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| 1 | NLRP3 inflammasome activation determines the fibrogenic potential of PM_(2.5) air pollution particles in the lung显示文摘Airborne fine particulate matter(PM_(2.5))is known to cause respiratory inflammation such as chronic obstructive pulmonary disease and lung fibrosis.NLRP3 inflammasome activation has been implicated in these diseases;however,due to the complexity in PM_(2.5)compositions,it is difficult to differentiate the roles of the components in triggering this pathway.We collected eight real-life PM_(2.5)samples for a comparative analysis of their effects on NLRP3 inflammasome activation and lung fibrosis.In vitro assays showed that although the PM_(2.5)particles did not induce significant cytotoxicity at the dose range of 12.5to 100μg/m L,they induced potent TNF-αand IL-1βproduction in PMA differentiated THP-1 human macrophages and TGF-β1 production in BEAS-2B human bronchial epithelial cells.At the dose of 100μg/m L,PM_(2.5)induced NLRP3 inflammasome activation by inducing lysosomal damage and cathepsin B release,leading to IL-1βproduction.This was confirmed by using NLRP3-and ASC-deficient cells as well as a cathepsin B inhibitor,ca-074 ME.Administration of PM_(2.5)via oropharyngeal aspiration at 2 mg/kg induced significant TGF-β1 production in the bronchoalveolar lavage fluid and collagen deposition in the lung at 21days post-exposure,suggesting PM_(2.5)has the potential to induce pulmonary fibrosis.The ranking of in vitro IL-1βproduction correlates well with the in vivo total cell count,TGF-β1 production,and collagen deposition.In summary,we demonstrate that the PM_(2.5)is capable of inducing NLRP3 inflammasome activation,which triggers a series of cellular responses in the lung to induce fibrosis. | Wei Cao Xiang Wang Jiulong Li Ming Yan Chong Hyun Chang Joshua Kim Jinhong Jiang Yu-Pei Liao Shannon Tseng Sydney Kusumoputro Candice Lau Marissa Huang Pengli Han Pengju Lu Tian Xia | 2022 | Journal of Environmental Sciences2022，34，1： | 3 |
| 2 | Aberrant cholesterol metabolic signaling impairs antitumor immunosurveillance through natural killer T cell dysfunction in obese liver显示文摘Obesity is a major risk factor for cancers including hepatocellular carcinoma(HCC)that develops from a background of non-alcoholic fatty liver disease(NAFLD).Hypercholesterolemia is a common comorbidity of obesity.Although cholesterol biosynthesis mainly occurs in the liver,its role in HCC development of obese people remains obscure.Using high-fat high-carbohydrate diet-associated orthotopic and spontaneous NAFLD-HCC mouse models,we found that hepatic cholesterol accumulation in obesity selectively suppressed natural killer T(NKT)cell-mediated antitumor immunosurveillance.Transcriptome analysis of human liver revealed aberrant cholesterol metabolism and NKT cell dysfunction in NAFLD patients.Notably,cholesterol-lowering rosuvastatin restored NKT expansion and cytotoxicity to prevent obesogenic diet-promoted HCC development.Moreover,suppression of hepatic cholesterol biosynthesis by a mammalian target of rapamycin(mTOR)inhibitor vistusertib preceded tumor regression,which was abolished by NKT inactivation but not CD8^(+)T cell depletion.Mechanistically,sterol regulatory element-binding protein 2(SREBP2)-driven excessive