Journal of Biomedical Research最新文献

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Upregulated inwardly rectifying K + current-mediated hypoactivity of parvalbumin interneuron underlies autism-like deficits in Bod1-deficient mice. 内向整流 K + 电流介导的副发光体中间神经元低活性上调是 Bod1 缺陷小鼠自闭症样缺陷的基础。
IF 2.2 4区 医学
Journal of Biomedical Research Pub Date : 2025-03-25 DOI: 10.7555/JBR.38.20240394
Chen Li, Kerui Wang, Xingfeng Mao, Xiuxiu Liu, Yingmei Lu
{"title":"Upregulated inwardly rectifying K <sup>+</sup> current-mediated hypoactivity of parvalbumin interneuron underlies autism-like deficits in <i>Bod1</i>-deficient mice.","authors":"Chen Li, Kerui Wang, Xingfeng Mao, Xiuxiu Liu, Yingmei Lu","doi":"10.7555/JBR.38.20240394","DOIUrl":"https://doi.org/10.7555/JBR.38.20240394","url":null,"abstract":"<p><p>Parvalbumin-positive (PV <sup>+</sup>) interneuron dysfunction is believed to be linked to autism spectrum disorder (ASD), a neurodevelopmental disorder, characterized by social deficits and stereotypical behaviors. However, the underlying mechanisms of PV <sup>+</sup> interneuron dysfunction remain largely unclear. Here, we found that a deficiency of biorientation defective 1 ( <i>Bod1</i>) in PV <sup>+</sup> interneuron led to an ASD-like phenotype in <i>Pvalb-Cre</i>; <i>Bod1</i> <sup><i>f/f</i></sup> mice. Mechanistically, we identified that <i>Bod1</i> deficiency induced hypoactivity of PV <sup>+</sup> interneuron and hyperactivity of calcium/calmodulin-dependent protein kinase Ⅱ alpha (CaMKⅡα) neurons in the medial prefrontal cortex (mPFC), as determined by whole-cell patch-clamp recording. Additionally, it concurrently decreased the power of high gamma oscillation, as assessed by <i>in vivo</i> multi-channel electrophysiological recording. Furthermore, we found that <i>Bod1</i> deficiency enhanced inwardly rectifying K <sup>+</sup> current, leading to an increase in the resting membrane potential of PV <sup>+</sup> interneurons. Importantly, the gain-of-function of <i>Bod1</i> improved social deficits and stereotypical behaviors in <i>Pvalb-Cre</i>; <i>Bod1</i> <sup><i>f/f</i></sup> mice. These findings provide mechanistic insights into the PV <sup>+</sup> interneuron dysfunction and suggest new strategies for developing PV <sup>+</sup> interneuron therapies for ASD.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-13"},"PeriodicalIF":2.2,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752769","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
Molecular pathways in cardiovascular disease under hypoxia: Mechanisms, biomarkers, and therapeutic targets.
IF 2.2 4区 医学
Journal of Biomedical Research Pub Date : 2025-03-20 DOI: 10.7555/JBR.38.20240387
Izzatullo Ziyoyiddin O G Li Abdullaev, Ulugbek Gapparjanovich Gayibov, Sirojiddin Zoirovich Omonturdiev, Sobirova Fotima Azamjonovna, Sabina Narimanovna Gayibova, Takhir Fatikhovich Aripov
{"title":"Molecular pathways in cardiovascular disease under hypoxia: Mechanisms, biomarkers, and therapeutic targets.","authors":"Izzatullo Ziyoyiddin O G Li Abdullaev, Ulugbek Gapparjanovich Gayibov, Sirojiddin Zoirovich Omonturdiev, Sobirova Fotima Azamjonovna, Sabina Narimanovna Gayibova, Takhir Fatikhovich Aripov","doi":"10.7555/JBR.38.20240387","DOIUrl":"https://doi.org/10.7555/JBR.38.20240387","url":null,"abstract":"<p><p>Chronic hypoxia is a key factor in the pathogenesis of cardiovascular diseases, including ischemia, heart failure, and hypertension. Under hypoxic conditions, oxygen deficiency disrupts oxidative phosphorylation in mitochondria, impairing ATP production and generating reactive oxygen species (ROS). These reactive species induce mitochondrial dysfunction, leading to oxidative stress, calcium imbalance, and activation of apoptosis pathways. Mitochondrial K-ATP (mitoK-ATP) and mitochondrial permeability transition pore (mPTP) channels are particularly affected, contributing to membrane potential loss, cytochrome C release, and cell death. This review explores the molecular mechanisms underlying