首页 > 最新文献

Brain and Behavior最新文献

英文 中文
Five-Decade Mortality Trends in Ischemic Stroke in the United States: A CDC WONDER Analysis 美国缺血性中风50年死亡率趋势:CDC WONDER分析
IF 2.7 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-12-31 DOI: 10.1002/brb3.71177
Rameez Qasim, Laiba Muzammil, Bilal Qammar, Areej Dar, Laiba Sultan, Mubashir Raza, Umama Alam, Raheel Ahmed, Hasibullah Aminpoor, Muhammad Khalid Afridi, Saad Ahmed Waqas

Introduction

Ischemic stroke, comprising nearly 85% of all strokes, remains a leading cause of death and disability worldwide. Annually, about 795,000 individuals in the United States (US) experience a new or recurrent stroke. Despite advancements in diagnosis, treatment, and prevention, significant disparities and geographic variability persist, highlighting the need for targeted strategies to address these ongoing challenges.

Methods

We analyzed US death certificate data from Centers for Disease Control and Prevention Wide-ranging Online Data for Epidemiologic Research (1968-2023) for ischemic stroke mortality using International Classification of Diseases (ICD-8, ICD-9, and ICD-10) codes. Demographics included age, sex, and race/ethnicity. Crude and age-adjusted mortality rates (AAMRs), annual percent change (APC), and average annual percent changes (AAPC) were calculated using joinpoint regression, and a p-value less than 0.05 defined significance.

Results

From 1968 to 2023, ischemic stroke mortality declined substantially, with 1,363,668 total deaths and the AAMR decreasing from 76.2 to 10.0 per 100,000 (AAPC: −3.59%). Early steep declines occurred from 1968 to 1982 and continued through 2014, followed by pronounced increases between 2014–2017 (APC 38.69) and 2017–2023 (APC 7.48). Men consistently exhibited higher AAMRs than women, with long-term declines, yet both experienced recent upward trends. Racial disparities persisted, with Black adults declining from 85.9 to 14.2 (AAPC: −3.30%) and White from 75.5 to 9.8 (AAPC: −3.63%), but both showed reversals after 2014. Older adults (≥65 years) bore the greatest burden (AAPC: −3.91%), while younger age groups exhibited smaller reductions.

Conclusion

Despite long-term declines in mortality, recent increases and persistent disparities by age, sex, and race underscore the need for targeted prevention and equitable healthcare interventions in particularly high-risk populations.

缺血性中风占所有中风的近85%,仍然是全世界死亡和残疾的主要原因。每年,美国约有79.5万人经历新的或复发性中风。尽管在诊断、治疗和预防方面取得了进步,但显著的差异和地域差异仍然存在,这突出表明需要制定有针对性的战略来应对这些持续的挑战。方法:我们使用国际疾病分类(ICD-8、ICD-9和ICD-10)代码分析了美国疾病控制和预防中心广泛在线流行病学研究数据(1968-2023)中缺血性卒中死亡率的死亡证明数据。人口统计包括年龄、性别和种族/民族。采用连接点回归计算粗死亡率和年龄调整死亡率(AAMRs)、年变化百分数(APC)和平均年变化百分数(AAPC), p值小于0.05。结果:1968年至2023年,缺血性脑卒中死亡率大幅下降,总死亡人数为1,363,668人,AAMR从76.2 / 10万下降到10.0 / 10万(AAPC: -3.59%)。早期的急剧下降发生在1968年至1982年,并持续到2014年,随后在2014-2017年(APC 38.69)和2017-2023年(APC 7.48)期间显著上升。男性的aamr一直比女性高,长期下降,但最近都有上升趋势。种族差异仍然存在,黑人成年人从85.9下降到14.2 (AAPC: -3.30%),白人从75.5下降到9.8 (AAPC: -3.63%),但在2014年之后两者都出现了逆转。老年人(≥65岁)的AAPC负担最大(-3.91%),而年轻年龄组的下降幅度较小。结论:尽管死亡率长期下降,但近期的上升和年龄、性别和种族之间的持续差异强调了在高危人群中进行有针对性的预防和公平的医疗干预的必要性。
{"title":"Five-Decade Mortality Trends in Ischemic Stroke in the United States: A CDC WONDER Analysis","authors":"Rameez Qasim,&nbsp;Laiba Muzammil,&nbsp;Bilal Qammar,&nbsp;Areej Dar,&nbsp;Laiba Sultan,&nbsp;Mubashir Raza,&nbsp;Umama Alam,&nbsp;Raheel Ahmed,&nbsp;Hasibullah Aminpoor,&nbsp;Muhammad Khalid Afridi,&nbsp;Saad Ahmed Waqas","doi":"10.1002/brb3.71177","DOIUrl":"10.1002/brb3.71177","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Ischemic stroke, comprising nearly 85% of all strokes, remains a leading cause of death and disability worldwide. Annually, about 795,000 individuals in the United States (US) experience a new or recurrent stroke. Despite advancements in diagnosis, treatment, and prevention, significant disparities and geographic variability persist, highlighting the need for targeted strategies to address these ongoing challenges.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We analyzed US death certificate data from Centers for Disease Control and Prevention Wide-ranging Online Data for Epidemiologic Research (1968-2023) for ischemic stroke mortality using International Classification of Diseases (ICD-8, ICD-9, and ICD-10) codes. Demographics included age, sex, and race/ethnicity. Crude and age-adjusted mortality rates (AAMRs), annual percent change (APC), and average annual percent changes (AAPC) were calculated using joinpoint regression, and a <i>p</i>-value less than 0.05 defined significance.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>From 1968 to 2023, ischemic stroke mortality declined substantially, with 1,363,668 total deaths and the AAMR decreasing from 76.2 to 10.0 per 100,000 (AAPC: −3.59%). Early steep declines occurred from 1968 to 1982 and continued through 2014, followed by pronounced increases between 2014–2017 (APC 38.69) and 2017–2023 (APC 7.48). Men consistently exhibited higher AAMRs than women, with long-term declines, yet both experienced recent upward trends. Racial disparities persisted, with Black adults declining from 85.9 to 14.2 (AAPC: −3.30%) and White from 75.5 to 9.8 (AAPC: −3.63%), but both showed reversals after 2014. Older adults (≥65 years) bore the greatest burden (AAPC: −3.91%), while younger age groups exhibited smaller reductions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Despite long-term declines in mortality, recent increases and persistent disparities by age, sex, and race underscore the need for targeted prevention and equitable healthcare interventions in particularly high-risk populations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"16 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71177","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Add-On Telitacicept Significantly Improves Outcome of Patients With Refractory Ocular Myasthenia Gravis a Real-World Case Series 附加泰利他塞普显著改善难治性重症肌无力患者的预后:现实世界病例系列。
IF 2.7 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-12-31 DOI: 10.1002/brb3.71157
Jing Lin, Yue Li, Mengcui Gui, Bitao Bu, Zhijun Li

Introduction

Refractory ocular myasthenia gravis (MG) represents a significant therapeutic challenge, as conventional immunotherapies often prove ineffective. Telitacicept, a recombinant B-lymphocyte stimulator receptor-antibody fusion protein, offers a novel immunomodulatory approach. This retrospective study evaluates its efficacy and safety in patients with MG-associated refractory ocular symptoms.

Methods

This is a single-center retrospective cohort study. evaluated patients with refractory ocular symptoms who received telitacicept weekly between August 2024 and January 2025. We evaluated treatment efficacy using Myasthenia Gravis Foundation of America post-intervention status (MGFA-PIS), Myasthenia Gravis Impairment Index-patient-reported outcome (MGII-PRO), quantitative MG (QMG), and MG activity of daily living (ADL) scores, as well as the reduction in daily prednisone dosage at baseline and each month following treatment. The safety assessment was also evaluated.

