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| 1 | 2018 Chinese Pediatric Cardiology Society(CPCS) guideline for diagnosis and treatment of syncope in children and adolescents显示文摘Syncope belongs to the transient loss of consciousness(TLOC), characterized by a rapid onset, short duration, and spontaneous complete recovery. It is common in children and adolescents, accounting for 1% to 2% of emergency department visits.Recurrent syncope can seriously affect children's physical and mental health, learning ability and quality of life and sometimes cardiac syncope even poses a risk of sudden death. The present guideline for the diagnosis and treatment of syncope in children and adolescents was developed for guiding a better clinical management of pediatric syncope. Based on the globally recent development and the evidence-based data in China, 2018 Chinese Pediatric Cardiology Society(CPCS) guideline for diagnosis and treatment of syncope in children and adolescents was jointly prepared by the Pediatric Cardiology Society, Chinese Pediatric Society, Chinese Medical Association(CMA)/Committee on Pediatric Syncope, Pediatricians Branch, Chinese Medical Doctor Association(CMDA)/Committee on Pediatric Cardiology, Chinese College of Cardiovascular Physicians, Chinese Medical Doctor Association(CMDA)/Pediatric Cardiology Society, Beijing Pediatric Society, Beijing Medical Association(BMA). The present guideline includes the underlying diseases of syncope in children and adolescents, the diagnostic procedures, methodology and clinical significance of standing test and headup tilt test, the clinical diagnosis vasovagal syncope, postural orthostatic tachycardia syndrome, orthostatic hypotension and orthostatic hypertension, and the treatment of syncope as well as follow-up. | Cheng Wang Yaqi Li Ying Liao Hong Tian Min Huang Xiangyu Dong Lin Shi Jinghui Sun Hongfang Jin Junbao Du Jindou An Jie Chen Mingwu Chen Qi Chen Sun Chen Yonghong Chen Zhi Chen Adolphus Kai-tung Chau Junbao Du Zhongdong Du Junkai Duan Hongyu Duan Xiangyu Dong Lin Feng Lijun Fu Fangqi Gong Yonghao Gui Ling Han Zhenhui Han Bing He Zhixu He Xiufen Hu Yimin Hua Guoying Huang Min Huang Ping Huang Yujuan Huang Hongfang Jin Mei Jin Bo Li Fen Li Tao Li Xiaohui Li Xiaoyan Liu Yan Li Haitao Lv Tiewei Lv Zipu Li Luyi Ma Silin Pan Yusheng Pang Hua Peng Yuming Qin Jie Shen Lin Shi Kun Sun Jinghui Sun Hong Tian Jie Tian Cheng Wang Hong Wang Lei Wang Jinju Wang Wendi Wang Yuli Wang Rongzhou Wu Tianhe Xia Yanyan Xiao Chunhong Xie Yanlin Xing Zhenyu Xiong Baoyuan Xu Yi Xu Hui Yan Shiwei Yang Qijian Yi Xia Yu Xianyi Yu Yue Yuan Hongyan Zhang Huili Zhang Li Zhang Qingyou Zhang Xi Zhang Yanmin Zhang Zhiwei Zhang Cuifen Zhao Bin Zhou Hua Zhu | 2018 | Science Bulletin2018，63，23： | 54 |
| 2 | Erianin,a novel dibenzyl compound in Dendrobium extract,inhibits lung cancer cell growth and migration via calcium/calmodulin-dependent ferroptosis显示文摘Ferroptosis,a novel form of programmed cell death,is characterized by iron-dependent lipid peroxidation and has been shown to be involved in multiple diseases,including cancer.Stimulating ferroptosis in cancer cells may be a potential strategy for cancer therapy.Therefore,ferroptosis-inducing drugs are attracting more attention for cancer treatment.Here,we showed that erianin,a natural product isolated from Dendrobium chrysotoxum Lindl,exerted its anticancer activity by inducing cell death and inhibiting cell migration in lung cancer cells.Subsequently,we demonstrated for the first time that erianin induced ferroptotic cell death in lung cancer cells,which was accompanied by ROS accumulation,lipid peroxidation,and GSH depletion.The ferroptosis inhibitors Fer-1 and Lip-1 but not Z-VAD-FMK,CQ,or necrostatin-1 rescued erianin-induced cell death,indicating that ferroptosis