期刊,中华医学杂志（英文版） 2024年卷22期_国家学术搜索

期刊信息/Journal information

中华医学杂志（英文版）

中华医学会

主办单位：中华医学会

主　　编：照日格图

出版周期：半月刊

国际刊号：0366-6999

电子邮箱：renlihua@cma.org.cn

电　　话：010-85158321

邮政编码：100710

地　　址：北京市东城区东四西大街42号

中华医学杂志（英文版）/Journal Chinese Medical JournalCSCDCSTPCD北大核心SCI

查看更多>>1887年创刊，中华医学会主办。中华医学杂志英文版(Chinese Medical Journal)是中华医学会会刊，是中国惟一被SCI核心版收录、具有百年以上历史的医学期刊。重点报道我国医学各学科最新进展和高水平科研成果，目前已被《科学引文索引（SCI）》、《医学索引（IM）》、Medline等国际著名检索系统收录。2009年SCI影响因子0.952，SCI被引频次3407。2010年被国际医学期刊编辑委员会（ICMJE）吸收为新成员。多次获得国家期刊奖、科协专项基金、自然基金等奖项和资助。实行全文上网（），网上投稿审稿()。

正式出版

收录年代

Related health burden with the improvement of air quality across China

Huaiyue XuQing WangHuanhuan ZhuYayi Zhang...

2726-2733页

查看更多>>摘要：Background:Substantial progress in air pollution control has brought considerable health benefits in China,but little is known about the spatio-temporal trends of economic burden from air pollution.This study aimed to explore their spatio-temporal features of disease burden from air pollution in China to provide policy recommendations for efficiently reducing the air pollution and related disease burden in an era of a growing economy.Methods:Using the Global Burden of Disease method and willingness to pay method,we estimated fine particulate matter(PM2.5)and/or ozone(O3)related premature mortality and its economic burden across China,and explored their spatio-temporal trends between 2005 and 2017.Results:In 2017,we estimated that the premature mortality and economic burden related to the two pollutants were RMB 0.94 million(68.49 per 100,000)and 1170.31 billion yuan(1.41％of the national gross domestic product[GDP]),respectively.From 2005 to 2017,the total premature mortality was decreasing with the air quality improvement,but the economic burden was increasing along with the economic growth.And the economic growth has contributed more to the growth of economic costs than the economic burden decrease brought by the air quality improvement.The premature mortality and economic burden from O3 in the total loss from the two pollutants was substantially lower than that of PM2.5,but it was rapidly growing.The O3-con-tribution was highest in the Yangtze River Delta region,the Fen-Wei Plain region,and some western regions.The proportion of economic burden from PM2.5 and O3 to GDP significantly declined from 2005 to 2017 and showed a decreasing trend pattern from northeast to southwest.Conclusion:The disease burden from O3 is lower than that of PM2.5,the O3-contribution has a significantly increasing trend with the growth of economy and O3 concentration.

原文链接:

国家科技期刊平台
NETL
NSTL
万方数据

Severe acute respiratory syndrome coronavirus 2-specific T-cell responses are induced in people living with human immunodeficiency virus after booster vaccination

Xiuwen WangYongzheng LiJunyan JinXiaoran Chai...