Results

Seven MGFA class 1 patients (5 females, 2 males) were enrolled, with a median onset age of 6 years (interquartile range [IQR] 2–21) and a median disease duration of 98 months (IQR 46–121). MG-ADL scores showed significant reduction with prolonged follow-up. 6/7 patients achieved ≥2-point MG-ADL improvement by the third follow-up. 4/6 patients reached minimal symptom expression at the fifth follow-up. The average ocular MG-ADL, MGII-PRO, and QMG scores revealed statistically significant improvements at the third month of follow-up, sustained through the sixth month. The regimen exhibited excellent tolerability, with no severe adverse events (e.g., hypersensitivity reactions, infections) reported.

Conclusion

Our preliminary findings indicate that telitacicept represents a promising and well-tolerated adjunct therapy for refractory ocular symptoms in MG, providing significant clinical evidence to support this novel therapeutic approach.

导读:难治性重症肌无力(MG)是一项重大的治疗挑战,因为传统的免疫疗法往往被证明无效。Telitacicept是一种重组b淋巴细胞刺激受体-抗体融合蛋白,提供了一种新的免疫调节途径。本回顾性研究评估其在mg相关的难治性眼部症状患者中的有效性和安全性。方法:这是一项单中心回顾性队列研究。评估2024年8月至2025年1月期间每周接受telitacicept治疗的难治性眼部症状患者。我们使用美国重症肌无力基金会干预后状态(MGFA-PIS)、重症肌无力损害指数-患者报告结果(MGII-PRO)、定量MG (QMG)和MG日常生活活动(ADL)评分,以及基线和治疗后每个月每日泼尼松剂量的减少来评估治疗效果。并对安全性评价进行了评价。结果:7例MGFA 1级患者(5名女性,2名男性)入组,中位发病年龄为6岁(四分位数间距[IQR] 2-21),中位病程为98个月(IQR 46-121)。MG-ADL评分随随访时间延长而显著降低。6/7例患者在第三次随访时MG-ADL改善≥2点。4/6患者在第五次随访时达到最低症状表达。平均眼部MG-ADL、MGII-PRO和QMG评分在随访的第三个月显示了统计学上显著的改善,并持续到第六个月。该方案表现出良好的耐受性,没有严重的不良事件(例如,过敏反应,感染)的报道。结论:我们的初步研究结果表明,替利他塞普是一种治疗MG患者难治性眼部症状的有希望且耐受性良好的辅助疗法,为支持这种新的治疗方法提供了重要的临床证据。
{"title":"Add-On Telitacicept Significantly Improves Outcome of Patients With Refractory Ocular Myasthenia Gravis a Real-World Case Series","authors":"Jing Lin,&nbsp;Yue Li,&nbsp;Mengcui Gui,&nbsp;Bitao Bu,&nbsp;Zhijun Li","doi":"10.1002/brb3.71157","DOIUrl":"10.1002/brb3.71157","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Refractory ocular myasthenia gravis (MG) represents a significant therapeutic challenge, as conventional immunotherapies often prove ineffective. Telitacicept, a recombinant B-lymphocyte stimulator receptor-antibody fusion protein, offers a novel immunomodulatory approach. This retrospective study evaluates its efficacy and safety in patients with MG-associated refractory ocular symptoms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This is a single-center retrospective cohort study. evaluated patients with refractory ocular symptoms who received telitacicept weekly between August 2024 and January 2025. We evaluated treatment efficacy using Myasthenia Gravis Foundation of America post-intervention status (MGFA-PIS), Myasthenia Gravis Impairment Index-patient-reported outcome (MGII-PRO), quantitative MG (QMG), and MG activity of daily living (ADL) scores, as well as the reduction in daily prednisone dosage at baseline and each month following treatment. The safety assessment was also evaluated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Seven MGFA class 1 patients (5 females, 2 males) were enrolled, with a median onset age of 6 years (interquartile range [IQR] 2–21) and a median disease duration of 98 months (IQR 46–121). MG-ADL scores showed significant reduction with prolonged follow-up. 6/7 patients achieved ≥2-point MG-ADL improvement by the third follow-up. 4/6 patients reached minimal symptom expression at the fifth follow-up. The average ocular MG-ADL, MGII-PRO, and QMG scores revealed statistically significant improvements at the third month of follow-up, sustained through the sixth month. The regimen exhibited excellent tolerability, with no severe adverse events (e.g., hypersensitivity reactions, infections) reported.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our preliminary findings indicate that telitacicept represents a promising and well-tolerated adjunct therapy for refractory ocular symptoms in MG, providing significant clinical evidence to support this novel therapeutic approach.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"16 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71157","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mapping the Scientific Landscape of Schizophrenia Genetics (2020–2025): A Bibliometric and Scientometric Study of Global Trends and Collaborations 绘制精神分裂症遗传学的科学景观(2020-2025):全球趋势和合作的文献计量学和科学计量学研究。
IF 2.7 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-12-31 DOI: 10.1002/brb3.71171
Niloofar Mikaeili, Mahdi Naeim, Mohammad Narimani

Background and objective

This study provides a comprehensive bibliometric and scientometric analysis of research trends in schizophrenia genetics from 2020 to 2025. Driven by rapid technological advances such as genome-wide association studies (GWAS) and next-generation sequencing (NGS), the field has experienced significant growth. The objective was to map the thematic evolution, key contributors, and collaboration networks shaping psychiatric genomics research.

Methods

An integrated bibliometric and scientometric approach was employed. A dataset of 5001 English-language publications authored by 27,692 researchers was retrieved from PubMed, Scopus, and web of science (Wos) databases. Following deduplication and eligibility screening, VOSviewer (version 1.6.20) was used to generate network visualizations analyzing co-authorship, keyword co-occurrence, citation, and co-citation patterns.

Results

The analysis revealed a notable surge in publications after 2022, increasing from 431 articles in 2020 to 1,645 articles in 2022, before stabilizing above 900 publications annually in 2023 and 2024. Six major thematic clusters were identified: (1) genetic and cellular mechanisms; (2) neurochemical and behavioral studies; (3) neuroimaging; (4) clinical and epidemiological features including polygenic risk scoring; (5) methodological approaches; and (6) comorbidities with pharmacogenetic implications. Prominent contributors included Ole A. Andreassen and Vince D. Calhoun, while the United States, China, and the United Kingdom emerged as central hubs of international collaboration.

Conclusion

This study elucidates the leading researchers, prevailing themes, and collaborative networks driving schizophrenia genetics research from 2020 to 2025. The findings demonstrate the efficacy of bibliometric and scientometric methods, particularly VOSviewer, in revealing the dynamic landscape of psychiatric genomics and guiding future multidisciplinary research efforts.This graphical abstract illustrates the integrated workflow of the study “mapping the scientific landscape of schizophrenia genetics (2020–2025)”. The process combines bibliometric and scientometric analyses of 5,001 publications using VOSviewer to identify thematic clusters, key contributors, and international collaboration networks that define global research trends in schizophrenia genetics.

