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Retrovirus-mediated gene transfer of human endostatin inhibits growth of human liver carcinoma cells SMMC7721 in nude mice

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World Journal of Gastroenterology 2002年第6期8卷 1045-1049页

作者： XuanWang Fu-KunLiu XiLi Jie-ShouLi Gen-XinXu DepartmentofMolecularBiology NanjingMilitaryMedicalSchoolNanjing210002JiangsuProvinceChina ResearchInstituteofGeneralSurgery ClinicalSchoolofMedicineNanjingUniversityNanjing210002JiangsuProvince

AIM: To study the effect of human endostatin mediated by retroviral gene transfer on the growth of human hepatocarcinoma cell line SMMC7721 in nude mice. METHODS: Human endostatin gene together with rat serum albumin signal peptide was transferred into human liver carcinoma SMMC7721 cells by retroviral vector pLncx to build a stable transfectant (SMMC-endo). PCR and Western blot analysis were used to verify the transfection and secretion of human endostatin gene in SMMC7721 cells. The endothelial cell proliferation assay in vitro was conducted to test the biological activity of the expressed human *** inhibitory effect of endostatin expressed by transfected 5MMC7721 on the growth rates of tumor cells in vivo was observed. The mean microvessel density in the specimen was also ***: PCR amplification proved that the genome of SMMC-endo cells contained a 550bp specific fragment of endostatin gene. Western blot analysis confirmed the secretion of human endostatin gene in the conditioned medium of transfected SMMC-endo cells. The endothelial proliferation assay showed that the conditioned medium of SMMC-endo cells significantly inhibited the proliferation of human umbilical vein endothelial cells by 48 %, significantly higher than that of SMMC-pLncx (10.2 %, P＜0.01). In vivo experiments revealed that only in 3 out of 5 mice tumors were formed and the mean size of flank tumors from SMMC-endo cells was 94.5 % smaller than that from the control SMMC-pLncx cells 22 days after tumor inoculation (P＜0.001).The mean microvessel density in tumor samples from SMMC-endo cells was only 8.6±1.1, much fewer than that of 22.6±4.5 from SMMC-pLncx cells (P＜0.01).CONCLUSION: Human endostatin mediated by retroviral gene transfer can inhibit human liver carcinoma cell SMMC7721 growth in nude mice.

关键词：逆转录病毒介导基因转染抗血管生成蛋白 Endostatin 裸鼠肝癌细胞生长 SMMC7721细胞系抑制作用

Cholesteryl ester transfer protein levels and gene deficiency in Chinese patients with cardio-cerebrovascular diseases

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中华医学杂志(英文版) 2002年第3期115卷 52-55页

作者：庄一义汪俊军强宏娟李勇刘小传李露言陈光辉 China 210002 China 210002 China 210002

Objective To detect cholesteryl ester transfer protein (CETP) levels, frequencies of CETP D442G and Ⅰ14A mutations and characteristics of abnormal lipids in patients wit h cardio-cerebro vascular diseases. Methods Ninety-four myocardial infarction (MI) patients,110 stroke patients and 335 hea lthy controls were selected. The CETP concentration was determined using ELISA . The CETP activity was measured using a substrate of 14 C-radiol abeled discoidal bilayer particles. The CETP gene mutations were detected by PC R-RFLP. Results The CETP concentrations in the MI and stroke group, were higher than those in th e controls. The gene mutation frequencies of D442G in the MI, stroke and contro l group were 3.5%, 3.6% and 5%, respectively, and the frequencies of Ⅰ14A wer e 1.05%, 0.91% and 1%, respectively. One case of D442G homozygote was detected in the healthy group. The frequency of two CETP gene mutations showed no signi ficant difference among the patients and controls. The CETP concentration and a ctivity in subjects with CETP mutations were one-third of those in the control group. The level of HDL-C, apo-A1 increased in the mutation subjects, while t he TG level decreased. Conclusions The CETP level increased significantly in patients with cardio-cerebrovascular diseases. The carriers of CETP deficiency had CETP and lipid abnormalities.

