Journal of Biomedical Research最新文献_第4页

Author Correction: CircPVT1 promotes silica-induced epithelial-mesenchymal transformation by modulating the miR-497-5p/TCF3 axis. 作者更正：CircPVT1通过调节miR-497-5p/TCF3轴促进二氧化硅诱导的上皮-间质转化。

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

引用次数: 0

Prophylactic cranial irradiation in small cell lung cancer: A review of evidence. 预防性颅照射治疗小细胞肺癌：证据综述。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2025-01-07 DOI: 10.7555/JBR.38.20240293

Femi Williams Adeoye

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

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. 重组S100A9中谷胱甘肽s转移酶的存在改变了其对人类精子功能的影响。

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

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 via 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":"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 Sirt6 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 Cyp7A1 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.","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

AdipoR1 promotes pathogenic Th17 differentiation by regulating mitochondrial function through FUNDC1. AdipoR1通过FUNDC1调节线粒体功能，促进致病性Th17分化。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-11-07 DOI: 10.7555/JBR.38.20240244

Hui Wang, Qian Zhang, Yuankai Sun, Wenfeng Tan, Miaojia Zhang

{"title":"AdipoR1 promotes pathogenic Th17 differentiation by regulating mitochondrial function through FUNDC1.","authors":"Hui Wang, Qian Zhang, Yuankai Sun, Wenfeng Tan, Miaojia Zhang","doi":"10.7555/JBR.38.20240244","DOIUrl":"10.7555/JBR.38.20240244","url":null,"abstract":"Adiponectin receptor 1 ( Adipor1) deficiency has been shown to inhibit Th17 cell differentiation and reduce joint inflammation and bone erosion in antigen-induced arthritis mice. Additional emerging evidence indicates that Th17 cells may differentiate into pathogenic (pTh17) and non-pathogenic (npTh17) cells, with the pTh17 cells playing a crucial role in numerous autoimmune and inflammatory conditions. In the current study, we found that Adipor1 deficiency inhibited pTh17 differentiation in vitro and induced mitochondrial dysfunction in pTh17 cells. RNA sequencing demonstrated a significant increase in the expression levels of Fundc1, a gene related to mitochondrial function, in Adipor1-deficient CD4 + T cells. Fundc1 knockdown in Adipor1-deficient CD4 + T cells partially reversed the effects of Adipor1 deficiency on mitochondrial function and pTh17 differentiation. In conclusion, the current study demonstrated a novel role of Adipor1 in regulating mitochondrial function via Fundc1 to promote pTh17 cell differentiation, providing some insight into potential therapeutic targets for autoimmune and inflammatory diseases.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"305-316"},"PeriodicalIF":2.2,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of amino acids in skeletal muscle health and sarcopenia: A narrative review. 氨基酸在骨骼肌健康和肌肉疏松症中的作用：综述。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-10-22 DOI: 10.7555/JBR.38.20240167

Ramendu Hom Chaudhuri

{"title":"The role of amino acids in skeletal muscle health and sarcopenia: A narrative review.","authors":"Ramendu Hom Chaudhuri","doi":"10.7555/JBR.38.20240167","DOIUrl":"10.7555/JBR.38.20240167","url":null,"abstract":"The skeletal muscle is the largest organ present in the body and is responsible for mechanical activities like maintaining posture, movement, respiratory function, and support for the health and functioning of other systems of the body. Skeletal muscle atrophy is a condition characterized by a reduction in muscle size, strength, and activity, which leads to an increased dependency on others for movement, an increased risk of falls, and a reduced quality of life. Various conditions like osteoarthritis, osteoporosis, and fractures are directly associated with increased muscle atrophy. Additionally, numerous risk factors, like aging, malnutrition, physical inactivity, and certain disease conditions, through distinct pathways, negatively affect skeletal muscle health and lead to muscle atrophy. Among various determinants of overall muscle health, the rate of muscle protein synthesis and degradation is an important parameter that eventually alters the fate of overall muscle health. In conditions of excessive skeletal muscle atrophy, including sarcopenia, the rate of muscle protein degradation usually exceeds the rate of protein synthesis. The availability of amino acids in the systemic circulation is a crucial step in muscle protein synthesis. The current review aims to consolidate the existing evidence on amino acids, highlight their mechanisms of action, and assess their roles and effectiveness in enhancing skeletal muscle health.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"229-241"},"PeriodicalIF":2.2,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Palmitoylethanolamide, an endogenous fatty acid amide, and its pleiotropic health benefits: A narrative review. 棕榈酰乙醇酰胺（一种内源性脂肪酸酰胺）及其对健康的多重益处：叙述性综述。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-10-22 DOI: 10.7555/JBR.38.20240053