背景与目的:本研究对2020 - 2025年精神分裂症遗传学的研究趋势进行了全面的文献计量学和科学计量学分析。在全基因组关联研究(GWAS)和下一代测序(NGS)等快速技术进步的推动下,该领域经历了显着增长。目的是绘制精神病学基因组学研究的主题演变、关键贡献者和合作网络。方法:采用文献计量学和科学计量学相结合的方法。从PubMed、Scopus和web of science (Wos)数据库中检索了27,692名研究人员撰写的5001篇英语出版物的数据集。在重复数据删除和资格筛选之后,使用VOSviewer(版本1.6.20)生成网络可视化,分析共同作者、关键词共现、引用和共同引用模式。结果:分析显示,2022年之后的出版物数量显著增加,从2020年的431篇增加到2022年的1645篇,然后在2023年和2024年稳定在每年900篇以上。确定了六个主要专题集群:(1)遗传和细胞机制;(2)神经化学和行为研究;(3)神经影像;(4)临床和流行病学特征,包括多基因风险评分;(5)方法方法;(6)具有药物遗传学意义的合并症。杰出的贡献者包括Ole A. Andreassen和Vince D. Calhoun,而美国、中国和英国则成为国际合作的中心枢纽。结论:本研究阐明了2020年至2025年精神分裂症遗传学研究的主要研究人员、流行主题和合作网络。这些发现证明了文献计量学和科学计量学方法,特别是VOSviewer,在揭示精神病学基因组学的动态景观和指导未来多学科研究工作方面的有效性。这个图形摘要说明了“绘制精神分裂症遗传学的科学景观(2020-2025)”研究的综合工作流程。该过程结合了文献计量学和科学计量学分析,使用VOSviewer对5,001份出版物进行分析,以确定确定精神分裂症遗传学全球研究趋势的主题集群、关键贡献者和国际合作网络。
{"title":"Mapping the Scientific Landscape of Schizophrenia Genetics (2020–2025): A Bibliometric and Scientometric Study of Global Trends and Collaborations","authors":"Niloofar Mikaeili,&nbsp;Mahdi Naeim,&nbsp;Mohammad Narimani","doi":"10.1002/brb3.71171","DOIUrl":"10.1002/brb3.71171","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and objective</h3>\u0000 \u0000 <p>This study provides a comprehensive bibliometric and scientometric analysis of research trends in schizophrenia genetics from 2020 to 2025. Driven by rapid technological advances such as genome-wide association studies (GWAS) and next-generation sequencing (NGS), the field has experienced significant growth. The objective was to map the thematic evolution, key contributors, and collaboration networks shaping psychiatric genomics research.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>An integrated bibliometric and scientometric approach was employed. A dataset of 5001 English-language publications authored by 27,692 researchers was retrieved from PubMed, Scopus, and web of science (Wos) databases. Following deduplication and eligibility screening, VOSviewer (version 1.6.20) was used to generate network visualizations analyzing co-authorship, keyword co-occurrence, citation, and co-citation patterns.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The analysis revealed a notable surge in publications after 2022, increasing from 431 articles in 2020 to 1,645 articles in 2022, before stabilizing above 900 publications annually in 2023 and 2024. Six major thematic clusters were identified: (1) genetic and cellular mechanisms; (2) neurochemical and behavioral studies; (3) neuroimaging; (4) clinical and epidemiological features including polygenic risk scoring; (5) methodological approaches; and (6) comorbidities with pharmacogenetic implications. Prominent contributors included Ole A. Andreassen and Vince D. Calhoun, while the United States, China, and the United Kingdom emerged as central hubs of international collaboration.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study elucidates the leading researchers, prevailing themes, and collaborative networks driving schizophrenia genetics research from 2020 to 2025. The findings demonstrate the efficacy of bibliometric and scientometric methods, particularly VOSviewer, in revealing the dynamic landscape of psychiatric genomics and guiding future multidisciplinary research efforts.This graphical abstract illustrates the integrated workflow of the study “mapping the scientific landscape of schizophrenia genetics (2020–2025)”. The process combines bibliometric and scientometric analyses of 5,001 publications using VOSviewer to identify thematic clusters, key contributors, and international collaboration networks that define global research trends in schizophrenia genetics.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"16 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71171","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Identifying Immune Cells as Mediators in the Impact of Gut Microbiota on Congenital Malformations of the Nervous System 鉴定免疫细胞在肠道微生物群对先天性神经系统畸形影响中的中介作用。
IF 2.7 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-12-31 DOI: 10.1002/brb3.71150
Haokun Tian, Xiaolan Guo, Jialu Yu, Yuanfang Lu, Wensen Cao, Xiuwei Wang, Zhiqiang Zhu, Zhen Guan, Aiyun Yang, Shen Li, Xiaochun Xu, Caihua Wang, Jianhua Wang

Introduction

Congenital malformations of the nervous system, such as neural tube defects, are significant contributors to infant morbidity and mortality. This study aimed to assess the causal influence of gut microbiota on nervous system malformations and to identify immune cells as potential mediators in this relationship, utilizing a two-step Mendelian randomization (TSMR) approach.

Methods

Using genome-wide association studies data on gut microbiota, immune cells, and congenital malformations of the nervous system, we applied TSMR to evaluate the total, direct, and mediating effects. Gut microbiota indicators served as exposures, congenital malformations of the nervous system as outcomes, and immune cell markers as mediators. Statistical analyses included MR Egger, inverse variance weighted, and so forth.

Results

Our analysis identified 19 gut microbiota indicators causally associated with congenital malformations of the nervous system. Notably, Eubacteriaceae and Eubacterium genera exhibited protective effects, while Escherichia and Bacteroides genera showed positive correlations with malformation risk. Nine immune cell indicators significantly mediated these effects. For example, CD20+ B cells were negatively associated with malformation risk, suggesting a protective immune response, whereas CD25+ B cells were positively correlated, indicating increased malformation risk.

Conclusions

This study demonstrated a significant link between gut microbiota composition and congenital nervous system malformations, mediated by specific immune cells. These findings highlighted the potential for gut microbiota modulation and immune-targeted therapies as preventive or therapeutic strategies in reducing malformation risks. Future investigations should aim to replicate these results across diverse populations and further elucidate the underlying biological mechanisms of gut–immune–neural interactions.

Trial Registration

The authors have nothing to report.

