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T3098C and T53C Mutations of HBV Genotype C Is Associated with HBV Infection Progress

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Biomedical and Environmental Sciences 2009年第6期22卷 511-517页

作者： su-zhen jiang ZHI-YONG GAO TONG LI ,YA-JUAN LI XIANO-MEI CHEN LING WANG FENG-MIN LU HUI ZHUANG Department of Microbiology Peking University Health Science Center Beijing 100191 China

Objective To analyze the association between mutation（s） in preS region of HBV and hepatitis B disease progress in Chinese patients with genotype C chronic HBV infection. Methods Ninety-three patients with chronic genotype C HBV infection, including 24 asymptomatic carriers （ASC）, 26 patients with chronic hepatitis B （CHB）, 22 patients with liver cirrhosis （LC） and 21 HCC patients were investigated. Levels of HBV DNA, HBeAg, alanine aminotransferase （ALT）, asparate transaminase （AST） were measured. HBV preS region was analyzed by PCR direct sequencing. Results The prevalence of preS T3098C and T53C mutations ofgenotype C HBV was significantly higher in LC and HCC patients than ASC and CHB patients. The rate ofT3098C mutation in ASC, CHB, LC, and HCC patients were 0.00% （0/24）, 3.85% （1/26）, 9.09% （2/22）, and 30.77% （8/22）, respectively （P=0.0015）, while the rate of T53C mutation was I2.50% （3/24）, 3.85% （1/26）, 40.91% （9/22）, and 42.31% （11/26）, respectively （P=0.0012）. Conclusion The frequency of genotype C HBV preS T3098C and T53C mutations is associated with hepatitis B infection progression.

关键词： Hepatitis B virus (HBV) Genotype C pre S Mutation Hepatocellular carcinoma (HCC)

Lower alanine aminotransferase levels are associated with increased all-cause and cardiovascular mortality in nonalcoholic fatty liver patients

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World Journal of Hepatology 2023年第6期15卷 813-825页

作者： Jia-Rui zheng Zi-Long Wang su-zhen jiang Hong-Song Chen Bo Feng Peking University Hepatology Institute Peking University People's HospitalBeijing 100044China

BACKGROUND Serum alanine aminotransferase(ALT) levels are often considered a marker to evaluate liver disease and its *** To investigate the association between ALT levels and all-cause and cause-specific mortality in patients with nonalcoholic fatty liver disease(NAFLD).METHODS The Third National Health and Nutrition Examination survey(NHANES-Ⅲ) from 1988 to 1994 and NHANES-Ⅲ-related mortality data from 2019 onward were used to obtain the necessary data for the study. NAFLD was defined as hepatic steatosis, as diagnosed by ultrasound, with no other liver diseases. ALT levels were categorized into four groups according to the different recommended upper limits of normal(ULN) in men and women: sults could be found in both men and women. Univariate analysis showed that severe NAFLD with normal ALT levels had the highest allcause and cause-specific mortality, but the difference was not statistically significant after adjustment for age and multivariate *** The risk of NAFLD was positively correlated with ALT level, but all-cause and cardiovascular mortality were the highest when ALT was < 0.5 ULN. Regardless of the severity of NAFLD, normal or lower ALT levels were associated with higher mortality than elevated ALT levels. Clinicians should be aware that high ALT levels indicate liver injury, but low ALT levels are associated with a higher risk of death.

关键词： Non-alcoholic fatty liver disease Alanine aminotransferase Mortality NHANES-Ⅲ

Hepatitis B Virus S Promoter Deletion in Hepatocellular Carcinoma

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国际感染病学（电子版） 2012年第1期1卷 14-24页

作者： su-zhen jiang Jia-jia zheng Xiang-Mei Chen Ting Zhang Qiang Xu Hui Zhuang Feng-min Lu Centers for the Infectious Disease & the Department of Microbiology Peking University Health Science Center Department of Infectious Disease Nanfang HospitalSouthern Medical University

Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue *** HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of hepatocellular carcinoma(HCC) patients were screened by PCR and direct *** patients carried HBV with genotype C,except for one B/C *** expression,localization and excretion of LHBs mutant carrying pre-S deletions were characterized in *** expression of endoplasmic reticulum(ER) GRP78 mRNA was *** Four patterns of pre-S mutations were identified:pre-S 1 in-frame deletion involving the first start codon;pre-S2 in-frame deletion;pre-S2 start codon mutation with or without in-frame deletion;and S promoter in-frame deletion(ASP).The first two types were evenly found in both tumor and non-tumor *** were rarely present as dominant *** last two types were frequently found in the dominant strains in tumor *** overall prevalence of HBV carrying ASP was 17.64%(6/34) in tumor tissues,but none were dominant in nontumor *** carrying ASP was unable to produce S protein in *** assay showed that the ASP LHBs mutant aggregated in the cytoplasm,accumulating mainly in the *** transfection and expression of ASP mutant caused GRP78 up-regulation in *** HBV S promoter deletion was found dominantly in HCC tumor *** aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.

关键词： Hepatitis B virus S promoter deletion ER stress Hepatocellular carcinoma

Hepatitis B Virus S Promoter Deletion in Hepatocellular Carcinoma

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国际感染病学（电子版） 2017年第1期6卷 69-72页

作者： su-zhen jiang Jia-jia zheng Xiang-Mei Chen Ting Zhang Qiang Xu Hui Zhuang Feng-min Lu 不详

Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue *** HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression, localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 m RNA was *** Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion; pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in *** HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.