contributed to erianin-induced cell death.Furthermore,we demonstrated that Ca^(2+)/CaM signaling was a critical mediator of erianin-induced ferroptosis and that blockade of this signaling significantly rescued cell death induced by erianin treatment by suppressing ferroptosis.Taken together,our data suggest that the natural product erianin exerts its anticancer effects by inducing Ca^(2+)/CaMdependent ferroptosis and inhibiting cell migration,and erianin will hopefully serve as a prospective compound for lung cancer treatment. | Peng Chen Qibiao Wu Jiao Feng Lili Yan Yitian Sun Shuiping Liu Yu Xiang Mingming Zhang Ting Pan Xiaying Chen Ting Duan Lijuan Zhai Bingtao Zhai Wengang Wang Ruonan Zhang Bi Chen Xuemeng Han Yicong Li Liuxi Chen Ying Liu Xingxing Huang Ting Jin Wenzheng Zhang Hong Luo Xiaohui Chen Yongqiang Li Qiujie Li Guohua Li Qin Zhang Lvjia Zhuo Zuyi Yang Huifen Tang Tian Xie Xiaoping Ouyang Xinbing Sui | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 42 |
| 3 | Correction of a genetic disease by CRISPR-Cas9-mediated gene editing in mouse spermatogonial stem cells显示文摘Spermatogonial 干细胞(SSC ) 能在移植以后生产众多的男配偶子进接受者睾丸,介绍为基因治疗和修改基因的动物的连续生产的一条珍贵途径。然而, SSC 的成功的基因操作被限制了,部分由于复杂性和当前可得到的基因编辑技术的低效率。这里,我们证明有效基因修正能用 CRISPR-Cas9 系统被介绍进 SSC。我们使用了 CRISPR-Cas9 系统变异在 SCC 的 EGFP transgene 或内长的 Crygc 基因。变异的 SSC 在移植以后经历了精子发生进不肥沃的老鼠睾丸的生精的小管。圆 spermatids 被产生并且在进成熟卵母细胞的注射以后,支持了显示相应变异的显型的异质接合的后代的生产。而且,在 Crygc 的一个引起疾病的变化(在 SSC 先存在的 Crygc −/−) 能乐意地到加入的 CRISPR-Cas9-induced nonhomologous 结束(NHEJ ) 或指导相同的修理(HDR ) 被修理,导致没有是的离开目标修正的证据带改正的基因的 SSC 线由整个染色体的定序出现。用从这些线产生的圆 spermatids 的授精在 100% 的效率与改正的显型产生了后代。我们的结果表明有效基因由 CRISPR-Cas9 系统在老鼠 SSC 编辑,并且提供在 SSC 经由基因修正治好基因疾病的原则的证明。 | Yuxuan Wu Hai Zhou Xiaoying Fan Ying Zhang Man Zhang Yinghua Wang Zhenfei Xie Meizhu Bai Qi Yin Dan Liang Wei Tang Jiaoyang Liao Chikai Zhou Wujuan Liu Ping Zhu Hongshan Guo Hong Pan Chunlian Wu Huijuan Shi Ligang Wu Fuchou Tang Jinsong Li | 2015 | Cell Research2015，25，1： | 37 |
| 4 | Anti-SARS-CoV-2 activities in vitro of Shuanghuanglian preparations and bioactive ingredients显示文摘Human infection with severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)causes coronavirus disease 2019(COVID-19)and there is no cure currently.The 3CL protease(3CLpro)is a highly conserved protease which is indispensable for CoVs replication,and is a promising target for development of broad-spectrum antiviral drugs.In this study we investigated the anti-SARS-CoV-2 potential of Shuanghuanglian preparation,a Chinese traditional patent medicine with a long history for treating respiratory tract infection in China.We showed that either the oral liquid of Shuanghuanglian,the lyophilized powder of Shuanghuanglian for injection or their bioactive components dose-dependently inhibited SARS-CoV-23CLpro as well as the replication of SARS-CoV-2 in Vero E6 cells.Baicalin and baicalein,two ingredients of Shuanghuanglian,were characterized as the first noncovalent,nonpeptidomimetic inhibitors of SARS-CoV-23CLpro and exhibited potent antiviral activities in a cell-based system.Remarkably,the binding mode of baicalein with SARS-CoV-23CLpro determined by X-ray protein crystallography was distinctly different from those of known 3CLpro inhibitors.Baicalein was productively ensconced in the core of the substrate-binding pocket by interacting with two catalytic residues,the crucial S1/S2 subsites and the oxyanion loop,acting as a“shield”in front of the catalytic dyad to effectively prevent substrate access to the catalytic dyad within the active site.Overall,this study provides an example for exploring the in vitro potency of Chinese traditional patent medicines and effectively identifying bioactive ingredients toward a specific target,and gains evidence supporting the in vivo studies of Shuanghuanglian oral liquid as well as two natural products for COVID-19 treatment. | Hai-xia Su Sheng Yao Wen-feng Zhao Min-jun Li Jia Liu Wei-juan Shang Hang Xie Chang-qiang Ke Hang-chen Hu Mei-na Gao Kun-qian Yu Hong Liu Jing-shan Shen Wei Tang Lei-ke Zhang Geng-fu Xiao Li Ni Dao-wen Wang Jian-ping Zuo Hua-liang Jiang Fang Bai Yan Wu Yang Ye Ye-chun Xu | 2020 | Acta Pharmacologica Sinica2020，41，9： | 32 |