hypoxia-induced cardiovascular diseases, with a focus on mitochondrial impairment, ion channel dysfunction, and ROS overproduction. Additionally, we examine hypoxia-inducible factor 1-alpha (HIF-1α) as a biomarker of cellular adaptation and discuss therapeutic strategies targeting mitochondrial function and oxidative stress. Antioxidants and compounds modulating key ion channels, such as K-ATP and mPTP, are highlighted as promising interventions for mitigating hypoxia-induced damage. Furthermore, we emphasize the potential of integrating <i>in vitro</i>, <i>in vivo</i>, and <i>in silico</i> studies to develop novel therapies aimed at preserving mitochondrial integrity and preventing cardiovascular diseases.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-16"},"PeriodicalIF":2.2,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692233","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
Bidirectional Mendelian randomization and mediation analysis of million-scale data reveal causal relationships between thyroid-related phenotypes, smoking, and lung cancer.
IF 2.2 4区 医学
Journal of Biomedical Research Pub Date : 2025-02-25 DOI: 10.7555/JBR.38.20240421
Xiang Wang, Xuan Wang, Mengsheng Zhao, Lijuan Lin, Yi Li, Ning Xie, Yanru Wang, Aoxuan Wang, Xiaowen Xu, Can Ju, Qiuyuan Chen, Jiajin Chen, Ruili Hou, Zhongwen Zhang, David C Christiani, Feng Chen, Yongyue Wei, Ruyang Zhang
{"title":"Bidirectional Mendelian randomization and mediation analysis of million-scale data reveal causal relationships between thyroid-related phenotypes, smoking, and lung cancer.","authors":"Xiang Wang, Xuan Wang, Mengsheng Zhao, Lijuan Lin, Yi Li, Ning Xie, Yanru Wang, Aoxuan Wang, Xiaowen Xu, Can Ju, Qiuyuan Chen, Jiajin Chen, Ruili Hou, Zhongwen Zhang, David C Christiani, Feng Chen, Yongyue Wei, Ruyang Zhang","doi":"10.7555/JBR.38.20240421","DOIUrl":"https://doi.org/10.7555/JBR.38.20240421","url":null,"abstract":"<p><p>Emerging evidence highlights the role of thyroid hormones in cancer, though findings are controversial. Research on thyroid-related traits in lung carcinogenesis is limited. Using UK Biobank data, we conducted bidirectional Mendelian randomization (MR) to assess causal links between lung cancer risk and thyroid dysfunction (hypothyroidism/hyperthyroidism) or function traits (free thyroxine [FT4], normal-range TSH). Furthermore, in the smoking-behavior stratified MR analysis, we evaluated the mediating effect of thyroid-related phenotypes on the association between smoking phenotype and lung cancer. We confirmed significant associations between lung cancer risk and hypothyroidism (hazards ratio [HR] = 1.14, 95% confidence interval [CI] = 1.03-1.26, <i>P</i> = 0.009) as well as hyperthyroidism (HR = 1.55, 95% CI = 1.29-1.87, <i>P</i> = 1.90×10 <sup>-6</sup>) in the UKB. Moreover, the MR analysis indicated a causal effect of thyroid dysfunction on lung cancer risk (OR <sub>inverse variance weighted [IVW]</sub> = 1.09, 95% CI = 1.05-1.13, <i>P</i> = 3.12×10 <sup>-6</sup> for hypothyroidism; OR <sub>IVW</sub> = 1.08, 95% CI = 1.04-1.12, <i>P</i> = 8.14×10 <sup>-5</sup> for hyperthyroidism). We found that FT4 levels were protective against lung cancer risk (OR <sub>IVW</sub> = 0.93, 95% CI = 0.87-0.99, <i>P</i> = 0.030). Additionally, the stratified MR analysis demonstrated the distinct causal effect of thyroid dysfunction on lung cancer risk among smokers. Hyperthyroidism mediated the effect of smoking behavior, especially the age of smoking initiation (17.66% mediated), on lung cancer risk. Thus, thyroid dysfunction phenotypes play causal roles in lung cancer development exclusively among smokers and act as mediators in the causal pathway from smoking to lung cancer.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-11"},"PeriodicalIF":2.2,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596977","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
Hypothyroidism affects cholelithiasis causally: A two-sample bidirectional Mendelian randomization study.
