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Interaction of Hepatitis B Virus X Protein with the Pregnane X Receptor Enhances the Synergistic Effects of Aflatoxin B1 and Hepatitis B Virus on Promoting Hepatocarcinogenesis

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Journal of Clinical and Translational Hepatology 2021年第4期9卷 466-476页

作者： Yongdong Niu Shaohua Fan Qin Luo Liming Chen Danmei Huang Wenjun Chang Wenxin Qin ganggang shi Department of Pharmacology Shantou University Medical CollegeShantouGuangdongChina Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province School of Life ScienceJiangsu Normal UniversityXuzhouJiangsuChina State Key Laboratory of Oncogenes and Related Genes Shanghai Cancer InstituteRenji HospitalShanghai Jiao Tong University School of MedicineShanghaiChina Department of Oncology First Affiliated Hospital of Shantou University Medical CollegeShantouGuangdongChina Department of Environmental Hygiene Second Military Medical UniversityShanghaiChina

Background and Aims:Hepatitis B virus(HBV)infection has been found to increase hepatocellular sensitivity to carcinogenic xenobiotics,by unknown mechanisms,in the generation of hepatocellular carcinoma.The pregnane X receptor(PXR)is a key regulator of the body’s defense against xenobiotics,including xenobiotic carcinogens and clinical drugs.In this study,we aimed to investigate the molecular mechanisms of HBV X protein(HBx)-PXR signaling in the synergistic effects of chemical carcinogens in HBV-associated hepatocarcinogenesis.Methods:The expression profile of PXR-cytochrome p4503A4(CYP3A4)signaling was determined by PCR,western blotting,and tissue microarray.Cell viability and aflatoxin B1(AFB1)cytotoxicity were measured using the cell counting kit-8 assay.Target gene expression was evaluated using transient transfection and real time-PCR.The genotoxicity of AFB1 was assessed in newborn mice with a single dose of AFB1.Results:HBx enhanced the hepatotoxicity of AFB1 by activating CYP3A4 and reducing glutathione Stransferase Mu 1(GSTM1)in cell lines.Activation of PXR by pregnenolone 16α-carbonitrile increased AFB1-induced liver tumor incidence by up-regulating oncogenic KRAS to enhance interleukin(IL)-11:IL-11 receptor subunit alpha-1(IL11RA-1)-mediated inflammation in an HBx transgenic model.Conclusions:Our finding regarding AFB1 toxicity enhancement by an HBx-PXR-CYP3A4/GSTM1-KRASIL11:IL11RA signaling axis provides a rational explanation for the synergistic effects of chemical carcinogens in HBV infection-associated hepatocarcinogenesis.

关键词： Liver cancer Hepatitis B virus X protein Pregnane X receptor Aflatoxin B1 Hepatotoxicity

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基于磁场模型的矿用钢丝绳检测信号特性试验研究

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煤炭科学技术 2024年第2期52卷 279-291页

作者：田劼白强王兴军孙钢钢师彰文李鹏博中国矿业大学(北京)机械与电气工程学院北京100083 中国矿业大学(北京)煤矿智能化与机器人创新应用应急管理部重点实验室北京100083

电磁检测是矿用钢丝绳缺陷可靠的检测手段之一。基于电磁法的矿用钢丝绳缺陷检测,目前存在缺陷与信号特性表征规律不明确的问题,定量识别时存在无关信号特性,影响识别准确性。采用三维磁偶极子理论计算、Maxwell模拟仿真与试验相互验证... 详细信息

电磁检测是矿用钢丝绳缺陷可靠的检测手段之一。基于电磁法的矿用钢丝绳缺陷检测,目前存在缺陷与信号特性表征规律不明确的问题,定量识别时存在无关信号特性,影响识别准确性。采用三维磁偶极子理论计算、Maxwell模拟仿真与试验相互验证的方法,总结漏磁信号特性与缺陷变化之间的表征关系。首先建立磁场环境下的钢丝绳三维磁偶极子理论模型,应用模型对标准缺陷处进行磁场理论计算并进行Maxwell模拟仿真;分别提取理论值与仿真值的峰/谷绝对值、波宽、峰谷差值、峰谷值宽度四项信号特性,进行缺陷与信号的表征分析;最后设计缺陷进行试验验证,得到试验数值的斯皮尔曼相关系数。试验结果表明:缺陷的宽度、深度与峰/谷绝对值、波宽、峰谷差值3个信号特征值呈正相关,与峰谷值宽度无明显相关性;缺陷长度与峰/谷绝对值呈先上升后下降的趋势,与波宽、峰谷差值、峰谷值宽度呈正相关。并且发现宽度缺陷信号幅值最强,长度缺陷信号幅值最弱,深度信号幅值居中,峰谷差值和峰谷绝对值与缺陷相关性最高。该研究具有一定的工程指导价值。

