Biological & pharmaceutical bulletin最新文献_第6页

Myofibroblasts Acquire Steroid Resistance via Bcl-xL in Asthmatic Lung Fibrosis. 哮喘肺纤维化中肌成纤维细胞通过Bcl-xL获得类固醇抵抗。

IF 1.7 4区医学

Biological & pharmaceutical bulletin Pub Date : 2026-01-01 DOI: 10.1248/bpb.b26-00099

Masaya Matsuda, Hayato Shimora, Hiroto Maeyama, Yuma Takatani, Yukino Nagatani, Momoka Makishima, Yuya Sannomiya, Yuichiro Kaibori, Nobuyuki Yamagishi, Osamu Kaminuma, Takeshi Nabe

{"title":"Myofibroblasts Acquire Steroid Resistance via Bcl-xL in Asthmatic Lung Fibrosis.","authors":"Masaya Matsuda, Hayato Shimora, Hiroto Maeyama, Yuma Takatani, Yukino Nagatani, Momoka Makishima, Yuya Sannomiya, Yuichiro Kaibori, Nobuyuki Yamagishi, Osamu Kaminuma, Takeshi Nabe","doi":"10.1248/bpb.b26-00099","DOIUrl":"10.1248/bpb.b26-00099","url":null,"abstract":"Severe asthma is characterized by both steroid resistance and fibrotic remodeling. We hypothesized that myofibroblasts in fibrotic lung tissue acquire glucocorticoid resistance through the upregulation of the anti-apoptotic factor B-cell lymphoma-extra large (Bcl-xL). This study aimed to determine whether myofibroblasts become steroid-resistant via Bcl-xL expression in vivo and in vitro. A steroid-resistant asthma model was developed by repeatedly challenging sensitized BALB/c mice intratracheally with a high dose of ovalbumin (OVA). Myofibroblasts were identified by flow cytometry as α-smooth muscle actin (α-SMA)+ CD31- CD45- CD326- cells. Lung mesenchymal stem cells (MSCs; platelet-derived growth factor receptor α+ CD31- CD45- CD326- cells) were isolated and differentiated into myofibroblasts by culturing them with 15% fetal bovine serum (FBS) for 6 d. In asthmatic lungs, α-SMA+ myofibroblasts showed increased Bcl-xL expression, which was unaffected by dexamethasone (DEX) treatment. However, co-treatment with the Bcl-xL inhibitor navitoclax significantly restored steroid sensitivity. In vitro, MSCs were susceptible to DEX-induced early apoptosis, whereas differentiated myofibroblasts were resistant to DEX-induced apoptosis and strongly expressed Bcl-xL. In other words, navitoclax treatment overcame steroid resistance in cultured myofibroblasts. These findings indicate that Bcl-xL-expressing myofibroblasts contribute to the development of glucocorticoid resistance in fibrotic lungs in severe asthma. Targeting Bcl-xL may provide a novel therapeutic strategy to restore steroid responsiveness in severe asthma.","PeriodicalId":8955,"journal":{"name":"Biological & pharmaceutical bulletin","volume":"49 6","pages":"919-924"},"PeriodicalIF":1.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148155058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

In Vivo and in Vitro Characterization of the Anti-inflammatory and Neuroprotective Effects of TPNA10168. TPNA10168抗炎和神经保护作用的体内外研究

IF 1.8 4区医学

Biological & pharmaceutical bulletin Pub Date : 2026-01-01 DOI: 10.1248/bpb.b25-00678

Yasuhiko Izumi, Kana Hirai, Sayuka Moro, Sonoka Inoue, Mari Nonaka, Saori Ikawa, Kouya Yamaki, Norihiko Takeda, Takahiro Yamada, Masafumi Ueda, Toshiaki Kume, Yutaka Koyama