神经系统的先天性畸形,如神经管缺陷,是婴儿发病率和死亡率的重要因素。本研究旨在评估肠道微生物群对神经系统畸形的因果影响,并利用两步孟德尔随机化(TSMR)方法确定免疫细胞作为这种关系的潜在介质。方法:利用肠道微生物群、免疫细胞和先天性神经系统畸形的全基因组关联研究数据,我们应用TSMR来评估总效应、直接效应和中介效应。肠道微生物群指标作为暴露,神经系统先天性畸形作为结果,免疫细胞标记作为介质。统计分析包括MR Egger、逆方差加权等。结果:我们的分析确定了19种肠道微生物指标与先天性神经系统畸形有因果关系。值得注意的是,真杆菌科和真杆菌属具有保护作用,而埃希菌属和拟杆菌属与畸形风险呈正相关。九种免疫细胞指标显著介导了这些作用。例如,CD20+ B细胞与畸形风险呈负相关,提示保护性免疫反应,而CD25+ B细胞呈正相关,提示畸形风险增加。结论:本研究证明了特异性免疫细胞介导的肠道微生物群组成与先天性神经系统畸形之间的显著联系。这些发现强调了肠道微生物群调节和免疫靶向治疗作为减少畸形风险的预防或治疗策略的潜力。未来的研究应该旨在在不同的人群中复制这些结果,并进一步阐明肠道-免疫-神经相互作用的潜在生物学机制。试验注册:作者无报告。
{"title":"Identifying Immune Cells as Mediators in the Impact of Gut Microbiota on Congenital Malformations of the Nervous System","authors":"Haokun Tian,&nbsp;Xiaolan Guo,&nbsp;Jialu Yu,&nbsp;Yuanfang Lu,&nbsp;Wensen Cao,&nbsp;Xiuwei Wang,&nbsp;Zhiqiang Zhu,&nbsp;Zhen Guan,&nbsp;Aiyun Yang,&nbsp;Shen Li,&nbsp;Xiaochun Xu,&nbsp;Caihua Wang,&nbsp;Jianhua Wang","doi":"10.1002/brb3.71150","DOIUrl":"10.1002/brb3.71150","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Congenital malformations of the nervous system, such as neural tube defects, are significant contributors to infant morbidity and mortality. This study aimed to assess the causal influence of gut microbiota on nervous system malformations and to identify immune cells as potential mediators in this relationship, utilizing a two-step Mendelian randomization (TSMR) approach.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using genome-wide association studies data on gut microbiota, immune cells, and congenital malformations of the nervous system, we applied TSMR to evaluate the total, direct, and mediating effects. Gut microbiota indicators served as exposures, congenital malformations of the nervous system as outcomes, and immune cell markers as mediators. Statistical analyses included MR Egger, inverse variance weighted, and so forth.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our analysis identified 19 gut microbiota indicators causally associated with congenital malformations of the nervous system. Notably, <i>Eubacteriaceae</i> and <i>Eubacterium</i> genera exhibited protective effects, while <i>Escherichia</i> and <i>Bacteroides</i> genera showed positive correlations with malformation risk. Nine immune cell indicators significantly mediated these effects. For example, CD20<sup>+</sup> B cells were negatively associated with malformation risk, suggesting a protective immune response, whereas CD25<sup>+</sup> B cells were positively correlated, indicating increased malformation risk.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study demonstrated a significant link between gut microbiota composition and congenital nervous system malformations, mediated by specific immune cells. These findings highlighted the potential for gut microbiota modulation and immune-targeted therapies as preventive or therapeutic strategies in reducing malformation risks. Future investigations should aim to replicate these results across diverse populations and further elucidate the underlying biological mechanisms of gut–immune–neural interactions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>The authors have nothing to report.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"16 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12754823/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145861943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Baishaoluoshi Decoction Mitigates Post-Stroke Spasticity by Targeting Synaptic Plasticity Through the Nogo-A/NgR Signaling Pathway 白芍络石汤通过Nogo-A/NgR信号通路靶向突触可塑性减轻脑卒中后痉挛
IF 2.7 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-12-31 DOI: 10.1002/brb3.71170
Xiongxing Sun, Shanshan Zeng, Shigao Lin, Lingying Wu, Xukun Tang, Jiajian Zhu, Yuhui Zhang, Lu Li, Ziming Chen, Xinyu Deng, Dahua Wu, Le Xie

Objective:

This study systematically investigated the effects and molecular mechanisms of Baishaoluoshi Decoction (BD) on synaptic plasticity in rats with post-stroke spasticity (PSS).

Methods

A rat model of PSS was established using middle cerebral artery occlusion. Behavioral assessments, including modified neurological severity scores, rotarod tests, and the Modified Ashworth Scale, were employed. Synaptic ultrastructure was analyzed using transmission electron microscopy (TEM). The molecular mechanisms were explored using immunofluorescence and western blot analyses to evaluate protein expression (Nogo-A, Nogo receptor (NgR), RhoA, Collapsin Response Mediator Protein 2 (CRMP2), and AGG) and NgR/Olig2 colocalization. BD was also tested in combination with the NgR antagonist NEP1-40.

Results

BD significantly ameliorated the neurological deficits, prolonged rotarod fall latency, and reduced spasticity. TEM revealed that BD restored the synaptic ultrastructure in the peri-infarct regions by increasing postsynaptic density (PSD) thickness and length, and narrowing synaptic clefts. BD downregulates synaptic-plasticity-related proteins (Nogo-A, NgR, RhoA, AGG, and CRMP2) and attenuates oligodendrocyte-mediated inhibitory signaling via reduced NgR/Olig2 co-localization. BD combined with NEP1-40 exhibits synergistic therapeutic efficacy.

Conclusion

BD alleviates PSS by enhancing synaptic plasticity and suppressing inhibitory signaling through multitarget modulation of neuron–glia interactions. These findings highlight BD as a promising therapeutic intervention for PSS, which is supported by molecular evidence of its effects on synaptic remodeling and functional recovery.

目的:系统探讨白芍络石汤对脑卒中后痉挛大鼠突触可塑性的影响及其分子机制。方法:采用大脑中动脉闭塞法建立大鼠PSS模型。行为评估,包括改进的神经严重程度评分、旋转测试和改进的Ashworth量表。透射电镜观察突触超微结构。利用免疫荧光和western blot分析探讨了分子机制,以评估蛋白表达(Nogo- a、Nogo受体(NgR)、RhoA、Collapsin Response Mediator protein 2 (CRMP2)和AGG)和NgR/Olig2共定位。BD还与NgR拮抗剂NEP1-40联合进行了试验。结果:BD可显著改善神经功能缺损,延长旋转跌倒潜伏期,减轻痉挛。透射电镜显示,BD通过增加突触后密度(PSD)厚度和长度,缩小突触间隙,恢复了梗死周围区域的突触超微结构。BD下调突触可塑性相关蛋白(Nogo-A、NgR、RhoA、AGG和CRMP2),并通过减少NgR/Olig2共定位减弱少突胶质细胞介导的抑制信号。BD联合NEP1-40具有协同治疗效果。结论:BD通过多靶点调节神经元-胶质细胞相互作用,增强突触可塑性,抑制抑制性信号传导,从而减轻PSS。这些发现强调了双酚d作为一种有希望的PSS治疗干预措施,其对突触重塑和功能恢复的影响得到了分子证据的支持。
{"title":"Baishaoluoshi Decoction Mitigates Post-Stroke Spasticity by Targeting Synaptic Plasticity Through the Nogo-A/NgR Signaling Pathway","authors":"Xiongxing Sun,&nbsp;Shanshan Zeng,&nbsp;Shigao Lin,&nbsp;Lingying Wu,&nbsp;Xukun Tang,&nbsp;Jiajian Zhu,&nbsp;Yuhui Zhang,&nbsp;Lu Li,&nbsp;Ziming Chen,&nbsp;Xinyu Deng,&nbsp;Dahua Wu,&nbsp;Le Xie","doi":"10.1002/brb3.71170","DOIUrl":"10.1002/brb3.71170","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective:</h3>\u0000 \u0000 <p>This study systematically investigated the effects and molecular mechanisms of Baishaoluoshi Decoction (BD) on synaptic plasticity in rats with post-stroke spasticity (PSS).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A rat model of PSS was established using middle cerebral artery occlusion. Behavioral assessments, including modified neurological severity scores, rotarod tests, and the Modified Ashworth Scale, were employed. Synaptic ultrastructure was analyzed using transmission electron microscopy (TEM). The molecular mechanisms were explored using immunofluorescence and western blot analyses to evaluate protein expression (Nogo-A, Nogo receptor (NgR), RhoA, Collapsin Response Mediator Protein 2 (CRMP2), and AGG) and NgR/Olig2 colocalization. BD was also tested in combination with the NgR antagonist NEP1-40.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>BD significantly ameliorated the neurological deficits, prolonged rotarod fall latency, and reduced spasticity. TEM revealed that BD restored the synaptic ultrastructure in the peri-infarct regions by increasing postsynaptic density (PSD) thickness and length, and narrowing synaptic clefts. BD downregulates synaptic-plasticity-related proteins (Nogo-A, NgR, RhoA, AGG, and CRMP2) and attenuates oligodendrocyte-mediated inhibitory signaling via reduced NgR/Olig2 co-localization. BD combined with NEP1-40 exhibits synergistic therapeutic efficacy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>BD alleviates PSS by enhancing synaptic plasticity and suppressing inhibitory signaling through multitarget modulation of neuron–glia interactions. These findings highlight BD as a promising therapeutic intervention for PSS, which is supported by molecular evidence of its effects on synaptic remodeling and functional recovery.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"16 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12755059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145861983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Demographic and Behavioral Correlates of Social Media Addiction and Loneliness Among Young Adults in Kyrgyzstan 吉尔吉斯斯坦年轻人社交媒体成瘾与孤独感的人口统计学和行为学相关性
IF 2.7 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-12-31 DOI: 10.1002/brb3.71166
Niyazi Ayhan, Bedir Eroğlu

Introduction:

Digital technologies now shape nearly every aspect of daily life, raising growing concern about how they influence people's psychological and social well-being, especially among youth in developing societies. This study examines the relationship between social media addiction and perceived loneliness among young adults in Kyrgyzstan, a rapidly digitizing Central Asian country, with a particular focus on demographic differences such as age and gender.