关键词： myocardial infarction · stroke · cholest eryl ester transfer protein · gene frequency

Targeting the ubiquitination/deubiquitination process to regulate immune checkpoint pathways

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Signal Transduction and Targeted Therapy 2021年第2期6卷 425-435页

作者： Jiaxin Liu Yicheng Cheng Ming Zheng Bingxiao Yuan Zimu Wang Xinying Li Jie Yin Mingxiang Ye Yong Song Department of Respiratory and Critical Care Medicine Afliated Jinling HospitalMedical School of Nanjing University210002 NanjingJiangsuChina Department of Respiratory and Critical Care Medicine Jining HospitalNanjing University School of Medicine210002 NanjingChina Department of Stomatology Jining HospitalMedical School of Nanjing UniversityNanjing 210002China Department of Respiratory and Critical Care Medicine Jinling HospitalNanjing Medical University210002 NanjingJiangsuChina

The immune system initiates robust immune responses to defend against invading pathogens or tumor cells and protect the body from damage,thus acting as a fortress of the ***,excessive responses cause detrimental effects,such as inflammation and autoimmune *** balance the immune responses and maintain immune homeostasis,there are immune checkpoints to terminate overwhelmed immune *** and tumor cells can also exploit immune checkpoint pathways to suppress immune responses,thus escaping immune *** a consequence,therapeutic antibodies that target immune checkpoints have made great breakthroughs,in particular for cancer *** the overall efficacy of immune checkpoint blockade(ICB)is unsatisfactory since only a small group of patients benefted from ICB ***,there is a strong need to search for other targets that improve the efficacy of *** is a highly conserved process which participates in numerous biological activities,including innate and adaptive immunity.A growing body of evidence emphasizes the importance of ubiquitination and its reverse process,deubiquitination,on the regulation of immune responses,providing the rational of simultaneous targeting of immune checkpoints and ubiquitination/deubiquitination pathways to enhance the therapeutic *** review will summarize the latest findings of ubiquitination/deubiquitination pathways for anti-tumor immunity,and discuss therapeutic significance of targeting ubiquitination/deubiquitination pathways in the future of immunotherapy.

关键词： ubiquitin immunity process

Compensatory Head Posture Changes in Patients with Obstructive Sleep Apnea

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2000年第1期20卷 66-69页

作者：童茂荣夏锡荣 Department of Respirology General Hospital of Nanjing Army Nanjing 210002

Summary: The upper airway narrowing and changes in head posture and their relationship with apnea seventy in patients with obstructive sleep apnea (OSA) were investigated. In 86 male OSA patients and 37 healthy men, one-night polysomnographic examination was performed and a lateral cephalogram by digital image processing system was taken in each subject. Fifteen variables concerning the upper airway dimensions, area and head postures were measured by using a computer software (NIH Image). The results showed that upper airway dimensions in the OSA group at all levels were significantly smaller than those in the control group and the results hold true when the age and body mass index were well controlled in these two groups. Significant forward inclination of the cervical column was found in the patients with an apnea index (AI) greater than 35 episodes/h. And changes in the head posture variables in the whole study group were significantly correlated with AI and airway dimensions at various levels. It was suggested that there exist significant and extensive upper airway narrowing in OSA patients even in upright position and awake state; And as the apnea seventy progresses, patients may assume certain compensatory head postures in an attempt to maintain an adequate airway patency.

关键词： sleep apnea, obstructive cephalometry pathogenesis

CXCR4 antagonist AMD3100 attenuates colonic damage in mice with experimental colitis

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World Journal of Gastroenterology 2010年第23期16卷 2873-2880页

作者： Xia, Xian-Ming Wang, Fang-Yu Xu, Wen-An Wang, Zhen-Kai Liu, Jiong Lu, You-Ke Jin, Xin-Xin Lu, Heng Shen, Yun-Zhu Jinling Hosp Dept Gastroenterol & Hepatol Nanjing 210002 Jiangsu Prov Peoples R China

AIM:To investigate the effects of the chemokine stromal cell-derived factor-1(CXCL12) receptor(CXCR4) antagonist AMD3100 on colonic inflammation and epithelial barrier in dextran sulfate sodium(DSS)-induced colitis in ***:Experimental colitis was induced by administration of 5% DSS for 7 d,and assays performed on intestinal segments from the ileocecal valve to the *** morphology was examined by hematoxylin and eosin *** cytokines were determined by enzyme-linked immunosorbent ***(MPO) activity(indicator of inflammatory infiltration) was observed *** permeability was assessed by mucosal-to-serosal clearance of fluorescein isothiocyanate-conjugated dextran 4000(FD4) in everted gut *** apoptosis of colonic epithelium was assessed by Hoechst-33342 *** further elucidate the role of CXCR4 in colonic inflammation,we also investigated the effect of AMD3100 on migration and cytokine production of isolated peripheral blood mononuclear cells(PBMCs).RESULTS:DSS-induced colitis was characterized by morphologic changes,as well as increased colonic cytokines,inflammatory infiltration,epithelial apoptosis,and intestinal permeability in *** AMD3100-treated mice,epithelial destruction,inflammatory infiltration,and submucosal edema were markedly reduced;colonic tumor necrosis factor-α(TNF-α),interleukin-6(IL-6) and interferon-γ(IFN-γ) levels,as well as MPO activity were significantly *** intestinal permeability in DSS-treated mice was signif icantly reduced by *** number of apoptotic cells in colitis mice was markedly increased after DSS administration,and decreased when treated with the CXCR4 antagonist *** pre-activated PBMCs,CXCL12 stimulation signif icantly increased the migration of PBMCs,and was inhibited by *** increased TNF-α,IL-6,and IFN-γ from CXCL12-treated PBMCs were also reduced by ***:The CXCR4 antagonist AMD3100 exerts the