{"title":"In Vivo and in Vitro Characterization of the Anti-inflammatory and Neuroprotective Effects of TPNA10168.","authors":"Yasuhiko Izumi, Kana Hirai, Sayuka Moro, Sonoka Inoue, Mari Nonaka, Saori Ikawa, Kouya Yamaki, Norihiko Takeda, Takahiro Yamada, Masafumi Ueda, Toshiaki Kume, Yutaka Koyama","doi":"10.1248/bpb.b25-00678","DOIUrl":"10.1248/bpb.b25-00678","url":null,"abstract":"Neuroinflammation contributes to the pathogenesis of various central nervous system disorders. TPNA10168, a novel nuclear factor erythroid 2-related factor 2 activator, exhibits neuroprotective effects in vitro and in vivo and anti-inflammatory activity in vitro. In this study, we examined the in vivo efficacy of TPNA10168 in a mouse model of systemic inflammation established by lipopolysaccharide (LPS) treatment. TPNA10168 attenuated the LPS-induced expression of several proinflammatory cytokines, such as tumor necrosis factor-α in the liver and interleukin-1β in the brain, and upregulated heme oxygenase-1 in both tissues. Although it did not suppress microglial activation in the brain, TPNA10168 reduced LPS-induced motor deficits without affecting anxiety-like or anhedonic behavior. In primary mesencephalic cultures, TPNA10168 inhibited microglial activation and nitric oxide production and protected dopaminergic neurons against LPS/interferon-γ-induced toxicity. The results suggest that TPNA10168 exerts partial anti-inflammatory effects in vivo and protects dopaminergic neurons from inflammation-induced damage in vitro, which indicates its potential as a therapeutic agent for inflammation-related neurological disorders.","PeriodicalId":8955,"journal":{"name":"Biological & pharmaceutical bulletin","volume":"49 1","pages":"201-212"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Strain-Dependent and Site-Specific Differences in Irinotecan-Induced Skin Pigmentation in Mice. 伊立替康诱导小鼠皮肤色素沉着的菌株依赖性和位点特异性差异。

IF 1.8 4区医学

Biological & pharmaceutical bulletin Pub Date : 2026-01-01 DOI: 10.1248/bpb.b26-00047

Masashi Imai, Keiichi Hiramoto, Kazuya Ooi

{"title":"Strain-Dependent and Site-Specific Differences in Irinotecan-Induced Skin Pigmentation in Mice.","authors":"Masashi Imai, Keiichi Hiramoto, Kazuya Ooi","doi":"10.1248/bpb.b26-00047","DOIUrl":"10.1248/bpb.b26-00047","url":null,"abstract":"Skin pigmentation induced by irinotecan-an anticancer drug-is clinically recognized; however, strain-dependent and skin site-specific differences in its manifestation have not been sufficiently investigated in mice. In this study, we compared melanocyte activation in plantar and genital skin following repeated irinotecan administration in three mouse strains: ICR (Slc:ICR), C57BL/6 (C57BL/6JmsSlc), and C3H (C3H/HeSlc). Melanocyte activation was assessed by 3,4-dihydroxyphenylalanine (DOPA) staining and immunofluorescence staining for microphthalmia-associated transcription factor (MITF). Although no obvious macroscopic pigmentation was observed in any strain or skin site, DOPA staining revealed an increased number of DOPA-positive cells in the plantar skin of all three mouse strains. By contrast, marked strain-dependent differences were observed in the genital skin: DOPA-positive cells were detected in ICR (Slc:ICR) and C57BL/6 (C57BL/6JmsSlc) mice but not in C3H (C3H/HeSlc) mice. MITF immunofluorescence staining results were consistent with the DOPA staining findings, demonstrating enhanced MITF signals in skin sites exhibiting melanocyte activation. Notably, the induction of DOPA-positive cells in the genital skin of albino ICR mice was an unexpected finding, suggesting that drug-induced melanocyte activation may occur independently of intrinsic melanin-producing capacity and instead involve upstream regulatory pathways. Collectively, these findings demonstrate clear strain-dependent and skin site-specific differences in irinotecan-induced melanocyte responses and provide important insights into the heterogeneity of drug-induced skin pigmentation.","PeriodicalId":8955,"journal":{"name":"Biological & pharmaceutical bulletin","volume":"49 4","pages":"720-724"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147687537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Claims-Based Identification of Urinary Tract Infections among Patients in Long-Term Care Wards: A Retrospective Validation Study. 长期护理病房患者尿路感染的基于索赔识别：一项回顾性验证研究。