cholesterol production from hepatocytes induced lipid peroxide accumulation and deficient cytotoxicity in NKT cells,which were supported by findings in people with obesity,NAFLD and NAFLD-HCC.This study highlights mTORC1/SREBP2/cholesterol-mediated NKT dysfunction in the tumor-promoting NAFLD liver microenvironment,providing intervention strategies that invigorating NKT cells to control HCC in the obesity epidemic. | Wenshu Tang Jingying Zhou Weiqin Yang Yu Feng Haoran Wu Myth T.S.Mok Lingyun Zhang Zhixian Liang Xiaoyu Liu Zhewen Xiong Xuezhen Zeng Jing Wang Jiahuan Lu Jingqing Li Hanyong Sun Xiaoyu Tian Philip Chun Yeung Yong Hou Heung Man Lee Candice C.H.Lam Howard H.W.Leung Anthony W.H.Chan Ka Fai To John Wong Paul B.S.Lai Kelvin K.C.Ng Simon K.H.Wong Vincent W.S.Wong Alice P.S.Kong Joseph J.Y.Sung Alfred S.L.Cheng | 2022 | Cellular & Molecular Immunology2022，19，7： | 3 |
| 3 | Source characterization of ozone precursors by complementary approaches of vehicular indicator and principal component analysis显示文摘 | Chih-Chung Chang Jia-Lin Wang Shih-Chun Candice Lung Shaw-Chen Liu Chein-Jung Shiu | 2008 | Atmospheric Environment2008，，10： | 1 |
| 4 | Smoking influences outcome in patients who had thrombolysed ischaemic stroke:the ENCHANTED study显示文摘Background and purpose As studies vary in defining the prognostic significance of smoking in acute ischaemic stroke(AIS),we aimed to determine the relation of smoking and key outcomes in patient participants who had thrombolysed AIS of the international quasi-factorial randomised Enhanced Control of Hypertension and Thrombolysis Stroke Study(ENCHANTED).Methods Post-hoc analyses of ENCHANTED,an international quasi-factorial randomised evaluation of intravenous alteplase-dose comparison and levels of blood pressure control in patients who had thrombolysed AIS.Multivariable logistic regression models with inverse probability of treatment weighting(IPTW)propensity scores were used to determine associations of self-reported smoking status and clinical outcomes,according to 90-day modified Rankin Scale(mRS)scores and symptomatic intracerebral haemorrhage(sICH).Results Of 4540 patients who had an AIS,there were 1008(22.2%)current smokers who were younger and predominantly male,with more comorbidities of hypertension,coronary artery disease,atrial fibrillation and diabetes mellitus,and greater baseline neurological impairment,compared with non-smokers.In univariate analysis,current smokers had a higher likelihood of a favourable shift in mRS scores(OR 0.88,95%CI 0.77 to 0.99;p=0.038)but this association reversed in a fully adjusted model with IPTW(adjusted OR 1.15,95%CI 1.04 to 1.28;p=0.009).A similar trend was also apparent for dichotomised poor outcome(mRS scores 2–6:OR 1.18,95%CI 1.05 to 1.33;p=0.007),but not with the risk of sICH across standard criteria.Conclusion Smoking predicts poor functional recovery in patients who had thrombolysed AIS.Trial registration number NCT01422616. | Lingli Sun Lili Song Jie Yang Richard I Lindley Thompson Robinson Pablo M Lavados Candice Delcourt Hisatomi Arima Bruce Ovbiagele John Chalmers Craig S Anderson Xia Wang | 2021 | Stroke & Vascular Neurology2021，6，3： | 1 |
