Pharmacovigilance Study Using WHO Safety Database. 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. The journal of medical investigation : JMI 71 1.2 134 140 20240000 10.2152/jmi.71.134 38735709 yukiishizawa/published_papers/43518421 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 Keisuke Ishizawa Angiogenesis inhibitor-specific hypertension increases the risk of developing aortic dissection. 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. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 167 115504 115504 20230916 10.1016/j.biopha.2023.115504 37722188 yukiishizawa/published_papers/43479583 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 Keisuke Ishizawa Valproic acid treatment attenuates cisplatin-induced kidney injury by suppressing proximal tubular cell damage. 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 kidney by suppressing proximal tubular cell damage. However, prospective controlled trials need to evaluate these findings before their practical application. Clinical and translational science 16 11 2369 2381 20230912 10.1111/cts.13638 37700528 yukiishizawa/published_papers/46932876 Takahiro Niimura Mitsuhiro Goda Koji Miyata Jun Matsumoto Toshihiko Yoshioka Hirofumi Hamano Fuka Aizawa Kenta Yagi Yuki Izawa-Ishizawa Yoshito Zamami Keisuke Ishizawa Evaluation of cardiovascular toxicity of the atezolizumab and bevacizumab combination Introduction: The combination of atezolizumab, an immune checkpoint inhibitor (ICI), and bevacizumab, a vascular endothelial growth factor (VEGF) inhibitor, is the first choice for systemic therapy in hepatocellular carcinoma. Immune-related cardiovascular toxicity—myocarditis and pericarditis—are known to occur during ICI treatment. By contrast, VEGF inhibitors (VEGFIs) cause cardiovascular complications such as hypertension and heart failure. Thus, different cardiovascular toxicities have been recognized for ICIs and VEGFIs, but the impact of their combination remains unclear. Here, we aimed to investigate the cardiovascular toxicity profile of atezolizumab in combination with bevacizumab using the World Health Organization adverse event reporting database—VigiBase.Methods: We analyzed data included in VigiBase till December 2022. To evaluate the frequency of reports related to atezolizumab, bevacizumab, and their combinations for 21 adverse events, we calculated the reporting odds ratio and information component. Analyses of the fatality of various cardiovascular toxicities associated with the use of each drug were performed.Results: The database included 84,951, 10,595, and 2,092 reports of treatment with bevacizumab, atezolizumab, and their combination, respectively. The disproportionality signal of hypertension, arterial embolism and thrombosis, supraventricular tachyarrhythmias, heart failure, myocarditis, hemorrhage-related clinical events, venous embolism and thrombosis, cardiomyopathy, respiratory failure with combination regimen of atezolizumab and bevacizumab was detected. Signals of these adverse events were also detected treatment with either atezolizumab or bevacizumab alone. Venous embolism and thrombosis exhibited the highest fatality rate in the two drug combination (12.82%) relative to those of atezolizumab (6.19%) and bevacizumab (4.54%).Discussion: Cardiovascular toxicity, owing to the combination of atezolizumab and bevacizumab, was similar to that of each single agent, and no new safety concerns were observed. Caution should be exercised when combining the two drugs since the fatality rate of thromboembolism increases with combination treatment. Frontiers in Drug Safety and Regulation 2674-0869 null null 20230804 10.3389/fdsfr.2023.1213771 yukiishizawa/published_papers/42415267 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 Keisuke Ishizawa Cardiovascular Toxicities Associated with Anaplastic Lymphoma Kinase Inhibitors: A Disproportionality Analysis of the WHO Pharmacovigilance Database (VigiBase). INTRODUCTION: Recently, cases of cardiovascular toxicities, such as pericarditis, caused by anaplastic lymphoma kinase (ALK) inhibitors have been reported; however, whether these adverse events are common among all ALK inhibitors remains unclear. AIMS: This study aimed to clarify the cardiovascular toxicity profile of ALK inhibitors using an adverse event spontaneous report database. METHODS: We analyzed data from VigiBase, the WHO global database of individual safety reports, from its inception in 1968 to December 2021. We calculated the reporting odds ratio to evaluate the association between ALK inhibitors (crizotinib, ceritinib, alectinib, brigatinib, and lorlatinib) and 21 cardiovascular adverse events. Time to onset of pericarditis from ALK inhibitor administration was analyzed. RESULTS: Of the 27,994,584 reports, 19,911 involved treatment with ALK inhibitors. Among the 21 cardiovascular toxicities, only pericarditis signals were detected with all five ALK inhibitors (crizotinib [reporting odds ratios (ROR), 4.7; 95% CI 3.63-6.15], ceritinib [ROR, 12.9; 95% CI 9.37-17.79], alectinib [ROR, 4.8; 95% CI 3.15-7.42], brigatinib [ROR, 3.5; 95% CI 1.33-9.46], and lorlatinib [ROR, 6.4; 95% CI 3.60-11.22]). For torsade de pointes/QT prolongation, signals were detected with crizotinib (ROR, 5.0; 95% CI 3.72-6.77) and ceritinib (ROR, 4.2; 95% CI 2.17-8.05), whereas for hypertension, they were identified only with brigatinib (ROR, 3.9; 95% CI 2.88-5.20), and for heart failure, they were detected with alectinib (ROR, 2.2; 95% CI 1.60-2.90), crizotinib (ROR, 2.1; 95% CI 1.72-2.48), and lorlatinib (ROR, 2.0; 95% CI 1.27-3.23). Regarding time-to-onset analysis from drug administration to adverse event reporting, for pericarditis, it ranged from 52.5 days for alectinib to 166.5 days for crizotinib. CONCLUSIONS: 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. Drug safety 46 6 545 552 20230600 10.1007/s40264-023-01300-9 37106270 yukiishizawa/published_papers/41441933 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 Keisuke Ishizawa Effects of vonoprazan and proton pump inhibitors on the efficacy of bevacizumab: a multicentre retrospective study. 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. Clinical and experimental medicine 23 6 2799 2804 20230204 10.1007/s10238-023-01008-1 36738305 yukiishizawa/published_papers/40881640 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 Keisuke Ishizawa Differential effects of proton pump inhibitors and vonoprazan on vascular endothelial growth factor expression in cancer cells. 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. Drug development research 84 1 75 83 20221209 10.1002/ddr.22013 36484282 yukiishizawa/published_papers/41212970 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 Keisuke Ishizawa Characterization of Immune Checkpoint Inhibitor-Induced Myasthenia Gravis Using the United States Food and Drug Administration Adverse Event Reporting System. Myasthenia gravis (MG) is a rare but fatal adverse event of immune checkpoint inhibitors (ICI). We assessed whether patient characteristics differed between those with immune checkpoint inhibitor-related MG and those with idiopathic MG. Reports from the United States 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 MG. Among 5,464,099 cases between 2011 to 2019, 53,447 were treated with ICIs. MG was reported more often in ICI user. Multiple logistic regression analyses showed that the reporting rate of ICI-related MG did not differ significantly between male and female; however, it was higher in older people than in younger people (adjusted odds ratio, 2.4 [95% confidence interval: 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 MG. Patients with elevated serum creatine kinase or troponin levels were more likely to have concurrent myositis and myocarditis. Unlike idiopathic MG, there was no sex difference in the development of ICI-related MG, 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 MG more closely in older people. This article is protected by copyright. All rights reserved. Journal of clinical pharmacology 63 4 473 479 20221201 10.1002/jcph.2187 36453166 yukiishizawa/published_papers/40144724 Masayuki Chuma Hirofumi Hamano Takashi Bando Masateru Kondo Naoto Okada Yuki Izumi Shunsuke Ishida Toshihiko Yoshioka Mizuho Asada Takahiro Niimura Yoshito Zamami Kenshi Takechi Mitsuhiro Goda Koji Miyata Kenta Yagi Sachiko Kasamo Yuki Izawa-Ishizawa Momoyo Azuma Hiroaki Yanagawa Yoshikazu Tasaki Keisuke Ishizawa Non-recovery of vancomycin-associated nephrotoxicity is related to worsening survival outcomes-combined retrospective analyses of two real-world databases. There has been growing concern in worsening survival and renal outcomes following vancomycin-associated nephrotoxicity (VAN) onset, but the factors associated with these phenomena remain unclear. To examine these factors, we performed a retrospective study combining the analysis of two real-world databases. Initially, the FDA Adverse Event Reporting System (FAERS) was used to evaluate the relationship between VAN and mortality using odds ratios (ORs) and 95% confidence intervals (CIs). Next, electronic medical records (EMRs) were examined in a more robust cohort for evaluation of the association between renal outcomes and worsening survival using Cox proportional hazards regression models. FAERS analysis revealed a significant correlation between VAN occurrence and increased mortality (OR: 1.30; 95% CI: 1.17-1.46). EMR analysis showed that non-recovery of VAN was associated with increased hospital mortality (hazard ratio [HR]: 4.05; 95% CI: 2.42-6.77) and one-year mortality (HR: 3.03, 95% CI: 1.98-4.64). The HR for VAN recovery was lower for patients with acute kidney injury (AKI) stage ≥ 2 (HR: 0.09; 95% CI: 0.02-0.40). Thus, worsening survival outcomes were associated with non-recovery of VAN, whereby AKI stage ≥ 2 was a significant risk factor. Progression to severe VAN should be prevented for better survival outcomes. Basic & clinical pharmacology & toxicology 131 6 525 535 20220928 10.1111/bcpt.13799 36169161 yukiishizawa/published_papers/37966124 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 Keisuke Ishizawa Investigation of drugs for the prevention of doxorubicin-induced cardiac events using big data analysis. AIM: Doxorubicin, an anthracycline anti-tumour agent, is an essential chemotherapeutic drug; however, the adverse events associated with doxorubicin usage, including cardiotoxicity, prevent patients from continuing treatment. Here, we used databases to explore existing approved drugs with potential preventative effects against doxorubicin-induced cardiac events and examined their efficacy and mechanisms. METHODS: 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. RESULTS: GEO analysis showed that doxorubicin administration upregulated 490 genes and downregulated 862 genes, and LINCS data identified sirolimus, verapamil, minoxidil, prednisolone, guanabenz, and mosapride as drugs capable of counteracting these genetic alterations. Examination of the effects of these drugs on cardiac toxicity using FAERS identified sirolimus and mosapride as new prophylactic drug candidates. In model mice, mosapride and sirolimus suppressed the Bax/Bcl-2 mRNA ratio, which is elevated in doxorubicin-induced cardiotoxicity. These drugs also suppressed the expression of inflammatory cytokines Il1b and Il6 and markers associated with myocardial fibrosis, including Lgal3 and Timp1. CONCLUSION: These findings suggest that doxorubicin-induced cardiac events are suppressed by the administration of mosapride and sirolimus. European journal of pharmacology 928 175083 175083 20220531 10.1016/j.ejphar.2022.175083 35659512 yukiishizawa/published_papers/37928602 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 Keisuke Ishizawa Discovery of preventive drugs for cisplatin-induced acute kidney injury using big data analysis. 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. Clinical and translational science 15 7 1664 1675 20220420 10.1111/cts.13282 35445533 yukiishizawa/published_papers/37928595 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 Keisuke Ishizawa A web-based survey of educational opportunities of medical professionals based on changes in conference design during the COVID-19 pandemic. Owing to the coronavirus disease 2019 (COVID-19) pandemic, understanding how to hold future online academic conferences effectively is imperative. We assessed the impact of COVID-19 on academic conferences, including facilities and settings for attendance, participation status, cost burden, and preferences for future styles of holding conferences, through a web-based questionnaire survey of 2,739 Japanese medical professionals, from December 2020 to February 2021. Of the participants, 28% preferred web conferences, 60% preferred a mix of web and on-site conferences, and 12% preferred on-site conferences. Additionally, 27% of the presenters stopped presenting new findings at web conferences. The proportion of participants who audio-recorded or filmed the sessions, despite prohibition, was six times higher at web than face-to-face conferences. Since the COVID-19 outbreak, the percentage of participants attending general presentations decreased from 91 to 51%. While web conferencing offers advantages, these are offset by a decrease in presentations pertaining to novel findings and data. Supplementary Information: The online version contains supplementary material available at 10.1007/s10639-022-11032-5. Education and information technologies 27 7 1 16 20220418 10.1007/s10639-022-11032-5 35464114 yukiishizawa/published_papers/37795068 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 Keisuke Ishizawa Identification of prophylactic drugs for oxaliplatin-induced peripheral neuropathy using big data. BACKGROUND: Drug repositioning is a cost-effective method to identify novel disease indications for approved drugs; it requires a shorter developmental period than conventional drug discovery methods. We aimed to identify prophylactic drugs for oxaliplatin-induced peripheral neuropathy by drug repositioning using data from large-scale medical information and life science information databases. METHODS: Herein, we analyzed the reported data between 2007 and 2017 retrieved from the FDA's database of spontaneous adverse event reports (FAERS) and the LINCS database provided by the National Institute of Health. The efficacy of the drug candidates for oxaliplatin-induced peripheral neuropathy obtained from the database analysis was examined using a rat model of peripheral neuropathy. Additionally, we compared the incidence of peripheral neuropathy in patients who received oxaliplatin at the Tokushima University Hospital, Japan. The effects of statins on the animal model were examined in six-week-old male Sprague-Dawley rats and seven or eight-week-old male BALB/C mice. Retrospective medical chart review included clinical data from Tokushima University Hospital from April 2009 to March 2018. RESULTS: Simvastatin, indicated for dyslipidemia, significantly reduced the severity of peripheral neuropathy and oxaliplatin-induced hyperalgesia. In the nerve tissue of model rats, the mRNA expression of Gstm1 increased with statin administration. A retrospective medical chart review using clinical data revealed that the incidence of peripheral neuropathy decreased with statin use. CONCLUSION AND RELEVANCE: 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. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 148 112744 112744 20220400 10.1016/j.biopha.2022.112744 35240525 yukiishizawa/published_papers/37783371 Masayuki Chuma Aki Nakamoto Takashi Bando Takahiro Niimura Yutaka Kondo Hirofumi Hamano Naoto Okada Mizuho Asada Yoshito Zamami Kenshi Takechi Mitsuhiro Goda Koji Miyata Kenta Yagi Toshihiko Yoshioka Yuki Izawa-Ishizawa Hiroaki Yanagawa Yoshikazu Tasaki Keisuke Ishizawa Association between statin use and daptomycin-related musculoskeletal adverse events: A mixed approach combining a meta-analysis and a disproportionality analysis. BACKGROUND: There is a growing concern about the association between the combined use of daptomycin (DAP) and statins and the occurrence of musculoskeletal adverse events (MAEs), but this remains controversial. This study aimed to clarify the association between statin use and DAP-related MAEs. METHODS: We used a mixed approach that combines two methodologies. First, we conducted a meta-analysis to examine the effects of statin use on DAP-related MAEs. Second, we conducted a disproportionality analysis using the FDA Adverse Events Reporting System (FAERS) to further confirm the results of the meta-analysis and to examine the effect of each type of statin on DAP-related MAEs in a large population. RESULTS: In the meta-analysis, statin use significantly increased the incidence of DAP-related rhabdomyolysis (odds ratio [OR]: 3.83, 95% confidence interval [CI]: 1.43-10.26) but not DAP-related myopathy (OR: 1.72, 95% CI: 0.95-3.12). In the disproportionality analysis using the FAERS, the use of statin significantly increased the reporting OR (ROR) for DAP-related myopathy (ROR: 5.69, 95% CI: 4.31-7.51) and rhabdomyolysis (ROR: 5.77, 95% CI: 4.33-7.68). Atorvastatin, rosuvastatin, and simvastatin all increased the incidence of DAP-related myopathy and rhabdomyolysis. CONCLUSION: The mixed approach combining a meta-analysis and disproportionality analysis showed that statin use was associated with the occurrence of DAP-related rhabdomyolysis. The appropriate use of statins and DAP should be performed with careful consideration of its safety. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 75 8 1416 1422 20220309 10.1093/cid/ciac128 35262686 yukiishizawa/published_papers/34680620 Hirofumi Hamano Yasumasa Ikeda Mitsuhiro Goda Keijo Fukushima Seiji Kishi Masayuki Chuma Michiko Yamashita Takahiro Niimura Kenshi Takechi Masaki Imanishi Yoshito Zamami Yuya Horinouchi Yuki Izawa-Ishizawa Licht Miyamoto Keisuke Ishizawa Hiromichi Fujino Toshiaki Tamaki Ken-Ichi Aihara Koichiro Tsuchiya Diphenhydramine may be a preventive medicine against cisplatin-induced kidney toxicity. Cisplatin is widely used as an anti-tumor drug for the treatment of solid tumors. Unfortunately, it causes kidney toxicity as a critical side effect, limiting its use, given that no preventive drug against cisplatin-induced kidney toxicity is currently available. Here, based on a repositioning analysis of the Food and Drug Administration Adverse Events Reporting System, we found that a previously developed drug, diphenhydramine, may provide a novel treatment for cisplatin-induced kidney toxicity. To confirm this, the actual efficacy of diphenhydramine was evaluated in in vitro and in vivo experiments. Diphenhydramine inhibited cisplatin-induced cell death in kidney proximal tubular cells. Mice administered cisplatin developed kidney injury with significant dysfunction (mean plasma creatinine: 0.43 vs 0.15 mg/dl) and showed augmented oxidative stress, increased apoptosis, elevated inflammatory cytokines, and MAPKs activation. However, most of these symptoms were suppressed by treatment with diphenhydramine. Furthermore, the concentration of cisplatin in the kidney was significantly attenuated in diphenhydramine-treated mice (mean platinum content: 70.0 vs 53.4 μg/g dry kidney weight). Importantly, diphenhydramine did not influence or interfere with the anti-tumor effect of cisplatin in any of the in vitro or in vivo experiments. In a selected cohort of 98 1:1 matched patients from a retrospective database of 1467 patients showed that patients with malignant cancer who had used diphenhydramine before cisplatin treatment exhibited significantly less acute kidney injury compared to ones who did not (6.1 % vs 22.4 %, respectively). Thus, diphenhydramine demonstrated efficacy as a novel preventive medicine against cisplatin-induced kidney toxicity. Kidney international 99 4 885 899 20210400 10.1016/j.kint.2020.10.041 33307103 yukiishizawa/published_papers/27559156 Yasumasa Ikeda Hiroaki Watanabe Tetsuya Shiuchi Hirofumi Hamano Yuya Horinouchi Masaki Imanishi Mitsuhiro Goda Yoshito Zamami Kenshi Takechi Yuki Izawa-Ishizawa Licht Miyamoto Keisuke Ishizawa Ken-Ichi Aihara Koichiro Tsuchiya Toshiaki Tamaki Deletion of H-ferritin in macrophages alleviates obesity and diabetes induced by high-fat diet in mice. AIMS/HYPOTHESIS: Iron accumulation affects obesity and diabetes, both of which are ameliorated by iron reduction. Ferritin, an iron-storage protein, plays a crucial role in iron metabolism. H-ferritin exerts its cytoprotective action by reducing toxicity via its ferroxidase activity. We investigated the role of macrophage H-ferritin in obesity and diabetes. METHODS: Conditional macrophage-specific H-ferritin (Fth, also known as Fth1) knockout (LysM-Cre Fth KO) mice were used and divided into four groups: wild-type (WT) and LysM-Cre Fth KO mice with normal diet (ND), and WT and LysM-Cre Fth KO mice with high-fat diet (HFD). These mice were analysed for characteristics of obesity and diabetes, tissue iron content, inflammation, oxidative stress, insulin sensitivity and metabolic measurements. RAW264.7 macrophage cells were used for in vitro experiments. RESULTS: Iron concentration reduced, and mRNA expression of ferroportin increased, in macrophages from LysM-Cre Fth KO mice. HFD-induced obesity was lower in LysM-Cre Fth KO mice than in WT mice at 12 weeks (body weight: KO 34.6 ± 5.6 g vs WT 40.1 ± 5.2 g). mRNA expression of inflammatory cytokines and infiltrated macrophages and oxidative stress increased in the adipose tissue of HFD-fed WT mice, but was not elevated in HFD-fed LysM-Cre Fth KO mice. However, WT mice fed an HFD had elevated iron concentration in adipose tissue and spleen, which was not observed in LysM-Cre Fth KO mice fed an HFD (adipose tissue [μmol Fe/g protein]: KO 1496 ± 479 vs WT 2316 ± 866; spleen [μmol Fe/g protein]: KO 218 ± 54 vs WT 334 ± 83). Moreover, HFD administration impaired both glucose tolerance and insulin sensitivity in WT mice, which was ameliorated in LysM-Cre Fth KO mice. In addition, energy expenditure, mRNA expression of thermogenic genes, and body temperature were higher in KO mice with HFD than WT mice with HFD. In vitro experiments showed that iron content was reduced, and lipopolysaccharide-induced Tnf-α (also known as Tnf) mRNA upregulation was inhibited in a macrophage cell line transfected with Fth siRNA. CONCLUSIONS/INTERPRETATION: Deletion of macrophage H-ferritin suppresses the inflammatory response by reducing intracellular iron levels, resulting in the prevention of HFD-induced obesity and diabetes. The findings from this study highlight macrophage iron levels as a potential therapeutic target for obesity and diabetes. Diabetologia 63 8 1588 1602 20200800 10.1007/s00125-020-05153-0 32430665 yukiishizawa/published_papers/27559166 Masaki Imanishi Yusuke Yamakawa Keijo Fukushima Raiki Ikuto Akiko Maegawa Yuki Izawa-Ishizawa Yuya Horinouchi Masateru Kondo Masatoshi Kishuku Mitsuhiro Goda Yoshito Zamami Kenshi Takechi Masayuki Chuma Yasumasa Ikeda Koichiro Tsuchiya Hiromichi Fujino Koichi Tsuneyama Keisuke Ishizawa Fibroblast-specific ERK5 deficiency changes tumor vasculature and exacerbates tumor progression in a mouse model. The roles of cancer-associated fibroblasts (CAFs) have been studied in the tumor progression, and CAFs are expected to become the new targets for cancer pharmacotherapies. CAFs contribute to tumor cell survival and proliferation, tumor angiogenesis, immune suppression, tumor inflammation, tumor cell invasion and metastasis, and extracellular matrix remodeling. However, detailed mechanisms of how CAFs function in the living system remain unclear. CAFs include α-smooth muscle actin, expressing activated fibroblasts similar to myofibroblasts, and are highly capable of producing collagen. Several reports have demonstrated the contributions of extracellular-signal-regulated kinase 5 (ERK5) in fibroblasts to the fibrotic processes; however, the roles of CAF-derived ERK5 remain unclear. To investigate the roles of CAF-derived ERK5 in the tumor progression, we created mice lacking the ERK5 gene specifically in fibroblasts. Colon-26 mouse colon cancer cells were implanted into the mice subcutaneously, and the histological analyses of the tumor tissue were performed after 2 weeks. Immunofluorescence analyses showed that recipient-derived fibroblasts existed within the tumor tissue. The present study demonstrated that fibroblast-specific ERK5 deficiency exacerbated tumor progression and it was accompanied with thicker tumor vessel formation and the increase in the number of activated fibroblasts. We combined the results of The Cancer Genome Atlas (TCGA) database analysis with our animal studies, and indicated that regulating ERK5 activity in CAFs or CAF invasion into the tumor tissue can be important strategies for the development of new targets in cancer pharmacotherapies. Naunyn-Schmiedeberg's archives of pharmacology 393 7 1239 1250 20200419 10.1007/s00210-020-01859-5 32307577 yukiishizawa/published_papers/24878624 Tatsuya Tsuda Masaki Imanishi Mizuho Oogoshi Mitsuhiro Goda Yoshitaka Kihira Yuya Horinouchi Yoshito Zamami Keisuke Ishizawa Yasumasa Ikeda Ichiro Hashimoto Toshiaki Tamaki Yuki Izawa-Ishizawa Rho-associated protein kinase and cyclophilin a are involved in inorganic phosphate-induced calcification signaling in vascular smooth muscle cells. Arterial calcification, a risk factor of cardiovascular events, develops with differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. Cyclophilin A (CypA) is a peptidyl-prolyl isomerase involved in cardiovascular diseases such as atherosclerosis and aortic aneurysms, and rho-associated protein kinase (ROCK) is involved in the pathogenesis of vascular calcification. CypA is secreted in a ROCK activity-dependent manner and works as a mitogen via autocrine or paracrine mechanisms in VSMCs. We examined the involvement of the ROCK-CypA axis in VSMC calcification induced by inorganic phosphate (Pi), a potent cell mineralization initiator. We found that Pi stimulated ROCK activity, CypA secretion, extracellular signal-regulated protein kinase (ERK) 1/2 phosphorylation, and runt-related transcription factor 2 expression, resulting in calcium accumulation in rat aortic smooth muscle cells (RASMCs). The ROCK inhibitor Y-27632 significantly suppressed Pi-induced CypA secretion, ERK1/2 phosphorylation, and calcium accumulation. Recombinant CypA was found to be associated with increased calcium accumulation in RASMCs. Based on these results, we suggest that autocrine CypA is mediated by ROCK activity and is involved in Pi-induced ERK1/2 phosphorylation following calcification signaling in RASMCs. Journal of pharmacological sciences 142 3 109 115 20200300 10.1016/j.jphs.2019.12.005 31882204 yukiishizawa/published_papers/24878640 Hirofumi Hamano Takahiro Niimura Yuya Horinouchi Yoshito Zamami Kenshi Takechi Mitsuhiro Goda Masaki Imanishi Masayuki Chuma Yuki Izawa-Ishizawa Licht Miyamoto Keijo Fukushima Hiromichi Fujino Koichiro Tsuchiya Keisuke Ishizawa Toshiaki Tamaki Yasumasa Ikeda Proton pump inhibitors block iron absorption through direct regulation of hepcidin via the aryl hydrocarbon receptor-mediated pathway. Proton pump inhibitors (PPIs) have been used worldwide to treat gastrointestinal disorders. A recent study showed that long-term use of PPIs caused iron deficiency; however, it is unclear whether PPIs affect iron metabolism directly. We investigated the effect of PPIs on the peptide hepcidin, an important iron regulatory hormone. First, we used the FDA Adverse Event Reporting System database and analyzed the influence of PPIs. We found that PPIs, as well as H2 blockers, increased the odds ratio of iron-deficient anemia. Next, HepG2 cells were used to examine the action of PPIs and H2 blockers on hepcidin. PPIs augmented hepcidin expression, while H2 blockers did not. In fact, the PPI omeprazole increased hepcidin secretion, and omeprazole-induced hepcidin upregulation was inhibited by gene silencing or the pharmacological inhibition of the aryl hydrocarbon receptor. In mouse experiments, omeprazole also increased hepatic hepcidin mRNA expression and blood hepcidin levels. In mice treated with omeprazole, protein levels of duodenal and splenic ferroportin decreased. Taken together, PPIs directly affect iron metabolism by suppressing iron absorption through the inhibition of duodenal ferroportin via hepcidin upregulation. These findings provide a new insight into the molecular mechanism of PPI-induced iron deficiency. Toxicology letters 318 86 91 20200100 10.1016/j.toxlet.2019.10.016 31669099 yukiishizawa/published_papers/13730602 Hirofumi Hamano Marin Mitsui Yoshito Zamami Kenshi Takechi Takahiro Nimura Naoto Okada Keijo Fukushima Masaki Imanishi Masayuki Chuma Yuya Horinouchi Yuki Izawa-Ishizawa Yasushi Kirino Toshimi Nakamura Kazuhiko Teraoka Yasumasa Ikeda Hiromichi Fujino Hiroaki Yanagawa Toshiaki Tamaki Keisuke Ishizawa Irinotecan-induced neutropenia is reduced by oral alkalization drugs: analysis using retrospective chart reviews and the spontaneous reporting database. PURPOSE: SN-38, an active metabolite of irinotecan, is reabsorbed by the intestinal tract during excretion, causing diarrhoea and neutropenia. In addition, the association between blood levels of SN-38 and neutropenia has been reported previously, and the rapid excretion of SN-38 from the intestinal tract is considered to prevent neutropenia. Oral alkalization drugs are used as prophylactic agents for suppressing SN-38 reabsorption. The relationship between oral alkalization drugs and neutropenia, however, has not been well studied. The aim of this study was to investigate the relationship between oral alkalization drugs and neutropenia in irinotecan-treated patients. METHODS AND RESULTS: Patients with cervical or ovarian cancer were administered irinotecan and investigated by medical chart reviews to determine whether oral alkalization drugs were effective at ameliorating irinotecan-induced neutropenia. The drug combination in the oral alkalization drugs-ursodeoxycholic acid, magnesium oxide, and sodium hydrogen carbonate-significantly improved neutrophil counts and reduced dose intensity compared with those of non-users. In the large-scale Japanese Adverse Drug Event Report database, the reporting odds ratio of irinotecan-induced neutropenia was significantly lower when irinotecan had been given in combination with oral alkalization drugs. CONCLUSIONS: These data indicate that oral alkalization drugs may reduce the frequency of neutropenia caused by irinotecan administration, making it possible to increase the dose safely. Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer 1433-7339 27 3 849 856 20190300 10.1007/s00520-018-4367-y 30062585 yukiishizawa/published_papers/13730601 Masateru Kondo Masaki Imanishi Keijo Fukushima Raiki Ikuto Yoichi Murai Yuya Horinouchi Yuki Izawa-Ishizawa Mitsuhiro Goda Yoshito Zamami Kenshi Takechi Masayuki Chuma Yasumasa Ikeda Hiromichi Fujino Koichiro Tsuchiya Keisuke Ishizawa Xanthine Oxidase Inhibition by Febuxostat in Macrophages Suppresses Angiotensin II-Induced Aortic Fibrosis. BACKGROUND: Several reports from basic researches and clinical studies have suggested that xanthine oxidase (XO) inhibitors have suppressive effects on cardiovascular diseases. However, the roles of a XO inhibitor, febuxostat (FEB), in the pathogenesis of vascular remodeling and hypertension independent of the serum uric acid level remain unclear. METHODS: To induce vascular remodeling in mice, angiotensin II (Ang II) was infused for 2 weeks with a subcutaneously implanted osmotic minipump. FEB was administered every day during Ang II infusion. Aortic fibrosis was assessed by elastica van Gieson staining. Mouse macrophage RAW264.7 cells (RAW) and mouse embryonic fibroblasts were used for in vitro studies. RESULTS: FEB suppressed Ang II-induced blood pressure elevation and aortic fibrosis. Immunostaining showed that Ang II-induced macrophage infiltration in the aorta tended to be suppressed by FEB, and XO was mainly colocalized in macrophages, not in fibroblasts. Transforming growth factor-β1 (TGF-β1) mRNA expression was induced in the aorta in the Ang II alone group, but not in the Ang II + FEB group. Ang II induced α-smooth muscle actin-positive fibroblasts in the aortic wall, but FEB suppressed them. XO expression and activity were induced by Ang II stimulation alone but not by Ang II + FEB in RAW. FEB suppressed Ang II-induced TGF-β1 mRNA expression in RAW. CONCLUSIONS: Our results suggested that FEB ameliorates Ang II-induced aortic fibrosis via suppressing macrophage-derived TGF-β1 expression. American journal of hypertension 1941-7225 32 3 249 256 20190212 10.1093/ajh/hpy157 30351343 yukiishizawa/published_papers/24878635 Yoshito Zamami Takahiro Niimura Toshihiro Koyama Yuta Shigemi Yuki Izawa-Ishizawa Mizuki Morita Ayako Ohshima Keisaku Harada Toru Imai Hiromi Hagiwara Naoto Okada Mitsuhiro Goda Kenshi Takechi Masayuki Chuma Yutaka Kondo Koichiro Tsuchiya Shiro Hinotsu Mitsunobu R Kano Keisuke Ishizawa Search for Therapeutic Agents for Cardiac Arrest Using a Drug Discovery Tool and Large-Scale Medical Information Database. The survival rate of cardiac arrest patients is less than 10%; therefore, development of a therapeutic strategy that improves their prognosis is necessary. Herein, we searched data collected from medical facilities throughout Japan for drugs that improve the survival rate of cardiac arrest patients. Candidate drugs, which could improve the prognosis of cardiac arrest patients, were extracted using "TargetMine," a drug discovery tool. We investigated whether the candidate drugs were among the drugs administered within 1 month after cardiac arrest in data of cardiac arrest cases obtained from the Japan Medical Data Center. Logistic regression analysis was performed, with the explanatory variables being the presence or absence of the administration of those candidate drugs that were administered to ≥10 patients and the objective variable being the "survival discharge." Adjusted odds ratios for survival discharge were calculated using propensity scores for drugs that significantly improved the proportion of survival discharge; the influence of covariates, such as patient background, medical history, and treatment factors, was excluded by the inverse probability-of-treatment weighted method. Using the search strategy, we extracted 165 drugs with vasodilator activity as candidate drugs. Drugs not approved in Japan, oral medicines, and external