关键词：电磁检测无损检测信号特性磁偶极子损伤缺陷矿用钢丝绳

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预灌封灭菌注射用水在ACYW135群脑膜炎球菌多糖疫苗中的应用

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微生物学免疫学进展 2024年第1期52卷 55-61页

作者：张冉孙刚刚石献华北京智飞绿竹生物制药有限公司生产中心生产三部北京100176

目的研究预灌封灭菌注射用水作为ACYW135群脑膜炎球菌多糖疫苗稀释剂的质量和稳定性,探索疫苗的新型组合包装形式。方法依据《中华人民共和国药典》2020版(简称《中国药典》)要求,连续生产3批次预灌封灭菌注射用水并检定合格,将其与3... 详细信息

目的研究预灌封灭菌注射用水作为ACYW135群脑膜炎球菌多糖疫苗稀释剂的质量和稳定性,探索疫苗的新型组合包装形式。方法依据《中华人民共和国药典》2020版(简称《中国药典》)要求,连续生产3批次预灌封灭菌注射用水并检定合格,将其与3批次检定合格的ACYW135群脑膜炎球菌多糖疫苗进行组合包装。检测预灌封灭菌注射用水和组合包装中以稀释剂复溶后的脑膜炎球菌多糖疫苗的质量和稳定性。结果 3批次预灌封灭菌注射用水在(40±2)℃、相对湿度(75±5)%条件下放置6个月的加速稳定性试验中,分别按规定于0、1、2、3、6个月取样检测;在(30±2)℃、相对湿度(65±5)%条件下放置48个月的长期稳定性试验中,于0、3、6、9、12、18、24、36、48个月取样检测;各取样节点的检测结果均符合《中国药典》“灭菌注射用水”标准。3批次脑膜炎球菌多糖疫苗在37℃放置6个月的加速稳定性试验中,分别按规定于0、1、2、3、6个月以稀释剂复溶后取样检测;在2~8℃放置48个月的长期稳定性试验中,于0、3、6、9、12、18、24、36、48个月以稀释剂复溶后取样检测;各项检测结果均符合《中国药典》“ACYW135群脑膜炎球菌多糖疫苗”标准。结论预灌封灭菌注射用水作为ACYW135群脑膜炎球菌多糖疫苗稀释剂具备适用性,该组合包装形式可为疫苗包装提供新选择。

关键词：预灌封灭菌注射用水疫苗稀释剂 ACYW135群脑膜炎球菌多糖疫苗组合包装稳定性

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煤化工净化装置节能降耗对策研究

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山东化工 2024年第4期53卷 277-279页

作者：骆建国石磊张林通张青杨刚刚华亭华煤清能煤化工有限责任公司甘肃平凉744100

疫情过后随着全国经济回暖,各地掀起了煤化工项目启动建设的浪潮,节能减排、低碳绿色在新型的煤化工行业成为新的焦点。本文主要介绍了甘肃某煤化工公司60万t/a煤制甲醇项目净化装置采取的一系列节能减排、低碳的技术措施。净化装置采... 详细信息

疫情过后随着全国经济回暖,各地掀起了煤化工项目启动建设的浪潮,节能减排、低碳绿色在新型的煤化工行业成为新的焦点。本文主要介绍了甘肃某煤化工公司60万t/a煤制甲醇项目净化装置采取的一系列节能减排、低碳的技术措施。净化装置采用大连理工大学的低温甲醇洗技术,包括CO_(2)吸收塔、H_(2)S浓缩塔、热再生塔、甲醇\水分离塔、尾气水洗塔等五塔工艺,研究表明:对再生系统进行技术改造、硫化氢浓缩塔顶增设尾气分液技术、系统增设两台甲醇过滤器、贫甲醇泵出口增设自控切断阀、进料冷却器入口增设甲醇排液管道、尾气二氧化碳回收利用技术、废水管线改造去制备煤浆和净化气氢碳比优化调整。通过以上技术改造和调整,降低了系统甲醇自身消耗,实现了CO_(2)回收利用,废水达到了零排放,满足了节能减排的要求。降低了产品单耗,提高了企业经济效益和竞争力。

关键词：煤化工净化工艺节能减排低碳绿色低温甲醇洗产品单耗技术改造零排放

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Positional cloning and characterization reveal the role of a miRNA precursor gene ZmLRT in the regulation of lateral root number and drought tolerance in maize

