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Mechanistic research:Selenium regulates virulence factors,reducing adhesion ability and inflammatory damage of Helicobacter pylori

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World Journal of Gastroenterology 2024年第1期30卷 91-107页

作者： Chun Qin Gan-Rong huang Ai-Xing Guan Wen-Ting Zhou Hao Chen Pei-Pei Luo Xian-Ke Luo Yan-Qiang huang zan-Song huang Guangxi Technology Innovation Cooperation Base of Prevention and Control Pathogenic Microbes with Drug Resistance Youjiang Medical University for NationalitiesBaise 533000Guangxi Zhuang Autonomous RegionChina Department of Digestive Diseases Affiliated Hospital of Youjiang Medical University for NationalitiesBaise 533000Guangxi Zhuang Autonomous RegionChina Key Laboratory of the Prevention and Treatment of Drug Resistant Microbial Infecting Youjiang Medical University for NationalitiesBaise 533000Guangxi Zhuang Autonomous RegionChina Department of Pathology Wannan Medical CollegeWuhu 241002Anhui ProvinceChina Department of Gastroenterology Wujin People’s Hospital affiliated to Jiangsu UniversityChangzhou 213004Jiangsu ProvinceChina Department of Gastroenterology Guangzhou Liwan District People's HospitalGuangzhou 510370Guangdong ProvinceChina

BACKGROUND The pathogenicity of Helicobacter pylori is dependent on factors including the environment and the host.Although selenium is closely related to pathogenicity as an environmental factor,the specific correlation between them remains unclear.AIM To investigate how selenium acts on virulence factors and reduces their toxicity.METHODS H.pylori strains were induced by sodium selenite.The expression of cytotoxin-associated protein A(CagA)and vacuolating cytotoxin gene A(VacA)was determined by quantitative PCR and Western blotting.Transcriptomics was used to analyze CagA,CagM,CagE,Cag1,Cag3,and CagT.C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction,and H.pylori colonization,inflammatory reactions,and the cell adhesion ability of H.pylori were assessed.RESULTS CagA and VacA expression was upregulated at first and then downregulated in the H.pylori strains after sodium selenite treatment.Their expression was significantly and steadily downregulated after the 5th cycle(10 d).Transcriptome analysis revealed that sodium selenite altered the levels affect H.pylori virulence factors such as CagA,CagM,CagE,Cag1,Cag3,and CagT.Of these factors,CagM and CagE expression was continuously downregulated and further downregulated after 2 h of induction with sodium selenite.Moreover,CagT expression was upregulated before the 3rd cycle(6 d)and significantly downregulated after the 5th cycle.Cag1 and Cag3 expression was upregulated and downregulated,respectively,but no significant change was observed by the 5th cycle.C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction.The extent of H.pylori colonization in the stomach increased;however,sodium selenite also induced a mild inflammatory reaction in the gastric mucosa of H.pylori-infected mice,and the cell adhesion ability of H.pylori was significantly weakened.CONCLUSION These results demonstrate that H.pylori displayed virulence attenuation after the 10th d of sodium selenite treatment.Sodium s

关键词： Helicobacter pylori Sodium selenite Virulence factors Adherence Inflammation

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Circulating copeptin level and the clinical prognosis of patients with chronic liver disease

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世界胃肠病学杂志:英文版 2023年第31期29卷 4797-4808页

作者： Hao-Qian Tan Ming Zhao zan huang Yang Liu Han Li Long-Hui Ma Jun-Ying Liu Department of Gastroenterology Zhoukou Central Hospital Affiliated to Xinxiang Medical UniversityZhoukou 466000Henan ProvinceChina Department of Gastroenterology Zhoukou Central HospitalZhoukou 466000Henan ProvinceChina Department of Teaching and Research Zhoukou Central HospitalZhoukou 466000Henan ProvinceChina