medicines were excluded. Then, we investigated whether the candidate drugs were administered to the 2,227 cardiac arrest patients included in this study. The results of the logistic regression analysis showed that three (isosorbide dinitrate, nitroglycerin, and nicardipine) of seven drugs that were administered to ≥10 patients showed significant association with improvement in the proportion of survival discharge. Further analyses using propensity scores revealed that the adjusted odds ratios for survival discharge for patients administered isosorbide dinitrate, nitroglycerin, and nicardipine were 3.35, 5.44, and 4.58, respectively. Thus, it can be suggested that isosorbide dinitrate, nitroglycerin, and nicardipine could be novel therapeutic agents for improving the prognosis of cardiac arrest patients. Frontiers in pharmacology 10 1257 1257 20190000 10.3389/fphar.2019.01257 31780928 yukiishizawa/published_papers/13730603 Yuya Horinouchi Yasumasa Ikeda Keijo Fukushima Masaki Imanishi Hirofumi Hamano Yuki Izawa-Ishizawa Yoshito Zamami Kenshi Takechi Licht Miyamoto Hiromichi Fujino Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Renoprotective effects of a factor Xa inhibitor: fusion of basic research and a database analysis. Renal tubulointerstitial injury, an inflammation-associated condition, is a major cause of chronic kidney disease (CKD). Levels of activated factor X (FXa), a blood coagulation factor, are increased in various inflammatory diseases. Therefore, we investigated the protective effects of an FXa inhibitor against renal tubulointerstitial injury using unilateral ureteral obstruction (UUO) mice (a renal tubulointerstitial fibrosis model) and the Food and Drug Administration Adverse Events Reporting System (FAERS) database. The renal expression levels of FX and the FXa receptors protease-activated receptor (PAR)-1 and PAR-2 were significantly higher in UUO mice than in sham-operated mice. UUO-induced tubulointerstitial fibrosis and extracellular matrix expression were suppressed in UUO mice treated with the FXa inhibitor edoxaban. Additionally, edoxaban attenuated UUO-induced macrophage infiltration and inflammatory molecule upregulation. In an analysis of the FAERS database, there were significantly fewer reports of tubulointerstitial nephritis for patients treated with FXa inhibitors than for patients not treated with inhibitors. These results suggest that FXa inhibitors exert protective effects against CKD by inhibiting tubulointerstitial fibrosis. Scientific reports 2045-2322 8 1 10858 10858 20180718 10.1038/s41598-018-29008-2 30022146 yukiishizawa/published_papers/13730607 Hirofumi Hamano Yasumasa Ikeda Hiroaki Watanabe Yuya Horinouchi Yuki Izawa-Ishizawa Masaki Imanishi Yoshito Zamami Kenshi Takechi Licht Miyamoto Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki The uremic toxin indoxyl sulfate interferes with iron metabolism by regulating hepcidin in chronic kidney disease. Background: Hepcidin secreted by hepatocytes is a key regulator of iron metabolism throughout the body. Hepcidin concentrations are increased in chronic kidney disease (CKD), contributing to abnormalities in iron metabolism. Levels of indoxyl sulfate (IS), a uremic toxin, are also elevated in CKD. However, the effect of IS accumulation on iron metabolism remains unclear. Methods: We used HepG2 cells to determine the mechanism by which IS regulates hepcidin concentrations. We also used a mouse model of adenine-induced CKD. The CKD mice were divided into two groups: one was treated using AST-120 and the other received no treatment. We examined control mice, CKD mice, CKD mice treated using AST-120 and mice treated with IS via drinking water. Results: In the in vitro experiments using HepG2 cells, IS increased hepcidin expression in a dose-dependent manner. Silencing of the aryl hydrocarbon receptor (AhR) inhibited IS-induced hepcidin expression. Furthermore, IS induced oxidative stress and antioxidant drugs diminished IS-induced hepcidin expression. Adenine-induced CKD mice demonstrated an increase in hepcidin concentrations; this increase was reduced by AST-120, an oral adsorbent of the uremic toxin. CKD mice showed renal anemia, decreased plasma iron concentration, increased plasma ferritin and increased iron content in the spleen. Ferroportin was decreased in the duodenum and increased in the spleen. These changes were ameliorated by AST-120 treatment. Mice treated by direct IS administration showed hepatic hepcidin upregulation. Conclusions: IS affects iron metabolism in CKD by participating in hepcidin regulation via pathways that depend on AhR and oxidative stress. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 1460-2385 33 4 586 597 20180401 10.1093/ndt/gfx252 28992067 yukiishizawa/published_papers/13730604 Takahiro Niimura Yoshito Zamami Toshihiro Koyama Yuki Izawa-Ishizawa Masashi Miyake Tadashi Koga Keisaku Harada Ayako Ohshima Toru Imai Yutaka Kondo Masaki Imanishi Kenshi Takechi Keijo Fukushima Yuya Horinouchi Yasumasa Ikeda Hiromichi Fujino Koichiro Tsuchiya Toshiaki Tamaki Shiro Hinotsu Mitsunobu R Kano Keisuke Ishizawa Hydrocortisone administration was associated with improved survival in Japanese patients with cardiac arrest. There are few reports on hydrocortisone administration after cardiac arrest, and those that have been published included few subjects. This study aimed to evaluate the effect of hydrocortisone administration on the outcomes of patients who experienced cardiac arrest. We investigated the survival discharge rates and the length of hospital stay from cardiac arrest to discharge, stratified by use of hydrocortisone, using a Japanese health-insurance claims dataset that covers approximately 2% of the Japanese population. The study included the data of 2233 subjects who experienced either in-hospital or out-of-hospital cardiac arrest between January 2005 and May 2014. These patients were divided into two groups, based on the administration of hydrocortisone. We adjusted the baseline characteristics, medical treatment, and drug administration data of the two groups using propensity scores obtained via the inverse probability of treatment weighted method. The hydrocortisone group had a significantly higher survival discharge rate (13/61 [21.1%] vs. 240/2172 [11.0%], adjusted odds ratio: 4.2, 95% CI: 1.60-10.98, p = 0.004). In addition, the administration of hydrocortisone was independent predictor of survival to discharge (hazard ratio: 4.6, p < 0.001). The results demonstrate a correlation between hydrocortisone administration and the high rates of survival to discharge. Scientific reports 2045-2322 7 1 17919 17919 20171220 10.1038/s41598-017-17686-3 29263333 yukiishizawa/published_papers/13730605 Shiho Sato Yoshito Zamami Toru Imai Satoshi Tanaka Toshihiro Koyama Takahiro Niimura Masayuki Chuma Tadashi Koga Kenshi Takechi Yasuko Kurata Yutaka Kondo Yuki Izawa-Ishizawa Toshiaki Sendo Hironori Nakura Keisuke Ishizawa Meta-analysis of the efficacies of amiodarone and nifekalant in shock-resistant ventricular fibrillation and pulseless ventricular tachycardia SCIENTIFIC REPORTS 2045-2322 7 1 null null 20171000 10.1038/s41598-017-13073-0 28978927 yukiishizawa/published_papers/13730606 Yasumasa Ikeda Yuya Horinouchi Hirofumi Hamano Tasuku Hirayama Seiji Kishi Yuki Izawa-Ishizawa Masaki Imanishi Yoshito Zamami Kenshi Takechi Licht Miyamoto Keisuke Ishizawa Ken-Ichi Aihara Hideko Nagasawa Koichiro Tsuchiya Toshiaki Tamaki Dietary iron restriction alleviates renal tubulointerstitial injury induced by protein overload in mice. Increased proteinuria causes tubulointerstitial injury due to inflammation in chronic kidney disease (CKD). Iron restriction exhibits protective effects against renal dysfunction; however, its effects against protein overload-induced tubulointerstitial damage remain unclear. Here, we investigated dietary iron restriction effect on tubulointerstitial damage in mice with protein-overload tubulointerstitial injury. Renal tubulointerstitial injury in animal model was induced by intraperitoneal injection of an overdose of bovine serum albumin (BSA). We divided mice into three groups: normal saline + normal diet (ND), BSA + ND, and BSA + iron-restricted diet (IRD). BSA overload induced renal tubulointerstitial injury in the ND mice, which was ameliorated in the IRD mice. Inflammatory cytokines and extracellular matrix mRNA expression was upregulated in BSA + ND mice kidneys and was inhibited by IRD. BSA-induced increase in renal superoxide production, NADPH oxidase activity, and p22phox expression was diminished in the IRD mice. IRD suppression increased BSA-induced renal macrophage infiltration. Moreover, BSA mice exhibited nucleotide-binding oligomerisation domain-like receptor pyrin domain-containing protein (NLRP) inflammasome activation, which was inhibited by IRD. Ferrous iron increased in kidneys with BSA overload and was inhibited by IRD. Thus, iron restriction inhibited oxidative stress and inflammatory changes, contributing to the protective effect against BSA overload-induced tubulointerstitial injury. Scientific reports 2045-2322 7 1 10621 10621 20170906 10.1038/s41598-017-11089-0 28878231 yukiishizawa/published_papers/13730608 Keisuke Oshima Yasumasa Ikeda Yuya Horinouchi Hiroaki Watanabe Hirofumi Hamano Yoshitaka Kihira Seiji Kishi Yuki Izawa-Ishizawa Licht Miyamoto Tasuku Hirayama Hideko Nagasawa Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Iron suppresses erythropoietin expression via oxidative stress-dependent hypoxia-inducible factor-2 alpha inactivation. Renal anemia is a major complication in chronic kidney disease (CKD). Iron supplementation, as well as erythropoiesis-stimulating agents, are widely used for treatment of renal anemia. However, excess iron causes oxidative stress via the Fenton reaction, and iron supplementation might damage remnant renal function including erythropoietin (EPO) production in CKD. EPO gene expression was suppressed in mice following direct iron treatment. Hypoxia-inducible factor-2 alpha (HIF-2α), a positive regulator of the EPO gene, was also diminished in the kidney of mice following iron treatment. Anemia-induced increase in renal EPO and HIF-2α expression was inhibited by iron treatment. In in vitro experiments using EPO-producing HepG2 cells, iron stimulation reduced the expression of the EPO gene, as well as HIF-2α. Moreover, iron treatment augmented oxidative stress, and iron-induced reduction of EPO and HIF-2α expression was restored by tempol, an antioxidant compound. HIF-2α interaction with the Epo promoter was inhibited by iron treatment, and was restored by tempol. These findings suggested that iron supplementation reduced EPO gene expression via an oxidative stress-HIF-2α-dependent signaling pathway. Laboratory investigation; a journal of technical methods and pathology 1530-0307 97 5 555 566 20170500 10.1038/labinvest.2017.11 28263291 yukiishizawa/published_papers/13730609 Yutaka Fukunaga Yuki Izawa-Ishizawa Yuya Horinouchi Eriko Sairyo Yasumasa Ikeda Keisuke Ishizawa Koichiro Tsuchiya Yoshiro Abe Ichiro Hashimoto Toshiaki Tamaki Topical application of nitrosonifedipine, a novel radical scavenger, ameliorates ischemic skin flap necrosis in a mouse model. Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO-NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO-NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO-NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO-NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO-NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p < 0.01). NO-NIF reduced oxidative stress, apoptosis and endothelial dysfunction, which were evidenced by the decrease of malondialdehyde, p22phox protein expression, number of apoptotic cells, phosphorylated p38 MAPK protein expression, and vascular cell adhesion molecule-1 protein expression while endothelial nitric oxide synthase protein expression was increased. In conclusion, they demonstrated that NO-NIF ameliorated ischemic skin flap necrosis by reducing oxidative stress, apoptosis, and endothelial dysfunction. NO-NIF is considered to be a candidate for the treatment of ischemic flap necrosis. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society 1524-475X 25 2 217 223 20170400 10.1111/wrr.12510 28090711 yukiishizawa/published_papers/13730610 Yasumasa Ikeda Mizuki Imao Akiho Satoh Hiroaki Watanabe Hirofumi Hamano Yuya Horinouchi Yuki Izawa-Ishizawa Yoshitaka Kihira Licht Miyamoto Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Iron-induced skeletal muscle atrophy involves an Akt-forkhead box O3-E3 ubiquitin ligase-dependent pathway. Skeletal muscle wasting or sarcopenia is a critical health problem. Skeletal muscle atrophy is induced by an excess of iron, which is an essential trace metal for all living organisms. Excessive amounts of iron catalyze the formation of highly toxic hydroxyl radicals via the Fenton reaction. However, the molecular mechanism of iron-induced skeletal muscle atrophy has remained unclear. In this study, 8-weeks-old C57BL6/J mice were divided into 2 groups: vehicle-treated group and the iron-injected group (10 mg iron day(-1)mouse(-1)) during 2 weeks. Mice in the iron-injected group showed an increase in the iron content of the skeletal muscle and serum and ferritin levels in the muscle, along with reduced skeletal muscle mass. The skeletal muscle showed elevated mRNA expression of the muscle atrophy-related E3 ubiquitin ligases, atrogin-1 and muscle ring finger-1(MuRF1), on days 7 and 14 of iron treatment. Moreover, iron-treated mice showed reduced phosphorylation of Akt and forkhead box O3 (FOXO3a) in skeletal muscles. Inhibition of FOXO3a using siRNA in vitro in C2C12 myotube cells inhibited iron-induced upregulation of atrogin-1 and MuRF1 and reversed the reduction in myotube diameters. Iron-load caused oxidative stress, and an oxidative stress inhibitor abrogated iron-induced muscle atrophy by reactivating the Akt-FOXO3a pathway. Iron-induced skeletal muscle atrophy is suggested to involve the E3 ubiquitin ligase mediated by the reduction of Akt-FOXO3a signaling by oxidative stress. Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) 1878-3252 35 5 66 76 20160500 10.1016/j.jtemb.2016.01.011 27049128 yukiishizawa/published_papers/26416025 Kishibuchi Reina Kihira Yoshitaka Yamaguchi Kunihisa Izawa-Ishizawa Yuki Ikeda Yasumasa Ishizawa Keisuke Tomita Shuhei Tsuchiya Koichiro Tamaki Toshiaki HIF-1 alpha is involved in recovery from renal ischemia-reperfusion injury through regulations of apoptotic factors Bcl-2 and CHAC1 JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 130 3 S247 null 20160300 yukiishizawa/published_papers/28151602 Yasumasa Ikeda Mizuki Imao Akiho Satoh Hiroaki Watanabe Hirofumi Hamano Yuya Horinouchi Yuki Izawa-Ishizawa Yoshitaka Kihira Licht Miyamoto Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Iron-induced skeletal muscle atrophy involves an Akt-forkhead box O3-E3 ubiquitin ligase-dependent pathway JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY 0946-672X 35 66 76 20160000 10.1016/j.jtemb.2016.01.011 yukiishizawa/published_papers/13730611 Yasumasa Ikeda Hirofumi Hamano Akiho Satoh Yuya Horinouchi Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawa Ken-Ichi Aihara Koichiro Tsuchiya Toshiaki Tamaki Bilirubin exerts pro-angiogenic property through Akt-eNOS-dependent pathway. Low serum bilirubin levels are associated with the risk of cardiovascular diseases including peripheral artery disease. Bilirubin is known to exert its property such as antioxidant effect or the enhancement of flow-mediated vasodilation, however, bilirubin action on angiogenesis remains unclear. To investigate the molecular mechanism of bilirubin on angiogenic effect, we first employed C57BL/6J mice with unilateral hindlimb ischemia surgery and divided the mice into two groups (vehicle-treated group and bilirubin-treated group). The analysis of laser speckle blood flow demonstrated the enhancement of blood flow recovery in response to ischemia of mice with bilirubin treatment. The density of capillaries was significantly higher in ischemic-adductor muscles of bilirubin-treated mice. The phosphorylated levels of endothelial nitric oxide synthase (eNOS) and Akt were increased in ischemic skeletal muscles of mice with bilirubin treatment compared with vehicle treatment. In in vitro experiments by using human aortic endothelial cells, bilirubin augmented eNOS and Akt phosphorylation, cell proliferation, cell migration and tube formation. These bilirubin actions on endothelial cell activation were inhibited by LY294002, a phosphatidylinositol 3-kinase inhibitor. In conclusion, bilirubin promotes angiogenesis through endothelial cells activation via Akt-eNOS-dependent manner. Hypertension research : official journal of the Japanese Society of Hypertension 1348-4214 38 11 733 40 20151100 10.1038/hr.2015.74 26134126 yukiishizawa/published_papers/13730612 Soichiro Tajima Yasumasa Ikeda Hideaki Enomoto Mizuki Imao Yuya Horinouchi Yuki Izawa-Ishizawa Yoshitaka Kihira Licht Miyamoto Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Angiotensin II alters the expression of duodenal iron transporters, hepatic hepcidin, and body iron distribution in mice Dr. Dietrich Steinkopff Verlag GmbH and Co. KG European Journal of