关键词： Ulcerative colitis Chemokine stromal cellderived factor-1 receptor Inflammation Apoptosis Intestinal permeability Epithelial barrier

Emodin enhances alveolar epithelial barrier function in rats with experimental acute pancreatitis

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World Journal of Gastroenterology 2010年第24期16卷 2994-3001页

作者： Xia, Xian-Ming Wang, Fang-Yu Wang, Zhen-Kai Wan, Hai-Jun Xu, Wen-An Lu, Heng Jinling Hosp Dept Gastroenterol & Hepatol Nanjing 210002 Jiangsu Prov Peoples R China

AIM: To investigate the effect of emodin on expression of claudin4, claudin5 and occludin, as well as the alveolar epithelial barrier in rats with pancreatitis induced by sodium taurocholate. METHODS: Experimental pancreatitis was induced by retrograde injection of 5% sodium taurocholate into the biliopancreatic duct. Emodin was injected via the external jugular vein 3 h after induction of acute pancreatitis. Rats from sham operation group and acute pancreatitis group were injected with normal saline (an equivalent volume as emodin) at the same time point. Samples of lung and serum were obtained 6 h after drug administration. Pulmonary morphology was examined with HE staining. Pulmonary edema was estimated by measuring water content in lung tissue samples. Tumor necrosis factorα (TNFα) and interleukin6 (IL6) level were measured by enzymelinked immunospecific assay. Serum amylase and pulmonary myeloperoxidase (MPO) activity were detected by spectrophotometry. Alveolar epithelial barrier was assessed by pulmonary dye extravasation. Expression of claudin4, claudin5 and occludin in lung tissue samples was examined by immunohistology, quantitative realtime reverse transcription polymerase chain reaction and Western blotting analysis, ***: Pancreatitis-associated lung injury was char-acterized by pulmonary edema, leukocyte infiltration, alveolar collapse, and elevated serum amylase level. The pulmonary damage, pulmonary pathological scores, serum amylase and MPO activity, TNF-α and IL-6 levels, and wet/dry ratio were decreased in rats after treatment with emodin. Immunostaining of claudin-4, claudin-5 and occludin was detected in lung tissue samples from rats in sham operation group, which was distributed in alveolar epithelium, vascular endothelium, and bron-chial epithelium, respectively. The mRNA and protein expression levels of claudin-4, claudin-5 and occludin in lung tissue samples were markedly decreased, the expression level of claudin-4, claudin-

关键词： Acute pancreatitis Emodin Lung injury Claudin Occludin Epithelial barrier

Arctigenin attenuates paraquat-induced human lung epithelial A549 cell injury by suppressing ROS/p38 mitogen-activated protein kinases-mediated apoptosis

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World Journal of Emergency Medicine 2022年第5期13卷 373-378页

作者： Chao Liu Zhao-rui Sun Meng-meng Wang Zhi-zhou Yang Wei Zhang Yi Ren Xiao-qin Han Rui Liu Quan Li Shi-nan Nie Department of Emergency Medicine Jinling HospitalMedical School of Nanjing UniversityNanjing 210002China