IF 2.2 4区 医学
Journal of Biomedical Research Pub Date : 2025-01-25 DOI: 10.7555/JBR.38.20240264
Xu Han, Hong Zhu
{"title":"Hypothyroidism affects cholelithiasis causally: A two-sample bidirectional Mendelian randomization study.","authors":"Xu Han, Hong Zhu","doi":"10.7555/JBR.38.20240264","DOIUrl":"https://doi.org/10.7555/JBR.38.20240264","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-4"},"PeriodicalIF":2.2,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390981","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
Chromosomal passenger complex-cyclin/CDK axis correlated with poor lung cancer prognosis.
IF 2.2 4区 医学
Journal of Biomedical Research Pub Date : 2025-01-25 DOI: 10.7555/JBR.38.20240296
Prerna Vats, Sakshi Nirmal, Ashok Kumar, Rajeev Nema
{"title":"Chromosomal passenger complex-cyclin/CDK axis correlated with poor lung cancer prognosis.","authors":"Prerna Vats, Sakshi Nirmal, Ashok Kumar, Rajeev Nema","doi":"10.7555/JBR.38.20240296","DOIUrl":"https://doi.org/10.7555/JBR.38.20240296","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-4"},"PeriodicalIF":2.2,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390979","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
Author Correction: CircPVT1 promotes silica-induced epithelial-mesenchymal transformation by modulating the miR-497-5p/TCF3 axis.
IF 2.2 4区 医学
Journal of Biomedical Research Pub Date : 2025-01-25 DOI: 10.7555/JBR.39.20250900
Siyun Zhou, Yan Li, Wenqing Sun, Dongyu Ma, Yi Liu, Demin Cheng, Guanru Li, Chunhui Ni
{"title":"Author Correction: <i>CircPVT1</i> promotes silica-induced epithelial-mesenchymal transformation by modulating the miR-497-5p/TCF3 axis.","authors":"Siyun Zhou, Yan Li, Wenqing Sun, Dongyu Ma, Yi Liu, Demin Cheng, Guanru Li, Chunhui Ni","doi":"10.7555/JBR.39.20250900","DOIUrl":"https://doi.org/10.7555/JBR.39.20250900","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1"},"PeriodicalIF":2.2,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390976","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
Author Correction: X-ray irradiation selectively kills thymocytes of different stages and impairs the maturation of donor-derived CD4 +CD8 + thymocytes in recipient thymus. 作者更正:x射线照射选择性地杀死不同阶段的胸腺细胞,并损害受体胸腺中供体来源的CD4 +CD8 +胸腺细胞的成熟。
IF 2.2 4区 医学
Journal of Biomedical Research Pub Date : 2024-12-25 DOI: 10.7555/JBR.38.20249001
Jinbo Li, Hongquan Cai, Jianliang Jin, Qian Wang, Dengshun Miao
{"title":"Author Correction: X-ray irradiation selectively kills thymocytes of different stages and impairs the maturation of donor-derived CD4 <sup>+</sup>CD8 <sup>+</sup> thymocytes in recipient thymus.","authors":"Jinbo Li, Hongquan Cai, Jianliang Jin, Qian Wang, Dengshun Miao","doi":"10.7555/JBR.38.20249001","DOIUrl":"https://doi.org/10.7555/JBR.38.20249001","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1"},"PeriodicalIF":2.2,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949182","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
Intermediate filaments and their associated molecules.