Nutrition 1436-6215 54 5 709 719 20150823 10.1007/s00394-014-0749-1 25096756 2-s2.0-84937513465 yukiishizawa/published_papers/26416020 Kishibuchi Reina Kihira Yoshitaka Yamaguchi Kunihisa Izawa-Ishizawa Yuki Ishizawa Keisuke Ikeda Yasumasa Tomita Shuuhei Tsuchiya Koichiro Tamaki Toshiaki Hypoxia-inducible factor-1 alpha. participates in induction of apoptosis in renal reperfusion injury JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 128 3 S204 null 20150700 yukiishizawa/published_papers/13730613 Yoshitaka Kihira 木平孝高 Ariunzaya Burentogtokh Mari Itoh Yuki Izawa-Ishizawa 石澤有紀 Keisuke Ishizawa 石澤啓介 Yasumasa Ikeda 池田康将 Koichiro Tsuchiya 土屋浩一郎 Toshiaki Tamaki 玉置俊晃 Hypoxia decreases glucagon-like peptide-1 secretion from GLUTag cell line Glucagon-like peptide-1 (GLP-1), an incretin hormone, is secreted from L cells located in the intestinal epithelium. It is known that intestinal oxygen tension is decreased postprandially. In addition, we found that the expression of hypoxia-inducible factor-1α (HIF-1α), which accumulates in cells under hypoxic conditions, was significantly increased in the colons of mice with food intake, indicating that the oxygen concentration is likely reduced in the colon after eating. Therefore, we hypothesized that GLP-1 secretion is affected by oxygen tension. We found that forskolin-stimulated GLP-1 secretion from GLUTag cells, a model of intestinal L cells, is suppressed in hypoxia (1% O2). Forskolin-stimulated elevations of preproglucagon (ppGCG) and proprotein convertase 1/3 (PC1/3) mRNA expression were decreased under hypoxic conditions. The finding that H89, a protein kinase A (PKA) inhibitor, inhibited the forskolin-stimulated increase of ppGCG and PC1/3 indicated that the cAMP-PKA pathway is involved in the hypoxia-induced suppression of the genes. Hypoxia decreased hexokinase 2 mRNA and protein expression and increased lactate dehydrogenase A mRNA and protein expression. Concomitantly, lactate production was increased and ATP production was decreased. Together, the results indicate that hypoxia decreases glucose utilization for ATP production, which probably causes a decrease in cAMP production and in subsequent GLP-1 production. Our findings suggest that the postprandial decrease in oxygen tension in the intestine attenuates GLP-1 secretion. Biological & Pharmaceutical Bulletin 1347-5215 38 4 514 521 20150400 10.1248/bpb.b14-00612 25832631 yukiishizawa/published_papers/13730614 Noriko Yamano Yasumasa Ikeda Minoru Sakama Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawa Licht Miyamoto Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki A long-term high-fat diet changes iron distribution in the body, increasing iron accumulation specifically in the mouse spleen Center for Academic Publications Japan Journal of Nutritional Science and Vitaminology 1881-7742 61 1 20 27 20150000 10.3177/jnsv.61.20 25994136 2-s2.0-84929747372 yukiishizawa/published_papers/13730615 Nhat-Tu Le Yuichiro Takei Yuki Izawa-Ishizawa Kyung-Sun Heo Hakjoo Lee Alan V. Smrcka Benjamin L. Miller Kyung Ae Ko Sara Ture Craig Morrell Keigi Fujiwara Masashi Akaike Jun-Ichi Abe Identification of activators of erk5 transcriptional activity by high-throughput screening and the role of endothelial ERK5 in vasoprotective effects induced by statins and antimalarial agents American Association of Immunologists Journal of Immunology 1550-6606 193 7 3803 3815 20141001 10.4049/jimmunol.1400571 25187658 2-s2.0-84907202543 yukiishizawa/published_papers/26036969 Masaki Imanishi Keisuke Ishizawa Takumi Sakurada Yuki Ishizawa Noriko Yamano Yoshitaka Kihira Yasumasa Ikeda Koichiro Tsuchiya Toshiaki Tamaki Drug Development for Cardiorenal Disease Based on Oxidative Stress Control YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN 0031-6903 134 6 715 719 20140600 24882646 yukiishizawa/published_papers/13730616 Masaki Imanishi Shuhei Tomita Keisuke Ishizawa Yoshitaka Kihira Masaki Ueno Yuki Izawa-Ishizawa Yasumasa Ikeda Noriko Yamano Koichiro Tsuchiya Toshiaki Tamaki Smooth muscle cell-specific Hif-1 alpha deficiency suppresses angiotensin II-induced vascular remodelling in mice CARDIOVASCULAR RESEARCH 1755-3245 102 3 460 468 20140600 10.1093/cvr/cvu061 24623277 yukiishizawa/published_papers/29590992 Atsushi Morimoto Shuhei Tomita Masaki Imanishi Go Shioi Yoshitaka Kihira Yuki Izawa-Ishizawa Mitsuru Takaku Ichiro Hashimoto Yasumasa Ikeda Hideki Nakanishi Toshiaki Tamaki Overexpressed HIF-2α in endothelial cells promotes vascularization and improves random pattern skin flap survival Lippincott Williams and Wilkins Plastic and Reconstructive Surgery 0032-1052 2 4 null null 20140404 10.1097/GOX.0000000000000083 2-s2.0-84897362750 yukiishizawa/published_papers/13730619 Yoshitaka Kihira 木平孝高 Mariko Miyake Manami Hirata Yoji Hoshina Kana Kato Hitoshi Shirakawa Hiroshi Sakaue 阪上浩 Noriko Yamano 山野範子 Yuki Izawa-Ishizawa 石澤有紀 Keisuke Ishizawa 石澤啓介 Yasumasa Ikeda 池田康将 Koichiro Tsuchiya 土屋浩一郎 Toshiaki Tamaki 玉置俊晃 Shuhei Tomita 冨田修平 Deletion of Hypoxia-Inducible Factor-1 alpha in Adipocytes Enhances Glucagon-Like Peptide-1 Secretion and Reduces Adipose Tissue Inflammation Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation. PLOS ONE PLoS ONE 1932-6203 9 4 e93856 e93856 20140400 10.1371/journal.pone.0093856 24705496 yukiishizawa/published_papers/13730620 Yasumasa Ikeda Iori Ozono Soichiro Tajima Mizuki Imao Yuya Horinouchi Yuki Izawa-Ishizawa Yoshitaka Kihira Licht Miyamoto Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Iron Chelation by Deferoxamine Prevents Renal Interstitial Fibrosis in Mice with Unilateral Ureteral Obstruction PLOS ONE 1932-6203 9 2 e89355 e89355 20140200 10.1371/journal.pone.0089355 24586712 yukiishizawa/published_papers/13730622 Keisuke Ishizawa Yuki Izawa-Ishizawa Noriko Yamano Maki Urushihara Takumi Sakurada Masaki Imanishi Shoko Fujii Asami Nuno Licht Miyamoto Yoshitaka Kihira Yasumasa Ikeda Shoji Kagami Hiroyuki Kobori Koichiro Tsuchiya Toshiaki Tamaki Nitrosonifedipine Ameliorates the Progression of Type 2 Diabetic Nephropathy by Exerting Antioxidative Effects PLOS ONE 1932-6203 9 1 e86335 e86335 20140100 10.1371/journal.pone.0086335 yukiishizawa/published_papers/25104934 Ikeda Y Tajima S Izawa-Ishizawa Y Kihira Y Ishizawa K Yoshida S Aihara K Tsuchiya K Tamaki T Bovine milk-derived lactoferrin exerts proangiogenic effects in an Src-Akt-eNOS-dependent manner in response to ischemia. Journal of cardiovascular pharmacology 0160-2446 61 5 423 429 20130500 10.1097/FJC.0b013e318287d526 23364610 yukiishizawa/published_papers/25104931 Yasumasa Ikeda Hideaki Enomoto Soichiro Tajima Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawa Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki Dietary iron restriction inhibits progression of diabetic nephropathy in db/db mice AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY 1931-857X 304 7 F1028 F1036 20130400 10.1152/ajprenal.00473.2012 23389454 yukiishizawa/published_papers/13730625 Takumi Sakurada Keisuke Ishizawa Masaki Imanishi Yuki Izawa-Ishizawa Shoko Fujii Erika Tominaga Teppei Tsuneishi Yuya Horinouchi Yoshitaka Kihira Yasumasa Ikeda Shuhei Tomita Ken-Ichi Aihara Kazuo Minakuchi Koichiro Tsuchiya Toshiaki Tamaki Nitrosonifedipine ameliorates angiotensin II-induced vascular remodeling via antioxidative effects Naunyn-Schmiedeberg's Archives of Pharmacology 0028-1298 386 1 29 39 20130100 10.1007/s00210-012-0810-7 23149861 2-s2.0-84872316103 yukiishizawa/published_papers/27100471 Yusaku Maeda Shuhei Tomita Masaki Murakami Hisatsugu Kurobe Masaki Imanishi Yasushi Yoshida Yoichiro Hirata Yoshitaka Kihira Yuki Ishizawa Keisuke Ishizawa Yasumasa Ikeda Koichiro Tsuchiya Tetsuya Kitagawa Masataka Sata Toshiaki Tamaki Deficiency of Hypoxia Inducible Factor-1 alpha in SM-22 alpha-Expressing Bone Marrow-Derived Cells Alleviates Neointimal Formation Following Wire-induced Vascular Injury CIRCULATION 1524-4539 126 21 null null 20121100 yukiishizawa/published_papers/13730627 Yuki Izawa-Ishizawa 石澤有紀 Keisuke Ishizawa 石澤啓介 Takumi Sakurada Masaki Imanishi Licht Miyamoto Shoko Fujii Hironori Taira Yoshitaka Kihira 木平孝高 Yasumasa Ikeda 池田康将 Shuichi Hamano 濱野修一 Shuhei Tomita 冨田修平 Koichiro Tsuchiya 土屋浩一郎 Toshiaki Tamaki 玉置俊晃 Angiotensin II receptor blocker improves tumor necrosis factor-α-induced cytotoxicity via antioxidative effect in human glomerular endothelial cells Pharmacology 0031-7012 90 5-6 324 331 20121100 10.1159/000343244 23052181 2-s2.0-84867214872 yukiishizawa/published_papers/13730628 Yasumasa Ikeda Ken-Ichi Aihara Sumiko Yoshida Takashi Iwase Soichiro Tajima Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawa Shuhei Tomita Koichiro Tsuchiya Masataka Sata Masashi Akaike Shigeaki Kato Toshio Matsumoto Toshiaki Tamaki Heparin cofactor II, a serine protease inhibitor, promotes angiogenesis via activation of the AMP-activated protein kinase-endothelial nitric-oxide synthase signaling pathway Journal of Biological Chemistry 0021-9258 287 41 34256 34263 20121005 10.1074/jbc.M112.353532 22904320 2-s2.0-84867280833 yukiishizawa/published_papers/13730629 Yasumasa Ikeda Soichiro Tajima Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawa Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki Estrogen Regulates Hepcidin Expression via GPR30-BMP6-Dependent Signaling in Hepatocytes PLOS ONE 1932-6203 7 7 e40465 e40465 20120700 10.1371/journal.pone.0040465 22792339 yukiishizawa/published_papers/25104987 Soichiro Tajima Yasumasa Ikeda Kaori Sawada Noriko Yamano Yuya Horinouchi Yoshitaka Kihira Keisuke Ishizawa Yuki Izawa-Ishizawa Kazuyoshi Kawazoe Shuhei Tomita Kazuo Minakuchi Koichiro Tsuchiya Toshiaki Tamaki Iron reduction by deferoxamine leads to amelioration of adiposity via the regulation of oxidative stress and inflammation in obese and type 2 diabetes KKAy mice AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM 0193-1849 302 1 E77 E86 20120100 10.1152/ajpendo.00033.2011 21917632 yukiishizawa/published_papers/25105745 Yasumasa Ikeda Ken-ichi Aihara Sumiko Yoshida Yoshitaka Kihira Keisuke Ishizawa Yuki Izawa-Ishizawa Shuhei Tomita Masataka Sata Masashi Akaike Shigeaki Kato Toshio Matsumoto Toshiaki Tamaki Heparin Cofactor II Promotes Angiogenesis via an AMPK-eNOS Signaling Pathway HYPERTENSION 0194-911X 58 5 E97 E97 20111100 yukiishizawa/published_papers/13730632 Yoshitaka Kihira 木平孝高 Noriko Yamano 山野範子 Yuki Izawa-Ishizawa 石澤有紀 Keisuke Ishizawa 石澤啓介 Yasumasa Ikeda 池田康将 Koichiro Tsuchiya 土屋浩一郎 Toshiaki Tamaki 玉置俊晃 Shuhei Tomita 冨田修平 Basic fibroblast growth factor regulates glucose metabolism through glucose transporter 1 induced by hypoxia-inducible factor-1α in adipocytes Hypoxia-inducible factor-1 (HIF-1), which is a transcription factor that enhances glycolysis in cells in response to hypoxia, is induced in hypertrophied adipocytes in obesity. Recent studies have shown that growth factors are able to induce HIF-1 by mechanisms independent of hypoxia. Since basic fibroblast growth factor (bFGF), an angiogenic factor, is concentrated in expanding adipose tissue, the possible effects of bFGF on regulation of HIF-1 in adipocytes were investigated. Treatment of differentiated 3T3-L1 adipocytes with bFGF induced HIF-1. Concomitantly, glucose transporter 1 (GLUT1), which is a target gene of HIF-1, was induced at both mRNA and protein levels and was translocated to the plasma membrane. A chromatin immunoprecipitation assay and an RNA interference study indicated that bFGF-induced HIF-1 directly upregulates GLUT1. In addition, it was observed that bFGF increases lactate production of adipocytes. This result indicates that bFGF reprograms the metabolism toward glycolysis. Intraperitoneal injection of bFGF into mice upregulated HIF-1 and GLUT1 in adipose tissues, suggesting that bFGF regulates the metabolism of adipocytes via HIF-1-GLUT1 regulation in vivo. We also found that bFGF inhibits insulin-induced phosphorylation of insulin receptor substrate-1 and Akt, suggesting that bFGF attenuates the insulin signal in adipocytes. Taken together, the findings suggest that bFGF has a harmful effect on the development of type 2 diabetes through metabolism reprogramming and attenuation of the insulin signal. The International Journal of Biochemistry & Cell Biology 1878-5875 43 11 1602 1611 20111100 10.1016/j.biocel.2011.07.009 21810481 yukiishizawa/published_papers/25104992 Hirotsugu Kurobe Masahisa Urata Masaki Ueno Masaaki Ueki Shiro Ono Yuki Izawa-Ishizawa Yayoi Fukuhara Yu Lei Adiratna Mat Ripen Tamotsu Kanbara Ken-ichi Aihara Keisuke Ishizawa Masashi Akaike Frank J. Gonzalez Toshiaki Tamaki Yousuke Takahama Masanori Yoshizumi Tetsuya Kitagawa Shuhei Tomita Role of Hypoxia-Inducible Factor 1 alpha in T Cells as a Negative Regulator in Development of Vascular Remodeling ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY 1524-4636 30 2 210 217 20100200 10.1161/ATVBAHA.109.192666 20007912 yukiishizawa/published_papers/25104955 Keisuke Ishizawa Yuki Izawa-Ishizawa Narantungalag Dorjsuren Erika Miki Yoshitaka Kihira Yasumasa Ikeda Shuichi Hamano Kazuyoshi Kawazoe Kazuo Minakuchi Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki Angiotensin II receptor blocker attenuates PDGF-induced mesangial cell migration in a receptor-independent manner Nephrology Dialysis Transplantation 0931-0509 25 2 364 372 20100200 10.1093/ndt/gfp520 19812233 2-s2.0-75649123444 yukiishizawa/published_papers/25104960 Motobayashi Y Izawa-Ishizawa Y Ishizawa K Orino S Yamaguchi K Kawazoe K Hamano S Tsuchiya K Tomita S Tamaki T Adiponectin inhibits insulin-like growth factor-1-induced cell migration by the suppression of extracellular signal-regulated kinase 1/2 activation, but not Akt in vascular smooth muscle cells. Hypertension research : official journal of the Japanese Society of Hypertension 0916-9636 32 3 188 193 20090300 10.1038/hr.2008.19 19262481 yukiishizawa/published_papers/13730637 Keisuke Ishizawa Yuki Izawa-Ishizawa Sachiyo Ohnishi Yuki Motobayashi Kazuyoshi Kawazoe Shuichi Hamano Koichiro Tsuchiya Shuhei Tomita Kazuo Minakuchi Toshiaki Tamaki Quercetin Glucuronide Inhibits Cell Migration and Proliferation by Platelet-Derived Growth Factor in Vascular Smooth Muscle Cells JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 109 2 257 264 20090200 10.1254/jphs.08236FP 19202317 yukiishizawa/published_papers/25104958 Keisuke Ishizawa Narantungalag Dorjsuren Yuki Izawa-Ishizawa Rika Sugimoto Yasumasa Ikeda Yoshitaka Kihira Kazuyoshi Kawazoe Shuhei Tomita Koichiro Tsuchiya Kazuo Minakuchi Toshiaki Tamaki Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration Journal of Endocrinology 0022-0795 202 2 309 316 20090000 10.1677/JOE-08-0469 19460854 2-s2.0-70349242253 yukiishizawa/published_papers/29795157 Yasuhisa Kanematsu Kunihisa Yamaguchi Hideki Ohnishi Yuki Motobayashi Keisuke Ishizawa Yuki Izawa Kazuyoshi Kawazoe Shuji Kondo Shoji Kagami Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki Dietary doses of nitrite restore circulating nitric oxide level and improve renal injury in L-NAME-induced hypertensive rats American Journal of Physiology - Renal Physiology 0363-6127 295 5 F1457 F1462 20081100 10.1152/ajprenal.00621.2007 18753302 2-s2.0-57349179059 yukiishizawa/published_papers/13730639 Yuki Izawa Masanori Yoshizumi Keisuke Ishizawa Yoshiko Fujita Shuji Kondo Shoji Kagami Kazuyoshi Kawazoe Koichiro Tsuchiya Shuhei Tomita Toshiaki Tamaki Big mitogen-activated protein kinase 1 (BMKI)/extracellular signal regulated kinase 5 (ERK5) is involved in platelet-derived growth factor (PDGF)-induced vascular smooth muscle cell migration HYPERTENSION RESEARCH 0916-9636 30 11 1107 1117 20071100 10.1291/hypres.30.1107 18250560 yukiishizawa/published_papers/13730640 Yasuhisa Kanematsu 兼松康久 Koichiro Tsuchiya 土屋浩一郎 Hideki Ohnishi 大西秀樹 Yuki Motobayashi 元林有紀 Yuki Izawa 井澤有紀 Manabu Ishihara 石原学 Keisuke Ishizawa 石澤啓介 Shinji Abe 阿部真治 Kazuyoshi Kawazoe 川添和義 Toshiaki Tamaki 玉置俊晃 Effects of angiotensin II type 1 receptor blockade on the systemic blood nitric oxide dynamics in N-omega-nitro-L-arginine methyl ester-treated rats Effects of angiotensin II type 1 receptor blockade on the systemic blood nitric oxide dynamics in Nω-nitro-L-arginine methyl ester-treated rats HYPERTENSION RESEARCH Hypertension Research 0916-9636 29 5 369 374 20060500 10.1291/hypres.29.369 16832158 yukiishizawa/published_papers/13730642 Y Fujita Y Izawa N Ali Y Kanematsu K Tsuchiya S Hamano T Tamaki M Yoshizumi Pramipexole protects against H2O2-induced PC12 cell death NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY 0028-1298 372 4 257 266 20060100 10.1007/s00210-005-0025-2 16362428 yukiishizawa/published_papers/13730643 Hiroyuki Sakakibara Kaori Ishida Yuki Izawa Yuko Minami Satomi Saito Yoshichika Kawai Veronika Butterweck Toshiaki Tamaki Yutaka Nakaya Junji Terao Effects of forced swimming stress on rat brain function Journal of Medical Investigation 1343-1420 52 Suppl. 