| 5 | Effect of hepatocyte apoptosis induced by TNF-α on acute severe hepatitis in mouse models显示文摘AIM To study the effect of hepatocyteapoptosis and necrosis induced by TNF-α on thepathogenesis of acute severe hepatitis(ASH).METHODS The model of ASH was prepared inD-galactosamine(GAIN)sensitized BALB/c miceby injection of either endotoxin(ET)or tumornecrosis factor-α(TNF-α).Morphologicalchanges of apoptotic hepatocytes were studiedby both light and electron microscope and in siteend labeling method(ISEL).Molecular biologicalchanges of DNA ladder were observed byelectrophoresis of extract from liver tissues.Biochemical changes were measured by alanineaminotransferase(ALT),asparticaminotransferase(AST)and TNF-α.The relationbetween apoptosis and necrosis was evaluatedsimultaneously.RESULTS The sequence of hepatocyteapoptosis,necrosis,and final death from ASHwas observed both in GAIN/ET and GAIN/TNF-agroup.Apoptosis was prominent at 3.5 h and 5 hafter injection of inducer,while necrosis becamedominant at 9 h after challenge.The appearanceof apoptosis was earlier in GAIN/TNF-α groupthan that in GAIN/ ET group.Pretreatment ofmice with antiTNF IgG1 may completely preventthe liver injury induced by GalN/ET.CONCLUSION TNF-α can cause liver damageby inducing hepatic apoptosis and necrosis inmice with endotoxemia. | Guo Qing Zang Xia Qiu Zhou Hong Yu Qing Xie Guo Ming Zhao Bin Wang Qing Guo Yue Qin Xiang Dan Liao Department of Infectious Diseases,Rujin Hospital,Shanghai Second Medical University,Shanghai 200025,China | 2000 | World Journal of Gastroenterology2000，6，5： | 30 |
| 6 | Phytochromes Regulate SA and JA Signaling Pathways in Rice and Are Required for Developmentally Controlled Resistance to Magnaporthe grisea显示文摘野类型的米饭植物的旧叶子(Oryza sativa L。cv。Nipponbare ) 比新叶子对强风真菌(Magnaporthe grisea ) 更抵抗。相反,米饭 phytochrome 三元组异种(phyAphyBphyC ) 的旧、新的叶子产生强风真菌。我们表明那个致病相关的班 1 (PR1 ) 蛋白质很快并且强烈在 M 期间被导致。grisea 感染和后面的外长的 jasmonate (JA ) 或水杨酸酸(SA ) 在旧叶子,然而并非在新叶子的暴露野类型。相反, PR1 蛋白质的累积显著地在 phyAphyBphyC 异种的旧、新的叶子被稀释。这些结果建议 phytochromes 在米饭为 PR1 蛋白质的正式就职被要求。PR1a 和 PR1b 的基础抄写层次是实质地更高的在象与 phyAphyBphyC 异种相比野类型,也建议那 phytochromes 为 PR1 基因的基础表示被要求。而且,知道在 SA 依赖或 JA 依赖的防卫小径工作的基因的抄本层次到叶年龄和功能的 phytochromes 被调整。一起拿,我们的调查结果证明 phytochromes 为年龄相关的抵抗在米饭被要求到 M。grisea 并且可以间接地由调整 SA 依赖、 JA 依赖的防卫小径增加 PR1 基因表示。 | Xian-Zhi Xie Yan-Jiu Xue Jin-Jun Zhou Bin Zhang Hong Chang Makoto Takano | 2011 | Molecular Plant2011，4，4： | 28 |
| 7 | Sevoflurane post-conditioning protects isolated rat hearts against ischemia-reperfusion injury via activation of the ERK1/2 pathway显示文摘瞄准: 在 sevoflurane 调查细胞外的调整信号的 kinases (英皇家空军之阶级最低之兵) 的角色在 vitro 的调节以后的导致的 cardioprotection。 | Hong XIE Jing ZHANG Jiang ZHU Li-xin LIU Mario REBECCHI Su-mei HU Chen WANG | 2014 | Acta Pharmacologica Sinica2014，35，12： | 27 |
| 8 | Up-regulation of divalent metal transporter 1 in 6-hydroxydopamine intoxication is IRE/IRP dependent显示文摘铁在 Parkinson 的疾病(PD ) 起一个关键作用。substantia nigra (SN ) 的增加的铁内容在 PD 病人,和二价的金属 transporter 被发现了(DMT1 ) 1 被显示了在两个导致 MPTP 的 PD 模型和 PD 病人的 SN 起来调整。然而,位于 DMT1 起来规定下面的机制大部分是未知的。在现在的学习,我们观察到那在 6-hydroxydopamine ( 6-OHDA )的 SN 导致了 PD 老鼠,有铁的 DMT1 应答的元素(怒火, DMT1+IRE ),然而并非没有怒火( DMT1?IRE )的 DMT1 ,是起来调整的,建议那增加的 DMT1+IRE 表情可能在 PD 老鼠说明 nigral 铁累积。这可能性进一步被估计在一在里面 vitro 学习使用 6-OHDA-treated 和 DMT1+IRE-over-expressing MES23.5 房间。在 6-OHDA-treated MES23.5 房间,增加了铁规章的蛋白质(IRP ) 1 并且 IRP2 表示被观察,当 IRP 的 silencing 戏剧性地减少了时 6-OHDA-induced DMT1+IRE 起来规定。有 N-acetyl-L-cysteine 的预告的处理充分由 6-OHDA-induced 的抑制压制了 IRP 起来规定氧化应力。增加的 DMT1+IRE 表示由 MES23.5 房间导致了增加的铁流入。我们的数据提供 DMT1+IRE 起来规定能说明细胞内部的氧化应力和那增加了的 6-OHDA-induced 开始的 IRE/IRP-dependent 6-OHDA-induced 铁累积的直接证据细胞内部的铁的层次导致加重的氧化应力。这研究的结果提供在 PD 的处理支持抗氧化剂的使用的新奇证据,旨在禁止由 DMT1 表示的规定的铁累积。 | Hong Jiang Ning Song Huamin Xu Shuzhen Zhang Jun Wang Junxia Xie | 2010 | Cell Research2010，20，3： | 25 |