| 5 | Hematoma growth and outcomes in intracerebral hemorrhage: The INTERACT1 study显示文摘 | Candice Delcourt Yining Huang Hisatomi Arima John Chalmers Stephen M. Davis Emma L. Heeley Jiguang Wang Mark W. Parsons Guorong Liu Craig S. Anderson | 2012 | Neurology2012，，： | 1 |
| 6 | Earlier Blood Pressure-Lowering and Greater Attenuation of Hematoma Growth in Acute Intracerebral Hemorrhage: INTERACT Pilot Phase显示文摘 | Hisatomi Arima Yining Huang Ji Guang Wang Emma Heeley Candice Delcourt Mark Parsons Qiang Li Bruce Neal John Chalmers Craig Anderson | 2012 | Stroke2012，，8： | 1 |
| 7 | Biogenic isoprene in subtropical urban settings and implications for air quality显示文摘 | Jia-Lin Wang Clock Chew Chih-Yuan Chang Wei-Cheng Liao Shih-Chun Candice Lung Wei-Nai Chen Po-Ju Lee Po-Hsiung Lin Chih-Chung Chang | 2013 | Atmospheric Environment2013，，： | 1 |
| 8 | Severe distortion of the uterus associated with a B-Lynch suture显示文摘 | Candice Wang Manisha Mathur | 2013 | Iin J Gyne- col Obstet2013，122，1： | 1 |
| 9 | 2019年全球、地区和国家5岁以下儿童呼吸道合胞病毒引发急性下呼吸道感染疾病负担研究的系统分析显示文摘背景呼吸道合胞病毒(respiratory syncytial virus,RSV)是引起婴幼儿急性下呼吸道感染最常见的病原体。此前估计,2015年全球60月龄以下儿童共发生3 310万次RSV相关急性下呼吸道感染,导致118 200人死亡。此后,几项社区监测研究获得了对RSV相关社区死亡的更精确估计。本文旨在更新2019年全球、地区和国家层面60月龄以下儿童RSV相关急性下呼吸道感染的发病率和死亡率,重点关注总体死亡率和在研RSV免疫制剂针对的更窄的婴儿年龄组。方法 检索获得MEDLINE、Embase、Global Health、CINAHL、Web of Science、LILACS、OpenGrey、中国知网、万方和维普数据库2017—2020年发表文献中的新数据,并纳入RSV GEN合作者提供的未发表数据,以扩展全球RSV疾病负担数据集。纳入的研究符合以下条件:报告了社区中或需要住院治疗的60月龄以下儿童RSV原发性急性下呼吸道感染的数据;报告了至少连续12个月的数据,但院内病死率或RSV季节性定义明确的地区除外;报告了RSV相关急性下呼吸道感染的发病率、住院率、院内病死率或急性下呼吸道感染住院的RSV阳性比例。如果病例定义不明或应用不一致、RSV感染未经实验室确认或仅基于血清学检测、报告的急性下呼吸道感染病例少于50例,则排除该研究。本研究应用广义线性混合效应模型(generalized linear mixed-effects model,GLMM)估计了2019年全球和地区(按国家发展状况和世界银行收入分类)RSV相关急性下呼吸道感染的发病率、住院率和院内病死率;通过基于危险因素的模型估计了国家层面RSV相关急性下呼吸道感染的发病率;通过GLMM开发了新模型,纳入最新的RSV社区死亡率数据,用于估计RSV的总体死亡率。本综述已在PROSPERO注册(CRD42021252400)。结果 除了先前综述中纳入的317项研究外,还纳入了113项符合条件的新研究以及51项未发表的研究,共计481项研究。据估计,2019年全球60月龄以下儿童中,共发生3 300万(置信区间为2 540万~4 460万)次RSV相关急性下呼吸道感染,导致360万(290万~460万)例住院、26 300(15 100~49 100)例院内死亡以及101 400(84 500~125 200)例可归因于RSV的总死亡数。在0~6个月的婴儿中,共发生660万(460万~970万)次RSV相关急性下呼吸道感染,导致140万(100万~200万)例住院、13 300(6 800~28 100)例院内死亡以及45 700(38 400~55 900)例可归因于RSV的总死亡数。60月龄以下和28 d~6月龄儿童的死亡中分别有2.0%(置信区间为1.6%~2.4%)和3.6%(3.0%~4.4%)归因于RSV。在各年龄组中,95%以上的RSV相关急性下呼吸道感染事件和97%以上的可归因于RSV的死亡事件都发生在中低收入国家。结论 RSV显著增加了全球60月龄以下儿童的发病和死亡负担,尤其是在出生后前6个月和中低收入国家。本研究强调了全球RSV疾病的总体死亡率负担,60月龄以下儿童中,每50例死亡就有1例可归因于RSV;28 d至6个月大的婴儿中,每28例死亡就有1例可归因于RSV。每1例RSV相关急性下呼吸道感染院内死亡,对应社区中约3例可归因于RSV的死亡。对6月龄内婴儿提供保护的RSV被动免疫计划有望对减轻RSV疾病负担,但实施计划时,仍需要更多数据来了解RSV疾病负担高峰可能向大龄转移的影响。 | You Li Xin Wang Dianna M.Blau Mauricio T.Caballero Daniel R.Feikin Christopher J.Gill Shabir A.Madhi Saad B.Omer Eric A.F Simoes Harry Campbell Ana Bermejo Pariente Darmaa Bardach Quique Bassat Jean-Sebastien Casalegno Giorgi Chakhunashvili Nigel Crawford Daria Danilenko Lien Anh Ha Do Marcela Echavarria Angela Gentile Aubree Gordon Terho Heikkinen QSue Huang Sophie Jullien Anand Krishnan Eduardo Luis Lopez Josko Markic Ainara Mira-Iglesias Hannah CMoore Jocelyn Moyes Lawrence Mwananyanda DJames Nokes Faseeha Noordeen Evangeline Obodai Nandhini Palani Candice Romero Vahid Salimi Ashish Satav Euri Seo Zakhar Shchomak Rosalyn Singleton Kirill Stolyarov Sonia K Stoszek Anne von Gottberg Danielle Wurzel Lay-Myint Yoshida Chee Fu Yung Heather J Zar Harish Nair 张甜甜 从兵兵 邓舒予 | 2023 | 中国病毒病杂志2023，13，2： | 0 |
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