2734-2744页

查看更多>>摘要：Background:T-cell-mediated immunity is crucial for the effective clearance of viral infection,but the T-cell-mediated immune responses that are induced by booster doses of inactivated severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)vac-cines in people living with human immunodeficiency virus(PLWH)remain unclear.Methods:Forty-five PLWH who had received antiretroviral therapy(ART)for more than two years and 29 healthy controls(HCs)at Beijing Youan Hospital were enrolled to assess the dynamic changes in T-cell responses between the day before the third vaccine dose(week 0)and 4 or 12 weeks(week 4 or week 12)after receiving the third dose of inactivated SARS-CoV-2 vaccine.Flow cytometry,enzyme-linked immunospot(ELISpot),and multiplex cytokines profiling were used to assess T-cell responses at the three timepoints in this study.Results:The results of the ELISpot and activation-induced marker(AIM)assays showed that SARS-CoV-2-specific T-cell responses were increased in both PLWH and HCs after the third dose of the inactivated SARS-CoV-2 vaccine,and a similar magnitude of immune response was induced against the Omicron(B.1.1.529)variant compared to the wild-type strain.In detail,spike-specific T-cell responses(measured by the ELISpot assay for interferon γ[IFN-γ]release)in both PLWH and HCs significantly increased in week 4,and the spike-specific T-cell responses in HCs were significantly stronger than those in PLWH 4 weeks after the third vaccination.In the AIM assay,spike-specific CD4+T-cell responses peaked in both PLWH and HCs in week 12.Additionally,sig-nificantly higher spike-specific CD8+T-cell responses were induced in PLWH than in HCs in week 12.In PLWH,the release of the cytokines interleukin-2(IL-2),tumour necrosis factor-alpha(TNF-a),and IL-22 by peripheral blood mononuclear cells(PBMCs)that were stimulated with spike peptides increased in week 12.In addition,the levels of IL-4 and IL-5 were higher in PLWH than in HCs in week 12.Interestingly,the magnitude of SARS-CoV-2-specific T-cell responses in PLWH was negatively associated with the extent of CD8+T-cell activation and exhaustion.In addition,positive correlations were observed between the magnitude of spike-specific T-cell responses(determined by measuring IFN-γ release by ELISpot)and the amounts of IL-4,IL-5,IL-2 and IL-17F.Conclusions:Our findings suggested that SARS-CoV-2-specific T-cell responses could be enhanced by the booster dose of inactivated COVID-19 vaccines and further illustrate the importance of additional vaccination for PLWH.

原文链接:

国家科技期刊平台
NETL
NSTL
万方数据

Spatial transcriptomic analysis deciphers adipocyte-to-fibroblast transformation in bleomycin-induced murine skin fibrosis

Yixiang ZhangJiahao HeFangzhou XieShengzhou Shan...

2745-2757页

查看更多>>摘要：Background:Scleroderma is characterized by inflammation and fibrosis,predominantly occurring in the skin and extending to various parts of the body.The pathophysiology of scleroderma is multifaceted,with the current understanding including endo-thelial damage,inflammatory cell infiltration,and fibroblast activation in its progression.Nonetheless,the mechanism of cellular interactions and the precise spatial distribution of these cellular events within the fibrotic tissues remain elusive,highlighting a critical gap in our comprehensive understanding of scleroderma's pathogenesis.Methods:In this study,we administered bleomycin intradermally to the dorsal skin of four individual murine models.Subse-quently,skin tissues were harvested at predetermined intervals for comprehensive spatial transcriptomic analysis to determine the spatial dynamics influencing scleroderma pathogenesis.To validate the possible results from bioinformatic analysis,further in vitro and in vivo experiments were conducted.Results:Analysis of the spatial transcriptome revealed significant alterations in cell clusters during the progression of scleroderma.Gene Ontology analysis identified disruptions in lipid metabolism as the disease advanced.Pseudotime analysis provided evidence for a phenotypic transition from adipocytes to fibroblasts.In vitro studies demonstrated increased expression of Col1a1 andα-SMA as the disease progressed.These fibroblasts have been identified as key contributors to the increasing inflammation.Co-culturing TGF-β induced adipocytes with RAW264.7 cells resulted in overexpression of pro-inflammatory cytokines in the RAW264.7 cells.Both in vitro and in vivo experiments confirmed adipocyte loss and fibroblast formation,with transformed fibroblasts showing pronounced pro-inflammatory characteristics,highlighting their crucial role in the disease mechanism.Conclusions:Our study showed the spatial distribution and dynamic alterations of various cell types during scleroderma progres-sion.Crucially,we identified the transformation of adipocytes into fibroblasts as a key factor promoting disease advancement.These emergent fibroblasts intensify inflammation,indicating that research on these cell clusters could reveal key scleroderma mechanisms and guide future therapies.

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