| 9 | Furazolidone-based triple and quadruple eradication therapy for Helicobacter pylori infection显示文摘AIM: To evaluate the efficacy of furazolidone-based triple and quadruple therapy in eradicating Helicobacter pylori(H. pylori) in a multi-center randomized controlled trial.METHODS: A total of 720 H. pylori positive patients with duodenal ulcer disease were enrolled at 10 different hospitals in Jiangxi province in China. The patients were randomly assigned to four treatment groups as follows: patients in Groups 1 and 3 received rabeprazole(10 mg), amoxicillin(1000 mg) and furazolidone(100 mg) twice daily for 7 and 10 d, respectively; patients in Groups 2 and 4 received rabeprazole(10 mg), bismuth(220 mg), amoxicillin(1000 mg) and furazolidone(100 mg) twice daily for 7 and 10 d, respectively. The primary outcome measure was H. pylori eradication rate 4 wk after treatment by intention-to-treat and per protocol analysis, while the secondary outcome measures were symptom and sign changes at the end of treatment and 4 wk after the end of treatment, as well as the proportion of patients who developed adverse events.RESULTS: The demographic data of the four groups were not significantly different. Overall, 666 patients completed the scheme and were re-assessed with the 13C-urea breath test. The intention-to-treat analysis of the H. pylori eradication rates in Groups 1, 2, 3 and 4 were 74.44%, 82.78%, 78.89% and 86.11%, respectively. The H. pylori eradication rate in Group 4 was significantly higher than that in Group 1. According tothe per protocol analysis, the H. pylori eradication rates in Groups 1, 2, 3 and 4 were 81.21%, 89.22%, 85.54% and 92.26%, respectively. The H. pylori eradication rate in Group 4 was significantly higher than that in Group 1. The number of adverse events was 15(8.3%), 16(8.9%), 15(8.3%) and 17(9.4%) in Groups 1, 2, 3 and 4, respectively, including dizziness, vomiting, diarrhea, nausea, skin rash, itchy skin, and malaise. The symptoms were relieved without special treatment in all of the patients.CONCLUSION: Both 7- and 10-d quadruple furazolidone-based therapies achieve satisfactory H. pylori eradication rates. | Yong Xie Yin Zhu Hong Zhou Zhi-Fa Lu Zhen Yang Xu Shu Xiao-Bai Guo Hui-Zhen Fan Jian-Hua Tang Xue-Ping Zeng Jian-Bo Wen Xiao-Qing Li Xing-Xing He Jiu-Hong Ma Dong-Sheng Liu Cai-Bin Huang Ning-Jian Xu Nong-Rong Wang Nong-Hua Lu | 2014 | World Journal of Gastroenterology2014，20，32： | 24 |
| 10 | Antihepatoma effect of alpha-fetoprotein antisense phosphorothioate oligodeoxyribonucleotides in vitro and in mice显示文摘AIM To evaluate antihepatoma effect ofantisense phosphorothioate oligodeo-xyribonucleotides (S-ODNs) targeted to alpha-fetoprotein (AFP) genes in vitro and in nudemice.METHODS AFP gene expression was examinedby immunocytochemical method or enzyme-linked immunosorbent assay. Effect of S-ODNson SMMC-7721 human hepatoma cell growth invitro was determined using microculturetetrazolium assay. In vivo antitumor activitiesof S-ODNs were monitored by measuring tumorweight differences in treated and control micebearing SMMC-7721 xenografts. Induction of cellapoptosis was evaluated by fluorescence-activated cell sorter (FACS) analysis.RESULTS Antisense S-ODN treatment led toreduced AFP gene expression. Specificantisense S-ODNs, but not control S-ODNs,inhibited the growth of heaptoma cells in vitro.In vivo. only antisense S-ODNs exhibitedobvious