{"title":"The association between weekly mean temperature and the epidemic of influenza across 122 countries/regions, 2014-2019.","authors":"Xiaoxiao Cao, Wenhao Zhu, Zhenghan Luo, Ran He, Yihao Li, Shirong Hui, Sheng Yang, Rongbin Yu, Peng Huang","doi":"10.7555/JBR.39.20250010","DOIUrl":"https://doi.org/10.7555/JBR.39.20250010","url":null,"abstract":"<p><p>The study examined the association between weekly mean temperature and influenza cases across 122 countries/regions (2014-2019) using a distributed lag non-linear model (DLNM). We analyzed 3145206 cases of overall influenza (Flu-All), with influenza A (Flu-A) and influenza B (Flu-B) accounting for 73.49% and 26.51%, respectively. Within a lag of 2 weeks, Flu-All incidence demonstrated a bimodal temperature relationship, with peak relative risks (RR) of 6.02 (95% CI: 1.92-20.77) at -8 ℃ and 3.08 (95% CI: 1.27-7.49) at 22 ℃. Flu-A exhibited a similar bimodal pattern, with RRs of 3.76 (95% CI: 2.39-5.91) at -8 ℃ and 2.08 (95% CI: 1.55-2.80) at 22 ℃. Flu-B demonstrated a single risk peak at 1 ℃ (RR = 4.48, 95% CI: 1.74-11.55). Subgroup analyses of climate zones revealed variations: tropical zones peaked at 12 ℃ (RR = 1.37, 95% CI: 1.08-1.74), while dry and temperate zones exhibited the highest risk at -5 ℃, with RRs of 4.49 (95% CI: 2.46-7.15) and 5.23 (95% CI: 3.17-8.64), respectively. Cold zones peaked at 1 ℃ (RR = 5.96, 95% CI: 3.76-9.43). Subgroup analyses of influenza transmission zones (ITZs) revealed variations: Africa showed higher risk between 6 ℃-14 ℃, Asia showed higher risk below 3 ℃, and Europe exhibited distinct risks of influenza peaks at -1 ℃ (Eastern), 1 ℃ (Southwest), and -20 ℃ (Northern). Elevated risks above 11 ℃ were identified in the Americas and Oceania. These findings establish a predictive framework for influenza outbreak preparedness by integrating regional temperature patterns with global climate variability.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-10"},"PeriodicalIF":2.2,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144017990","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}
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}
{"title":"Molecular pathways in cardiovascular disease under hypoxia: Mechanisms, biomarkers, and therapeutic targets.","authors":"Izzatullo Abdullaev, Ulugbek Gayibov, Sirojiddin Omonturdiev, Sobirova Fotima, Sabina Gayibova, Takhir Aripov","doi":"10.7555/JBR.38.20240387","DOIUrl":"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 hypoxia, 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. The mitochondrial ATP-sensitive potassium channel (mitoK <sub>ATP</sub>) and mitochondrial permeability transition pore (mPTP) channels are particularly affected, contributing to membrane potential loss, cytochrome c release, and cell death. This review delves into 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 mitoK <sub>ATP</sub> 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":"254-269"},"PeriodicalIF":2.2,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239985/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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}
{"title":"Intermediate filaments and their associated molecules.","authors":"Jing Gao, Fumihiko Nakamura","doi":"10.7555/JBR.38.20240193","DOIUrl":"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. Therefore, this comprehensive review aims to 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 provide an overview of 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":"242-253"},"PeriodicalIF":2.2,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239979/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Prophylactic cranial irradiation in small cell lung cancer: A review of evidence.","authors":"Femi Williams Adeoye","doi":"10.7555/JBR.38.20240293","DOIUrl":"10.7555/JBR.38.20240293","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"128-131"},"PeriodicalIF":2.2,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11982683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949190","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}