IF 1.8 4区医学

Biological & pharmaceutical bulletin Pub Date : 2026-01-01 DOI: 10.1248/bpb.b25-00803

Kohei Kumagai, Ryo Inose, Asako Kimura, Yuichi Muraki

{"title":"Claims-Based Identification of Urinary Tract Infections among Patients in Long-Term Care Wards: A Retrospective Validation Study.","authors":"Kohei Kumagai, Ryo Inose, Asako Kimura, Yuichi Muraki","doi":"10.1248/bpb.b25-00803","DOIUrl":"10.1248/bpb.b25-00803","url":null,"abstract":"Claims data can be a resource for epidemiological evaluations in long-term care patients at increased risk of urinary tract infections (UTI) from antimicrobial-resistant bacteria. However, as claims data are primarily collected for administrative purposes, validating diagnostic accuracy is required. This study evaluated the validity of claims-based UTI identification in this patient population. This retrospective study included patients in long-term care wards between January 2023 and December 2024. Using diagnoses from electronic medical records as the gold standard, we evaluated the positive predictive value (PPV) of claims-based identification of UTI and catheter-associated UTI (CAUTI). Diagnoses were identified using International Classification of Diseases, 10th Revision (ICD-10) codes or urinalysis with microscopy, urine culture, antibiotic prescriptions, or indwelling bladder catheter procedures. Sensitivity analysis excluding suspected diagnoses was performed. Among 523 patients, 200 with at least one ICD-10 code for UTI were randomly selected. The PPV for identifying UTI using ICD-10 codes improved from 66.0 to 77.8% when additional codes were combined, and that for CAUTI improved from 45.5 to 86.8% with indwelling bladder catheter procedures. Excluding suspected diagnoses further improved the accuracy. Integrating ICD-10 codes, urinalysis with microscopy, urine culture, antibiotic prescriptions, and, when relevant, indwelling bladder catheter procedures while excluding suspected diagnoses enhances the validity of claims-based UTI identification and may be applicable to database studies using claims data.","PeriodicalId":8955,"journal":{"name":"Biological & pharmaceutical bulletin","volume":"49 4","pages":"738-742"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Involvement of Ca_v3.2 T-Type Ca²⁺ Channels and the Role of Endogenous Estrogen in Pruritus: Evidence from a Fundamental Study and Cross-Sectional Analysis of Pharmacy Claims Data. Cav3.2 t型Ca2+通道的参与和内源性雌激素在瘙痒症中的作用：来自基础研究和药学索赔数据横断面分析的证据

IF 1.8 4区医学

Biological & pharmaceutical bulletin Pub Date : 2026-01-01 DOI: 10.1248/bpb.b25-00671

Shotaro Kurahashi, Tomoyoshi Miyamoto, Hiroyuki Nishikawa, Emiri Mishima, Seira Matsunaga, Shiori Kino, Tomoya Ashida, Rina Minamino, Iyo Nishiyama, Maki Yamaguchi, Takashi Yamamoto, Mikio Sakakibara, Takuya Okada, Naoki Toyooka, Maho Tsubota, Fumiko Sekiguchi, Atsufumi Kawabata