antitumor activities. FACS analysisrevealed that the growth inhibition by antisenseS. ODNs was associated with their cell apoptosisinduction.CONCLUSION Antisense S-ODNs targeted toAFP genes inhibit the growth of human hepatomacells and solid hepatoma, which is related totheir cell apoptosis induction. | Xing Wang Wang~1 Jin Hui Yuan~1 Ru Gang Zhang~1 Li Xia Guo~1 Yong Xie~2 Hong Xie~1 ~1Department of Biotherapy,Shanghai Institute of Cell Biology,Chinese Academy of Sciences,Shanghai 200031,China ~2Department of Biology,Hong Kong University of Science and Technology,ChinaDr.Xing Wang Wang earned Ph.D.from Shanghai Institute of Materia Medical,Chinese Academy of Sciences in 1997.Now a professor at Shanghai Institute of Cell Biology,Chinese Academy of Sciences. | 2001 | World Journal of Gastroenterology2001，7，3： | 21 |
| 11 | Concurrent chemoradiotherapy combined with enteral nutrition support:a radical treatment strategy for esophageal squamous cell carcinoma patients with malignant istulae显示文摘Background: Concurrent chemoradiotherapy(CCRT) significantly increases the survival rate of esophageal squa?mous cell carcinoma(ESCC) patients with malignant fistulae. Recent clinical evidence has shown the benefits of enteral nutrition for malnourished cancer patients. In this study, we aimed to validate that, with the support of enteral nutrition, ESCC patients who develop malignant fistulae might be able to complete CCRT and achieve long?term survival.Methods: We reviewed the medical records of 652 patients with ESCC who received definitive CCRT at Sun Yat?sen University Cancer Center between January 2010 and December 2012. Treatment outcome and toxicity were ret?rospectively evaluated in 40 ESCC patients with malignant fistulae. All the 40 patients were treated with CCRT and evaluated by clinical nutritionists using nutrition risk screening(NRS) before, during, and after treatment. Twenty?two patients received a nasogastric tube, and 18 underwent percutaneous endoscopic gastrostomy feeding. The median energy intake was 2166 kcal/day. Treatment response was evaluated at 3 months after the completion of CCRT.Results: With a median follow?up of 18 months(range, 3–39 months), patients' 1?year overall survival(OS) rate was 62.5%, and the estimated OS time was 25.5 months. Univariate analysis showed that the NRS score(P n NRS score(P se to treatment(P < 0.001) were sig= 0.003), increase i= 0.024), fistula closure(P = 0.011), and responnifi?cantly associated with OS. Multivariate analysis showed that tumor response(P = 0.044) and increase in NRS score(P = 0.044) were independent predictors of OS. Grade 3 vomiting was observed in 8 patients(20.0%), grade 3 neutro?penia was observed in 11 patients(27.5%), and grade 3 cough was observed in 13 patients(32.5%); 2 patients(5.0%) died of massive bleeding during treatment.Conclusions: CCRT combined with enteral nutrition support is effective for ESCC patients with malignant fistulae. Patients have an increased potential to be cured, especially those who experience complete response and have an increase in NRS score. Careful observation and nutrition support are required for patients with advanced T?category ESCC who undergo CCRT. | Li Ma Guang-Yu Luo Yu-Feng Ren Bo Qiu Hong Yang Chun-Xia Xie Song-Ran Liu Shi-Liang Liu Zhao-Lin Chen Qun Li Jian-Hua Fu Meng-Zhong Liu Yong-Hong Hu Wen-Feng Ye Hui Liu | 2017 | Chinese Journal of Cancer2017，36，1： | 19 |