关键词： Hepatitis B virus (HBV) S promoter deletion ER stress Hepatocellular carcinoma(HCC)

Hepatitis B Virus S Promoter Deletion in Hepatocellular Carcinoma

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国际感染病学（电子版） 2016年第1期5卷 35-38页

作者： su-zhen jiang Jia-jia zheng Xiang-Mei Chen Ting Zhang Qiang Xu Hui Zhuang Feng-min Lu

Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue *** HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression,localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 mRNA was *** Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion;pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in *** HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.

关键词： Hepatitis B virus(HBV) S promoter deletion ER stress Hepatocellular carcinoma(HCC)

Hepatitis B Virus S Promoter Deletion in Hepatocellular Carcinoma

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国际感染病学（电子版） 2018年第2期7卷 37-40页

作者： su-zhen jiang Jia-jia zheng Xiang-Mei Chen Ting Zhang Qiang Xu Hui Zhuang Feng-min Lu

Objective To identify the difference and significance of dominant types of hepatitis B virus(HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue *** HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma(HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression, localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 m RNA was *** Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion; pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion(ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64%(6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in *** HBV S promoter deletion was found dominantly in HCC tumor tissue. The aggregation of mutant large surface proteins in the ER possibly involved in HBV-related HCC.

关键词： Hepatitis B virus(HBV) S promoter deletion ER stress Hepatocellular carcinoma(HCC)

Hepatitis B Virus S Promoter Deletion in Hepatocellular Carcinoma

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国际感染病学（电子版） 2015年第4期4卷 125-128页

作者： su-zhen jiang Jia-jia zheng Xiang-Mei Chen Ting Zhang Qiang Xu Hui Zhuang Feng-min Lu 不详

Objective To identify the difference and significance of dominant types of hepatitis B virus (HBV) pre-S mutation between liver tumor tissues and paired adjacent non-tumor tissues and to test if the mutations were tumor tissue *** HBV DNA isolated from 34 paired intratumoral and peritumoral tissues of Hepatocellular Carcinoma (HCC) patients were screened by PCR and direct sequencing. All patients carried HBV with genotype C, except for one B/C heterozygote. The expression,localization and excretion of LHBs mutant carrying pre-S deletions were characterized in vitro. The expression of endoplasmic reticulum(ER) GRP78 mRNA was *** Four patterns of pre-S mutations were identified: pre-S1 in-frame deletion involving the first start codon; pre-S2 in-frame deletion;pre-S2 start codon mutation with or without in-frame deletion; and S promoter in-frame deletion (ΔSP). The first two types were evenly found in both tumor and non-tumor tissues. They were rarely present as dominant strains. The last two types were frequently found in the dominant strains in tumor tissues. The overall prevalence of HBV carrying ΔSP was 17.64% (6/34) in tumor tissues, but none were dominant in non-tumor tissues. HBV carrying ΔSP was unable to produce S protein in vitro. Immunocytofluorescence assay showed that the ΔSP LHBs mutant aggregated in the cytoplasm, accumulating mainly in the ER. Transient transfection and expression of ΔSP mutant caused GRP78 up-regulation in vitro.

关键词： HCC HBV

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大方坯连铸结晶器浸入式水口结构优化

炼钢 2008年第2期24卷 42-45页

作者：高泽平苏振江湖南工业大学材料与冶金工程系湖南株洲412000

通过物理模拟实验,测定所设计的系列水口在不同工况条件下,结晶器内液面波动、冲击压力及保护渣覆盖情况,经优化后,找出较佳水口;再应用流场计算软件FLUENT及水力模型,对所选水口进行结晶器内钢液的流场和温度场特性分析,优选出适合大... 详细信息

通过物理模拟实验,测定所设计的系列水口在不同工况条件下,结晶器内液面波动、冲击压力及保护渣覆盖情况,经优化后,找出较佳水口;再应用流场计算软件FLUENT及水力模型,对所选水口进行结晶器内钢液的流场和温度场特性分析,优选出适合大方坯连铸工艺的浸入式水口结构形式,并在生产中得到了验证。

关键词：大方坯连铸结晶器浸入式水口结构优化

Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2

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Neural Regeneration Research 2025年第6期20卷 1776-1788页

作者： Zige jiang Dexiang Liu Tingting Li Chengcheng Gai Danqing Xin Yijing Zhao Yan Song Yahong Cheng Tong Li zhen Wang Department of Physiology School of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Medical Psychology and Ethics School of Basic Medicine SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Neurosurgery surgery Qingdao Municipal HospitalQingdaoShandong ProvinceChina

The pathophysiology of Huntington's disease involves high levels of the neurotoxin quinolinic acid. Quinolinic acid accumulation results in oxidative stress, which leads to neurotoxicity. However, the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington's disease pathology remain unknown. In this study, we established in vitro and in vivo models of Huntington's disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice, respectively. We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum, which was accompanied by down-regulation of cystathionine β-synthase, an enzyme responsible for hydrogen sulfide production. However, treatment with NaHS(a hydrogen sulfide donor) increased hydrogen sulfide levels in the neurons and in mouse serum, as well as cystathionine β-synthase expression in the neurons and the mouse striatum, while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum. These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression. Finally, treatment with the nuclear factor erythroid 2-related factor 2inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress. Taken together, our findings show that hydrogen sulfide reduces oxidative stress in Huntington's disease by activating nuclear factor erythroid 2-related factor 2,suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington's disease.

关键词： apoptosis cystathionine-β-synthase nuclear factor erythroid 2-related factor 2 Huntington's disease hydrogen sulfide mitochondrion neuroplasticity oxidative stress quinolinic acid reactive oxygen species