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Journal of Integrative Plant Biology 2023年第3期65卷 772-790页

作者： Ming Zhang Yanhong Chen Hongyan Xing Wensheng Ke Yunlu shi Zhipeng Sui Ruibin Xu Lulu Gao ganggang Guo Jiansheng Li Jiewen Xing Yirong Zhang State Key Laboratory for Agrobiotechnology Key Laboratory of Crop Heterosis and Utilization(MOE)Key Laboratory of Crop Genetic ImprovementChina Agricultural UniversityBeijing 100193China Agronomy College of Shandong Agricultural University Taian 271018China Key L aboratory of Crop Germplasm Resources and Utilization(MARA) Institute of Crop SciencesChinese Academy of Agricultural SciencesBeijing 100081China Center for Crop Functional Genomics and Molecular Breeding China Agricultural UniversityBeijing 100193China Yantai Science and Technology Innovation Promotion Center Yantai 264003China Beijing Key Laboratory of Maize DNA Fingerprinting and Molecular Breeding Maize Research InstituteBeijing Academy of Agriculture and Forestry SciencesBeijing 100097China National Maize Improvement Center of China China Agricultural UniversityBeijing 100193China

Lateral roots play essential roles in drought tolerance in maize(Zea mays L.). However, the genetic basis for the variation in the number of lateral roots in maize remains elusive. Here, we identified a major quantitative trait locus(QTL),q LRT5-1, controlling lateral root number using a recombinant inbred population from a cross between the maize lines Zong3(with many lateral roots) and 87-1(with few lateral roots).Fine-mapping and functional analysis determined that the candidate gene for qLRT5-1,ZmLRT, expresses the primary transcript for the microRNA miR166a. ZmLRT was highly expressed in root tips and lateral root primordia,and knockout and overexpression of ZmLRT increased and decreased lateral root number,respectively. Compared with 87-1, the ZmLRT gene model of Zong3 lacked the second and third exons and contained a 14 bp deletion at the junction between the first exon and intron,which altered the splicing site. In addition,ZmLRT expression was significantly lower in Zong3 than in 87-1, which might be attributed to the insertions of a transposon and over large DNA fragments in the Zong3 ZmLRT promoter region. These mutations decreased the abundance of mature miR166a in Zong3, resulting in increased lateral roots at the seedling stage.Furthermore, miR166a post-transcriptionally repressed five development-related class-Ⅲ homeodomain-leucine zipper genes. Moreover,knockout of ZmLRT enhanced drought tolerance of maize seedlings. Our study furthers our understanding of the genetic basis of lateral root number variation in maize and highlights ZmLRT as a target for improving drought tolerance in maize.

关键词： drought tolerance lateral root number maize miRNA precursor QTL mapping

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The Effects of Liquor Spirits on RNA Pol III Genes and Cell Growth of Human Cancer Lines

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Food and Nutrition Sciences 2018年第3期9卷 208-220页

作者： Yunfeng Yi Junxia Lei ganggang shi Songlin Chen Yanmei Zhang Zaifa Hong Zhimin He Shuping Zhong Department of Cardiothoracic Surgery Xiamen University Affiliated Southeast Hospital Xiamen China School of Medicine South China University of Technology Guangzhou China Keck School of Medicine University of Southern California Los Angeles USA Department of Pharmacology Shantou University Medical College Shantou China Cancer Hospital and Institute of Guangzhou Medical University Guangzhou China

Alcohol consumption is a major health issue and associated with human cancers, such as liver and breast cancers. Alcohol was classed as carcinogen to human by IARC. We have performed in vivo and in vitro studies which demonstrate that diluted ethanol promotes cell proliferation and transformation and tumor formation. Consumption of liquor spirits (white wines) is a popular behavior. However, it is unclear whether liquor spirits affect cellular phenotypes of human cancers. At present study, we used diluted ethanol and liquor spirits (Sample #1 and Sample #2) to determine the changes in RNA polymerase III-dependent gene (Pol III gene) transcription, cell growth and colony formation in the different human cancer lines. The results indicate that low concentration of ethanol increases RNA Pol III gene transcription and rate of cell growth. However, both liquor spirits (Sample #1 and Sample #2) inhibit the activity of RNA Pol III genes and repress cell proliferation of the cancer lines, compared to diluted ethanol. The liquor spirits reduce the rate of colony formation of human breast cancer cells and esophageal carcinoma cells. The inhibitions of the liquor spirits to RNA Pol III genes, cell growth and colony formation are in a dose-dependent manner. These new findings suggest that the liquor spirits contain some active components to repress Pol III gene transcription and cell growth caused by ethanol in different human cancer cells.