| 12 | Exogenous NADPH ameliorates myocardial ischemia–reperfusion injury in rats through activating AMPK/mTOR pathway显示文摘Our previous study shows that nicotinamide adenine dinucleotide phosphate(NADPH)plays an important role in protecting against cerebral ischemia injury.In this study we investigated whether NADPH exerted cardioprotection against myocardial ischemia/reperfusion(I/R)injury.To induce myocardial I/R injury,rats were subjected to ligation of the left anterior descending branch of coronary artery for 30 min followed by reperfusion for 2 h.At the onset of reperfusion,NADPH(4,8,16 mg·kg?1·d?1,iv)was administered to the rats.We found that NADPH concentrations in plasma and heart were signi?cantly increased at 4 h after intravenous administration.Exogenous NADPH(8?16 mg/kg)signi?cantly decreased myocardial infarct size and reduced serum levels of lactate dehydrogenase(LDH)and cardiac troponin I(cTn-I).Exogenous NADPH signi?cantly decreased the apoptotic rate of cardiomyocytes,and reduced the cleavage of PARP and caspase-3.In addition,exogenous NADPH reduced mitochondrial vacuolation and increased mitochondrial membrane protein COXIV and TOM20,decreased BNIP3L and increased Bcl-2 to protect mitochondrial function.We conducted in vitro experiments in neonatal rat cardiomyocytes(NRCM)subjected to oxygen–glucose deprivation/restoration(OGD/R).Pretreatment with NADPH(60,500 nM)signi?cantly rescued the cell viability and inhibited OGD/R-induced apoptosis.Pretreatment with NADPH signi?cantly increased the phosphorylation of AMPK and downregulated the phosphorylation of mTOR in OGD/R-treated NRCM.Compound C,an AMPK inhibitor,abolished NADPH-induced AMPK phosphorylation and cardioprotection in OGD/R-treated NRCM.In conclusion,exogenous NADPH exerts cardioprotection against myocardial I/R injury through the activation of AMPK/mTOR pathway and inhibiting mitochondrial damage and cardiomyocyte apoptosis.NADPH may be a potential candidate for the prevention and treatment of myocardial ischemic diseases. | Jiang Zhu Yi-fei Wang Xiao-ming Chai Ke Qian Ling-wei Zhang Peng Peng Pei-min Chen Jian-fang Cao Zheng-hong Qin Rui Sheng Hong Xie | 2020 | Acta Pharmacologica Sinica2020，41，4： | 19 |
| 13 | Clinical efficacy of 0.1% pranoprofen in treatment of dry eye patients:a multicenter, randomized, controlled clinical trial显示文摘 | Chen Jingyao Dong Fei Chen Wei Sun Xuguang Deng Yingping Hong Jing Zhang Mingchang Yang Wenzhao Liu Zuguo Xie Lixin | 2014 | Chinese Medical Journal2014，，13： | 18 |
| 14 | Growth-inhibiting effects of taxol on human liver cancer in vitro and in nude mice显示文摘AIM To investigate the effects of taxol onSMMC-7721 human hepatoma and itsmechanisms.METHODS In vitro cell growth was assessedby trypan blue exclusion method.Experimentalhepatoma model was established by seedingSMMC-7721 cells subcutaneously into Balb/c(nu/nu)nude mice.In vivo tumor growth wasdetermined by measurement of tumor diameterwith Vernier calipers.The syntheses of DNA,RNA and protein were analyzed by incorporationof ~3H-thymidine,~3H-uridine and ~3H-leucinerespectively.Using light and electronmicroscopes to observe the morphologicalchanges of cells including mitosis andapoptosis.RESULTS Taxol was effective against SMMC-7721 human hepatoma cell growth in the rangesof 2.5 nmol/L-10 nmol/L with mitotic arrestand apoptosis in vitro.DNA,RNA and proteinsyntheses in cells were also obviouslysuppressed by in vitro treatment of taxol for72 h.Taxol at 2.5 nmol/L reduced ~3H-thymidineuptake to about 34% of the control value(P<0.05).Increasing the dose of taxol to20 nmol/L resulted in a greater decrease in ~3H-thymidine incorporation to 60% of the controlvalue(P<0.01).At a concentration of 20 nmol/L,the ~3H-uridine and ~3H-leucine uptakeswere reduced to 52%(P<0.05)and 63%(P<0.01),respectively.In vivo,taxolsignificantly inhibited SMMC-7721 tumor growthat 10 mg/kg,i.p.,once daily for 10 d.A morethan 90% decrease in tumor volume wasobserved by day 11(P<0.01)similarly withmitotic arrest and cell apoptosis.CONCLUSION Taxol has a marked anticanceractivity in SMMC-7721 human hepatoma both invitro and in nude mice.Its mechanisms might beassociated with mitotic arrest,subsequently,apoptosis of the hepatoma cells.No obvioustoxicity was observed with in vivoadministration of taxoi. | Jin Hui Yuan Ru Ping Zhang Ru Gang Zhang Li Xia Guo Xing Wang Wang Dan Luo Yong Xie Hong Xie | 2000 | World Journal of Gastroenterology2000，6，2： | 18 |