Debasis Basu

{"title":"Palmitoylethanolamide, an endogenous fatty acid amide, and its pleiotropic health benefits: A narrative review.","authors":"Debasis Basu","doi":"10.7555/JBR.38.20240053","DOIUrl":"10.7555/JBR.38.20240053","url":null,"abstract":"The global nutritional transition has led to the increased frequency and severity of chronic degenerative diseases worldwide, primarily driven by chronic inflammatory stress. At mealtimes, various pharmaceutical products aim to prevent such inflammatory stress, but they usually cause various systemic side effects. Therefore, the supplementation of natural and safe ingredients is a promising strategy to reduce the risk and severity of inflammatory stress-related diseases. Palmitoylethanolamide (PEA), an endocannabinoid-like mediator, has been extensively studied for its diverse actions, including anti-inflammatory, antimicrobial, immunostimulatory, neuroprotective, and pain-reducing effects, with high tolerability and safety in both animals and humans. Because of its multiple molecular targets and mechanisms of action, PEA has demonstrated therapeutic benefits in various diseases, including neurological, psychiatric, ophthalmic, metabolic, oncological, renal, hepatic, immunological, rheumatological, and gastrointestinal conditions. The current review highlights the roles and functions of PEA in various physiological and pathological conditions, further supporting its use as an important dietary agent.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"215-228"},"PeriodicalIF":2.2,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LncRNA LINC01503 promotes angiogenesis in colorectal cancer by regulating VEGFA expression via miR-342-3p and HSP60 binding. LncRNA LINC01503通过miR-342-3p和HSP60结合调控VEGFA的表达，从而促进结直肠癌的血管生成。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-10-22 DOI: 10.7555/JBR.38.20240190

Dandan Zheng, Xiya Zhang, Jia Xu, Shuwen Chen, Bin Wang, Xiaoqin Yuan

{"title":"LncRNA LINC01503 promotes angiogenesis in colorectal cancer by regulating VEGFA expression via miR-342-3p and HSP60 binding.","authors":"Dandan Zheng, Xiya Zhang, Jia Xu, Shuwen Chen, Bin Wang, Xiaoqin Yuan","doi":"10.7555/JBR.38.20240190","DOIUrl":"10.7555/JBR.38.20240190","url":null,"abstract":"Colorectal cancer (CRC) ranks among the top five most common malignant tumors worldwide and has a high mortality rate. Angiogenesis plays an important role in CRC progression; however, anti-angiogenesis therapy still has many limitations. Long non-coding RNAs (lncRNAs) participate in tumor progression by regulating the expression of vascular endothelial growth factor in metastatic CRC. Thus, targeting specific lncRNAs may provide some new hope for anti-angiogenic strategies. Through analyzing data from both clinical samples and The Cancer Genome Atlas database, we found that the lncRNA LINC01503 was specifically upregulated in CRC tissues and was associated with tumor progression and poor overall survival. We also demonstrated that LINC01503 enhanced the capacity for tube formation and migration of vascular endothelial cells, thus promoting CRC tumorigenesis by upregulating vascular endothelial growth factor A (VEGFA) expression in CRC cells. Mechanistically, LINC01503 promoted the expression of VEGFA by simultaneously regulating both mRNA and protein stability of VEGFA by binding to miR-342-3p and the chaperone HSP60, respectively. The upregulation of LINC01503 in CRC cells was attributed to the CREB-binding protein CBP/p300-mediated H3K27 acetylation of the LINC01503 promoter region. Taken together, our findings clarify the mechanism by which LINC01503 may promote CRC angiogenesis, implying that LINC01503 may serve as a potential prognostic biomarker and therapeutic target for CRC.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"286-304"},"PeriodicalIF":2.2,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gold nanorods as biocompatible nano-agents for the enhanced photothermal therapy in skin disorders. 金纳米棒作为生物相容性纳米试剂，用于增强皮肤病的光热疗法。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-10-08 DOI: 10.7555/JBR.38.20240119

Yamei Gao, Shaohu Huo, Chao Chen, Shiyu Du, Ruiyuan Xia, Jian Liu, Dandan Chen, Ziyue Diao, Xin Han, Zhiqiang Yin

{"title":"Gold nanorods as biocompatible nano-agents for the enhanced photothermal therapy in skin disorders.","authors":"Yamei Gao, Shaohu Huo, Chao Chen, Shiyu Du, Ruiyuan Xia, Jian Liu, Dandan Chen, Ziyue Diao, Xin Han, Zhiqiang Yin","doi":"10.7555/JBR.38.20240119","DOIUrl":"10.7555/JBR.38.20240119","url":null,"abstract":"Rod-shaped gold nanomaterials, known as gold nanorods (GNRs), may undergo specific surface modification, because of their straightforward surface chemistry. This feature makes them appropriate for use as functional and biocompatible nano-formulations. By optimizing the absorption of longitudinally localized surface plasmon resonance in the near-infrared region, which corresponds to the near-infrared bio-tissue window, GNRs with appropriate modifications may improve the results of photothermal treatment (PTT). In dermatology, potential noninvasive uses of GNRs to enhance wound healing, manage infections, combat cutaneous malignancies, and remodel skin tissues via PTT have attracted research attention in recent years. The review discussed the basic properties of GNRs, such as their shape, size, optical performance, photothermal efficiency, and metabolism. Then, the disadvantages of using these particles in photodynamic therapy are highlighted. Next, biological applications of GNRs-based PTT are explored in detail. Finally, the limitations and future perspectives of this research are addressed, providing a comprehensive perspective on the potential GNRs with PTT.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-17"},"PeriodicalIF":2.2,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873593/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0