Methods:

A cross-sectional survey design was used. Data were gathered from 426 participants aged 18–26 using the Bergen Social Media Addiction Scale (BSMAS) and the UCLA Loneliness Scale. Along with correlation analysis, independent-samples t-tests, one-way analysis of variance (ANOVA), and multiple regression analyses were conducted to examine demographic variations and relational patterns.

Results:

The results showed a small yet meaningful link between social media addiction and loneliness (r = 0.161, p = 0.001). Women were more likely to display higher addiction levels, whereas men reported feeling lonelier. Participants aged 24–26 exhibited the highest loneliness scores.

Conclusion:

These findings suggest that digital behavior and demographic factors may be important considerations in psychological screening and intervention strategies for young people.

导言:数字技术现在几乎影响着日常生活的方方面面,人们越来越关注数字技术如何影响人们的心理和社会福祉,尤其是发展中社会的青年。本研究考察了吉尔吉斯斯坦(一个快速数字化的中亚国家)年轻人的社交媒体成瘾与感知孤独之间的关系,特别关注年龄和性别等人口统计学差异。方法:采用横断面调查设计。使用卑尔根社交媒体成瘾量表(BSMAS)和加州大学洛杉矶分校孤独量表从426名18-26岁的参与者中收集数据。除相关分析外,还进行了独立样本t检验、单因素方差分析(ANOVA)和多元回归分析,以检验人口统计学差异和相关模式。结果:结果显示社交媒体成瘾和孤独感之间存在微小但有意义的联系(r = 0.161, p = 0.001)。女性更有可能表现出更高的上瘾程度,而男性则报告感觉更孤独。24-26岁的参与者表现出最高的孤独感得分。结论:这些发现表明,数字行为和人口因素可能是青少年心理筛查和干预策略的重要考虑因素。
{"title":"Demographic and Behavioral Correlates of Social Media Addiction and Loneliness Among Young Adults in Kyrgyzstan","authors":"Niyazi Ayhan,&nbsp;Bedir Eroğlu","doi":"10.1002/brb3.71166","DOIUrl":"10.1002/brb3.71166","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction:</h3>\u0000 \u0000 <p>Digital technologies now shape nearly every aspect of daily life, raising growing concern about how they influence people's psychological and social well-being, especially among youth in developing societies. This study examines the relationship between social media addiction and perceived loneliness among young adults in Kyrgyzstan, a rapidly digitizing Central Asian country, with a particular focus on demographic differences such as age and gender.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods:</h3>\u0000 \u0000 <p>A cross-sectional survey design was used. Data were gathered from 426 participants aged 18–26 using the Bergen Social Media Addiction Scale (BSMAS) and the UCLA Loneliness Scale. Along with correlation analysis, independent-samples <i>t</i>-tests, one-way analysis of variance (ANOVA), and multiple regression analyses were conducted to examine demographic variations and relational patterns.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results:</h3>\u0000 \u0000 <p>The results showed a small yet meaningful link between social media addiction and loneliness (<i>r</i> = 0.161, <i>p</i> = 0.001). Women were more likely to display higher addiction levels, whereas men reported feeling lonelier. Participants aged 24–26 exhibited the highest loneliness scores.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion:</h3>\u0000 \u0000 <p>These findings suggest that digital behavior and demographic factors may be important considerations in psychological screening and intervention strategies for young people.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"16 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12755396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","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 Sphingolipid Metabolism and Neuron Death in Ischemic Stroke: A New Perspective from Bioinformatics 鞘脂代谢和神经元死亡在缺血性卒中中的作用:生物信息学的新视角。
IF 2.7 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-12-31 DOI: 10.1002/brb3.71172
Zhong-can Chen, Fang-biao Xu, Sen Hu, Qiang Cui, Hugo Andrade Barazarte, Jing Zhang, Li-na Suo, Jian-jun Gu, Jiang-yu Xue
<div> <section> <h3> Background</h3> <p>Ischemic stroke (IS) is a leading cause of death and disability worldwide, but traditional risk factors do not fully explain its pathophysiology. Neuronal death in IS is influenced by multiple pathways, including sphingolipid metabolism, which plays a significant role in neuronal function and survival. Ceramides, key sphingolipid molecules, are involved in various neuronal processes, including cell death. This study aims to explore the relationship between sphingolipid metabolism and neuron death in IS using bulk and single-cell transcriptomics.</p> </section> <section> <h3> Methods</h3> <p>We obtained sphingolipid metabolism gene sets from the GeneCard database and analyzed differential gene expression in IS datasets from the GEO database, including human peripheral blood bulk data (GSE16561) and MCAO mouse peripheral blood scRNA sequencing data (GSE225948). Gene set enrichment analysis (GSEA), immune infiltration analysis using CIBERSORT, and protein-protein interaction network construction were performed. Single-cell RNA sequencing (scRNA-seq) data were used to identify key genes and analyze cellular heterogeneity, differentiation, and cell interactions. In vivo validation of key gene expression was conducted in MCAO rats.</p> </section> <section> <h3> Results</h3> <p>GSEA revealed significant changes in the sphingolipid metabolism pathway in IS patients. Immune infiltration analysis showed altered immune cell profiles, with decreases in CD8 T cells and increases in monocytes and neutrophils. Enrichment analysis of sphingolipid metabolism-related genes highlighted pathways such as the sphingolipid signaling pathway and ceramide metabolism. Protein-protein interaction network analysis identified 19 key genes linked to sphingolipid metabolism and neuron death. scRNA-seq analysis revealed significant changes in sphingolipid metabolism in monocytes and neutrophils, with the App gene showing notable differential expression. Pseudotime analysis suggested diverse differentiation trajectories in monocytes, and cell interaction analysis indicated potential communication between monocytes and B cells. In vivo validation confirmed higher App gene expression in MCAO rats compared to sham controls.</p> </section> <section> <h3> Conclusion</h3> <p>This study provides comprehensive insights into the role of sphingolipid metabolism in ischemic stroke, identifying key genes and cellular mechanisms involved in neuron death. The findings suggest that sphingolipid metabolism, particularly through the App gene, may be a potent
背景:缺血性脑卒中(IS)是世界范围内导致死亡和残疾的主要原因,但传统的危险因素并不能完全解释其病理生理。IS的神经元死亡受多种途径影响,其中鞘脂代谢在神经元功能和存活中起重要作用。神经酰胺是神经鞘脂的关键分子,参与各种神经过程,包括细胞死亡。本研究旨在利用大量和单细胞转录组学研究IS鞘脂代谢与神经元死亡之间的关系。方法:从GeneCard数据库中获取鞘脂代谢基因集,并从GEO数据库中分析IS数据集中的差异基因表达,包括人外周血容量数据(GSE16561)和MCAO小鼠外周血scRNA测序数据(GSE225948)。基因集富集分析(GSEA)、免疫浸润分析(CIBERSORT)和蛋白相互作用网络构建。单细胞RNA测序(scRNA-seq)数据用于鉴定关键基因并分析细胞异质性、分化和细胞相互作用。在MCAO大鼠体内验证关键基因的表达。结果:GSEA显示IS患者鞘脂代谢途径发生显著变化。免疫浸润分析显示免疫细胞谱改变,CD8 T细胞减少,单核细胞和中性粒细胞增加。鞘脂代谢相关基因富集分析突出了鞘脂信号通路和神经酰胺代谢等途径。蛋白质-蛋白质相互作用网络分析确定了与鞘脂代谢和神经元死亡相关的19个关键基因。scRNA-seq分析显示,单核细胞和中性粒细胞鞘脂代谢发生显著变化,App基因表达差异显著。伪时间分析表明单核细胞的分化轨迹多样,细胞相互作用分析表明单核细胞与B细胞之间存在潜在的交流。体内验证证实,与假对照组相比,MCAO大鼠的App基因表达更高。结论:本研究为神经鞘脂代谢在缺血性卒中中的作用提供了全面的见解,确定了参与神经元死亡的关键基因和细胞机制。研究结果表明,鞘脂代谢,特别是通过App基因,可能是IS的潜在治疗靶点。进一步探索鞘脂的分子机制和细胞相互作用可能会导致缺血性卒中的新治疗策略。
{"title":"The Role of Sphingolipid Metabolism and Neuron Death in Ischemic Stroke: A New Perspective from Bioinformatics","authors":"Zhong-can Chen,&nbsp;Fang-biao Xu,&nbsp;Sen Hu,&nbsp;Qiang Cui,&nbsp;Hugo Andrade Barazarte,&nbsp;Jing Zhang,&nbsp;Li-na Suo,&nbsp;Jian-jun Gu,&nbsp;Jiang-yu Xue","doi":"10.1002/brb3.71172","DOIUrl":"10.1002/brb3.71172","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Ischemic stroke (IS) is a leading cause of death and disability worldwide, but traditional risk factors do not fully explain its pathophysiology. Neuronal death in IS is influenced by multiple pathways, including sphingolipid metabolism, which plays a significant role in neuronal function and survival. Ceramides, key sphingolipid molecules, are involved in various neuronal processes, including cell death. This study aims to explore the relationship between sphingolipid metabolism and neuron death in IS using bulk and single-cell transcriptomics.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;We obtained sphingolipid metabolism gene sets from the GeneCard database and analyzed differential gene expression in IS datasets from the GEO database, including human peripheral blood bulk data (GSE16561) and MCAO mouse peripheral blood scRNA sequencing data (GSE225948). Gene set enrichment analysis (GSEA), immune infiltration analysis using CIBERSORT, and protein-protein interaction network construction were performed. Single-cell RNA sequencing (scRNA-seq) data were used to identify key genes and analyze cellular heterogeneity, differentiation, and cell interactions. In vivo validation of key gene expression was conducted in MCAO rats.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;GSEA revealed significant changes in the sphingolipid metabolism pathway in IS patients. Immune infiltration analysis showed altered immune cell profiles, with decreases in CD8 T cells and increases in monocytes and neutrophils. Enrichment analysis of sphingolipid metabolism-related genes highlighted pathways such as the sphingolipid signaling pathway and ceramide metabolism. Protein-protein interaction network analysis identified 19 key genes linked to sphingolipid metabolism and neuron death. scRNA-seq analysis revealed significant changes in sphingolipid metabolism in monocytes and neutrophils, with the App gene showing notable differential expression. Pseudotime analysis suggested diverse differentiation trajectories in monocytes, and cell interaction analysis indicated potential communication between monocytes and B cells. In vivo validation confirmed higher App gene expression in MCAO rats compared to sham controls.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;This study provides comprehensive insights into the role of sphingolipid metabolism in ischemic stroke, identifying key genes and cellular mechanisms involved in neuron death. The findings suggest that sphingolipid metabolism, particularly through the App gene, may be a potent","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"16 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12755557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mobile Phone Addiction and Academic Procrastination in Adolescents: The Serial Mediating Roles of Self-Regulation and Psychological Resilience and the Moderating Role of the Parent-Child Relationship 青少年手机成瘾与学业拖延:自我调节、心理弹性的连续中介作用及亲子关系的调节作用
IF 2.7 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-12-31 DOI: 10.1002/brb3.71169
Yang Liu, Yan Lin, Shaokun Zhao, Fan Wang, Qingying Yuan, Yongsheng Tong