| 15 | Daclatasvir plus asunaprevir in treatment-na?ve patients with hepatitis C virus genotype 1b infection显示文摘AIM To assess daclatasvir plus asunaprevir(d UAL) in treatment-na?ve patients from China's Mainland, Russia and South Korea with hepatitis C virus(HCV) genotype 1 b infection. METHODS Patients were randomly assigned(3:1) to receive 24 wk of treatment with d UAL(daclatasvir 60 mg once daily and asunaprevir 100 mg twice daily) beginning on day 1 of the treatment period(immediate treatment arm) or following 12 wk of matching placebo(placebodeferred treatment arm). The primary endpoint was a comparison of sustained virologic response at posttreatment week 12(SVR12) compared with the historical SVR rate for peg-interferon plus ribavirin(70%) among patients in the immediate treatment arm. The first 12 wk of the study were blinded. Safety was assessed in d UAL-treated patients compared with placebo patients during the first 12 wk(doubleblind phase), and during 24 wk of d UAL in both arms combined.RESULTS In total, 207 patients were randomly assigned to immediate(n = 155) or placebo-deferred(n = 52) treatment. Most patients were Asian(86%), female(59%) and aged < 65 years(90%). Among them, 13% had cirrhosis, 32% had IL28 B non-CC genotypes and 53% had baseline HCV RNA levels of ≥ 6 million IU/m L. Among patients in the immediate treatment arm, SVR12 was achieved by 92%(95% confidence interval: 87.2-96.0), which was significantly higher than the historical comparator rate(70%). SVR12 was largely unaffected by cirrhosis(89%), age ≥ 65 years(92%), male sex(90%), baseline HCV RNA ≥ 6 million(89%) or IL28 B non-CC genotypes(96%), although SVR12 was higher among patients without(96%) than among those with(53%) baseline NS5 A resistanceassociated polymorphisms(at L31 or Y93 H). during the double-blind phase, aminotransferase elevations were more common among placebo recipients than among patients receiving d UAL. during 24 wk of d UAL therapy(combined arms), the most common adverse events(≥ 10%) were elevated alanine aminotransferase and upper respiratory tract infection; emergent grade 3-4 laboratory abnormalities were infrequently observed, and all grade 3-4 aminotransferase abnormalities(alanine aminotransferase, n = 9; aspartate transaminase, n = 6) reversed within 8-11 d. Two patients discontinued d UAL treatment; one due to aminotransferase elevations, nausea, and jaundice and the other due to a fatal adverse event unrelated to treatment. There were no treatment-related deaths.CONCLUSION d UAL was well-tolerated during this phase 3 study, and SVR12 with d UAL treatment(92%) exceeded thehistorical SVR rate for peg-interferon plus ribavirin of 70%. | Lai Wei Fu-Sheng Wang Ming-Xiang Zhang Ji-Dong Jia Alexey A Yakovlev Wen Xie Eduard Burnevich Jun-Qi Niu Yong Jin Jung Xiang-Jun Jiang Min Xu Xin-Yue Chen Qing Xie Jun Li Jin-Lin Hou Hong Tang Xiao-guang Dou Yash Gandhi Wen-Hua Hu Fiona McPhee Stephanie Noviello Michelle Treitel Ling Mo Jun Deng | 2018 | World Journal of Gastroenterology2018，24，12： | 17 |