300 301 20051100 10.2152/jmi.52.300 16366521 2-s2.0-30144437015 yukiishizawa/published_papers/13730645 Keisuke Ishizawa 石澤啓介 Yuki Izawa 井澤有紀 Hiroyuki Ito 伊藤浩敬 Chieko Miki Kayoko Miyama Yoshiko Fujita 藤田佳子 Yasuhisa Kanematsu 兼松康久 Koichiro Tsuchiya 土屋浩一郎 Toshiaki Tamaki 玉置俊晃 Akira Nishiyama 西山成 Masanori Yoshizumi 吉栖正典 Aldosterone stimulates vascular smooth muscle cell proliferation via big mitoten-activated protein kinase 1 activation The nongenomic effects of aldosterone have been implicated in the pathogenesis of various cardiovascular diseases. Aldosterone-induced nongenomic effects are attributable in part to the activation of extracellular signal-regulated kinase 1/2 (ERK1/2), a classical mitogen-activated protein (MAP) kinase. Big MAP kinase 1 (BMK1), a newly identified MAP kinase, has been shown to be involved in cell proliferation, differentiation, and survival. We examined whether aldosterone stimulates BMK1-mediated proliferation of cultured rat aortic smooth muscle cells (RASMCs). Mineralocorticoid receptor (MR) expression and localization were evaluated by Western blotting analysis and fluorolabeling methods. ERK1/2 and BMK1 activities were measured by Western blotting analysis with the respective phosphospecific antibodies. Cell proliferation was determined by Alamar Blue colorimetric assay. Aldosterone (0.1 to 100 nmol/L) dose-dependently activated BMK1 in RASMCs, with a peak at 30 minutes. To clarify whether aldosterone-induced BMK1 activation is an MR-mediated phenomenon, we examined the effect of eplerenone, a selective MR antagonist, on aldosterone-induced BMK1 activation. Eplerenone (0.1 to 10 micromol/L) dose-dependently inhibited aldosterone-induced BMK1 activation in RASMCs. Aldosterone also stimulated RASMC proliferation, which was inhibited by eplerenone. Aldosterone-mediated phenomena were concluded to be attributable to a nongenomic effect because cycloheximide failed to inhibit aldosterone-induced BMK1 activation. Transfection of dominant-negative MAP kinase/ERK kinase 5 (MEK5), which is an upstream regulator of BMK1, partially inhibited aldosterone-induced RASMC proliferation, which was almost completely inhibited by MEK inhibitor PD98059. In addition to the classical steroid activity, rapid nongenomic effects induced by aldosterone may represent an alternative etiology for vascular diseases such as hypertension. Hypertension 1524-4563 46 4 1046 1052 20050808 10.1161/01.HYP.0000172622.51973.f5 16087789 yukiishizawa/published_papers/13730646 Y Ikeda K Aihara T Sato M Akaike M Yoshizumi Y Suzaki Y Izawa M Fujimura S Hashizume M Kato S Yagi T Tamaki H Kawano T Matsumoto H Azuma S Kato T Matsumoto Androgen receptor gene knockout male mice exhibit impaired cardiac growth and exacerbation of angiotensin II-induced cardiac fibrosis JOURNAL OF BIOLOGICAL CHEMISTRY 0021-9258 280 33 29661 29666 20050800 10.1074/jbc.M411694200 15961403 yukiishizawa/published_papers/13730647 Nermin Ali Masanori Yoshizumi Yoshiko Fujita Yuki Izawa Yasuhisa Kanematsu Keisuke Ishizawa Koichiro Tsuchiya Seiji Yano Saburo Sone Toshiaki Tamaki A novel Src kinase inhibitor, M475271, inhibits VEGF-induced human umbilical vein endothelial cell proliferation and migration. Vascular endothelial growth factor (VEGF) was reported to be a potent proangiogenic factor that plays a pivotal role in both physiological and pathological angiogenesis. M475271, 4-quinazolinamine, N-(2-chloro-5-methoxyphenyl)-6-methoxy-7-[(1-methyl-4-piperidinyl) methoxy]-(9Cl), is a new anilinoquinazoline derivative that showed selective inhibition of Src kinase activity and tumor growth in vivo. Here, we examined the effect of M475271 on VEGF-induced human umbilical vein endothelial cell (HUVEC) proliferation and migration and their intracellular mechanisms. Our findings showed that M475271 pretreatment resulted in a significant inhibition of VEGF-induced HUVEC proliferation, [(3)H]thymidine incorporation, and migration. M475271 inhibited VEGF-induced Flk-1 and Src phosphorylation and their association. Confocal laser microscopic examination confirmed the inhibitory effect of M475271 on VEGF-induced Flk-1/Src association. M475271 inhibited VEGF-induced extracellular signal-regulated kinase1/2 (ERK1/2) and p38 but not Akt activation in a concentration-dependent manner. M475271, PI3-K inhibitor, and p38 inhibitor inhibited VEGF-induced HUVEC proliferation and migration. However, a MEK1/2 inhibitor inhibited VEGF-induced proliferation but not migration. These findings suggest that M475271 attenuates VEGF-induced HUVEC proliferation and migration through the inhibition of signaling pathways involving Src, ERK1/2, and/or p38. Taken together, these data indicate that M475271 may be a useful candidate for inhibition of endothelial cell proliferation and migration relevant to angiogenesis. Journal of pharmacological sciences 1347-8613 98 2 130 41 20050600 10.1254/jphs.FP0040850 15937404 yukiishizawa/published_papers/13730648 K Tsuchiya Y Kanematsu M Yoshizumi H Ohnishi K Kirima Y Izawa M Shikishima T Ishida S Kondo S Kagami Y Takiguchi T Tamaki Nitrite is an alternative source of NO in vivo AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 1522-1539 288 5 H2163 H2170 20050500 10.1152/ajpheart.00525.2004 15626692 yukiishizawa/published_papers/47984754 藤田佳子井澤有紀吉栖正典兼松康久玉置俊晃 LPCによるVEGFレセプターのtransactivation 徳島医学会四国医学雑誌 2758-3279 61 1∼2 60 60 20050400 yukiishizawa/published_papers/47984758 井澤有紀吉栖正典藤田佳子土屋浩一郎玉置俊晃血管平滑筋細胞における,アンジオテンシンIIによるERK1/2活性化を介したインスリンシグナルの抑制インスリン抵抗性の分子機構日本心脈管作動物質学会血管 2759-2286 28 1 7 7 20050100 yukiishizawa/published_papers/29709421 Masumi Okamoto Koichiro Tsuchiya Yasuhisa Kanematsu Yuki Izawa Masanori Yoshizumi Susumu Kagawa Toshiaki Tamaki Nitrite-derived nitric oxide formation following ischemia-reperfusion injury in kidney American Journal of Physiology - Renal Physiology 0363-6127 288 1 F182 F187 20050100 10.1152/ajprenal.00036.2004 15367387 2-s2.0-11144272001 yukiishizawa/published_papers/13730650 K Tsuchiya Y Takiguchi M Okamoto Y Izawa Y Kanematsu M Yoshizumi T Tamaki Malfunction of vascular control in lifestyle-related diseases: Formation of systemic hemoglobin-nitric oxide complex (HbNO) from dietary nitrite JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8648 96 4 395 400 20041200 10.1254/jphs.FMJ04006X3 15599101 yukiishizawa/published_papers/47984747 藤田佳子吉栖正典井澤有紀兼松康久土屋浩一郎玉置俊晃 LPC刺激による血管内皮細胞増殖へのVEGFレセプター(Flk-1/KDR)の関与 (NPO)日本高血圧学会日本高血圧学会総会プログラム・抄録集 27 68 68 20041000 yukiishizawa/published_papers/47984744 兼松康久土屋浩一郎藤田佳子井澤有紀吉栖正典玉置俊晃 ARB慢性投与によるL-NAME高血圧ラットの血中一酸化窒素(NO)量の増加 (NPO)日本高血圧学会日本高血圧学会総会プログラム・抄録集 27 113 113 20041000 yukiishizawa/published_papers/47984759 須崎友紀吉栖正典西山成井澤有紀兼松康久土屋浩一郎玉置俊晃糖尿病モデルラット糸球体および高血糖刺激によるラット腎メサギウム細胞におけるBMK1活性化 (公社)日本薬理学会日本薬理学雑誌 1347-8397 124 2 24P 24P 20040800 yukiishizawa/published_papers/13730652 M Kyaw M Yoshizumi K Tsuchiya Y Izawa Y Kanematsu T Tamaki Atheroprotective effects of antioxidants through inhibition of mitogen-activated protein kinases ACTA PHARMACOLOGICA SINICA 1671-4083 25 8 977 985 20040800 15301727 yukiishizawa/published_papers/13730655 M Kyaw M Yoshizumi K Tsuchiya S Kagami Y Izawa Y Fujita N Ali Y Kanematsu K Toida K Ishimura T Tamaki Src and Cas are essentially but differentially involved in angiotensin II-stimulated migration of vascular smooth muscle cells via extracellular signal-regulated kinase 1/2 and c-Jun NH2-terminal kinase activation MOLECULAR PHARMACOLOGY 0026-895X 65 4 832 841 20040400 10.1124/mol.65.4.832 15044612 yukiishizawa/published_papers/13730657 N Ali M Yoshizumi K Tsuchiya M Kyaw Y Fujita Y Izawa S Abe Y Kanematsu S Kagami T Tamaki Ebselen inhibits p38 mitogen-activated protein kinase-mediated endothelial cell death by hydrogen peroxide EUROPEAN JOURNAL OF PHARMACOLOGY 0014-2999 485 1-3 127 135 20040200 10.1016/j.ejphar.2003.11.079 14757132 yukiishizawa/published_papers/13730656 Masanori Yoshizumi 吉栖正典 Yoshiko Fujita 藤田佳子 Yuki Izawa 井澤有紀 Yuki Suzaki 須崎友紀 Moe Kyaw モーチョー Nermin Ali ネルミンアリ Koichiro Tsuchiya 土屋浩一郎 Shoji Kagami 香美祥二 Seiji Yano 矢野聖二 Saburo Sone 曽根三郎 Toshiaki Tamaki 玉置俊晃 Ebselen inhibits tumor necrosis factor-alpha-induced c-Jun N-terminal kinase activation and adhesion molecule expression in endothelial cells. Ebselen inhibits tumor necrosis factor-α-induced c-jun N-terminal kinase activation and adhesion molecule expression in endothelial cells Tumor necrosis factor-alpha (TNF-alpha) stimulates expression of endothelial cell (EC) genes that may promote atherosclerosis in part by an activation of mitogen-activated protein (MAP) kinases. Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one), a selenoorganic compound, is effective for acute ischemic stroke; however, its effect on EC has not yet been elucidated. We examined the effect of ebselen on TNF-alpha-induced MAP kinase activation and adhesion molecule expression in cultured human umbilical vein endothelial cells (HUVEC). Extracellular signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 were rapidly and significantly activated by TNF-alpha in HUVEC. TNF-alpha-induced JNK activation was inhibited by ebselen, whereas ERK1/2 and p38 were not affected. Apoptosis signal-regulated kinase 1 (ASK1) was suggested to be involved in TNF-alpha-induced JNK activation because transfection of kinase-inactive ASK1 inhibited TNF-alpha-induced JNK activation. Ebselen inhibited TNF-alpha-induced TNF receptor-associated factor 2 (TRAF2)-ASK1 complex formation and phosphorylation of stress-activated protein kinase ERK kinase 1 (SEK1), which is an upstream signaling molecule of JNK. Finally, TNF-alpha-induced activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) activation and resultant intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions were inhibited by ebselen. Specific inhibitors for JNK and NF-kappaB also inhibited TNF-alpha-induced ICAM-1 and VCAM-1 expressions in HUVEC. These findings suggest that ebselen prevents TNF-alpha-induced EC activation through the inhibition of TRAF2-ASK1-SEK1 signaling pathway, which leads to JNK activation. Inhibition of JNK by ebselen may imply its usefulness for the prevention of atherosclerosis relevant to EC activation. Experimental cell research Experimental Cell Research 0014-4827 292 1 1 10 20040101 10.1016/j.yexcr.2003.08.003 14720501 yukiishizawa/published_papers/13730654 Yuki Suzaki Masanori Yoshizumi Shoji Kagami Akira Nishiyama Yuichi Ozawa Moe Kyaw Yuki Izawa Yasuhisa Kanematsu Koichiro Tsuchiya Toshiaki Tamaki BMK1 is activated in glomeruli of diabetic rats and in mesangial cells by high glucose conditions Blackwell Publishing Inc. Kidney International 0085-2538 65 5 1749 1760 20040000 10.1111/j.1523-1755.2004.00576.x 15086914 2-s2.0-2342522648 yukiishizawa/misc/52863937 Mitsuhiro Goda Masaya Kanda Kei Kawada Atsushi Ogawa Mizusa Hyodo Kenta Yagi Fuka Aizawa Takahiro Niimura Yuki Izawa-Ishizawa Keisuke Ishizawa MATE ARE BOUND TO A MULTIPROTEIN COMPLEX CONTAINING NHE3, AND IT'S CAUSING FUNCTIONAL INTERACTIONS DRUG METABOLISM AND PHARMACOKINETICS 1880-0920 61 null null 20250600 yukiishizawa/misc/54165400 吉岡俊彦吉岡俊彦八木健太八木健太竹内大平新村貴博新村貴博相澤風花相澤風花合田光寛合田光寛川田敬川田敬石澤有紀石澤有紀滝沢宏光石澤啓介石澤啓介石澤啓介 Impact of surgical procedure on prognosis in lung cancer: a real-world data analysis 肺がん術式選択が予後に与える影響:リアルワールドデータ解析日本薬学会年会要旨集(Web) 0918-9823 145th null null 20250000 yukiishizawa/misc/54165394 新田綾香合田光寛新村貴博佐藤真希川田敬辻中海斗宮田晃志河野祐輝相澤風花石澤啓介石澤有紀新田綾香合田光寛辻中海斗相澤風花石澤啓介新村貴博八木健太石澤啓介中馬真幸川田敬石澤有紀股関節形成術の術後感染症における抗MRSA薬とリファンピシン併用の実臨床成績:診療報酬データベースを用いたレトロスペクティブ解析四国医学雑誌(Web) 2758-3279 80 5-6 null null 20250000 yukiishizawa/misc/54165376 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薗田悠平相澤風花合田光寛石澤啓介八木健太新村貴博石澤啓介川田敬石澤有紀胆汁酸製剤による多発性硬化症抑制効果の検討四国医学雑誌(Web) 2758-3279 81 1-2 null null 20250000 yukiishizawa/misc/54165371 佐川真琳八木健太八木健太高岡麻佑相澤風花相澤風花合田光寛合田光寛新村貴博新村貴博川田敬川田敬石澤有紀石澤有紀櫻田巧櫻田巧石澤啓介石澤啓介石澤啓介 Investigation of drugs that enhance the efficacy of hematopoietic stem cell pretransplantation drugs 造血幹細胞移植前処置薬の薬効を増強する薬剤の探索日本臨床腫瘍学会学術集会(CD-ROM) 22nd null null 20250000 yukiishizawa/misc/54165364 兵藤瑞紗石澤有紀石澤有紀糸数柊人宮田辰巳福岡媛乃山尾珠美相澤風花相澤風花新村貴博新村貴博堀川伊和堀川伊和八木健太八木健太川田敬川田敬合田光寛合田光寛石澤啓介石澤啓介石澤啓介大動脈疾患発症における血管内皮ERK5シグナルの役割検討日本薬理学雑誌 0015-5691 160 Supplement null null 20250000 yukiishizawa/misc/54165358 川田敬合田光寛合田光寛相澤風花新村貴博石澤有紀八木健太石澤啓介石澤啓介石澤啓介若手薬剤師とともに取り組む臨床研究~実臨床の問題解決と薬物療法の最適化~ 医療薬学フォーラム講演要旨集 1348-0863 33rd null null 20250000 yukiishizawa/misc/54165352 八木健太八木健太新村貴博新村貴博相澤風花相澤風花川田敬川田敬合田光寛合田光寛石澤有紀石澤有紀矢野貴久石澤啓介石澤啓介石澤啓介臨床・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講演要旨集 1348-0863 33rd null null 20250000 yukiishizawa/misc/54165346 相澤風花相澤風花西橋彩香薗田悠平薗田悠平谷田奨太八木健太八木健太新村貴博新村貴博山崎博輝山崎博輝合田光寛合田光寛川田敬川田敬石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介胆汁酸-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講演要旨集 1348-0863 33rd null null 20250000 yukiishizawa/misc/54165337 新村貴博新村貴博植田詩穂村川和奏奈阿部菜摘八木健太八木健太相澤風花相澤風花川田敬川田敬合田光寛合田光寛石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介 Development of a novel drug for sarcopenia utilizing medical data 医療データを用いたサルコペニア新薬の開発日本解剖学会総会・全国学術集会抄録集(CD-ROM) 130th null null 20250000 yukiishizawa/misc/54165331 相澤風花相澤風花岡林亜美新村貴博新村貴博武内香凛八木健太八木健太座間味義人合田光寛合田光寛川田敬川田敬石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介 HMG-CoA reductase inhibitors alleviate different types of chemotherapy induced-peripheral neuropathy via activation of GST HMG-CoA還元酵素阻害剤は,GSTの活性化を介して様々なタイプの化学療法誘発性末梢神経障害を軽減する日本解剖学会総会・全国学術集会抄録集(CD-ROM) 130th null null 20250000 yukiishizawa/misc/54165314 薗田悠平薗田悠平相澤風花相澤風花西橋彩香八木健太八木健太新村貴博新村貴博合田光寛合田光寛川田敬川田敬石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介多発性硬化症に対するウルソデオキシコール酸投与の影響日本薬理学雑誌 0015-5691 160 Supplement null null 20250000 yukiishizawa/misc/54165324 相澤風花相澤風花薗田悠平薗田悠平西橋彩香高橋志門八木健太八木健太新村貴博新村貴博合田光寛合田光寛川田敬石澤有紀石澤有紀石澤啓介石澤啓介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日本臨床薬理学会学術総会抄録集(Web) 2436-5580 45th null null 20240000 yukiishizawa/misc/54165319 新村貴博新村貴博植田詩穂村川和奏奈阿部菜摘八木健太八木健太相澤風花相澤風花合田光寛合田光寛石澤有紀石澤啓介石澤啓介石澤啓介糖尿病治療薬に関連した筋萎縮に関する検討日本臨床薬理学会学術総会抄録集(Web) 2436-5580 45th null null 20240000 yukiishizawa/misc/54165308 八木健太八木健太高岡麻佑佐川真琳相澤風花相澤風花新村貴博新村貴博合田光寛合田光寛川田敬川田敬石澤有紀石澤有紀石澤啓介石澤啓介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日本臨床薬理学会学術総会抄録集(Web) 2436-5580 45th null null 20240000 yukiishizawa/misc/49948969 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吉岡俊彦合田光寛神田将哉相澤風花櫻田巧桐野靖石澤啓介石澤有紀新村貴博八木健太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四国医学雑誌(Web) 2758-3279 79 5-6 null null 20240000 yukiishizawa/misc/49948961 糸数柊人宮田辰巳糸数柊人宮田晃志宮田辰巳近藤正輝相澤風花新村貴博八木健太合田光寛石澤啓介石澤有紀近藤正輝相澤風花合田光寛石澤啓介新村貴博八木健太石澤啓介川田敬杜仲葉エキスによる大動脈疾患発症抑制効果の検討四国医学雑誌(Web) 2758-3279 80 1-2 null null 20240000 yukiishizawa/misc/49948956 宮田辰巳糸数柊人福岡媛乃宮田辰巳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合田光寛石澤啓介石澤有紀辻中海斗相澤風花合田光寛石澤啓介新村貴博八木健太石澤啓介川田敬レボフロキサシンの血管炎症への影響四国医学雑誌(Web) 2758-3279 80 1-2 null null 20240000 yukiishizawa/misc/49948951 内田和志運天拡人運天拡人濱野裕章新村貴博新村貴博合田光寛合田光寛八木健太八木健太相澤風花相澤風花石澤有紀石澤有紀座間味義人石澤啓介石澤啓介石澤啓介 Development of mouse model for immune checkpoint inhibitor-related myocarditis and preventive effects of Calcitriol on model mice 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に対するカルシトリオール投与による心筋炎予防効果日本薬学会年会要旨集(Web) 0918-9823 144th null null 20240000 yukiishizawa/misc/49948925 新村貴博新村貴博合田光寛合田光寛八木健太八木健太相澤風花相澤風花石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介マクロライド系抗菌薬における心血管毒性プロファイルの網羅的解析医療薬学フォーラム講演要旨集 1348-0863 32nd null null 20240000 yukiishizawa/misc/49948920 八木健太八木健太鍛治園誠鍛治園誠丸尾陽成吉岡俊彦相澤風花相澤風花新村貴博新村貴博合田光寛合田光寛石澤有紀石澤有紀座間味義人石澤啓介石澤啓介石澤啓介医療費の削減に薬剤投与量の調整は有効性を示す医療薬学フォーラム講演要旨集 1348-0863 32nd null null 20240000 yukiishizawa/misc/49948914 石田朋奈合田光寛合田光寛神田将哉神田将哉加納菜々吉岡俊彦吉岡俊彦川田敬川田敬相澤風花相澤風花新村貴博新村貴博八木健太八木健太石澤有紀石澤有紀石澤啓介石澤啓介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プログラム・要旨集 2024 null null 20240000 yukiishizawa/misc/49948909 高岡麻佑八木健太八木健太合田光寛合田光寛相澤風花相澤風花新村貴博新村貴博川田敬川田敬石澤有紀石澤有紀石澤啓介石澤啓介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プログラム・要旨集 2024 null null 20240000 yukiishizawa/misc/49948904 新村貴博新村貴博植田詩穂村川和奏奈阿部菜摘八木健太八木健太相澤風花相澤風花合田光寛合田光寛石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介クリニカルフェノミクスによる筋萎縮抑制薬の創出次世代を担う若手のための創薬・医療薬理シンポジウムプログラム・要旨集 2024 null null 20240000 yukiishizawa/misc/49948899 神田将哉神田将哉合田光寛合田光寛石田朋奈石田俊介石田俊介櫻田巧櫻田巧坂東貴司坂東貴司川田敬川田敬相澤風花相澤風花新村貴博新村貴博八木健太八木健太石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介シスプラチン誘発腎障害の原因にアプローチする新たな予防戦略の開発日本薬理学雑誌 0015-5691 159 Supplement null null 20240000 yukiishizawa/misc/49948893 石澤有紀石澤有紀宮田晃志辻中海斗辻中海斗糸数柊人宮田辰巳近藤正輝近藤正輝新村貴博新村貴博吉岡俊彦吉岡俊彦相澤風花相澤風花八木健太八木健太川田敬合田光寛合田光寛石澤啓介石澤啓介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つの矛盾日本薬理学雑誌 0015-5691 159 Supplement null null 20240000 yukiishizawa/misc/49948888 相澤風花相澤風花岡林亜美森山大嗣八木健太八木健太新村貴博新村貴博合田光寛合田光寛石澤有紀石澤有紀川田敬川田敬石澤啓介石澤啓介石澤啓介 HMG-CoA還元酵素阻害剤はGSTを介して抗がん剤誘発性機械的刺激応答閾値低下を改善する日本薬理学雑誌 0015-5691 159 Supplement null null 20240000 yukiishizawa/misc/49948883 八木健太今若清香高岡麻佑岡本尚大岡本尚大相澤風花相澤風花新村貴博新村貴博合田光寛合田光寛川田敬川田敬石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介 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日本薬理学雑誌 0015-5691 159 Supplement null null 20240000 yukiishizawa/misc/49948878 新田綾香新田綾香合田光寛合田光寛新村貴博新村貴博佐藤真希中馬真幸宮田晃志河野祐輝川田敬石澤有紀石澤有紀八木健太八木健太相澤風花相澤風花櫻田巧櫻田巧桐野靖桐野靖石澤啓介石澤啓介石澤啓介 A comprehensive search for factors influencing the treatment of surgical site infections in orthopedic surgery 整形外科領域の手術部位感染症治療に影響を及ぼす因子の網羅的探索日本薬学会年会要旨集(Web) 0918-9823 144th null null 20240000 yukiishizawa/misc/49948871 新村貴博新村貴博植田詩穂阿部菜摘村川和奏奈八木健太八木健太相澤風花相澤風花合田光寛合田光寛石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介フェノミクス解析を用いたサルコペニア治療法の開発生体機能と創薬シンポジウム要旨集 2024 null null 20240000 yukiishizawa/misc/49949119 相澤風花相澤風花岡林亜美森山大嗣八木健太八木健太高橋志門新村貴博新村貴博合田光寛合田光寛石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介スタチンはOxaliplatinおよびPaclitaxcel誘発性末梢神経障害を改善する医療薬学フォーラム講演要旨集 1348-0863 31st null null 20230000 yukiishizawa/misc/49949113 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川田敬相澤風花八木健太石澤有紀新村貴博合田光寛石澤啓介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プログラム・要旨集 2023 null null 