关键词： Ethanol Liquor Spirits Cancer Cells Pol III Genes Cell Growth Colony Formation

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Nifedipine and Diltiazem Protect L-VDCC-/-H9c2 Cells against Hypoxia/Reoxygenation Injury via Regulating the Expression of Cyclooxygenase-2

Nifedipine and Diltiazem Protect L-VDCC-/-H9c2 Cells against...

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首届东方药理论坛暨2018年全国心脑血管药理学术会议、上海市药理学会第十九届学术年会

作者： Man Liu ganggang shi Department of Pharmacology Shantou University Medical College

Restoration of the coronary blood flow of ischemic heart induces additional cardiac damage and complications,such as inflammation,oxidative stress and apoptosis,named as myocardial ischemia/reperfusion（I/R） injury,also called hypoxia/reoxygenation（H/R） injury.Our previous work has indicated that nifedipine and diltiazem can protect myocardium against I/R injury through blocking L-type voltage-dependent calcium channel（L-VDCC）.However,it has been reported that nifedipine and diltiazem can also reduce I/R injury in a L-VDCC-independent way,which has been confirmed by our studies.Cyclooxygenase-2（COX-2）,which has been reported to be related to H/R injury,is a key enzyme for the production of prostanoids.This work is to study whether or not nifedipine and diltiazem can regulate the expression of COX-2 to alleviate cardiomyocytes H/R injury in a L-VDCC-independent way.Materials & Methods L-VDCC-/-H9 c2 cells were divided into:CON,H/R,H/R+DMSO,H/R+nifedipine,H/R+diltiazem,H/R+NS-398（selective inhibitor of COX-2） group.Hypoxia was achieved by placing the cells on a hypoxia chamber,containing 94% N2 and 5% CO21% O2 at 37℃ to mimic ischemia.Reoxygenation was achieved by exposing cell to normal medium and room air with atmosphere containing 5% CO2,95% O2 at 37 ℃.Nifdepine,diltiazem or NS-398 was added to the changed medium during H/R stimulation.Expression of COX-2 mRNA was detected by Quantitative PCR. COX-2 and cleaved-caspase3 protein expression was detected by Western Blot.Interleukin6（IL-6） concentration,malondialdehyde（MDA） content and superoxide dismutase（SOD） activity were measured by relative kits.Early apoptotic cells were measured by Annexin-V FITC/PI.Data were analyzed using one-way ANOVA followed by Tukey’s test.Results In H/R group,COX-2 mRNA and protein expression were up-regulated;IL-6 concentration,MDA content,cleaved-caspase3 protein expression and early apoptotic cells were increased and SOD activity group was decreased compared with CON group.In H/R+NS-398 group,IL-6 concentration,MDA content,cleaved-ca

关键词： nifedipine diltiazem L-VDCC-/-H9c2cells hypoxia/reoxygenation COX-2

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Angiotensin Ⅱ confers resistance to apoptosis in cardiac myofibroblasts through the AT1/ERK1/2/RSK1 pathway

Angiotensin Ⅱ confers resistance to apoptosis in cardiac my...

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首届东方药理论坛暨2018年全国心脑血管药理学术会议、上海市药理学会第十九届学术年会

作者： Wenfeng Cai ganggang shi Department of Pharmacology Shantou University Medical College

Myofibroblast apoptosis is essential for normal resolution of wound repair,including cardiac infarction repair.Impaired cardiac myofibroblast（CMF） apoptosis is associated with excessive extracellular matrix（ECM） deposition,which could be responsible for pathological cardiac fibrosis.Conventionally,angiotensin Ⅱ（Ang Ⅱ）,a soluble peptide,is implicated in fibrogenesis because it induces cardiac fibroblast（CFb） proliferation,differentiation and collagen synthesis.However,the role of AngⅡ in regulation of CMF survival and apoptosis has not been fully clarified.In this report,we cultured neonatal rat CFbs,which transform into CMFs after passage 3（6-8 days）,and investigated the effects of Ang Ⅱ on CMFs challenged by TNF-α combined with cycloheximide and the underlying mechanisms.Here,we show that Ang Ⅱrapidly activates MAPKs but not AKT in CMFs and confers apoptosis resistance,as evidenced by the inhibition of caspase-3 cleavage,early apoptotic cells and late apoptotic cells.This inhibitory effect of Ang Ⅱ was reversed by blockade of AT1 or inactivation of ERK1/2 or RSK1 but not AT2,indicating that activation of the pro-survival AT1/ERK1/2/RSK1 signaling pathway mediates apoptosis resistance.TGF-β,a latent fibrotic factor,was found to have no relation to Ang Ⅱ-induced apoptosis resistance in our study.Furthermore,Ang Ⅱ-mediated apoptosis resistance,which was conferred by activation of the AT1/ERK1/2/RSK1 signaling pathway,was also confirmed in human adult ventricular cardiac myofibroblasts.Collectively,our findings suggest a novel profibrotic mechanism of Ang Ⅱ in which it promotes myofibroblast resistance to apoptosis in addition to classical mechanisms,providing a potential novel therapeutic approach by targeting pro-survival signaling pathways.