BACKGROUND:Paraquat(PQ)-induced acute lung injury(ALI)and pulmonary fi brosis are common diseases with high mortality but without eff ective antidotes in emergency *** previous study has proved that arctigenin suppressed pulmonary fibrosis induced by *** wondered whether arctigenin could also have a protective eff ect on PQ-induced ***:A PQ-induced A549 cell injury model was used,and the effect of arctigenin was determined by a cell counting kit-8(CCK-8)cell viability *** addition,terminal deoxynucleotidyl transferase(TdT)-mediated dUTP nick-end labelling(TUNEL)staining assays and mitochondrial membrane potential assays were performed to evaluate the level of cell *** generation of reactive oxygen species(ROS)was refl ected by dihydroethidium(DHE)staining and a 2’,7’-dichlorodihy drofluorescein diacetate(DCFH-DA)***,immunoblotting studies were used to assess the expression of mitogen-activated protein kinases(MAPKs)and p38 ***:Arctigenin attenuated PQ-induced inhibition of A549 cell viability in a dose-dependent *** also significantly reduced PQ-induced A549 cell apoptosis,as refl ected by the TUNEL assay and mitochondrial membrane potential assay,which may result from suppressed ROS/p38 MAPK signaling because we found that arctigenin dramatically suppressed ROS generation and p38 MAPK ***:Arctigenin could attenuate PQ-induced lung epithelial A549 cell injury in vitro by suppressing ROS/p38 MAPK-mediated cell apoptosis,and arctigenin might be considered a potential candidate drug for PQ-induced ALI.

关键词： Paraquat A549 cells Arctigenin Reactive oxygen species Mitogen-activated protein kinases Apoptosis

Annexin A5 regulates Leydig cell testosterone production via ERK1/2 pathway

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Asian Journal of Andrology 2016年第3期18卷 456-461,I0010页

作者： Ze He Qin Sun Yuan-Jiao Liang Li Chen Yi-Feng Ge Shi-Feng Yun Bing Yao The Reproductive Medical Center Nanjing Jinling Hospital Nanjing University School of Medicine Nanjing Jiangsu 210002 China Department of Comparative Medicine Nanjing Jinling Hospital Nanjing University School of Medicine Nanjing Jiangsu 210002 China.

This study was to investigate the effect of annexin A5 on testosterone secretion from primary rat Leydig cells and the underlying mechanisms. Isolated rat Leydig ceils were treated with annexin A5. Testosterone production was detected by chemiluminescence assay. The protein and mRNA of Steroidogenic acute regulatory （STAR）, P450scc, 3β-hydroxysteroid dehydrogenase （3β-HSD）, 17β-hydroxysteroid dehydrogenase （17β-HSD）, and 17β-hydroxylase were examined by Western blotting and semi-quantitative RT-PCR, respectively. Annexin A5 significantly stimulated testosterone secretion from rat Leydig cells in dose- and time-dependent manners and increased mRNA and protein expression of STAR, P450scc, 3β-HSD, and 17β-HSD but not 17α-hydroxylase. Annexin A5 knockdown by siRNA significantly decreased the level of testosterone and protein expression of P450scc, 3β-HSD, and 17β-HSD. The significant activation of ERK1/2 signaling was observed at 5, 10, and 30 min after annexin A5 treatment. After the pretreatment of Leydig cells with ERK inhibitor PD98059 （50 μmol l^-1） for 20 min, the effects of annexin A5 on promoting testosterone secretion and increasing the expression of P450scc, 3β-HSD, and 17β-HSD were completely abrogated （P 〈 0.05）. Thus, ERK1/2 signaling is involved in the roles of annexin A5 in mediating testosterone production and the expression of P450scc, 3β-HSD, and 17β-HSD in Leydig cells.

关键词： 17β-HSD 3β-HSD annexin A5 P450scc STAR testosterone

系统论视阈下特别重大突发事件应急治理失灵模型研究

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灾害学 2025年第1期40卷 140-145页

作者：陈梁陈威王修来南京信息工程大学管理工程学院江苏南京210044 南京信息工程大学人才大数据研究院江苏南京210044 东部战区总医院医学信息数据室江苏南京210002

顺应韧性治理的发展潮流,基于系统论破解特别重大突发事件应急治理失灵困境。结合中国应急管理部官方网站公布的特别重大突发事件调查报告,从“失灵溯源”的视角综合审视突发事件应急治理过程,根据技术应用、情报协同、组织治理在应急... 详细信息

顺应韧性治理的发展潮流,基于系统论破解特别重大突发事件应急治理失灵困境。结合中国应急管理部官方网站公布的特别重大突发事件调查报告,从“失灵溯源”的视角综合审视突发事件应急治理过程,根据技术应用、情报协同、组织治理在应急治理过程中赋能与失灵的双重效应,构建特别重大突发事件应急治理失灵模型。研究发现,技术应用子系统、情报协同子系统和组织治理子系统分别通过技术支持、数据获取和信息整合;情报收集、分析协同和共享传递;指挥协调、资源调度和决策执行的作用路径,共同影响特别重大突发事件的应急治理效能。在实际治理过程中,需要解决系统和要素之间的失灵困境,才能更好地赋能特别重大突发事件应急治理韧性。

关键词：特别重大突发事件应急治理失灵模型系统论