Background

Mobile phone addiction and academic procrastination are two common behavioral challenges among adolescents. While prior research has documented their association, the underlying mechanisms—particularly the mediating roles of self-regulation and psychological resilience and the moderating role of the parent-child relationship —remain insufficiently examined.

Methods

This study involved 966 adolescents who completed the Mobile Phone Addiction Scale, Self-Regulation Scale, Brief Resilience Scale, Parent-Child Relationship Scale, and Academic Procrastination Scale–Short Form. Data were analyzed using partial least squares structural equation modeling (PLS-SEM).

Results

The results of the research showed that (1) mobile phone addiction had a significant positive effect on academic procrastination; (2) self-regulation mediated between mobile phone addiction and academic procrastination; (3) psychological resilience mediated between mobile phone addiction and academic procrastination; (4) self-regulation and psychological resilience served as serial mediators between mobile phone addiction and academic procrastination and (5) parent-child relationship significantly moderated the association of mobile phone addiction on academic procrastination.

Conclusion

This study describes the further relationships among mobile phone addiction, academic procrastination, and related factors in adolescents. The observed patterns suggest that approaches to adolescent well-being may benefit from integrated frameworks considering individual, familial, and educational dimensions—with a particular focus on the role of self-regulation, psychological resilience, and parent-child relationship.

背景:手机成瘾和学习拖延是青少年中常见的两种行为挑战。虽然先前的研究已经证明了它们之间的联系,但潜在的机制——特别是自我调节和心理弹性的中介作用以及亲子关系的调节作用——仍然没有得到充分的研究。方法:对966名青少年进行手机成瘾量表、自我调节量表、简易弹性量表、亲子关系量表和学业拖延量表(简表)的问卷调查。数据分析采用偏最小二乘结构方程模型(PLS-SEM)。结果:研究结果表明:(1)手机成瘾对学业拖延有显著的正向影响;(2)自我调节在手机成瘾与学业拖延之间起中介作用;(3)心理弹性在手机成瘾与学业拖延之间起中介作用;(4)自我调节和心理弹性在手机成瘾与学业拖延之间起串行中介作用;(5)亲子关系显著调节手机成瘾对学业拖延的影响。结论:本研究进一步描述了青少年手机成瘾、学业拖延及其相关因素之间的关系。观察到的模式表明,考虑到个人、家庭和教育维度的综合框架,特别是关注自我调节、心理弹性和亲子关系的作用,可以使青少年幸福的方法受益。
{"title":"Mobile Phone Addiction and Academic Procrastination in Adolescents: The Serial Mediating Roles of Self-Regulation and Psychological Resilience and the Moderating Role of the Parent-Child Relationship","authors":"Yang Liu,&nbsp;Yan Lin,&nbsp;Shaokun Zhao,&nbsp;Fan Wang,&nbsp;Qingying Yuan,&nbsp;Yongsheng Tong","doi":"10.1002/brb3.71169","DOIUrl":"10.1002/brb3.71169","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Mobile phone addiction and academic procrastination are two common behavioral challenges among adolescents. While prior research has documented their association, the underlying mechanisms—particularly the mediating roles of self-regulation and psychological resilience and the moderating role of the parent-child relationship —remain insufficiently examined.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study involved 966 adolescents who completed the Mobile Phone Addiction Scale, Self-Regulation Scale, Brief Resilience Scale, Parent-Child Relationship Scale, and Academic Procrastination Scale–Short Form. Data were analyzed using partial least squares structural equation modeling (PLS-SEM).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The results of the research showed that (1) mobile phone addiction had a significant positive effect on academic procrastination; (2) self-regulation mediated between mobile phone addiction and academic procrastination; (3) psychological resilience mediated between mobile phone addiction and academic procrastination; (4) self-regulation and psychological resilience served as serial mediators between mobile phone addiction and academic procrastination and (5) parent-child relationship significantly moderated the association of mobile phone addiction on academic procrastination.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study describes the further relationships among mobile phone addiction, academic procrastination, and related factors in adolescents. The observed patterns suggest that approaches to adolescent well-being may benefit from integrated frameworks considering individual, familial, and educational dimensions—with a particular focus on the role of self-regulation, psychological resilience, and parent-child relationship.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"16 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71169","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Unveiling the Genetic Association Between Hemoglobin Concentration and Amyotrophic Lateral Sclerosis 揭示血红蛋白浓度与肌萎缩性侧索硬化症之间的遗传关系。
IF 2.7 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-12-31 DOI: 10.1002/brb3.71152
Hongmei Luo, Yujie Yang, Xiaojian Cao, Chunchu Deng, Hong Chen