{"title":"Involvement of Cav3.2 T-Type Ca2+ Channels and the Role of Endogenous Estrogen in Pruritus: Evidence from a Fundamental Study and Cross-Sectional Analysis of Pharmacy Claims Data.","authors":"Shotaro Kurahashi, Tomoyoshi Miyamoto, Hiroyuki Nishikawa, Emiri Mishima, Seira Matsunaga, Shiori Kino, Tomoya Ashida, Rina Minamino, Iyo Nishiyama, Maki Yamaguchi, Takashi Yamamoto, Mikio Sakakibara, Takuya Okada, Naoki Toyooka, Maho Tsubota, Fumiko Sekiguchi, Atsufumi Kawabata","doi":"10.1248/bpb.b25-00671","DOIUrl":"10.1248/bpb.b25-00671","url":null,"abstract":"To clarify the roles of Cav3.2 T-type Ca2+ channels and endogenous estrogen in pruritus, we conducted a fundamental study employing mice and clinical cross-sectional analyses of pharmacy claims data. In mice, intradermal injection of sulfide (Na2S), a Cav3.2 enhancer, caused itch responses, an effect blocked by KTtp38, a T-type Ca2+ channel inhibitor, and deletion of Cav3.2 gene. KTtp38 also suppressed itch responses following intradermal histamine or chloroquine. The sulfide-induced itch responses in female mice decreased by ovariectomy and/or repeated treatment with letrozole, an aromatase inhibitor. Cross-sectional analyses of pharmacy claims data of 357972 female patients aged 18 years and older, obtained from nationwide branches of a chain pharmacy group, showed significantly lower prescription rates of topical steroids used for treatment of pruritus and/or dermatitis in women 55 years and older than in women under 55 years, and in the users than non-users of estrogen suppressants. Multivariate logistic regression analysis in the users and non-users of estrogen suppressants after propensity score matching indicated significant negative association of topical steroid prescription with the use of estrogen suppressants. Together, the present fundamental and clinical studies suggest the involvement of Cav3.2 and the promotive role of estrogen in pruritus in mice and/or humans.","PeriodicalId":8955,"journal":{"name":"Biological & pharmaceutical bulletin","volume":"49 3","pages":"480-490"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Organ Crosstalk in CKD-Associated Frailty: Mechanistic Insights, Translational Opportunities, and Clinical Implications. ckd相关衰弱的器官串扰：机制见解、转化机会和临床意义。

IF 1.8 4区医学

Biological & pharmaceutical bulletin Pub Date : 2026-01-01 DOI: 10.1248/bpb.b26-00057

Hiroshi Watanabe, Yutaka Kitazato, Shu Hirashima, Yuki Enoki, Hiromasa Kato, Wataru Ochiai, Hitoshi Maeda, Motoko Tanaka, Kazutaka Matsushita, Toru Maruyama

{"title":"Organ Crosstalk in CKD-Associated Frailty: Mechanistic Insights, Translational Opportunities, and Clinical Implications.","authors":"Hiroshi Watanabe, Yutaka Kitazato, Shu Hirashima, Yuki Enoki, Hiromasa Kato, Wataru Ochiai, Hitoshi Maeda, Motoko Tanaka, Kazutaka Matsushita, Toru Maruyama","doi":"10.1248/bpb.b26-00057","DOIUrl":"10.1248/bpb.b26-00057","url":null,"abstract":"Frailty in chronic kidney disease (CKD) is increasingly recognized as a manifestation of accelerated biological aging, characterized by systemic impairments that extend beyond the musculoskeletal domain. A distinctive yet underappreciated feature of CKD-associated frailty is its triple burden-the co-existence of sarcopenia, bone fragility, and cognitive impairment. Rather than isolated phenomena, these deficits share convergent pathophysiological drivers, including uremic toxicity, oxidative stress, hormonal dysregulation, and chronic inflammation. Accumulating evidence highlights the role of organ crosstalk-particularly along the muscle-bone and muscle-brain axes-as a key integrative mechanism linking these outcomes. This review synthesizes current understanding of the epidemiology, diagnostic approaches, and mechanistic underpinnings of this multisystem condition, emphasizing skeletal muscle as a central node in a dynamic physiological network. Recent advances in biomarker development, imaging technologies, and therapeutic strategies point toward a shift from compartmentalized to network-informed care. By framing CKD-related frailty as a disorder of disrupted inter-organ communication resulting in a triple burden of decline, we propose a unified pathophysiological model to guide earlier recognition and personalized, multimodal interventions. Importantly, this perspective also calls for a critical re-evaluation of current treatment targets in CKD management to ensure alignment with the goals of frailty prevention and long-term functional preservation.","PeriodicalId":8955,"journal":{"name":"Biological & pharmaceutical bulletin","volume":"49 6","pages":"896-909"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Phenylbutyrate-Derived Nitric Oxide Donor Induces Pancreatic Cancer Cell Death Accompanied by Impairment of Autophagy-Related Pathways and HIF-1α Reduction. 苯基丁酸衍生一氧化氮供体诱导胰腺癌细胞死亡并伴随自噬相关通路损伤和HIF-1α降低。