IF 2.2 4区 医学
Journal of Biomedical Research Pub Date : 2024-12-25 DOI: 10.7555/JBR.38.20240193
Jing Gao, Fumihiko Nakamura
{"title":"Intermediate filaments and their associated molecules.","authors":"Jing Gao, Fumihiko Nakamura","doi":"10.7555/JBR.38.20240193","DOIUrl":"https://doi.org/10.7555/JBR.38.20240193","url":null,"abstract":"<p><p>Intermediate filaments (IFs) in human cells are the products of six distinct gene families, all sharing homology in a core rod domain. These IFs assemble into non-polar polymers, providing cytoplasmic and nuclear mechanical support. Recent research has revealed the active and dynamic properties of IFs and their binding partners. This regulation extends beyond cell mechanics to include migration, mechanotransduction, and tumor growth. This comprehensive review will catalog all human IF genes and IF-associated proteins (IFAPs), detailing their names, sizes, functions, associated human diseases, relevant literature, and links to resources like Uniprot and the Protein Atlas database. These links provide access to additional information such as protein structure, subcellular localization, disease-causing mutations, and pathology. Using this catalog, we will overview the current understanding of the biological functions of IFs and IFAPs. This overview is crucial for identifying gaps in their characterization and understanding IF-mediated mechanotransduction. Additionally, we will consider potential future research directions.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-12"},"PeriodicalIF":2.2,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390892","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
Letter to the Editor The presence of glutathione S-transferase in recombinant S100A9 alters its effect on human sperm function.
IF 2.2 4区 医学
Journal of Biomedical Research Pub Date : 2024-12-25 DOI: 10.7555/JBR.38.20240155
Estefania Massa, Gastón Prez, Sergio Ghersevich
{"title":"Letter to the Editor The presence of glutathione S-transferase in recombinant S100A9 alters its effect on human sperm function.","authors":"Estefania Massa, Gastón Prez, Sergio Ghersevich","doi":"10.7555/JBR.38.20240155","DOIUrl":"https://doi.org/10.7555/JBR.38.20240155","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-4"},"PeriodicalIF":2.2,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390973","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
Hepatic SIRT6 protects against cholestatic liver disease primarily via inhibiting bile acid synthesis. 肝脏SIRT6主要通过抑制胆汁酸合成来预防胆汁淤积性肝病。
IF 2.2 4区 医学
Journal of Biomedical Research Pub Date : 2024-11-25 DOI: 10.7555/JBR.38.20240172
Wen Zhang, Jiahui Wang, Luyao Yang, Yuyun Shao, Hongjun Peng, Longfeng Jiang, Liang Sheng
{"title":"Hepatic SIRT6 protects against cholestatic liver disease primarily <i>via</i> inhibiting bile acid synthesis.","authors":"Wen Zhang, Jiahui Wang, Luyao Yang, Yuyun Shao, Hongjun Peng, Longfeng Jiang, Liang Sheng","doi":"10.7555/JBR.38.20240172","DOIUrl":"https://doi.org/10.7555/JBR.38.20240172","url":null,"abstract":"<p><p>Cholestatic liver disease, caused by the accumulation of hazardous bile acids in the liver, may result in cirrhosis, fibrosis, or liver failure. Activation of SIRT6 prevents cholestasis-associated pathological events, such as oxidative stress and mitochondrial biogenesis disorders, and inhibits bile acid synthesis to alleviate cholestatic liver injury. However, it is still uncertain which pathway is responsible for the therapeutic effect of SIRT6 in reducing cholestasis. Therefore, we treated liver-specific <i>Sirt6</i> knockout mice with N-Acetylcysteine, Keap1-Nrf2-IN-1, or acadesine to remove oxidative stress and/or trigger mitochondrial biogenesis after cholestatic liver disease modeling, but these measures did not significantly improve cholestatic symptoms. However, MDL801, a SIRT6 agonist that downregulating CYP7A1, the key enzyme in bile acid synthesis, exhibited favorable therapeutic effects. In addition, the hepatic knockdown of <i>Cyp7A1</i> further confirmed that inhibition of hepatic bile acid synthesis might be the main pathway by which SIRT6 alleviates cholestatic liver disease. These findings provide a solid basis for the potential application of SIRT6 agonists in the treatment of cholestatic liver disease.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-17"},"PeriodicalIF":2.2,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769215","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
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