Background

Although previous studies have suggested an association between hemoglobin (Hb) concentration and amyotrophic lateral sclerosis (ALS), the precise cause-and-effect relationship between them is still unclear. This study aims to investigate the causal correlation between Hb concentration and ALS, and explore the potential genes related to their association.

Methods

We extracted summary statistical data of Hb concentration and ALS from genome-wide association studies (GWAS), performed Mendelian randomization (MR) analyses, and conducted RNA sequencing of motor neurons different from ALS patient-derived induced pluripotent stem cells (iPSCs), followed by an intersection analysis between differentially expressed genes (DEGs) in ALS motor neurons and selected instrumental variables (IVs) associated with Hb concentration.

Results

As a result, Hb concentration had a negative causal relationship with the risk of ALS, established through IVW (OR = 0.854; 95% CI: 0.767–0.951; p = 0.00418) of the univariable MR analysis. A multivariable MR further confirmed that this causal link remained robust, even when accounting for confounders including systolic blood pressure, total cholesterol levels, body mass index, LDL cholesterol, diastolic blood pressure, and smoking. Importantly, genetically predicted ALS did not show a causal connection to Hb concentration. Additionally, RNA sequencing analysis and qRT-PCR results revealed that transcripts for BACH1 and FLVCR1 were upregulated, while those for TRIM58 were downregulated in SOD1D90A ALS motor neurons, compared to the control. In motor neurons differentiated from a sporadic ALS patient-derived iPSCs, qRT-PCR showed increased transcript levels of BACH1, and decreased transcript levels of FLVCR1 and TRIM58. These three genes were intersected with harmonized SNPs between Hb concentration and ALS.

Conclusion

Our study concludes that genetically predicted Hb concentration exhibited an independent inverse causal association with the risk of developing ALS, with potential involvement of genes such as BACH1, FLVCR1, and TRIM58.