20230000 yukiishizawa/misc/49949107 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吉岡俊彦合田光寛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プログラム・要旨集 2023 null null 20230000 yukiishizawa/misc/49949100 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坂東寛合田光寛新村貴博相澤風花八木健太石澤有紀櫻田巧石澤啓介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次世代を担う若手のための創薬・医療薬理シンポジウムプログラム・要旨集 2023 null null 20230000 yukiishizawa/misc/49949093 今若清香八木健太岡本尚大高岡麻佑合田光寛相澤風花新村貴博石澤有紀石澤啓介八木健太岡本尚大合田光寛相澤風花新村貴博石澤啓介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プログラム・要旨集 2023 null null 20230000 yukiishizawa/misc/49949087 西穂香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石澤有紀辻中海斗吉岡俊彦近藤正輝新村貴博相澤風花八木健太合田光寛石澤啓介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プログラム・要旨集 2023 null null 20230000 yukiishizawa/misc/49949081 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運天拡人新村貴博合田光寛八木健太相澤風花石澤有紀石澤啓介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プログラム・要旨集 2023 null null 20230000 yukiishizawa/misc/49949074 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相澤風花合田光寛八木健太新村貴博石澤有紀石澤啓介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プログラム・要旨集 2023 null null 20230000 yukiishizawa/misc/49949068 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合田光寛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石澤啓介シスプラチン誘発腎障害に対するSGLT2阻害薬の影響次世代を担う若手のための創薬・医療薬理シンポジウムプログラム・要旨集 2023 null null 20230000 yukiishizawa/misc/49949063 坂東寛坂東寛合田光寛合田光寛新村貴博新村貴博新田侑生中馬真幸北川航平相澤風花相澤風花八木健太八木健太石澤有紀石澤有紀櫻田巧櫻田巧石澤啓介石澤啓介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要旨集 2023 null null 20230000 yukiishizawa/misc/49949055 吉岡俊彦吉岡俊彦合田光寛合田光寛杉本祐悟石田朋奈神田将哉神田将哉櫻田巧櫻田巧相澤風花相澤風花新村貴博新村貴博八木健太八木健太石澤有紀石澤有紀石澤啓介石澤啓介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要旨集 2023 null null 20230000 yukiishizawa/misc/49949049 新村貴博新村貴博宮田晃志八木健太八木健太相澤風花相澤風花濱野裕章濱野裕章石澤有紀石澤有紀合田光寛合田光寛座間味義人座間味義人石澤啓介石澤啓介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要旨集 2023 null null 20230000 yukiishizawa/misc/49949042 宮田晃志石澤有紀濱野裕章濱野裕章新村貴博新村貴博相澤風花相澤風花八木健太八木健太座間味義人座間味義人合田光寛合田光寛石澤啓介石澤啓介石澤啓介 Arterial Diseases Associated with Phosphodiesterase 5 Inhibitors 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年会要旨集(Web) 0918-9823 143rd null null 20230000 yukiishizawa/misc/49949035 相澤風花相澤風花岡林亜美森山大嗣八木健太八木健太合田光寛合田光寛新田綾香新田綾香新村貴博新村貴博石澤有紀石澤啓介石澤啓介石澤啓介 Investigation of the novel effect of statins for the development of supportive care to chemotherapy-induced peripheral neuropathy 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年会要旨集(Web) 0918-9823 143rd null null 20230000 yukiishizawa/misc/49949028 合田光寛合田光寛糸林小友理神田将哉神田将哉吉岡俊彦吉岡俊彦杉本祐悟石田朋奈相澤風花相澤風花新村貴博新村貴博八木健太八木健太石澤有紀櫻田巧櫻田巧桐野靖桐野靖石澤啓介石澤啓介石澤啓介 Mechanism of the prophylactic effect of sodium valproate on cisplatin-induced renal injury. 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年会要旨集(Web) 0918-9823 143rd null null 20230000 yukiishizawa/misc/49949022 八木健太八木健太高岡麻佑吉武愛哉丸尾陽成安藤里英安藤里英相澤風花相澤風花新村貴博新村貴博石澤有紀濱野裕章濱野裕章合田光寛座間味義人座間味義人石澤啓介石澤啓介石澤啓介 Effect of proton pump inhibitors and Vonoprazan on VEGF expression 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年会要旨集(Web) 0918-9823 143rd null null 20230000 yukiishizawa/misc/49949015 新村貴博新村貴博運天拡人濱野裕章濱野裕章内田和志友近七海宮田晃志合田光寛合田光寛八木健太八木健太相澤風花相澤風花石澤有紀座間味義人座間味義人石澤啓介石澤啓介石澤啓介 Development of a immune checkpoint inhibitor-related myocarditis model mouse using genome-edited mice 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年会要旨集(Web) 0918-9823 143rd null null 20230000 yukiishizawa/misc/49949008 西内栞合田光寛新村貴博生田賢治八木健太相澤風花濱野裕章座間味義人石澤啓介西内栞合田光寛生田賢治相澤風花石澤啓介新村貴博八木健太石澤啓介濱野裕章座間味義人石澤有紀ドキソルビシン誘発心筋障害の予防薬探索四国医学雑誌(Web) 2758-3279 79 1-2 null null 20230000 yukiishizawa/misc/49949001 吉岡俊彦吉岡俊彦合田光寛合田光寛糸林小友理杉本祐悟石田朋奈神田将哉神田将哉小川敦小川敦櫻田巧櫻田巧相澤風花相澤風花新村貴博新村貴博八木健太八木健太石澤有紀石澤啓介石澤啓介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効果日本薬理学雑誌 0015-5691 158 Supplement null null 20230000 yukiishizawa/misc/49948995 西穂香石澤有紀辻中海斗辻中海斗大峯航平糸数柊人宮田晃志近藤正輝近藤正輝合田光寛合田光寛新村貴博新村貴博濱野裕章濱野裕章相澤風花相澤風花八木健太八木健太座間味義人座間味義人石澤啓介石澤啓介石澤啓介抗悪性腫瘍薬スニチニブが大動脈解離発症に及ぼす影響日本薬理学雑誌 0015-5691 158 Supplement null null 20230000 yukiishizawa/misc/49948988 西内栞西内栞合田光寛合田光寛新村貴博新村貴博座間味義人座間味義人八木健太八木健太相澤風花相澤風花濱野裕章濱野裕章石澤有紀石澤啓介石澤啓介石澤啓介ビッグデータ解析を基盤としたドキソルビシン誘発心筋炎の予防薬探索日本薬理学雑誌 0015-5691 158 Supplement null null 20230000 yukiishizawa/misc/49948979 川田敬川田敬石田智滉常風興平森沢惇平相澤風花相澤風花八木健太八木健太石澤有紀石澤有紀新村貴博新村貴博阿部真治合田光寛合田光寛石澤啓介石澤啓介石澤啓介植物由来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- 日本薬理学雑誌 0015-5691 158 Supplement null null 20230000 yukiishizawa/misc/49948974 岡本尚大岡本尚大八木健太八木健太今若清香高岡麻佑國木悠理香石澤有紀石澤有紀相澤風花相澤風花新村貴博新村貴博合田光寛合田光寛石澤啓介石澤啓介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日本薬理学雑誌 0015-5691 158 Supplement null null 20230000 yukiishizawa/misc/49948930 相澤風花岡林亜美森山大嗣八木健太八木健太合田光寛合田光寛新村貴博新村貴博石澤有紀石澤有紀石澤啓介石澤啓介石澤啓介 HMG-CoA還元酵素阻害剤-GSTシグナルはオキサリプラチンおよびパクリタキセルによる神経障害を抑制する日本医療薬学会年会講演要旨集(Web) 2424-2470 33rd null null 20230000 yukiishizawa/misc/47284127 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相澤風花薗田悠平合田光寛八木健太新村貴博石澤有紀石澤啓介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プログラム・要旨集 2023 null null 20230000 yukiishizawa/misc/46011181 川田敬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相澤風花八木健太八木健太石澤有紀石澤有紀新村貴博新村貴博合田光寛合田光寛石澤啓介石澤啓介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- 日本臨床薬理学会学術総会抄録集(Web) 2436-5580 44th null null 20230000 yukiishizawa/misc/44024836 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八木健太相澤風花新村貴博合田光寛座間味義人石澤啓介石澤啓介 VEGF発現にプロトンポンプ阻害剤が与える影響日本循環薬理学会口演要旨集 32nd null null 20230000 yukiishizawa/misc/44024824 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新村貴博濱野裕章合田光寛八木健太相澤風花座間味義人石澤啓介石澤啓介 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日本循環薬理学会口演要旨集 32nd null null 20230000 yukiishizawa/misc/52526602 合田光寛神田将哉神田将哉吉岡俊彦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座間味義人石澤啓介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血管(Web) 2759-2286 45 1 null null 20220000 yukiishizawa/misc/49949320 合田光寛合田光寛吉岡俊彦吉岡俊彦神田将哉神田将哉吉田愛美糸林小友理杉本祐悟相澤風花八木健太新村貴博石澤有紀座間味義人座間味義人石澤啓介石澤啓介石澤啓介 Effect of Eucommia leaf extract on cisplatin-induced renal injury シスプラチン誘発腎障害に対する杜仲葉エキスの有用性日本杜仲研究会定期大会講演要旨集 16th null null 20220000 yukiishizawa/misc/49949314 相澤風花森山大嗣岡林亜美高橋志門薗田悠平新村貴博合田光寛合田光寛八木健太石澤有紀座間味義人石澤啓介石澤啓介 Pharmacist-Scientistが目指すDry&Wet研究によるエビデンスの創出日本緩和医療薬学会年会プログラム・要旨集 15th null null 20220000 yukiishizawa/misc/49949308 坂東貴司坂東貴司中馬真幸合田光寛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座間味義人石澤啓介石澤啓介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プログラム・要旨集 2022 null null 20220000 yukiishizawa/misc/49949301 相澤風花岡林亜美森山大嗣薗田悠平薗田悠平高橋志門高橋志門新田綾香新田綾香合田光寛合田光寛八木健太新村貴博座間味義人座間味義人石澤有紀石澤啓介石澤啓介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プログラム・要旨集 2022 null null 20220000 yukiishizawa/misc/49949295 糸林小友理合田光寛合田光寛杉本祐悟石田朋奈神田将哉神田将哉吉岡俊彦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座間味義人石澤啓介石澤啓介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プログラム・要旨集 2022 null null 20220000 yukiishizawa/misc/49949287 神田将哉合田光寛吉岡俊彦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座間味義人石澤啓介石澤啓介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プログラム・要旨集 2022 null null 20220000 yukiishizawa/misc/49949241 國木悠理香八木健太高岡麻佑岡本尚大岡本尚大濱野裕章合田光寛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石澤啓介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講演要旨集 1348-0863 30th null null 20220000 yukiishizawa/misc/49949217 大峯航平近藤正輝近藤正輝合田光寛西穂香宮田晃志辻中海斗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啓介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講演要旨集 1348-0863 30th null null 20220000 yukiishizawa/misc/49949211 阪本淑華友近七海新村貴博合田光寛合田光寛相澤風花八木健太西内栞西内栞生田賢治濱野裕章石澤有紀座間味義人石澤啓介石澤啓介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講演要旨集 1348-0863 30th null null 20220000 yukiishizawa/misc/49949196 糸林小友理合田光寛合田光寛杉本祐悟神田将哉神田将哉吉岡俊彦吉岡俊彦小川敦櫻田巧相澤風花八木健太石澤有紀座間味義人座間味義人石澤啓介石澤啓介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講演要旨集 1348-0863 30th null null 20220000 yukiishizawa/misc/49949190 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合田光寛座間味義人座間味義人石澤啓介石澤啓介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講演要旨集 1348-0863 30th null null 20220000 yukiishizawa/misc/49949154 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石澤啓介石澤啓介臨床薬理の視点で実践する創薬研究:抗がん剤有害事象とターゲットとしたトランスレーショナルリサーチ日本医療薬学会年会講演要旨集(Web) 2424-2470 32 null null 20220000 yukiishizawa/misc/49949148 山川裕介八木健太吉岡俊彦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合田光寛座間味義人石澤啓介石澤啓介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日本医療薬学会年会講演要旨集(Web) 2424-2470 32 null null 20220000 yukiishizawa/misc/49949141 八木健太丸尾陽成石田俊介鍛治園誠相澤風花新村貴博石澤有紀濱野裕章合田光寛合田光寛座間味義人座間味義人石澤啓介石澤啓介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日本医療薬学会年会講演要旨集(Web) 2424-2470 32 null null 20220000 yukiishizawa/misc/49949127 合田光寛合田光寛神田将哉神田将哉吉岡俊彦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座間味義人石澤啓介石澤啓介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日本医療薬学会年会講演要旨集(Web) 2424-2470 32 null null 20220000 yukiishizawa/misc/44024885 大峯航平近藤正輝近藤正輝合田光寛合田光寛西穂香宮田晃志辻中海斗辻中海斗濱野裕章相澤風花相澤風花八木健太座間味義人石澤啓介石澤啓介石澤有紀杜仲葉エキスによる大動脈疾患発症抑制効果の検討日本薬理学雑誌 0015-5691 157 Supplement null null 20220000 yukiishizawa/misc/44024879 安藤里英安藤里英八木健太岡本尚大岡本尚大相澤風花濱野裕章石澤有紀合田光寛合田光寛座間味義人座間味義人石澤啓介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日本薬理学雑誌 0015-5691 157 Supplement null null 20220000 yukiishizawa/misc/44024868 宮田晃志石澤有紀近藤正輝近藤正輝辻中海斗辻中海斗大峯航平西穂香糸数柊人新村貴博相澤風花相澤風花濱野裕章濱野裕章八木健太座間味義人座間味義人合田光寛合田光寛石澤啓介石澤啓介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日本薬理学雑誌 0015-5691 157 Supplement null null 20220000 yukiishizawa/misc/44024860 運天拡人濱野裕章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合田光寛八木健太相澤風花石澤有紀座間味義人座間味義人石澤啓介石澤啓介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日本薬理学雑誌 0015-5691 157 Supplement null null 20220000 yukiishizawa/misc/44024853 吉田愛美合田光寛合田光寛杉本祐悟八木田ひかり神田将哉神田将哉吉岡俊彦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座間味義人石澤啓介石澤啓介シスプラチン誘発腎障害に対する新規予防薬候補の効果日本薬理学雑誌 0015-5691 157 Supplement null null 20220000 yukiishizawa/misc/40881652 宮田晃志石澤有紀近藤正輝近藤正輝辻中海斗辻中海斗大峯航平西穂香糸数柊人新村貴博相澤風花相澤風花濱野裕章濱野裕章八木健太座間味義人座間味義人合田光寛合田光寛石澤啓介石澤啓介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プログラム・要旨集 2022 null null 20220000 yukiishizawa/misc/40881646 國木悠理香八木健太高岡麻佑岡本尚大岡本尚大濱野裕章濱野裕章相澤風花新村貴博石澤有紀合田光寛合田光寛座間味義人座間味義人石澤啓介石澤啓介石澤啓介慢性骨髄性白血病に対する既存治療薬と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プログラム・要旨集 2022 null null 20220000 yukiishizawa/misc/39100662 宮田晃志合田光寛吉岡俊彦座間味義人石澤啓介坂東寛合田光寛吉岡俊彦小川淳石澤啓介濱野裕章中馬真幸新田侑生田崎嘉一座間味義人石澤有紀有害事象自発報告データベースを活用したラモトリギンによる皮膚障害発生リスクに影響を与える因子の探索四国医学雑誌 0037-3699 78 1-2 null null 20220000 yukiishizawa/misc/35045095 座間味義人新村貴博川尻雄大合田光寛濱野裕章八木健太相澤風花小林大介島添隆雄石澤有紀楊河宏章石澤啓介医療ビッグデータを活用したドラッグリポジショニングによるオキサリプラチン誘発末梢神経障害の予防薬開発 (公財)臨床薬理研究振興財団臨床薬理の進歩 0914-4366 42 72 84 20210600 yukiishizawa/misc/35045110 相澤風花座間味義人濱野裕章石澤啓介梶本春奈森山大嗣新村貴博合田光寛八木健太石澤有紀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徳島医学会四国医学雑誌 0037-3699 77 1-2 109 109 20210400 yukiishizawa/misc/35045102 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徳島医学会四国医学雑誌 0037-3699 77 1-2 57 62 20210400 yukiishizawa/misc/35045136 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第5回病院薬剤師が実践するリバーストランスレーショナルリサーチの最前線∼臨床情報を突破口とした創薬・育薬研究∼ 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 (公社)日本薬学会日本薬学会年会要旨集 0918-9823 141 S21 3 20210300 yukiishizawa/misc/35045131 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次世代の若手研究者が切り開く薬学研究の発展と医療への貢献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 (公社)日本薬学会日本薬学会年会要旨集 0918-9823 141 GS04 6 20210300 yukiishizawa/misc/35045127 坂東貴司中馬真幸新村貴博座間味義人石澤有紀合田光寛八木健太濱野裕章岡田直人泉侑希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バンコマイシン関連腎障害に対する薬剤性腎障害原因薬剤の多剤併用における影響 (公社)日本薬学会日本薬学会年会要旨集 0918-9823 141 27V11 pm01 20210300 yukiishizawa/misc/35045120 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 (公社)日本薬学会日本薬学会年会要旨集 0918-9823 141 27P02 198S 20210300 yukiishizawa/misc/52526593 辻中海斗辻中海斗石澤有紀新村貴博新村貴博吉岡俊彦吉岡俊彦合田光寛近藤正輝近藤正輝大峯航平西穂果宮田晃志濱野裕章相澤風花八木健太座間味義人座間味義人石澤啓介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血管(Web) 2759-2286 44 1 null null 20210000 yukiishizawa/misc/49949327 石澤有紀合田光寛近藤正輝近藤正輝大峯航平西穂香辻中海斗辻中海斗武智研志相澤風花相澤風花八木健太座間味義人座間味義人石澤啓介石澤啓介 Preventive effect of Eucommia leaf extract or quercetin on the onset of aortic dissection in mice 杜仲葉エキス及び含有フラボノイドによる大動脈解離発症抑制効果の検討日本杜仲研究会定期大会講演要旨集 15th null null 20210000 yukiishizawa/misc/49949224 座間味義人座間味義人座間味義人新村貴博濱野裕章合田光寛合田光寛相澤風花八木健太石澤有紀石澤啓介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日本医療薬学会年会講演要旨集(Web) 2424-2470 31 null null 20210000 yukiishizawa/misc/49949183 相澤風花梶本春奈森山大嗣新村貴博合田光寛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座間味義人座間味義人石澤啓介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日本医療薬学会年会講演要旨集(Web) 2424-2470 31 null null 20210000 yukiishizawa/misc/49949176 神田将哉神田将哉合田光寛合田光寛吉岡俊彦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座間味義人座間味義人八木健太濱野裕章石澤有紀石澤啓介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日本医療薬学会年会講演要旨集(Web) 2424-2470 31 null null 20210000 yukiishizawa/misc/37966138 神田将哉神田将哉合田光寛合田光寛吉岡俊彦吉岡俊彦前川晃子吉田愛美中馬真幸新村貴博相澤風花八木健太濱野裕章岡田直人石澤有紀座間味義人座間味義人石澤啓介石澤啓介大規模医療情報を用いたシスプラチン誘発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プログラム・要旨集 2021 null null 20210000 yukiishizawa/misc/37966131 坂東貴司坂東貴司中馬真幸合田光寛合田光寛新村貴博石澤有紀八木健太濱野裕章岡田直人泉侑希座間味義人座間味義人石澤啓介石澤啓介バンコマイシン関連腎障害に対する薬剤性腎障害原因薬剤の多剤併用による影響次世代を担う若手のための創薬・医療薬理シンポジウムプログラム・要旨集 2021 null null 20210000 yukiishizawa/misc/37935036 西内栞西内栞斎藤広海新村貴博座間味義人座間味義人座間味義人合田光寛合田光寛八木健太相澤風花濱野裕章石澤有紀石澤啓介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日本臨床薬理学会学術総会抄録集(Web) 2436-5580 42nd null null 20210000 yukiishizawa/misc/37935030 宮田晃志坂東寛合田光寛合田光寛中馬真幸新田侑生田崎嘉一吉岡俊彦吉岡俊彦小川淳座間味義人座間味義人座間味義人濱野裕章石澤有紀石澤啓介石澤啓介ラモトリギンの皮膚障害リスクに影響する因子の探索日本臨床薬理学会学術総会抄録集(Web) 2436-5580 42nd null null 20210000 yukiishizawa/misc/37935024 宮田晃志辻中海斗辻中海斗新村貴博新村貴博吉岡俊彦吉岡俊彦近藤正輝近藤正輝大峯航平西穂果濱野裕章濱野裕章相澤風花相澤風花座間味義人座間味義人石澤啓介石澤啓介石澤有紀合田光寛八木健太血管新生阻害剤による有害事象発症の関連要因探索四国医学雑誌 0037-3699 77 5-6 null null 20210000 yukiishizawa/misc/37836807 高橋志門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座間味義人座間味義人石澤有紀石澤啓介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新規抗てんかん薬の探索日本薬理学雑誌 0015-5691 156 Supplement null null 20210000 yukiishizawa/misc/37836800 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座間味義人石澤啓介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その有用性の検討日本薬理学雑誌 0015-5691 156 Supplement null null 20210000 yukiishizawa/misc/37829877 梶本春奈森山大嗣相澤風花新村貴博座間味義人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日本薬理学雑誌 0015-5691 156 Supplement null null 20210000 yukiishizawa/misc/37644232 相澤風花梶本春奈森山大嗣新村貴博新田綾香合田光寛八木健太濱野裕章石澤有紀座間味義人座間味義人座間味義人石澤啓介石澤啓介オキサリプラチン誘発性末梢神経障害克服を目指したデータサイエンスによるアプローチ鎮痛薬・オピオイドペプチドシンポジウムプログラム・抄録集 40th null null 20210000 yukiishizawa/misc/34581236 中馬真幸座間味義人合田光寛八木健太石澤有紀濱野裕章岡田直人近藤正輝楊河宏章石澤啓介臨床現場の疑問に応える(答える)腎臓病薬物療法研究臨床現場で勤務する薬剤師の視点を生かしたトランスレーショナルリサーチ日本腎臓病薬物療法学会日本腎臓病薬物療法学会誌 2187-0411 9 S81 S81 20201100 yukiishizawa/misc/34874246 石澤啓介合田光寛中馬真幸八木健太石澤有紀座間味義人データ駆動型薬理学・臨床薬理学研究有害事象自発報告データベースを活用した抗がん剤副作用に対する予防法の探索 (一社)日本臨床薬理学会臨床薬理 1882-8272 51 Suppl. S140 S140 20201000 yukiishizawa/misc/34874241 座間味義人川尻雄大牛尾聡一郎武智研志新村貴博合田光寛八木健太中馬真幸石澤有紀楊河宏章石澤啓介多施設・多職種連携による医薬品適正使用ならびに医療費削減の推進大規模医療情報データベースを活用した有害事象軽減のための多施設共同研究 (一社)日本臨床薬理学会臨床薬理 1882-8272 51 Suppl. S191 S191 20201000 yukiishizawa/misc/34581231 腫瘍循環器学(Cardio-Oncology)研究 ∼基礎-臨床間の双方向性研究を展開するためにビッグデータ解析と基礎研究を融合した新たな研究手法による腫瘍循環器学へのアプローチ日本癌学会日本癌学会総会記事 0546-0476 79 S8 2 20201000 yukiishizawa/misc/34493284 前川晃子吉田愛美村井陽一新村貴博座間味義人石澤啓介合田光寛神田将哉濱野裕章岡田直人石澤有紀中馬真幸武智研志堀ノ内裕也池田康将シスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証徳島医学会四国医学雑誌 0037-3699 76 1-2 116 116 20200400 yukiishizawa/misc/34493257 合田光寛座間味義人新村貴博川尻雄大武智研志中馬真幸萱野純史濱野裕章岡田直人小林大介島添隆雄石澤有紀石澤啓介第4回病院薬剤師が実践するリバーストランスレーショナルリサーチの最前線 ∼臨床薬剤師の視点から新たな薬物療法を提案する∼ 医療ビッグデータ解析と基礎研究を融合したオキサリプラチン誘発末梢神経障害に対する予防薬探索 (公社)日本薬学会日本薬学会年会要旨集 0918-9823 140 S37 3 20200300 yukiishizawa/misc/49949334 座間味義人座間味義人新村貴博合田光寛八木健太相澤風花石澤有紀石澤啓介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誘発副作用に対する予防法の開発次世代を担う若手のための医療薬科学シンポジウム講演要旨集 14th null null 20200000 yukiishizawa/misc/49949274 座間味義人座間味義人新村貴博石澤有紀合田光寛濱野裕章岡田直人八木健太中馬真幸桐野靖中村敏己石澤啓介石澤啓介医療ビッグデータを活用したドラッグリポジショニング研究日本医療薬学会年会講演要旨集(Web) 2424-2470 30 null null 20200000 yukiishizawa/misc/49949258 新村貴博座間味義人座間味義人合田光寛中馬真幸八木健太福島圭穣石澤有紀藤野裕道石澤啓介石澤啓介免疫チェックポイント阻害剤関連致死的有害事象のリスク因子評価日本医療薬学会年会講演要旨集(Web) 2424-2470 30 null null 20200000 yukiishizawa/misc/37829884 新村貴博座間味義人座間味義人川尻雄大合田光寛岡田直人萱野純史八木健太中馬真幸福島圭穣石澤有紀池田康将小林大介藤野裕道島添隆雄石澤啓介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薬剤性末梢神経障害に対する予防薬の探索日本薬理学雑誌 0015-5691 155 Supplement null null 20200000 yukiishizawa/misc/37526284 神田将哉神田将哉合田光寛合田光寛吉岡俊彦吉岡俊彦吉田愛美新村貴博石澤有紀座間味義人座間味義人中馬真幸濱野裕章岡田直人池田康将桐野靖中村敏己石澤啓介石澤啓介 5-HT3受容体拮抗薬併用によるシスプラチン誘発腎機能障害に与える影響日本薬理学雑誌 0015-5691 155 Supplement null null 20200000 yukiishizawa/misc/34722060 前川晃子合田光寛吉田愛美神田将哉神田将哉生田賢治新村貴博石澤有紀座間味義人座間味義人中馬真幸武智研志濱野裕章岡田直人堀ノ内裕也池田康将石澤啓介石澤啓介大規模医療情報データベースを活用したシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証日本薬理学雑誌 0015-5691 155 Supplement null null 20200000 yukiishizawa/misc/34722027 中馬真幸座間味義人座間味義人合田光寛八木健太石澤有紀濱野裕章岡田直人近藤正輝楊河宏章石澤啓介石澤啓介ビッグデータ解析を基盤としたバンコマイシン関連腎障害予防のためのドラッグリポジショニング研究日本感染症学会西日本地方会学術集会・日本感染症学会中日本地方会学術集会・日本化学療法学会西日本支部総会合同開催プログラム・抄録集 90th-63rd-68th null null 20200000 yukiishizawa/misc/34721980 相澤風花相澤風花相澤風花相澤風花合田光寛合田光寛神田将哉神田将哉吉岡俊彦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座間味義人石澤有紀石澤啓介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日本循環薬理学会口演要旨集 30th null null 20200000 yukiishizawa/misc/29516403 吉田愛美前川晃子村井陽一新村貴博座間味義人石澤啓介合田光寛神田将哉濱野裕章岡田直人石澤有紀中馬真幸武智研志堀ノ内裕也池田康将シスプラチン誘発腎障害に対する新規予防薬の探索徳島医学会四国医学雑誌 0037-3699 75 5-6 245 246 20191200 yukiishizawa/misc/29516385 堀ノ内裕也池田康将福島圭穣今西正樹濱野裕章石澤有紀座間味義人武智研志藤野裕道石澤啓介土屋浩一郎玉置俊晃認定薬剤師の科学力を考える基礎研究と医療ビッグデータ解析を融合させたドラッグ・リボジショニングへの試み (一社)日本臨床薬理学会臨床薬理 1882-8272 50 Suppl. S176 S176 20191100 yukiishizawa/misc/29516374 合田光寛神田将哉前川晃子新村貴博石澤有紀座間味義人中馬真幸武智研志濱野裕章岡田直人福島圭穰藤野裕道土屋浩一郎堀ノ内裕也池田康将楊河宏章石澤啓介大規模医療情報データベースを活用したシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証 (一社)日本臨床薬理学会臨床薬理 1882-8272 50 Suppl. S246 S246 20191100 yukiishizawa/misc/25105139 堀ノ内裕也池田康将福島圭穣今西正樹濱野裕章石澤有紀座間味義人武智研志藤野裕道石澤啓介土屋浩一郎玉置俊晃認定薬剤師の科学力を考える基礎研究と医療ビッグデータ解析を融合させたドラッグ・リボジショニングへの試み (一社)日本臨床薬理学会臨床薬理 1882-8272 50 Suppl. S176 S176 20191100 yukiishizawa/misc/25105131 合田光寛神田将哉前川晃子新村貴博石澤有紀座間味義人中馬真幸武智研志濱野裕章岡田直人福島圭穰藤野裕道土屋浩一郎堀ノ内裕也池田康将楊河宏章石澤啓介大規模医療情報データベースを活用したシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証 (一社)日本臨床薬理学会臨床薬理 1882-8272 50 Suppl. S246 S246 20191100 yukiishizawa/misc/25105123 新村貴博座間味義人内藤優太朗川尻雄大合田光寛武智研志中馬真幸堀ノ内裕也石澤有紀池田康将石澤啓介抗がん剤誘発末梢神経障害の予防薬開発を目的とした医療ビッグデータ解析および基礎研究 (一社)日本臨床薬理学会臨床薬理 1882-8272 50 Suppl. S265 S265 20191100 yukiishizawa/misc/29516414 中馬真幸合田光寛谷友歩座間味義人武智研志石澤有紀濱野裕章石田俊介新村貴博近藤正輝坂東貴司岡田直人福島圭穣藤野裕道土屋浩一郎堀ノ内裕也池田康将楊河宏章石澤啓介ドラッグリポジショニング手法を用いたバンコマイシン関連腎障害の予防薬探索とその有用性の検討日本腎臓病薬物療法学会日本腎臓病薬物療法学会誌 2187-0411 8 S138 S138 20191000 yukiishizawa/misc/24878680 中馬真幸合田光寛谷友歩座間味義人武智研志石澤有紀濱野裕章石田俊介新村貴博近藤正輝坂東貴司岡田直人福島圭穣藤野裕道土屋浩一郎堀ノ内裕也池田康将楊河宏章石澤啓介ドラッグリポジショニング手法を用いたバンコマイシン関連腎障害の予防薬探索とその有用性の検討日本腎臓病薬物療法学会日本腎臓病薬物療法学会誌 2187-0411 8 S138 S138 20191000 yukiishizawa/misc/29516392 中馬真幸座間味義人合田光寛武智研志石澤有紀新村貴博濱野裕章近藤正輝楊河宏章石澤啓介医療ビッグデータを活用した救急薬学研究 (一社)日本救急医学会日本救急医学会雑誌 1883-3772 30 9 506 507 20190900 yukiishizawa/misc/25105170 合田光寛斉家和仁神田将哉村井陽一吉田愛美新村貴博石澤有紀座間味義人中馬真幸武智研志生田賢治濱野裕章岡田直人堀ノ内裕也池田康将桐野靖中村敏己寺岡和彦石澤啓介ビッグデータを用いたシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証 (公社)日本薬学会日本薬学会年会要旨集 0918-9823 139 4 132 132 20190300 yukiishizawa/misc/25105154 武智研志中馬真幸石田俊介坂東寛座間味義人石澤有紀堀ノ内裕也池田康将石澤啓介楊河宏章第2回領域別専門薬剤師によるclinical questionの解決手段と，薬物療法のエビデンス創出に向けて向精神薬の副作用対策を基盤とした臨床研究とその活用 (公社)日本薬学会日本薬学会年会要旨集 0918-9823 139 1 261 261 20190300 yukiishizawa/misc/25105147 近藤正輝今西正樹生藤来希村井陽一福島圭穣堀ノ内裕也石澤有紀合田光寛座間味義人武智研志中馬正幸池田康将藤野裕道土屋浩一郎石澤啓介大学院生が期待するウェットからドライな薬学研究の未来キサンチンオキシダーゼ阻害剤による新規血管線維化抑制機構の検討 (公社)日本薬学会日本薬学会年会要旨集 0918-9823 139 1 328 328 20190300 yukiishizawa/misc/40881678 座間味義人座間味義人石澤有紀新村貴博小山敏広濱野裕章岡田直人合田光寛武智研志中馬真幸堀ノ内裕也桐野靖中村敏己寺岡和彦石澤啓介石澤啓介大規模医療情報データベースを活用した周術期領域における薬剤疫学研究日本医療薬学会年会講演要旨集(Web) 2424-2470 29 null null 20190000 yukiishizawa/misc/40881669 神田将哉神田将哉合田光寛合田光寛村井陽一吉田愛美新村貴博石澤有紀座間味義人座間味義人中馬真幸濱野裕章岡田直人武智研志堀ノ内裕也池田康将桐野靖中村敏己寺岡和彦石澤啓介石澤啓介シスプラチン誘発腎障害に対する各種5-HT3受容体拮抗薬の影響日本医療薬学会年会講演要旨集(Web) 2424-2470 29 null null 20190000 yukiishizawa/misc/40881664 合田光寛合田光寛座間味義人座間味義人新村貴博川尻雄大武智研志中馬真幸萱野純史濱野裕章岡田直人小林大介島添隆雄石澤有紀桐野靖中村敏己寺岡和彦石澤啓介石澤啓介大規模医療情報データベースを活用したオキサリプラチン誘発末梢神経障害に対する予防薬探索日本医療薬学会年会講演要旨集(Web) 2424-2470 29 null null 20190000 yukiishizawa/misc/37644259 合田光寛斉家和仁神田将哉神田将哉新村貴博石澤有紀座間味義人座間味義人中馬真幸濱野裕章生田賢治岡田直人武智研志堀ノ内裕也池田康将桐野靖中村敏己寺岡和彦石澤啓介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有効性の基礎的検証日本臨床腫瘍薬学会学術大会講演要旨集 2019 null null 20190000 yukiishizawa/misc/37644242 堀ノ内裕也池田康将濱野裕章今西正樹福島圭穣石澤有紀合田光寛座間味義人座間味義人武智研志宮本理人藤野裕道石澤啓介石澤啓介土屋浩一郎玉置俊晃慢性腎不全関連サルコペニアにおける鉄代謝異常日本サルコペニア・フレイル学会誌 2433-1805 3 2 null null 20190000 yukiishizawa/misc/35048564 Zamami Yoshito 座間味義人 Izawa-Ishizawa Yuki 石澤有紀 Ikeda Yasumasa 池田康将 Kobayashi Daisuke 小林大介 Shimazoe Takao 島添隆雄 Ishizawa Keisuke 石澤啓介 Kawajiri Takehiro 川尻雄大 Niimura Takahiro 新村貴博 Goda Mitsuhiro 合田光寛 Okada Naoto 岡田直人 Hamano Hiroaki 濱野裕章 Takechi Kenshi 武智研志 Chuma Masayuki 中馬真幸 Horinouchi Yuya 堀ノ内裕也 Search for preventive drugs against anticancer drug-induced side effects using a large-scale medical information database 大規模医療情報データベースを活用した抗がん剤誘発副作用に対する予防薬の探索 Treatment outcomes of cancer patients have improved with progress in oncology medication therapy, but side effects caused by anticancer agents are becoming widespread. Side effects caused by anticancer drugs not only significantly lower the patient's QOL but also often lead to dose reduction or discontinuation of the anticancer drugs. Addressing these side effects is important for improving patient prognosis. Therefore, improvement of the quality of cancer therapy through the development of preventive drugs against anticancer drug-induced side effects is an urgent goal. In recent years, clinical research has been carried out in Japan using large-scale medical information sources such as disease/side effect databases, in order to accurately evaluate the effects of drug used in clinical practice. Research utilizing such a large-scale medical information database can cover various patient parameters and a wide range of observation areas. Therefore, this approach is suitable for conducting clinical research on rare diseases and low-frequency side effects. In this symposium, we will introduce research conducted using drug discovery tools and cell/animal experiments based on a large-scale medical information database to search for preventive agents against anticancer drug-induced side effects, as well as consider future prospects for this approach. Japanese Pharmacological Society 公益社団法人日本薬理学会 Proceedings for Annual Meeting of The Japanese Pharmacological Society 日本薬理学会年会要旨集 92 2 AS1-3 20190000 10.1254/jpssuppl.92.0_2-AS1-3 yukiishizawa/misc/34721974 Goda Mitsuhiro 合田光寛 Hamano Hirofumi 濱野裕章 Ikuta Kenji 生田賢治 Okada Naoto 岡田直人 Takechi Kenshi 武智研志 Horinouchi Yuya 堀ノ内裕也 Ikeda Yasumasa 池田康将 Ishizawa Keisuke 石澤啓介 Saike Kazuhito 斉家和仁 Kanda Masaya 神田将哉 Murai Yoichi 村井陽一 Yoshida Ami 吉田愛美 Niimura Takahiro 新村貴博 Izawa-Ishizawa Yuki 石澤有紀 Zamami Yoshito 座間味義人 Chuma Masayuki 中馬真幸 Effect of the new preventive medicine on cisplatin-induced acute kidney injury シスプラチン誘発腎障害に対する新規予防薬の有効性の検証 OBJECTIVE: Cisplatin (CDDP)-induced acute kidney injury (AKI) is highly expressed. Forced hydration and diuresis may partially prevent nephrotoxicity, but it is still difficult to completely prevent kidney injury, so establishment of a new preventive method is required. Therefore, in this study, we elected to candidates for preventive drugs of CDDP-induced AKI using big data analysis, and to verify the effectiveness of the drugs.METHODS: Using FAERS (FDA Adverse Event Reporting System), existing drugs that may reduce CDDP-induced AKI were extracted. C57BL/6 mice were intraperitoneally administered with CDDP. Renal function was evaluated by serum creatinine and blood urea nitrogen. Histological damage in the cortex of kidney sections was scored. The effect of preventive drugs for CDDP-induced nephropathy was evaluated.Results: The drug X was extracted a candidate drug suggesting the protective effect of CDDP-induced AKI by FAERS analysis. It was revealed that administration of the drug X significantly suppressed CDDP-induced AKI.Conclusions: From the results of this study, it was suggested that existing pharmaceutical products elected by FAERS could be a preventive drug for CDDP-induced AKI. Japanese Pharmacological Society 公益社団法人日本薬理学会 Proceedings for Annual Meeting of The Japanese Pharmacological Society 日本薬理学会年会要旨集 92 0 3 P-076 20190000 10.1254/jpssuppl.92.0_3-P-076 yukiishizawa/misc/29516437 堀ノ内裕也池田康将渡邉大晃濱野裕章石澤有紀今西正樹座間味義人武智研志宮本理人石澤啓介土屋浩一郎玉置俊晃マクロファージフェリチン欠損は肥満・糖尿病における脂肪炎症を抑制する日本心脈管作動物質学会血管 0911-4637 42 1 44 44 20190100 yukiishizawa/misc/29516430 合田光寛斉家和仁神田将哉村井陽一吉田愛美新村貴博石澤有紀座間味義人中馬真幸武智研志濱野裕章岡田直人堀ノ内裕也池田康将石澤啓介シスプラチン誘発腎障害に対する各種5-HT3受容体拮抗薬の影響日本心脈管作動物質学会血管 0911-4637 42 1 49 49 20190100 yukiishizawa/misc/35048542 大島啓亮池田康将堀ノ内裕也渡邉大晃濱野裕章木平孝高岸誠司石澤有紀宮本理人平山祐永澤秀子石澤啓介土屋浩一郎玉置玉置 Iron suppresses erythropoietin expression via oxidative stress-dependent hypoxia-inducible factor-2 alpha inactivation. 鉄は酸化ストレス依存的低酸素誘導因子2 α不活性化を介してエリスロポエチンの発現を抑制する 0288724X 福山大学薬学部研究年報 = Annual report of the Faculty of Pharmacy & Pharmaceutical Sciences, Fukuyama University 0288-724X 36 52 53 20181225 yukiishizawa/misc/25105177 合田光寛濱野裕章岡田直人今西正樹座間味義人桐野靖中村敏己寺岡和彦石澤啓介斉家和仁新村貴博池田康将伊勢諒石澤有紀堀ノ内裕也中馬真幸武智研志シスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証徳島医学会四国医学雑誌 0037-3699 74 5-6 219 220 20181200 yukiishizawa/misc/24878684 新村貴博座間味義人石澤有紀石澤啓介大規模医療情報・生命科学データベースを活用したドラッグリポジショニング研究日本亜鉛栄養治療研究会亜鉛栄養治療 2187-9133 9 1 15 21 20181000 yukiishizawa/misc/34721952 Yuya Horinouchi Yasumasa Ikeda Keijo Fukushima Masaki Imanishi Hirofumi Hamano Yuki Izawa-Ishizawa Yoshito Zamami Hiromichi Fujino Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Utilizing Real-World Big Data in the Search for New Renoprotective Drugs HYPERTENSION 1524-4563 72 null null 20180900 yukiishizawa/misc/25105180 堀ノ内裕也池田康将福島圭穣石澤有紀藤野裕道玉置俊晃リアルワールドデータを活用した新規腎保護薬の探索 (一社)日本腎臓学会日本腎臓学会誌 1884-0728 60 6 744 744 20180800 yukiishizawa/misc/29516444 堀ノ内裕也池田康将石澤有紀玉置俊晃福島圭穣藤野裕道濱野裕章今西正樹座間味義人石澤啓介土屋浩一郎大規模医療情報データベース解析と基礎研究の融合による新規腎保護薬の探索徳島医学会四国医学雑誌 0037-3699 74 1-2 82 83 20180400 yukiishizawa/misc/24878542 新村貴博座間味義人石澤啓介今西正樹石澤有紀堀ノ内裕也池田康将玉置俊晃武智研志福島圭穣藤野裕道土屋浩一郎大規模医療情報を活用した心肺停止患者に対するニコランジルの有効性に関する検討徳島医学会四国医学雑誌 0037-3699 74 1-2 79 80 20180400 yukiishizawa/misc/24878536 武智研志楊河宏章座間味義人今西正樹石澤啓介堀ノ内裕也石澤有紀池田康将玉置俊晃てんかん誘発性精神症状の行動学的解析および治療薬の探索と作用機序の解明徳島医学会四国医学雑誌 0037-3699 74 1-2 80 80 20180400 yukiishizawa/misc/24878530 今西正樹近藤正輝座間味義人石澤啓介田中恭平生藤来希村井陽一武智研志堀ノ内裕也石澤有紀池田康将玉置俊晃藤野裕道土屋浩一郎 Febuxostatの尿酸合成抑制作用とは独立した血管線維化抑制機構の解明徳島医学会四国医学雑誌 0037-3699 74 1-2 80 80 20180400 yukiishizawa/misc/24878523 石澤有紀岩田悠佑堀ノ内裕也池田康将玉置俊晃鍵本優有座間味義人石澤啓介今西正樹武智研志マウス大動脈瘤形成に対するケルセチンの効果徳島医学会四国医学雑誌 0037-3699 74 1-2 81 82 20180400 yukiishizawa/misc/24878516 堀ノ内裕也池田康将石澤有紀玉置俊晃福島圭穣藤野裕道濱野裕章今西正樹座間味義人石澤啓介土屋浩一郎大規模医療情報データベース解析と基礎研究の融合による新規腎保護薬の探索徳島医学会四国医学雑誌 0037-3699 74 1-2 82 83 20180400 yukiishizawa/misc/37644278 堀ノ内裕也池田康将福島圭穣今西正樹濱野裕章石澤有紀座間味義人座間味義人藤野裕道石澤啓介石澤啓介土屋浩一郎玉置俊晃大規模医療情報データベースを活用した新規腎保護薬の探索医療薬学フォーラム講演要旨集 1348-0863 26th null null 20180000 yukiishizawa/misc/35048529 斉家和仁合田光寛伊勢諒新村貴博石澤有紀座間味義人座間味義人中馬真幸濱野裕章岡田直人武智研志今西正樹今西正樹堀ノ内裕也池田康将土屋浩一郎石澤啓介石澤啓介シスプラチン誘発腎障害に対するフェノフィブラートの有効性の検証日本医療薬学会年会講演要旨集(Web) 2424-2470 28 null null 20180000 yukiishizawa/misc/35048516 堀ノ内裕也池田康将福島圭穣濱野裕章今西正樹石澤有紀座間味義人座間味義人武智研志藤野裕道石澤啓介石澤啓介土屋浩一郎玉置俊晃リアルワールドビッグデータを活用した新規腎保護薬の探索日本医療薬学会年会講演要旨集(Web) 2424-2470 28 null null 20180000 yukiishizawa/misc/35048508 合田光寛斉家和仁伊勢諒新村貴博石澤有紀座間味義人座間味義人中馬真幸濱野裕章岡田直人武智研志今西正樹今西正樹堀ノ内裕也池田康将桐野靖中村敏己寺岡和彦石澤啓介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とその有効性の検証日本医療薬学会年会講演要旨集(Web) 2424-2470 28 null null 20180000 yukiishizawa/misc/34722006 堀ノ内裕也池田康将渡邉大晃濱野裕章石澤有紀今西正樹座間味義人座間味義人武智研志宮本理人石澤啓介石澤啓介土屋浩一郎玉置俊晃マクロファージ鉄の肥満・糖尿病における役割日本鉄バイオサイエンス学会学術集会プログラム・抄録集 42nd null null 20180000 yukiishizawa/misc/24878552 新村貴博座間味義人今西正樹石澤啓介武智研志堀ノ内裕也石澤有紀池田康将玉置俊晃藤野裕道土屋浩一郎新規心肺蘇生薬の開発を目的としたドラッグリポジショニング研究大規模医療情報を活用した検討徳島医学会四国医学雑誌 0037-3699 73 5-6 323 323 20171200 yukiishizawa/misc/28028830 Yuya Horinouchi Yasumasa Ikeda Hirofumi Hamano Masaki Imanishi Yuki Izawa-Ishizawa Yoshito Zamami Kenshi Takechi Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki The Effect of Iron on Skeletal Muscle Atrophy in Chronic Kidney Disease FREE RADICAL BIOLOGY AND MEDICINE 1873-4596 112 204 205 20171100 10.1016/j.freeradbiomed.2017.10.323 yukiishizawa/misc/24878559 新村貴博座間味義人石澤有紀今西正樹武智研志福島圭穣堀ノ内裕也池田康将藤野裕道土屋浩一郎玉置俊晃石澤啓介大規模医療情報を用いて新規心肺蘇生後症候群治療薬の開発を志向したドラッグリポジショニング研究 (一社)日本臨床薬理学会臨床薬理 0388-1601 48 Suppl. S344 S344 20171100 yukiishizawa/misc/25035440 池田康将堀ノ内裕也濱野裕章濱野裕章平山祐岸誠司石澤有紀今西正樹座間味義人座間味義人武智研志宮本理人石澤啓介石澤啓介粟飯原賢一永澤秀子土屋浩一郎玉置俊晃鉄摂取制限による尿細管間質障害の抑制効果の検討日本鉄バイオサイエンス学会学術集会プログラム・抄録集 41st 40 null 20170800 yukiishizawa/misc/29516454 濱野裕章池田康将渡邉大晃堀ノ内裕也石澤有紀石澤啓介土屋浩一郎玉置俊晃インドキシル硫酸はヘプシジンを介した鉄代謝異常に関与する (一社)日本腎臓学会日本腎臓学会誌 1884-0728 59 3 321 321 20170400 yukiishizawa/misc/28031092 Hirofumi Hamano Yasumasa Ikeda Hiroaki Watanabe Yuya Horinouchi Yuki Izawa-Ishizawa Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Indoxyl Sulfate Involves Abnormality of Iron Metabolism Through Hepcidin Regulation FASEB JOURNAL 1530-6860 31 null null 20170400 yukiishizawa/misc/37644271 濱野裕章濱野裕章池田康将渡邉大晃堀ノ内裕也石澤有紀今西正樹座間味義人座間味義人武智研志石澤啓介石澤啓介土屋浩一郎玉置俊晃慢性腎臓病における尿毒素蓄積によるヘプシジン制御と鉄代謝破綻のメカニズムの解明日本鉄バイオサイエンス学会学術集会プログラム・抄録集 41st null null 20170000 yukiishizawa/misc/34722016 濱野裕章濱野裕章池田康将渡邉大晃堀ノ内裕也石澤有紀今西正樹座間味義人座間味義人武智研志石澤啓介石澤啓介土屋浩一郎玉置俊晃インドキシル硫酸蓄積はヘプシジン制御を介して鉄代謝恒常性破綻に関与する日本薬理学会近畿部会プログラム・要旨集 131st null null 20170000 yukiishizawa/misc/34721998 渡邉大晃池田康将濱野裕章濱野裕章堀ノ内裕也石澤有紀今西正樹座間味義人座間味義人武智研志宮本理人土屋浩一郎玉置俊晃石澤啓介石澤啓介肥満・糖尿病におけるマクロファージ鉄制御機構の検討日本薬理学会近畿部会プログラム・要旨集 132nd null null 20170000 yukiishizawa/misc/29516461 濱野裕章池田康将渡邉大晃堀ノ内裕也佐藤明穂大島啓亮石澤有紀石澤啓介土屋浩一郎玉置俊晃慢性腎不全における尿毒素蓄積が生体内鉄代謝に与える影響の検討日本心脈管作動物質学会血管 0911-4637 40 1 40 40 20170100 yukiishizawa/misc/28139648 Yasumasa Ikeda Keisuke Oshima Yuya Horinouchi Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki The Involvement of Iron on Erythropoietin Expression FASEB JOURNAL 1530-6860 30 null null 20160400 yukiishizawa/misc/25106942 今西正樹石澤啓介櫻田巧小原祐介戸谷紘基長尾朋子細岡真由子土屋浩一郎壱岐豊石澤有紀木平孝高池田康将玉置俊晃ニフェジピン光分解産物による血管リモデリング抑制効果四国医学雑誌 0037-3699 72 1/2 67 null 20160400 yukiishizawa/misc/34721962 Hirofumi Hamano Yasumasa Ikeda Hiroaki Watanabe Akiho Satoh Keisuke Oshima Yuya Horinouchi Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki The impact of uremic toxin on hepcidin regulation JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8648 130 3 S141 S141 20160300 yukiishizawa/misc/34721941 Akiho Satoh Yasumasa Ikeda Yuya Horinouchi Hirofumi Hamano Mizuki Imao Hiroaki Watanabe Yuki Izawa-Ishizawa Yoshitaka Kihira Licht Miyamoto Keisuke Ishizawa Koichiro Tsuchiya Yoshiaki Tamaki The impact of iron deficiency on skeleta muscle atrophy JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8648 130 3 S105 S105 20160300 yukiishizawa/misc/29516473 渡邉大晃池田康将濱野裕章佐藤明穂堀之内裕也石澤有紀木平孝高宮本理人土屋浩一郎玉置俊晃石澤啓介慢性腎臓病におけるヘプシジン制御メカニズムの検討 (公社)日本薬学会日本薬学会年会要旨集 0918-9823 136 3 67 67 20160300 yukiishizawa/misc/29516468 佐藤明穂池田康将堀ノ内裕也濱野裕章今尾瑞季渡邉大晃石澤有紀木平孝高石澤啓介玉置俊晃宮本理人土屋浩一郎鉄過剰による骨格筋分化抑制作用の解明 (公社)日本薬学会日本薬学会年会要旨集 0918-9823 136 3 70 70 20160300 yukiishizawa/misc/25106947 今西正樹石澤啓介小原佑介櫻田巧戸谷紘基長尾朋子壱岐豊細岡真由子石澤有紀木平孝高池田康将土屋浩一郎玉置俊晃ニトロソニフェジピンによる抗大動脈瘤機序の検討血管 0911-4637 39 1 41 null 20160100 yukiishizawa/misc/28357160 Yasumasa Ikeda Yusuke Kanai Yuya Horinouchi Yuki Izawa-Ishizawa Yoshitaka Kihira Licht Miyamoto Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki The Effects of Bilirubin on Angiogenesis in Mice with Hindlimb Ischemia FASEB JOURNAL 1530-6860 29 null null 20150400 yukiishizawa/misc/37644287 濱野裕章濱野裕章池田康将堀ノ内裕也堀ノ内裕也佐藤明穂渡邉大晃大島啓亮石澤有紀木平孝高石澤啓介石澤啓介土屋浩一郎玉置俊晃慢性腎不全における尿毒素によるヘプシジン制御機構日本薬理学会近畿部会プログラム・要旨集 128th null null 20150000 yukiishizawa/misc/26416073 木平孝高岸渕麗奈山口邦久石澤有紀池田康将石澤啓介冨田修平土屋浩一郎玉置俊晃腎虚血再灌流障害において低酸素誘導因子が制御する因子の探索日本薬学会年会要旨集(CD-ROM) 135th ROMBUNNO.28PB-AM190 null 20150000 yukiishizawa/misc/26416084 岸渕麗奈木平孝高山口邦久石澤有紀池田康将冨田修平土屋浩一郎玉置俊晃低酸素誘導因子の機能不全は腎虚血再潅流障害からの回復を阻害する生体膜と薬物の相互作用シンポジウム講演要旨集 0919-2131 36th 123 124 20141120 yukiishizawa/misc/28091751 K. Ishizawa Y. Kohara T. Sakurada H. Toya Y. Iki Y. Izawa-Ishizawa Y. Kihira Y. Ikeda K. Tsuchiya T. Tamaki Nitrosonifedipine ameliorates the progression of aortic aneurysms by exerting antioxidative effects EUROPEAN HEART JOURNAL 1522-9645 35 786 786 20140900 yukiishizawa/misc/25106807 小原佑介石澤啓介櫻田巧戸谷紘基長尾朋子壱岐豊石澤有紀木平孝高池田康将土屋浩一郎玉置俊晃薬剤誘導性大動脈瘤モデルに対するニトロソニフェジピンの効果日本薬理学会近畿部会プログラム・要旨集 125th 96 null 20140500 yukiishizawa/misc/28037759 Yasumasa Ikeda Soichiro Tajima Mizuki Imao Yuya Horinouchi Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Ferritin induces IL-1 beta production through inflammasome activation via NF-kappa B-dependent manner in macrophages FASEB JOURNAL 1530-6860 28 1 null null 20140400 yukiishizawa/misc/28069852 Yuki Izawa-Ishizawa Nhat-Tu Le Yuichiro Takei Kyung-Sun Heo Hakjoo Lee Alan Smrcka Benjamin Miller Kyung-Ae Ko Sara Ture Craig Morrell Keigi Fujiwara Masashi Akaike Toshiaki Tamaki Jun-ichi Abe Anti-inflammatory effects of statins and anti-malarial agents via endothelial ERK5 activation JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8648 124 86P 86P 20140000 yukiishizawa/misc/28069606 Keisuke Ishizawa Yuki Ishizawa Noriko Yamano Asami Nuno Masaki Imanishi Takumi Sakurada Yoshitaka Kihira Yasumasa Ikeda Koichiro Tsuchiya Toshiaki Tamaki Nitrosonifedipine ameliorates the progression of renal disease associated with endothelial dysfunction independently of eNOS JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8648 124 223P 223P 20140000 yukiishizawa/misc/28069344 Mizuki Imao Yasumasa Ikeda Yuya Horinouchi Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawal Koichiro Tsuchiyal Toshiaki Tamaki The mechanism of skeletal muscle atrophy induced by iron JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8648 124 196P 196P 20140000 yukiishizawa/misc/26416093 岸渕麗奈木平孝高山口邦久石澤有紀池田康将冨田修平土屋浩一郎玉置俊晃低酸素誘導因子の腎虚血再灌流障害に対する役割日本薬理学会近畿部会プログラム・要旨集 126th 39 null 20140000 yukiishizawa/misc/25106812 小原佑介石澤啓介櫻田巧戸谷紘基長尾朋子壱岐豊細岡真由子石澤有紀木平孝高池田康将土屋浩一郎玉置俊晃ニトロソニフェジピンは大動脈瘤の形成を抑制する次世代を担う創薬・医療薬理シンポジウムプログラム・要旨集 2014 81 null 20140000 yukiishizawa/misc/25105003 Masaki Imanishi 今西正樹 Keisuke Ishizawa 石澤啓介 Takumi Sakurada 櫻田巧 Yuki Ishizawa 石澤有紀 Noriko Yamano 山野範子 Yoshitaka Kihira 木平孝高 Yasumasa Ikeda 池田康将 Koichiro Tsuchiya 土屋浩一郎 Toshiaki Tamaki 玉置俊晃 Drug development for cardiorenal disease based on oxidative stress control 酸化ストレス制御を基盤とする新規心腎血管障害治療薬の開発 (公社)日本薬学会 Yakugaku Zasshi 薬学雑誌 1347-5231 134 6 715 719 20140000 10.1248/yakushi.13-00255-4 24882646 2-s2.0-84922245064 yukiishizawa/misc/28258107 Nhat-Tu Le Yuichiro Takei Yuki Izawa-Ishizawa Kyung-Sun Heo Hakjoo Lee Carolyn McClain Hannah Cushman Alan V. Smrcka Renjamin Miller Kyung Ae Ko Craig Morrell Keigi Fujiwara Masashi Akaike Jun-ichi Abe A Hmg-Coa Reductase Inhibitor (Statin) Directly Activates Endothelial Erk5 and Prevents Endothelial Dysfunction and Acute Cardiac Allograft Rejection CIRCULATION 1524-4539 128 22 null null 20131100 yukiishizawa/misc/25106817 