BACKGROUND The relationship between copeptin and the severity of circulatory dysfunction and systemic stress response in patients with chronic liver disease(CLD)has been established.Nevertheless,the potential of serum copeptin levels to predict the prognosis of CLD patients remains unclear.AIM To conduct a systematic review and meta-analysis to investigate the correlation between serum copeptin and transplant-free survival(TFS)in this population.METHODS To achieve the objective of the meta-analysis,PubMed,Embase,the Cochrane Library,and the Web of Science were searched to identify observational studies with longitudinal follow-up.The Cochrane Q test was utilized to assess betweenstudy heterogeneity,and the I2 statistic was estimated.Random-effects models were employed to combine the outcomes,taking into account the potential influence of heterogeneity.RESULTS Ten datasets including 3133 patients were involved.The follow-up durations were 1 to 48 mo(mean:12.5 mo).Overall,it was shown that a high level of serum copeptin was associated with a poor TFS[risk ratio(RR):1.82,95%confidence interval:1.52-2.19,P0.05).CONCLUSION Patients with CLD who have high serum copeptin concentrations may be associated with a poor clinical prognosis.

关键词： Chronic liver disease Liver cirrhosis Copeptin Prognosis Mortality Meta-analysis

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大学生身体活动和睡眠质量与焦虑及抑郁情绪的关系

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中国学校卫生 2024年第5期45卷 684-688页

作者：陈保祥周玉兰黄赞浙江师范大学体育与健康科学学院金华321004

目的探讨大学生身体活动、睡眠质量与焦虑、抑郁情绪的关系,以期为大学生心理健康干预提供实证支持与理论指导。方法于2023年3—4月,采用方便抽样的方法选取中国6所不同省份高校的2099名大学生进行调查,采用国际体育活动问卷简表(IPAQ-... 详细信息

目的探讨大学生身体活动、睡眠质量与焦虑、抑郁情绪的关系,以期为大学生心理健康干预提供实证支持与理论指导。方法于2023年3—4月,采用方便抽样的方法选取中国6所不同省份高校的2099名大学生进行调查,采用国际体育活动问卷简表(IPAQ-SF)、匹兹堡睡眠质量指数(PSQI)、流调中心用抑郁量表(CES-D)和焦虑自评量表(SAS)评估参与者的身体活动量、睡眠质量、抑郁和焦虑情绪。采用描述性统计、Logistic回归模型对数据进行分析。结果高体力活动的大学生比例为30.3%,中等和低体力活动的大学生分别为45.3%和24.4%。62.3%的大学生睡眠质量较差,焦虑和抑郁情绪的检出率分别为21.6%和39.9%。与男生(42.8%)相比,女生参加高体力活动的比例较低(22.3%),而参加中等体力活动(48.1%)和低体力活动(29.5%)的比例则高于男生(40.8%,16.4%);女生(65.0%)睡眠质量差的比例高于男生(58.0%)(χ^(2)值分别为110.15,10.70,P值均<0.05)。女生有抑郁情绪的比例(43.8%)高于男生(33.9%)(χ^(2)=20.48,P<0.05)。Logistic回归分析结果显示,高体力活动与大学生焦虑和抑郁情绪均呈负相关(OR值分别为0.45,0.33),睡眠质量差与大学生焦虑和抑郁情绪呈正相关(OR值分别为3.89,3.94)(P值均<0.01);身体活动和睡眠质量与大学生的焦虑、抑郁情绪存在交互效应关系,即与低体力活动且睡眠质量差相比,高体力活动和睡眠质量好的共同作用与大学生焦虑和抑郁情绪的降低均相关(OR值分别为0.14,0.08,P值均<0.01)。结论身体活动和睡眠质量与大学生的焦虑、抑郁情绪存在相关性。提高身体活动量和睡眠质量有益于改善大学生抑郁和焦虑等心理健康问题。

关键词：运动活动睡眠焦虑抑郁精神卫生回归分析学生

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Mitochondrial ROS promote macrophage pyroptosis by inducing GSDMD oxidation

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Journal of Molecular Cell Biology 2019年第12期11卷 1069-1082页