IF 1.8 4区医学

Biological & pharmaceutical bulletin Pub Date : 2026-01-01 DOI: 10.1248/bpb.b26-00297

Kaho Takasaki, Takuro Beppu, Shuhei Imoto, Kenji Tsukigawa, Masahiro Tokuno, Masaki Otagiri, Keishi Yamasaki, Keiko Ueno-Shuto, Koji Nishi

{"title":"A Phenylbutyrate-Derived Nitric Oxide Donor Induces Pancreatic Cancer Cell Death Accompanied by Impairment of Autophagy-Related Pathways and HIF-1α Reduction.","authors":"Kaho Takasaki, Takuro Beppu, Shuhei Imoto, Kenji Tsukigawa, Masahiro Tokuno, Masaki Otagiri, Keishi Yamasaki, Keiko Ueno-Shuto, Koji Nishi","doi":"10.1248/bpb.b26-00297","DOIUrl":"https://doi.org/10.1248/bpb.b26-00297","url":null,"abstract":"4-[4-(Bis(2-(nitrooxy)ethyl)amino)phenyl]butanoic acid (NPB), a phenylbutyrate-derived nitric oxide (NO) donor, has been developed as a potential anticancer agent for pancreatic cancer. In the present study, we investigated the cytotoxic effects of NPB under cellular stress conditions and examined its effects on autophagy-related pathways and hypoxia-inducible factor-1α (HIF-1α) signaling. NPB-induced cell death was enhanced under nutrient-deprived conditions in PANC-1 cells. In addition, NPB induced greater cell death under hypoxic conditions than under normoxic conditions in PANC-1 cells, whereas in BxPC-3 cells, NPB-induced cell death was slightly but significantly lower under hypoxic conditions than under normoxic conditions. Using GFP-LC3-RFP-LC3ΔG reporter cells, NPB suppressed starvation-induced autophagic flux. In pancreatic cancer cells, NPB decreased DAPGreen fluorescence, an indicator of autophagy-related vesicular activity, and increased propidium iodide-positive cells under hypoxic conditions. Western blot analysis showed that NPB induced the accumulation of p62 and LC3 under both normoxic and hypoxic conditions. Under hypoxic conditions, NPB also reduced HIF-1α expression. Under cobalt chloride (CoCl2)-induced HIF-1α-accumulating conditions, NPB and the NO donor NONOate suppressed HIF-1α expression, whereas OH-PB, a non-NO-releasing analog, showed little effect. Furthermore, the proteasome inhibitor MG132 restored HIF-1α accumulation in NPB-treated cells. Time-course analysis under CoCl2-treated conditions showed that NPB reduced HIF-1α expression concomitantly with p62 accumulation. These findings suggest that NPB induces pancreatic cancer cell death, particularly under nutrient-deprived and hypoxic conditions, accompanied by impairment of autophagy-related pathways and NO-dependent, proteasome-associated reduction of HIF-1α.","PeriodicalId":8955,"journal":{"name":"Biological & pharmaceutical bulletin","volume":"49 7","pages":"1161-1168"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Oxidative Stress-Sensitive Ca²⁺ Channel, TRPM2, Contributes to Diabetes Progression Accompanied by ER Stress. 氧化应激敏感Ca2+通道，TRPM2，有助于糖尿病进展伴内质网应激。

IF 1.8 4区医学

Biological & pharmaceutical bulletin Pub Date : 2026-01-01 DOI: 10.1248/bpb.b26-00216

Shinichiro Yamamoto, Tomomi Ishida, Sayuri Shido, Tomohiro Numata, Shunichi Shimizu