背景:虽然以前的研究表明血红蛋白(Hb)浓度与肌萎缩侧索硬化症(ALS)之间存在关联,但它们之间确切的因果关系尚不清楚。本研究旨在探讨Hb浓度与ALS之间的因果关系,并探索其关联的潜在基因。方法:我们从全基因组关联研究(GWAS)中提取Hb浓度和ALS的汇总统计数据,进行孟德尔随机化(MR)分析,并对ALS患者来源的诱导多能干细胞(iPSCs)不同的运动神经元进行RNA测序,随后对ALS运动神经元中差异表达基因(DEGs)和选定的与Hb浓度相关的工具变量(IVs)进行交叉分析。结果:通过单变量MR分析的IVW (OR = 0.854; 95% CI: 0.767-0.951; p = 0.00418), Hb浓度与ALS的风险呈负因果关系。多变量磁共振进一步证实,即使考虑到包括收缩压、总胆固醇水平、体重指数、低密度脂蛋白胆固醇、舒张压和吸烟在内的混杂因素,这种因果关系仍然很明显。重要的是,基因预测的ALS没有显示出与Hb浓度的因果关系。此外,RNA测序分析和qRT-PCR结果显示,与对照组相比,SOD1D90A ALS运动神经元中BACH1和FLVCR1转录本上调,而TRIM58转录本下调。在散发性ALS患者来源的iPSCs分化的运动神经元中,qRT-PCR显示BACH1转录水平升高,FLVCR1和TRIM58转录水平降低。这三个基因在Hb浓度和ALS之间有统一的snp相交。结论:我们的研究得出结论,基因预测的Hb浓度与ALS发生风险呈独立的负相关,可能与BACH1、FLVCR1和TRIM58等基因有关。
{"title":"Unveiling the Genetic Association Between Hemoglobin Concentration and Amyotrophic Lateral Sclerosis","authors":"Hongmei Luo,&nbsp;Yujie Yang,&nbsp;Xiaojian Cao,&nbsp;Chunchu Deng,&nbsp;Hong Chen","doi":"10.1002/brb3.71152","DOIUrl":"10.1002/brb3.71152","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Although previous studies have suggested an association between hemoglobin (Hb) concentration and amyotrophic lateral sclerosis (ALS), the precise cause-and-effect relationship between them is still unclear. This study aims to investigate the causal correlation between Hb concentration and ALS, and explore the potential genes related to their association.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We extracted summary statistical data of Hb concentration and ALS from genome-wide association studies (GWAS), performed Mendelian randomization (MR) analyses, and conducted RNA sequencing of motor neurons different from ALS patient-derived induced pluripotent stem cells (iPSCs), followed by an intersection analysis between differentially expressed genes (DEGs) in ALS motor neurons and selected instrumental variables (IVs) associated with Hb concentration.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>As a result, Hb concentration had a negative causal relationship with the risk of ALS, established through IVW (OR = 0.854; 95% CI: 0.767–0.951; <i>p</i> = 0.00418) of the univariable MR analysis. A multivariable MR further confirmed that this causal link remained robust, even when accounting for confounders including systolic blood pressure, total cholesterol levels, body mass index, LDL cholesterol, diastolic blood pressure, and smoking. Importantly, genetically predicted ALS did not show a causal connection to Hb concentration. Additionally, RNA sequencing analysis and qRT-PCR results revealed that transcripts for <i>BACH1</i> and <i>FLVCR1</i> were upregulated, while those for <i>TRIM58</i> were downregulated in <i>SOD1</i><sup>D90A</sup> ALS motor neurons, compared to the control. In motor neurons differentiated from a sporadic ALS patient-derived iPSCs, qRT-PCR showed increased transcript levels of <i>BACH1</i>, and decreased transcript levels of <i>FLVCR1</i> and <i>TRIM58</i>. These three genes were intersected with harmonized SNPs between Hb concentration and ALS.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our study concludes that genetically predicted Hb concentration exhibited an independent inverse causal association with the risk of developing ALS, with potential involvement of genes such as <i>BACH1</i>, <i>FLVCR1</i>, and <i>TRIM58</i>.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"16 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12755399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Genetic Association Between Polymyositis/Dermatomyositis and Epilepsy: Insights From Mendelian Randomization and Bioinformatic Analyses 多肌炎/皮肌炎与癫痫的遗传关联:孟德尔随机化和生物信息学分析的见解。
IF 2.7 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-12-29 DOI: 10.1002/brb3.71148
Ying Liu, Yuhang Yu, Chulong Fang, Qingzhong Wu, Lingli Ou, Jianhao Xiao, Kui Duan, Ting Jiang, Lan Ye, Xiao Hu, Zhanhui Feng
<div> <section> <h3> Background:</h3> <p>Idiopathic inflammatory myositis (IIM), comprising polymyositis (PM) and dermatomyositis (DM), is a collective term for immune-mediated diseases characterized by skeletal muscle inflammation. Emerging evidence points to an increased incidence of epilepsy in patients with PM/DM. However, the causality and underlying mechanisms behind this association are unclear. Our study aimed to explore the potential causal link between PM/DM and epilepsy, with a focus on immune-mediated mechanisms, using Mendelian randomization (MR) and transcriptome analyses.</p> </section> <section> <h3> Methods:</h3> <p>Initially, summary data from genome-wide association studies (GWAS) related to polymyositis (PM; finn-b-M13_POLYMYO), dermatomyositis (DM; finn-b-DERMATOPOLY_FG), and epilepsy (ebi-a-GCST90018840) were obtained from the Integrative Epidemiology Unit Open GWAS database. These data were utilized for Mendelian randomization (MR) analysis and generalized summary data based Mendelian randomization (GSMR). To ensure the robustness of the findings, sensitivity analyses were conducted to corroborate the results of the MR analyses. Subsequently, the study leveraged publicly accessible databases and bioinformatics tools to conduct comprehensive analyses of gene expression data. This included differential expression analysis, immune infiltration analysis, and gene enrichment analysis. Differentially expressed SNP-related genes (DE-SRGs) were further analyzed using single-cell transcriptomics. Finally, the expression of four key genes (IER3, TNF, GPANK1, and ATF6B) in the hippocampus of epilepsy mouse model was quantified using PCR.</p> </section> <section> <h3> Results:</h3> <p>The MR analysis disclosed a causal association between PM and epilepsy, whereas the reverse MR analysis did not identify a significant causal effect of epilepsy on PM. However, there was no association between DM and epilepsy of MR analysis. The Transcriptome analysis not only identified DE-SRGs but also revealed distinct immune cell infiltration patterns in epilepsy patients. Specifically, we observed SRGs are mainly expressed in endothelial cells, microglia, and T cells, indicative of a proinflammatory state. Furthermore, the gene set variation analysis (GSVA) highlighted the differential activation of pathways in these cell types, including inflammatory response and allograft rejection, which were significantly upregulated. PCR results show the expression of IER3, TNF, GPANK1, and ATF6B in hippocampus of epilepsy model largely consistent with bioinformatics predictions.</p> </section> <section>
背景:特发性炎症性肌炎(IIM),包括多发性肌炎(PM)和皮肌炎(DM),是以骨骼肌炎症为特征的免疫介导疾病的总称。新出现的证据表明PM/DM患者癫痫发病率增加。然而,这种关联背后的因果关系和潜在机制尚不清楚。我们的研究旨在探索PM/DM与癫痫之间的潜在因果关系,重点是免疫介导的机制,使用孟德尔随机化(MR)和转录组分析。方法:最初,从综合流行病学单位开放GWAS数据库中获得与多肌炎(PM; fin -b- m13_polymyo)、皮肌炎(DM; fin -b- dermatopoly_fg)和癫痫(ebi-a-GCST90018840)相关的全基因组关联研究(GWAS)的汇总数据。这些数据被用于孟德尔随机化(MR)分析和基于孟德尔随机化的广义汇总数据(GSMR)。为了确保研究结果的稳健性,进行了敏感性分析以证实MR分析的结果。随后,该研究利用可公开访问的数据库和生物信息学工具对基因表达数据进行了全面分析。这包括差异表达分析、免疫浸润分析和基因富集分析。差异表达的snp相关基因(DE-SRGs)进一步使用单细胞转录组学进行分析。最后,采用PCR方法定量分析癫痫小鼠模型海马中四个关键基因(IER3、TNF、GPANK1、ATF6B)的表达。结果:MR分析揭示了PM和癫痫之间的因果关系,而反向MR分析没有发现癫痫对PM的显著因果影响。然而,在MR分析中没有发现糖尿病与癫痫之间的关联。转录组分析不仅鉴定了DE-SRGs,还揭示了癫痫患者独特的免疫细胞浸润模式。具体来说,我们观察到SRGs主要在内皮细胞、小胶质细胞和T细胞中表达,表明促炎状态。此外,基因集变异分析(GSVA)强调了这些细胞类型中通路的差异激活,包括炎症反应和同种异体移植排斥反应,这些通路显着上调。PCR结果显示癫痫模型海马中IER3、TNF、GPANK1、ATF6B的表达与生物信息学预测基本一致。结论:本研究显示PM与癫痫之间存在因果关系,癫痫对PM无显著影响。糖尿病和癫痫之间没有因果关系。DM与癫痫之间联系的缺失可能反映了免疫病理的根本差异:PM是由T细胞介导的肌肉侵袭驱动的,而DM主要涉及体液免疫和补体沉积,表明不同的神经炎症影响。我们的研究结果确定免疫介导的神经炎症是PM和癫痫发生之间的中心机制联系。这些发现暗示了共同的免疫致病机制,并提示了多发性肌炎相关癫痫的治疗靶点。
{"title":"Genetic Association Between Polymyositis/Dermatomyositis and Epilepsy: Insights From Mendelian Randomization and Bioinformatic Analyses","authors":"Ying Liu,&nbsp;Yuhang Yu,&nbsp;Chulong Fang,&nbsp;Qingzhong Wu,&nbsp;Lingli Ou,&nbsp;Jianhao Xiao,&nbsp;Kui Duan,&nbsp;Ting Jiang,&nbsp;Lan Ye,&nbsp;Xiao Hu,&nbsp;Zhanhui Feng","doi":"10.1002/brb3.71148","DOIUrl":"10.1002/brb3.71148","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background:&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Idiopathic inflammatory myositis (IIM), comprising polymyositis (PM) and dermatomyositis (DM), is a collective term for immune-mediated diseases characterized by skeletal muscle inflammation. Emerging evidence points to an increased incidence of epilepsy in patients with PM/DM. However, the causality and underlying mechanisms behind this association are unclear. Our study aimed to explore the potential causal link between PM/DM and epilepsy, with a focus on immune-mediated mechanisms, using Mendelian randomization (MR) and transcriptome analyses.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods:&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Initially, summary data from genome-wide association studies (GWAS) related to polymyositis (PM; finn-b-M13_POLYMYO), dermatomyositis (DM; finn-b-DERMATOPOLY_FG), and epilepsy (ebi-a-GCST90018840) were obtained from the Integrative Epidemiology Unit Open GWAS database. These data were utilized for Mendelian randomization (MR) analysis and generalized summary data based Mendelian randomization (GSMR). To ensure the robustness of the findings, sensitivity analyses were conducted to corroborate the results of the MR analyses. Subsequently, the study leveraged publicly accessible databases and bioinformatics tools to conduct comprehensive analyses of gene expression data. This included differential expression analysis, immune infiltration analysis, and gene enrichment analysis. Differentially expressed SNP-related genes (DE-SRGs) were further analyzed using single-cell transcriptomics. Finally, the expression of four key genes (IER3, TNF, GPANK1, and ATF6B) in the hippocampus of epilepsy mouse model was quantified using PCR.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results:&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The MR analysis disclosed a causal association between PM and epilepsy, whereas the reverse MR analysis did not identify a significant causal effect of epilepsy on PM. However, there was no association between DM and epilepsy of MR analysis. The Transcriptome analysis not only identified DE-SRGs but also revealed distinct immune cell infiltration patterns in epilepsy patients. Specifically, we observed SRGs are mainly expressed in endothelial cells, microglia, and T cells, indicative of a proinflammatory state. Furthermore, the gene set variation analysis (GSVA) highlighted the differential activation of pathways in these cell types, including inflammatory response and allograft rejection, which were significantly upregulated. PCR results show the expression of IER3, TNF, GPANK1, and ATF6B in hippocampus of epilepsy model largely consistent with bioinformatics predictions.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 ","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"16 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12748525/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145854398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Brain and Behavior
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1