作者： Yufang Wang Peiliang Shi Qin Chen zan huang Dayuan Zou Jingzi Zhang Xiang Gao Zhaoyu Lin State Key Laboratory of Pharmaceutical Biotechnology Department of Hepatopancreatobiliary SurgeryNanjing Drum Tower HospitalThe Affiliated Hospital of Nanjing University Medical SchoolMOE Key Laboratory of Model Animals for Disease StudyModel Animal Research CenterNanjing UniversityNanjing 210061China Jiangsu Province Key Laboratory of Gastrointestinal Nutrition and Animal Health Nanjing Agriculture UniversityNanjing 210095China

Disrupted mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) generation are often associated with macrophage pyroptosis. It remains unclear how these forms of mitochondrial dysfunction relate to inflammasome activation and gasdermin-D (Gsdmd) cleavage, two central steps of the pyroptotic process. Here, we also found MMP collapse and ROS generation induced by Nlrp3 inflammasome activation as previous studies reported. The elimination of ROS alleviated the cleavage of Gsdmd, suggesting that Gsdmd cleavage occurs downstream of ROS release. Consistent with this result, hydrogen peroxide treatment augmented the cleavage of Gsdmd by caspase-1. Indeed, four amino acid residues of Gsdmd were oxidized under oxidative stress in macrophages. The efficiency of Gsdmd cleavage by inflammatory caspase-1 was dramatically reduced when oxidative modification was blocked by mutation of these amino acid residues. These results demonstrate that Gsdmd oxidation serves as a de novo mechanism by which mitochondrial ROS promote Nlrp3 inflammasome-dependent pyroptotic cell death.

关键词： ROS Nlrp3 gasdermin-D oxidation mitochondria

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GSDMB promotes non-canonical pyroptosis by enhancing caspase-4 activity

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Journal of Molecular Cell Biology 2019年第6期11卷 496-508页

作者： Qin Chen Peiliang Shi Yufang Wang Dayuan Zou Xiuwen Wu Dingyu Wang Qiongyuan Hu Yujie Zou zan huang Jianan Ren Zhaoyu Lin Xiang Gao State Key Laboratory of Pharmaceutical Biotechnology and Nanjing Drum Tower Hospital Model Animal Research Center Nanjing University Nanjing 210061 China Department of Surgery Jinling Hospital Medical School of Nanjing University Nanjing 210061 China Jiangsu Province Key Laboratory of Gastrointestinal Nutrition and Animal Health Nanjing Agriculture University Nanjing 210095 China

Gasdermin B (GSDMB) has been reported to be associated with immune diseases in humans, but the detailed molecular mechanisms remain unsolved. The N-terminus of GSDMB by itself, unlike other gasdermin family proteins, does not induce cell death. Here, we show that GSDMB is highly expressed in the leukocytes of septic shock patients, which is associated with increased release of the gasdermin D (GSDMD) N-terminus. GSDMB expression and the accumulation of the N-terminal fragment of GSDMD are induced by the activation of the non-canonical pyroptosis pathway in a human monocyte cell line. The downregulation of GSDMB alleviates the cleavage of GSDMD and cell death. Consistently, the overexpression of GSDMB promotes GSDMD cleavage, accompanied by increased LDH release. We further found that GSDMB promotes caspase-4 activity, which is required for the cleavage of GSDMD in non-canonical pyroptosis, by directly binding to the CARD domain of caspase-4. Our study reveals a GSDMB-mediated novel regulatory mechanism for non-canonical pyroptosis and suggests a potential new strategy for the treatment of inflammatory diseases.