石澤啓介山野範子石澤有紀櫻田巧今西正樹布あさ美木平孝高池田康将土屋浩一郎玉置俊晃ニトロソニフェジピンは血管内皮保護作用を示して糖尿病性腎症進展を抑制する日本腎臓学会誌 0385-2385 55 3 378 null 20130425 yukiishizawa/misc/28203754 Yasumasa Ikeda Hideaki Enomoto Soichiro Tajima Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawa Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki The effect of dietary iron restriction against diabetic nephropathy in db/db mice FASEB JOURNAL 0892-6638 27 null null 20130400 yukiishizawa/misc/25106827 石澤有紀石澤啓介山野範子櫻田巧今西正樹藤井聖子布あさ美木平孝高池田康将土屋浩一郎玉置俊晃ニトロソニフェジピンは血管内皮細胞障害を伴う糖尿病性腎症の進展を抑制する血管 0911-4637 36 1 44 null 20130131 yukiishizawa/misc/25106822 土肥紗希子石澤有紀石澤啓介櫻田巧今西正樹小原佑介長尾朋子木平孝高池田康将土屋浩一郎玉置俊晃無機リン刺激による血管平滑筋細胞石灰化におけるRho‐kinaseの関与血管 0911-4637 36 1 27 null 20130131 yukiishizawa/misc/28262766 Yuki Izawa-Ishizawa Keisuke Ishizawa Sakiko Doi Masaki Imanishi Takumi Sakurada Noriko Yamano Yusuke Kohara Tomoko Nagao Yoshitaka Kihira Yasumasa Ikeda Koichiro Tsuchiya Toshiaki Tamaki Y-27632, a rho-kinase inhibitor, inhibits inorganic phosphate-induced ERK1/2 phosphorylation and ALP activity in vascular smooth muscle cells JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 121 205P 205P 20130000 yukiishizawa/misc/28251939 Noriko Yamano Keisuke Ishizawa Shoko Fujii Asami Nuno Masaki Imanishi Takumi Sakurada Yuta Suzuki Furi Endo Yuki Ishizawa Yoshitaka Kihira Yasumasa Ikeda Koichiro Tsuchiya Toshiaki Tamaki Effects of nitrosonifedipine on the diabetic nephropathy with the endothelial dysfunction JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 121 76P 76P 20130000 yukiishizawa/misc/28237095 Mari Itoh Yoshitaka Kihira Noriko Yamano Yuki Ishizawa Keisuke Ishizawa Yasumasa Ikeda Koichiro Tsuchiya Shuhei Tomita Toshiaki Tamaki Secretion of glucagon-like peptide-1 from intestinal L cell in hypoxia JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 121 229P 229P 20130000 yukiishizawa/misc/28211478 Yoji Hoshina Yoshitaka Kihira Shuhei Tomita Mariko Miyake Noriko Yamano Yuki Ishizawa Keisuke Ishizawa Yasumasa Ikeda Koichiro Tsuchiya Toshiaki Tamaki Adipocyte-specific hypoxia-inducible factor-1alpha knockout stimulated GLP-1 and insulin secretions in mice JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 121 151P 151P 20130000 yukiishizawa/misc/25106832 今西正樹石澤啓介櫻田巧石澤有紀山野範子木平孝高池田康将土屋浩一郎玉置俊晃酸化ストレスに起因する心腎血管障害の克服を目指す新規治療薬開発日本薬学会年会要旨集(CD-ROM) 133rd ROMBUNNO.GS-1-4 null 20130000 yukiishizawa/misc/28662409 Masaki Imanishi Shuhei Tomita Keisuke Ishizawa Yoshitaka Kihira Yasumasa Ikeda Noriko Yamano Yuki Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Hypoxia-inducible Factor-1 alpha in Vascular Smooth Muscle Cells Regulates Angiotensin II-induced Vascular Remodeling and AT1 Receptor Expression in Mouse Aortic Media CIRCULATION 1524-4539 126 21 null null 20121100 yukiishizawa/misc/28634984 Yasumasa Ikeda Hideaki Enomoto Soichiro Tajima Yuki Izawa-Ishizawa Yoshitaka Kihira Keisuke Ishizawa Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki Iron Restriction Prevents the Progression of Diabetic Nephropathy in db/db Mice CIRCULATION 1524-4539 126 21 null null 20121100 yukiishizawa/misc/25106844 田島壮一郎池田康将土屋浩一郎堀ノ内裕也櫻田巧木平孝高石澤有紀石澤啓介川添和義冨田修平水口和生玉置俊晃十二指腸からの鉄吸収に対するAngiotensin IIの影響日本鉄バイオサイエンス学会学術集会プログラム・抄録集 36th 35 null 20120800 yukiishizawa/misc/25106850 藤井聖子石澤啓介櫻田巧山野範子石澤有紀今西正樹布あさ美鈴木雄太木平孝高池田康将冨田修平土屋浩一郎玉置俊晃ニフェジピン光分解産物による糖尿病性腎症進展抑制作用医療薬学フォーラム講演要旨集 1348-0863 20th 215 null 20120700 yukiishizawa/misc/25106856 石澤啓介櫻田巧今西正樹藤井聖子石澤有紀宮本理人山野範子木平孝高池田康将冨田修平土屋浩一郎玉置俊晃 Nitrosonifedipineはangiotensin II誘発のマウス血管リモデリングを改善する日本酸化ストレス学会学術集会プログラム・抄録集 65th 49 null 20120605 yukiishizawa/misc/25105112 池田康将 Tajima Soichiro Izawa-Ishizawa Yuki 2012(博慈会オープンセサミ賞) Estrogen regulates hepcidin expression via GPR30-BMP6-dependent signaling in hepatocytes (平成24年度助成研究論文) 博慈会老人病研究所未病と抗老化 : 財団法人博慈会老人病研究所紀要 1347-667X 21 0 61 68 20120600 yukiishizawa/misc/25106862 藤井聖子石澤啓介櫻田巧今西正樹石澤有紀木平孝高池田康将冨田修平土屋浩一郎玉置俊晃糖尿病モデルマウスにおいてニトロソニフェジピンは腎症の進展を抑制する日本腎臓学会誌 0385-2385 54 3 346 null 20120425 yukiishizawa/misc/28635518 Takumi Sakurada Keisuke Ishizawa Shoko Fujii Yuki Izawa-Ishizawa Masaki Imanishi Asami Nuno Yoshitaka Kihira Yasumasa Ikeda Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki Effects of nitrosonifedipine, a photodegradation product of nifedipine, on diabetic nephropathy in type II diabetic mice FASEB JOURNAL 0892-6638 26 null null 20120400 yukiishizawa/misc/25106868 布あさ美石澤啓介藤井聖子石澤有紀今西正樹櫻田巧木平孝高池田康将冨田修平土屋浩一郎玉置俊晃 2型糖尿病性腎症に対するニトロソニフェジピンの効果日本薬学会年会要旨集 0918-9823 132nd 3 116 null 20120305 yukiishizawa/misc/25106674 田島壮一郎池田康将土屋浩一郎堀ノ内裕也櫻田巧石澤有紀木平孝高石澤啓介川添和義冨田修平水口和生玉置俊晃鉄キレート剤は肥満の脂肪肥大進展を抑制する (公社)日本薬理学会日本薬理学雑誌 0015-5691 139 3 30P 30P 20120300 yukiishizawa/misc/25106874 石澤啓介藤井聖子布あさ美石澤有紀今西正樹櫻田巧木平孝高池田康将冨田修平土屋浩一郎玉置俊晃 Nitrosonifedipineは2型糖尿病モデルマウスにおける腎症進展を抑制する血管 0911-4637 35 1 56 null 20120131 yukiishizawa/misc/28667085 Noriko Yamano Yasumasa Ikeda Minoru Sakama Yuki Ishizawa Yoshitaka Kihira Keisuke Ishizawa Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki Accumulated iron storage in high fat diet-induced obese and diabetic mice JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 118 215P 215P 20120000 yukiishizawa/misc/28663071 Hideaki Enomoto Yasumasa Ikeda Soichiro Tajima Yuki Ishizawa Yoshitaka Kihira Keisuke Ishizawa Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki Protective effect of dietary iron restriction on diabetic nephropathy JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 118 247P 247P 20120000 yukiishizawa/misc/28626844 Shuhei Tomita Mitsuru Takaku Noriko Yamano Yuki Ishizawa Yoshitaka Kihira Keisuke Ishizawa Yasumasa Ikeda Koichiro Tsuchiya Toshiaki Tamaki Preoperative stabilization of HIF-1 by systemic introduction of dimethyloxalylglycine (DMOG), improves skin flap survival JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 118 86P 86P 20120000 yukiishizawa/misc/28620593 Manami Hirata Yoshitaka Kihira Mariko Miyake Yuki Izawa-Ishizawa Keisuke Ishizawa Yasumasa Ikeda Koichiro Tsuchiya Toshiaki Tamaki Shuhei Tomita High fat diet-induced inflammation in adipose tissues is reduced in adipocyte-specific hypoxia-inducible factor-1 alpha knockout mice. JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 118 71P 71P 20120000 yukiishizawa/misc/28619310 Masaki Imanishi Keisuke Ishizawa Yoshitaka Kihira Yasumasa Ikeda Noriko Yamano Yuki Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Shuhei Tomita The inhibitory effects of smooth muscle cell-specific hypoxia-inducible factor-1 alpha deficiency on angiotensin II-induced vascular remodeling in mice JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 118 77P 77P 20120000 yukiishizawa/misc/28612248 Shoko Fujii Keisuke Ishizawa Takumi Sakurada Yuki Izawa-Ishizawa Masaki Imanishi Asami Nuno Yuta Suzuki Yoshitaka Kihira Yasumasa Ikeda Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki Nitrosonifedipine prevents the progression of diabetic nephropathy in type II diabetic mice JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 118 92P 92P 20120000 yukiishizawa/misc/25106879 布あさ美石澤啓介藤井聖子櫻田巧山野範子石澤有紀今西正樹鈴木雄太木平孝高池田康将土屋浩一郎玉置俊晃糖尿病性腎症進展に対するニトロソニフェジピンの抑制作用次世代を担う創薬・医療薬理シンポジウムプログラム・要旨集 2012 67 null 20120000 yukiishizawa/misc/28341855 Yuki Ishizawa Keisuke Ishizawa Takumi Sakurada Masaki Imanishi Shoko Fujii Yoshitaka Kihira Yasumasa Ikeda Shuhei Tomita Koichiro Tsuchiya Toshiaki Tamaki Angiotensin II-Induced Vascular Remodeling Is Improved by Nitorosonifedipine, a Possible New Class Drug Against Oxidative Stress HYPERTENSION 0194-911X 58 5 E43 E44 20111100 yukiishizawa/misc/28322371 Kazuyuki Yamaguchi Yoshitaka Kihira Noriko Yamano Yuki Izawa-Ishizawa Keisuke Ishizawa Yasumasa Ikeda Koichiro Tsuchiya Shuhei Tomita Toshiaki Tamaki Glucose Metabolism of Adipocytes is Regulated by Basic Fibroblast Growth Factor Via Hypoxia-Inducible Factor-1 alpha HYPERTENSION 0194-911X 58 5 E166 E166 20111100 yukiishizawa/misc/28316792 Masaki Imanishi Keisuke Ishizawa Yoshitaka Kihira Yasumasa Ikeda Noriko Yamano Yuki Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Shuhei Tomita Smooth Muscle Cell-Specific Hypoxia-Inducible Factor-1 alpha Deficiency Attenuates Angiotensin II-Induced Vascular Remodeling in Mice CIRCULATION 0009-7322 124 21 null null 20111100 yukiishizawa/misc/28309634 Masaki Imanishi Keisuke Ishizawa Yoshitaka Kihira Yasumasa Ikeda Noriko Yamano Yuki Ishizawa Koichiro Tsuchiya Toshiaki Tamaki Shuhei Tomita Hypoxia-Inducible Factor-1 alpha Deficiency in Smooth Muscle Cells Suppresses Angiotensin II-Induced Vascular Remodeling in Mice HYPERTENSION 0194-911X 58 5 E145 E145 20111100 yukiishizawa/misc/28248072 Soichiro Tajima Yasumasa Ikeda Noriko Yamano Koichiro Tsuchiya Yuki Ishizawa Yoshitaka Kihira Keisuke Ishizawa Kazuyoshi Kawazoe Shuhei Tomita Kazuo Minakuchi Toshiaki Tamaki Inhibition of Adipocyte Hypertrophy by Deferoxamine in Diabetic KKAy Mice HYPERTENSION 0194-911X 58 5 E166 E166 20111100 yukiishizawa/misc/28300383 K. Ishizawa T. Sakurada M. Imanishi F. Fujii Y. Ishizawa Y. Kihira Y. Ikeda S. Tomita K. Tsuchiya T. Tamaki Nitorosonifedipine is a new class drug to improves angiotensin II-induced vascular remodeling EUROPEAN HEART JOURNAL 0195-668X 32 33 33 20110800 yukiishizawa/misc/25106903 櫻田巧石澤啓介今西正樹谷口順平藤井聖子布あさ美鈴木雄太石澤有紀土屋浩一郎玉置俊晃 Nitrosonifedipineによるマウス血管リモデリング抑制機構の解明次世代を担う創薬・医療薬理シンポジウムプログラム・要旨集 2011 49 null 20110000 yukiishizawa/misc/29911991 冨田修平黒部裕嗣浦田将久福原弥生石澤有紀神原保石澤啓介土屋浩一郎北川哲也吉栖正典玉置俊晃動脈硬化の病態進展におけるT細胞のHIF-1αの役割 (公社)日本薬理学会日本薬理学雑誌 1347-8397 133 3 25P 25P 20090300 yukiishizawa/misc/25109042 Yuki Motobayashi Yuki Izawa-Ishizawa Keisuke Ishizawa Sakiko Orino Kunihisa Yamaguchi Kazuyoshi Kawazoe Shuichi Hamano Koichiro Tsuchiya Shuhei Tomita Toshiaki Tamaki Adiponectin inhibits vascular smooth muscle cell migration via the suppression of extracellular signal-regulated kinase 1/2 activation, but not Akt Hypertens Res 32 188 193 20090000 10.1038/hr.2008.19 yukiishizawa/misc/26870314 Hiroyuki Sakakibara Yuki Izawa Jun-Ichiro Nakajima Shujiro Seo Toshiaki Tamaki Yoshichika Kawai Junji Terao Effects of polyphenol rich herbal medicine, ginkgo biloba extracts on neurotransmitter levels in rat brain American Chemical Society ACS Symposium Series 1947-5918 993 429 434 20080919 10.1021/bk-2008-0993.ch037 2-s2.0-84905562818 yukiishizawa/misc/41525628 ISHIZAWA Keisuke 石澤啓介 MIKI Erika 三木恵里加 IZAWA ISHIZAWA Yuki 石澤井澤 OHNISHI Hideki 有 DORJSUREN Narantungalag 大西秀樹 MOTOBAYASHI Yuki DORJSUREN Narantungalag YAMAGUCHI Kunihisa 元林有紀 TSUCHIYA Koichiro 山口邦久 TOMITA Shuhei 土屋浩一郎 TAMAKI Toshiaki 冨田修平玉置俊晃 Inhibitory effects of angiotensin II receptor blocker on PDGF-induced cell migration in rat mesangial cells PDGFによるメサンギウム細胞遊走に対するオルメサルタンの抑制効果とその分子機構血管 0911-4637 31 2 59 64 20080430 10.1093/ndt/gfp520 yukiishizawa/misc/28783110 Hirotsugu Kurobe Masahisa Urata Yuki Izawa Yayoi Fukuhara Tamotsu Kanbara Kenichi Aihara Masashi Akaike Frank Gonzalez Toshio Matsumoto Toshiaki Tamaki Tetsuya Kitagawa Masanori Yoshizumi Shuhei Tomita Hif-1 alpha in T cells pathway plays a crucial role in the progression of arteriosclerosis and artery intimal thickening CIRCULATION 0009-7322 116 16 246 246 20071000 yukiishizawa/misc/28790684 H. Kurobe M. Urata Y. Izawa Y. Fukuhara T. Kanbara K. Aihara T. Tamaki T. Matsumoto T. Kitagawa M. Yoshizumi S. Tomita HIF-1 signaling pathway plays a crucial role in the progression of atherosclerosis ATHEROSCLEROSIS SUPPLEMENTS 1567-5688 8 1 216 216 20070600 yukiishizawa/misc/28772112 Hironori Taira Keisuke Ishizawa Narantungalag Dorjsuren Yuki Izawa Erika Miki Arisa Hironaga Yuki Motobayashi Kazuyoshi Kawazoe Kazuo Minakuchi Toshiaki Tamaki RNH-6270, angiotensin II receptor blocker inhibits TNF-alpha-induced cytotoxicity in endothelial cells JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 103 78P 78P 20070000 yukiishizawa/misc/27671330 Hiroyuki Sakakibara Yuki Izawa Jun-ichiro Nakajima Shujiro Seo Toshiaki Tamaki Yoshichika Kawai Junji Terao Antidepressant effects of polyphenol rich herbal medicine, Ginkgo biloba extracts, in behavioral models ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY 0065-7727 232 275 275 20060900 yukiishizawa/misc/38448316 Kurobe Hirotsugu Izawa Yuki Fukuhara Yayoi Kanbara Tamotsu Kurushima Atsushi Aihara Ken-ichi Akaike Masashi Kano Masashi Kitaichi Takashi Masuda Yutaka Azuma Hiroyuki Tamaki Toshiaki Matsumoto Toshio Kitagawa Tetsuya Tomita Shuhei Yoshizumi Masanori OJ-211 HIF-ARNT Transcriptional System in T Cells Has a Pivotal Role in Vascular Inflammation and Remodeling(Atherosclerosis, basic-2 (H) OJ36,Oral Presentation (Japanese),The 70th Anniversary Annual Scientific Meeting of the Japanese Circulation Society) Japanese Circulation Society 社団法人日本循環器学会 Circulation journal : official journal of the Japanese Circulation Society 1346-9843 70 287 287 20060301 yukiishizawa/misc/28733227 H Kurobe Y Izawa Y Fukuhara T Kanbara K Aihara M Akaike H Azuma T Kitagawa T Tamaki T Matsumoto M Ueno S Tomita M Yoshizumi T cell-specific HIF-1alpha-deficient mice, but not ARNT-deficient mice, exhibit exacerbated inflammation and vascular remodeling in response to cuff injury CIRCULATION 0009-7322 112 17 U73 U74 20051000 yukiishizawa/misc/13730658 Yoshiko Fujita 藤田佳子 Masanori Yoshizumi 吉栖正典 Yuki Izawa 井澤有紀 Yasuhisa Kanematsu 兼松康久 Toshiaki Tamaki 玉置俊晃 Lysophosphatidylcholine(LPC)transactivates vascular endothelial growth factor(VEGF) receptor via c-Src in HUVEC ヒト臍帯静脈内皮細胞(HUVEC)における Lysophosphatidylcholine(LPC)刺激によるVEGFレセプターのトランスアクチベーション One of the major lipid components of oxidized low density lipoprotein, lysophosphatidylcholine(LPC)is involved in numerous biological processes as a bioactive lipid molecule and has beenshown to be involved in the progression of atherosclerosis. As counter-ligands, G2A and GPR4wereidentified with high binding affinity for LPC that are belonging to orphan G-protein-coupledreceptors(GPCRs)at plasma membranes. Although several GPCR ligands transactivate receptortyrosine kinases (RTKs), such as epidermal growth factor receptor, transactivation of RTK byLPC has not yet been reported. Here we observed for the first time that LPC treatment inducestyrosyl phosphorylation of vascular endothelial growth factor(VEGF)receptor2(fetal liverkinase-1/kinase-insert domain-containing receptor, Flk-1/KDR)in human umbilical vein endothelialcells(HUVEC). VEGF receptor tyrosine kinase inhibitors, SU1498and VTKi inhibited Flk-1/KDRtransactivation by LPC. Furthermore, we examined the effect of the Src family kinases inhibitors,Herbimycin A and PP2 on LPC-induced Flk-1/KDR transactivation. Herbimycin A and PP2inhibited Flk-1/KDR transactivation in HUVEC, suggesting that c-Src is involved in LPC-inducedFlk-1/KDR transactivation. Kinase-inactive(KI)Src transfection also inhibited LPC-induced Flk-1/KDR transactivation. In addition, LPC activated extracellular signal-regulated kinase1/2and Akt,which are downstream effectors of Flk-1/KDR, and these were inhibited by SU1498，VTKi,Herbimycin A, PP2and KI Src transfection in HUVEC. LPC-mediated HUVEC proliferation wasshown to be secondary to transactivation because it was suppressed by SU1498，VTKi, HerbimycinA, PP2and KI Src transfection. It is concluded that c-Src-mediated Flk-1/KDR transactivation byLPC may have important implications for the progression of atherosclerosis. 徳島医学会 Shikoku Acta Medica 四国医学雑誌 0037-3699 61 3,4 91 94 20050825 yukiishizawa/misc/28731212 Toshiaki Tamaki Masumi Okamoto Yasuhisa Kanematsu Yuki Izawa Shoji Kagami Shuji Kondo Masanori Yoshizumi Koichiro Tsuchiya DIETARY DOSE OF NITRITE ATTENUATES L-NAME-INDUCED RENAL INJURY IN RATS NEPHROLOGY 1320-5358 10 A256 A257 20050600 yukiishizawa/misc/28731150 Y Fujita M Yoshizumi N Ali Y Izawa K Tsuchiya T Tamaki Neuroprotective effect of pramipexole against H2O2-induced PC12 cell death JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 97 69P 69P 20050000 yukiishizawa/misc/28505724 Y Izawa M Yoshizumi M Kyaw S Abe H Onishi M Shikishima Y Kanematsu K Tsuchiya T Tamaki PDGF stimulates Big Mitogen-Activated Protein Kinase 1 (BMK1) in vascular smooth muscle cells JOURNAL OF PHARMACOLOGICAL SCIENCES 1347-8613 94 91P 91P 20040000 yukiishizawa/misc/47740456 吉栖正典ネルミン・アリ藤田佳子井澤有紀チョー・モー土屋浩一郎玉置俊晃酸化ストレスによる血管内皮細胞死に対するEbselenの抑制効果とその分子機構 (NPO)日本高血圧学会日本高血圧学会総会プログラム・抄録集 26 193 193 20031000 yukiishizawa/misc/28542440 M Yoshizumi Y Izawa Y Suzaki M Kyaw N Ali Y Fujita K Tsuchiya T Tamaki PDGF stimulates big mitogen-activated protein kinase 1 (BMK1) in vascular smooth muscle cells CIRCULATION 0009-7322 108 17 25 25 20031000 yukiishizawa/misc/47740464 Kyaw Moe 吉栖正典土屋浩一郎 Ali Nermin 須崎友紀石澤啓介井澤有紀玉置俊晃 Angiotensin IIによる培養ラット大動脈平滑筋細胞のmigrationにおけるSrc tyrosine kinaseとCasアダプター蛋白の役割 (公社)日本薬理学会日本薬理学雑誌 1347-8397 122 2 6P 6P 20030800 臨床薬理研究振興財団 2024年度臨床薬理研究振興財団賞学術奨励賞性差を考慮した薬物有害事象マネジメントの確立に向けたデータ駆動型臨床薬理学研究 20241200 Yuki Izawa-Ishizawa 石澤有紀 Tokushima Medical Association 徳島医学会第40回徳島医学会賞マウス大動脈瘤形成に対するケルセチンの効果 20180211 Yuki Izawa-Ishizawa 石澤有紀大越瑞穂徳島大学医学部Student Lab運営委員会医学科3年医学研究実習 2014年実験ノート/ベストインストラクター賞 20141226 Yuki Izawa-Ishizawa 石澤有紀日本循環薬理学会第24回日本循環薬理学会 Young Investigator Award 新規薬剤誘発性大動脈解離モデルを用いたスタチンの効果の検討 20141205 Yuki Izawa-Ishizawa 石澤有紀 The Japanese Pharmacological Society 日本薬理学会第87回日本薬理学会年会優秀発表賞内皮細胞におけるERK5活性化を介したスタチン・抗マラリア薬の抗炎症作用の検討 20140320 Yuki Izawa-Ishizawa 石澤有紀三木産業株式会社財団法人三木康楽会平成19年度康楽賞 20080118 Yuki Izawa 井澤有紀徳島大学医学部平成17年度岡奨学賞インスリン抵抗性および糖尿病性血管障害によるMAPキナーゼファミリーの病態生理学的意義と細胞内分子機構の解明 20060302 Yuki Izawa 井澤有紀 The Japanese Pharmacological Society 日本薬理学会第77回日本薬理学会年会優秀発表賞ラット血管平滑筋細胞においてPDGFはBig MAP Kinase 1 (BMK1)を活性化させる 20040309