关键词： cardiacfibrosis myofibroblast apoptosis angiotensinⅡ ERK1/2

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Calcium channel blockers of the subthreshold dose protect against myocardial ischemia reperfusion injury in mice

Calcium channel blockers of the subthreshold dose protect ag...

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首届东方药理论坛暨2018年全国心脑血管药理学术会议、上海市药理学会第十九届学术年会

作者： Qing Zhu ganggang shi Department of Pharmacology Shantou University Medical College

Efficient prevention of myocardial ischemia/reperfusion（I/R） injury has not been completely resolved yet.Calcium channel blockers is one approach to solve this problem due to calcium overload.And L-type voltage dependent calcium channel（L-VDCC） is the major target of classical calcium channel blockers.However,some literature indicated that new targets and the new mechanisms of calcium channel blockers might exist result from the calcium channel blockers not entirely worked through blocking L-VDCC in recent years.Maybe they have the new targets and the new mechanisms.Our previous studies suggested that verapamil（Ver）, nifedipine（Nif）which widely used as the calcium channel blockers in clinical and F2（N-n-butyl haloperidol iodide,a new compound researched and synthesized by our drug research lab） could protect cardiomyocytes against hypoxia/reoxygenation（H/R） injury through non L-VDCC.Ischemic heart disease,also known as coronary atherosclerotic heart disease,has become a leading cause of death worldwide.Ischemic heart disease is a leading cause of death worldwide.Previously,we and others reported that calcium channel blockers exerted a solid protective effect against myocardial I/R injury.So,we aimed to investigate the effect of subthreshold dose calcium channel blockers which against the myocardial I/R injury and we further confirmed calcium channel blockers could protect against myocardial I/R injury in non L-VDCC manner.

关键词： Ischemia-reperfusion Calciumchannelblocker Subthresholddose

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Nifedipine protects Cacna1C-/-H9c2 cells against hypoxia/reoxygenation injury by regulating JunB

Nifedipine protects Cacna1C-/-H9c2 cells against hypoxia/reo...

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首届东方药理论坛暨2018年全国心脑血管药理学术会议、上海市药理学会第十九届学术年会

作者： Shanna Feng ganggang shi Department of Pharmacology Shantou University Medical College

JunB,one major member of activator protein-1（AP-1） family,always works through forming both homodimers and heterodimers.The studies have reported that myocardial ischemia and hypoxia led to a significant increase of JunB expression up to 2-7 times,and JunB is involved in cell proliferation,apoptosis,oxidative stress,protein synthesis,inflammation,etc.Myocardial ischemia/reperfusion（I/R） causes breakage of cell membrane,Ca2+-overload,inflammation,oxidative stress,metabolic disorder of energy,etc.Calcium channel blockers（CCB） alleviate myocardial ischemia/reperfusion injury（MIRI） by protecting cardiac myocytes and improving cardiac function.CCB,the drugs that can attenuate MIRI through lowering the level of intracellular Ca2+ by blocking L-type calcium channel（LTCC） and inhibiting the influx of Ca2+,is divided into three categories,nifedipine（Nif）,verapamil（Ver）,diltiazem（Dil） for represent respectively.N-n-butyl haloperidol iodide（F2）,a novel CCB developed by our own teams,produces protective effects on MIRI and hypoxia/reoxygenation（H/R） injury by blocking LTCC.A study reported that Nif ameliorated ischemia-induced endothelial cell permeability through preventing translocation of PKC,while had no effect on Ca2+level induced by ischemia.It indicates that Nif exerts a direct protective effect which is independent of Ca2+channels.Our research group have proved that CCB can restrain the cell apoptosis,reduce inflammatory cytokine and MDA,decrease activity of LDH and enhance activity of SOD by a LTCC-independent way in H/R models of Cacna1 C-/-H9 c2 cells,cardiac microvascular endothelial cells without LTCC,and H9 c2 cells cultured in Ca2+-free buffer solution.

关键词： nifedipine hypoxia/reoxygenation JunB Cacna1C-/-H9c2cells

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