关键词： GSDMB GSDMD pyroptosis sepsis

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CD4+T cells memorize obesity and promote weight regain

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Cellular & Molecular Immunology 2018年第6期15卷 630-639页

作者： Jianghuan Zou Beibei Lai Mingzhu Zheng Qin Chen Shujun Jiang Anying Song zan huang Peiliang Shi Xin Tu Di Wang Linrong Lu Zhaoyu Lin Xiang Gao State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study Model Animal Research CenterNanjing Biomedical Research InstituteNanjing University12 Xuefu RoadPukou DistrictNanjingJiangsu 210061China Institute of Immunology Program in Molecular and Cellular BiologyZhejiang University School of MedicineHangzhouZhejiang 310058China

Body weight regain often causes failure of obesity therapies while the underlying mechanism remains largely unknown.In this study,we report that immune cells,especially CD4+T cells,mediate the‘memory’of previous obese status.In a weight gain-loss-regain model,we found that C57BL/6J mice with an obesity history showed a much faster rate of body weight regain.This obesity memory could last for at least 2 months after previously obese mice were kept at the same body weight as non-obese mice.Surprisingly,such obesity memory was abrogated by dexamethasone treatment,whereas immunodeficient Rag1−/−and H2A−/−mice failed to establish such memory.Rag1−/−mice repossessed the obesity memory when immune cells or CD4+T cells isolated from previously obese mice were transferred.Furthermore,depletion of CD4+T cells led to obesity memory ablation.Taken together,we conclude that CD4+T cells mediate obesity memory and promote weight regain.

关键词： CD4+T cell immunodeficiency metabolism obesity memory weight regain

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照明电子镇流器的简化

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今日电子 2007年第7期 43-44页

作者： zan huang 国际整流器公司

HVIC技术使得控制、驱动和PFC集成成为现实电子镇流器IC已经成为荧光照明设计中的一个关键因素，尤其在制造商致力简化电路、减少开发时间、提高效率和降低成本的时候。为满足这些需求，市面上出现了一系列的IC，从简单的自振荡半桥驱... 详细信息

HVIC技术使得控制、驱动和PFC集成成为现实电子镇流器IC已经成为荧光照明设计中的一个关键因素，尤其在制造商致力简化电路、减少开发时间、提高效率和降低成本的时候。为满足这些需求，市面上出现了一系列的IC，从简单的自振荡半桥驱动器到高集成、管脚少的器件（带有高级控制特性，如软开关功能，以及预热、启辉和运行模式频率控制）。这些器件还具备一些集成的保护特性，包括低共振和过热保护。

关键词：电子镇流器照明设计半桥驱动器 IC技术控制特性高集成简化电路开关功能

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STAT1 signaling is required for optimal Th1 cell differentiation in mice

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Chinese Science Bulletin 2010年第11期55卷 1032-1040页

作者： MA Da huang Hua huang zan The Key Laboratory of Developmental Genes and Human Disease of Education Ministry School of Basic Medical Science Southeast University Nanjing 210009 China Department of Cell Biology Neurology and Anatomy Stritch School of Medicine Loyola University Chicago Maywood IL 60153 USA

Although IFN-γ alone does not prime type I T helper cell (Th1) differentiation, the loss of IFN-γ signaling leads to impaired Th1 phenotype: IFN-γ receptor-deficient (Ifngr-/-) Th1 cells fail to permanently repress IL-4 expression. They can differentiate into IL-4-producing cells under Th2-inducing conditions. These observations suggest that IFN-γ signaling plays a critical role in si- lencing Il4 gene in Th1 cells and stabilizing Th1 phenotype. IFN-γ signaling has been further shown to inhibit IL-4 expression by inhibiting STAT6 phosphorylation. This work aims to study the mechanism by which STAT1, the downstream molecule that transduces IFN-γ signaling, may mediate suppression of IL-4 expression in Th1 cells. The results show that STAT1-deficient naive CD4+ T cells express a reduced level of IFN-γ as well as an elevated level of IL-4. These cells exhibit bias to differentiate into Th2 cells under unpolarized conditions. Under Th1-inducing conditions, STAT1-deficient naive CD4+ T cells show impaired Th1 differentiation: Stat1-/- Th1 cells express reduced levels of IFN-γ and T-bet. These cells also fail to repress the expression of IL-4 and GATA-3 and retain STAT6 signaling. More importantly, Stat1-/- Th1 cells can be effectively induced to differentiate into IL-4-producing cells under Th2-inducing conditions. Ectopic expression of T-bet in Stat1-/- Th1 cells dramatically represses their ability to do so and drastically restores IFN-γ expression, suggesting that STAT1 may inhibit IL-4 expression through T-bet. Finally, histone H3 acetylation (H3AC) and histone H3 K4 dimethylation (H3K4dim) were observed in two enhancer regions of Il4 gene locus in Stat1-/- Th1 cells, suggesting a permissive status of Il4 gene locus in these cells. Thus, this study reveals new mechanisms by which STAT1 signaling may mediate repression of Il4 gene in Th1 cells: upregulating T-bet that subsequently represses GATA3 and IL-4 expression, antagonizing STAT6 signaling, and inhibiting epigenetic modifications in Il4 gene locus.