{"title":"The Oxidative Stress-Sensitive Ca2+ Channel, TRPM2, Contributes to Diabetes Progression Accompanied by ER Stress.","authors":"Shinichiro Yamamoto, Tomomi Ishida, Sayuri Shido, Tomohiro Numata, Shunichi Shimizu","doi":"10.1248/bpb.b26-00216","DOIUrl":"https://doi.org/10.1248/bpb.b26-00216","url":null,"abstract":"Beta cell dysfunction is a critical factor contributing to decreases in insulin secretion. A growing body of evidence suggests the involvement of endoplasmic reticulum (ER) stress in beta cell dysfunction, which leads to the development of diabetes. On the other hand, oxidative stress also plays a role in the development of diabetes with beta cell dysfunction. Transient receptor potential melastatin 2 (TRPM2) is a Ca2+-permeable channel activated by oxidative stress and is highly expressed in beta cells. Some studies have claimed that Ca2+ influxes via TRPM2 in response to oxidative stress are involved in beta cell dysfunction accompanied by cell death. Although ER stress and oxidative stress form a mutually reinforcing cycle, the relationship in diabetes development between ER stress and the oxidative stress-sensitive TRP channel, TRPM2, has yet to be investigated. Therefore, we herein examined this relationship using Akita mice. Akita mice develop diabetes by ER stress-induced beta cell dysfunction accompanied by cell death. We found that increases in blood glucose in Akita mice were attenuated by the disruption of Trpm2. Additionally, in a glucose tolerance test, abnormal blood glucose increases with glucose loading in Akita mice were attenuated by the disruption of Trpm2. The results of this study using Akita mice suggest that the oxidative stress-sensitive channel, TRPM2, contributes to diabetes progression associated with ER stress.","PeriodicalId":8955,"journal":{"name":"Biological & pharmaceutical bulletin","volume":"49 7","pages":"1204-1209"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rapid Screening for Detecting Genetically Modified Wheat by Loop-Mediated Isothermal Amplification. 环介导等温扩增检测转基因小麦的快速筛选

IF 1.8 4区医学

Biological & pharmaceutical bulletin Pub Date : 2026-01-01 DOI: 10.1248/bpb.b25-00586

Shinya Kimata, Takumi Daimon, Miwa Takahashi, Kiyoko Miyatake, Yoshiki Ishida, Ken Iijima, Reona Takabatake

{"title":"Rapid Screening for Detecting Genetically Modified Wheat by Loop-Mediated Isothermal Amplification.","authors":"Shinya Kimata, Takumi Daimon, Miwa Takahashi, Kiyoko Miyatake, Yoshiki Ishida, Ken Iijima, Reona Takabatake","doi":"10.1248/bpb.b25-00586","DOIUrl":"10.1248/bpb.b25-00586","url":null,"abstract":"We developed a loop-mediated isothermal amplification (LAMP)-based detection method for screening glyphosate-tolerant genetically modified (GM) wheat by targeting nucleotide sequences of the cauliflower mosaic virus 35S promoter (P35S) and 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) from Agrobacterium tumefaciens strain CP4. LAMP products were detected using a Genie II real-time fluorometer. The limit of detection (LOD) was found to be ≤0.05% corresponding to 14 copies of target DNA. We also designed primer sets for detecting the endogenous reference sequences of wheat, proline-rich protein (PRP), and Waxy-D1. The combination of two LAMP primer sets targeting the PRP and Waxy-D1 sequences was useful for distinguishing common wheat from durum wheat. Single-stranded tag hybridization (STH) on a chromatography printed-array strip (C-PAS) system, a lateral-flow DNA chromatography technology, was used to improve efficiency. LAMP amplification was clearly detected by the STH C-PAS system at the LOD level, and duplex detection of P35S and PRP, and EPSPS and PRP was successfully achieved. This simple and quick method for screening GM wheat will be useful for preventing food and environmental contamination by unauthorized GM crops.","PeriodicalId":8955,"journal":{"name":"Biological & pharmaceutical bulletin","volume":"49 3","pages":"557-563"},"PeriodicalIF":1.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Foreword. 前言。

IF 1.8 4区医学

Biological & pharmaceutical bulletin Pub Date : 2026-01-01 DOI: 10.1248/bpb.b26-ctf4908

Kayoko Takeda Mamiya

引用次数: 0