关键词： STAT1 Th1/Th2 房间 T 赌注 STAT6 信号 transduction

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SH-2-containing protein tyro-sine phosphatase 1 is required for IL-4-induced IL-4R expression in spleen cells

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Chinese Science Bulletin 2005年第14期50卷 1456-1461页

作者： CAO Xin huang zan FAN Jingyi Department of Cell Biology and Medical Genetics Nanjing Medical University Nanjing 210029 China Molecular Biology Program Stritch School of Medicine Loyola University at Chicago Maywood IL 60153 USA Department of Organismal Biology and Anatomy University of Chicago Chicago IL 60637 USA

To investigate the role of SH-2-containing pro- tein tyrosine phosphatase 1, SHP-1, in IL-4-induced IL-4 receptor (IL-4R) expression, we examined IL-4 receptor α-chain (IL-4Rα) mRNA expression in Na3VO4-treated wild type (WT) spleen cells and measured IL-4R mRNA in IL-4-stimulated spleen cells of viable motheaten mice (mev/mev). It is found that IL-4-induced IL-4R mRNA ex- pression was impaired in Na3VO4-treated WT spleen cells and IL-4-stimulated mev/mev spleen cells. Here we show that the impaired IL-4-induced IL-4Rα mRNA expression was due to reduced expression of IL-4R that led to impaired STAT6 signaling. We further demonstrate that reduction of IL-4Rα protein expression in mev/mev spleen cells was due to alteration in cell compositions. In mev/mev spleen, the per- centages of CD4+, CD8+, and CD19+ cells expressing rela- tively high levels of IL-4R were reduced dramatically while the percentages of Mac-1+ and Gr-1+ cells with relative low levels of IL-4R increased greatly. Despite the profound effect of reduced expression of IL-4R protein, the IL-4Rα mRNA expression was comparable in spleen cells of littermate con- trol mice (+/?) and mev/mev mice and no differences were found in B cells, T cells, and macrophages, suggesting cell type-specific downregulation of IL-4R expression in macro- phages through a posttranscriptional mechanism. Our study suggests that SHP-1 is required for IL-4-meidated function and indirectly regulates IL-4-meidated function in spleen cells by affecting hematopoiesis.

关键词：蛋白质酪氨酸磷酸酶脾细胞

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Further Investigation on the Rearrangement Mechanism of Reactions of 1,5-Benzothiazepines with Ethoxycarbonylcarbene

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Chemical Research in Chinese Universities 2006年第1期22卷 36-39页

作者： WU Chun-zan huang Jia-xing ZHANG Qi-han XU Jia-xi Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education College of Chemistry and Molecular Engineering Peking University Beijing 100871 P. R. China

The reactions of 2,3-dihydro-1,5-benzothiazepines with ethoxyearbonylcarbene undergo complex rearrangements to produce rlng-opening and ring contraction products. Previously it was presumed that the different products were formed via different mechanisms depending on the kind of substituents at the 2-position of 1,5-benzothiazepines. However, on the basis of the further detailed investigation, it was found that all 1,5-benzothiazepines can undergo the same rearrangement to yield both ring-opening and ring contraction products.

关键词： 1,5-Benzothiazepine Ethoxycarbonylcarbene Rearrangement Ring-contraction Ring-opening

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