| 16 | An HBV-encoded miRNA activates innate immunity to restrict HBV replication显示文摘We previously identified that hepatitis B virus(HBV)encodes a microRNA(HBV-miR-3)that restrains HBV replication by targeting the HBV transcript.However,whether HBV-miR-3 affects host innate immunity to modulate HBV replication remains unclear.Here,we examined the vital functions of HBV-miR-3 in the innate immune response after HBV infection.We found that HBV-miR-3 expression gradually increased in a dose-and time-dependent manner in HBV-infected HepG2-NTCP cells.HBV-miR-3 activated the JAK/STAT signaling pathway by downregulating SOCS5 in hepatocytes,thereby enhancing the IFN-induced anti-HBV effect.In addition,HBVmiR-3 in exosomes facilitated the Ml polarization of macrophages.Furthermore,exosomes containing HBV-miR-3 enhanced the secretion of IL-6 via inhibiting the SOCS5-mediated ubiquitination of EGFR.In short,these results demonstrate that HBV-miR-3 activates the innate immune response to restrain HBV replication by multiple pathways,which may suppress HBV-induced acute liver cell injury and affect the progression of persistent HBV infection. | Xiaoqing Zhao Lu Sun Ting Mu Jianying Yi Chaoqun Ma Hong Xie Min Liu Hua Tang | 2020 | Journal of Molecular Cell Biology2020，12，4： | 17 |
| 17 | Minimally invasive surgery alone compared with intensity-modulated radiotherapy for primary stage I nasopharyngeal carcinoma显示文摘Background:The National Comprehensive Cancer Network guidelines recommend intensity-modulated radiotherapy(IMRT)as the primary curative treatment for newly diagnosed nasopharyngeal carcinoma(NPC),but the radiation-related complications and relatively high medical costs remain a consequential burden for the patients.Endoscopic nasopharyngectomy(ENPG)was successfully applied in recurrent NPC with radiation free and relatively low medical costs.In this study,we examined whether ENPG could be an effective treatment for localized stage I NPC.Methods:Ten newly diagnosed localized stage I NPC patients voluntarily received ENPG alone from June 2007 to September 2017 in Sun Yat-sen University Cancer Center.Simultaneously,the data of 329 stage I NPC patients treated with IMRT were collected and used as a reference cohort.The survival outcomes,quality of life(QOL),and medical costs between two groups were compared.Results:After a median follow-up of 59.0 months(95%CI 53.4-64.6),no death,locoregional recurrence,or distant metastasis was observed in the 10 patients treated with ENPG.The 5-year overall survival,local relapse-free survival,regional relapse-free survival,and distant metastasis-free survival among the ENPG-treated patients was similar to that among the IMRT-treated patients(100%vs.99.1%,100%vs.97.7%,100%vs.99.0%,100%vs.97.4%,respectively,P>0.05).In addition,compared with IMRT,ENPG was associated with decreased total medical costs($4090.42±1502.65 vs.$12620.88±4242.65,P<0.001)and improved QOL scores including dry mouth(3.3±10.5 vs.34.4±25.8,P<0.001)and sticky saliva(3.3±10.5 vs.32.6±23.3,P<0.001).Conclusions:ENPG alone was associated with promising long-term survival outcomes,low medical costs,and satisfactory QOL and might therefore be an alternative strategy for treating newly diagnosed localized stage I NPC patients who refused radiotherapy.However,the application of ENPG should be prudent,and prospective clinical tri-als were needed to further verify the results. | You-Ping Liu Xing Lv Xiong Zou Yi-Jun Hua Rui You Qi Yang Le Xia Shao-Yan Guo Wen Hu Meng-Xia Zhang Si-Yuan Chen Mei Lin Yu-Long Xie Li-Zhi Liu Rui Sun Pei-Yu Huang Wei Fan Xiang Guo Ming-Huang Hong Ming-Yuan Chen | 2019 | Cancer Communications2019，39，1： | 17 |
| 18 | Puerarin enhances superoxide dismutase activity and inhibits RAGE and VEGF expression in retinas of STZ-induced early diabetic rats显示文摘Objective:To investigate the effects of puerarin on the activity of superoxide dismutase(SOD), and expressions of advanced glycation end-product(AGE) receptor(RAGE) and vascular endothelial growth factor(VEGF) in retinas of streptozotocin(STZ)-induced early diabetic rats. Methods:Diabetic rat models were established by inducing diabetes via intra-peritoneal injection of STZ.Rats were randomly divided into normal(control),diabetic(DM),and DM+ puerarin groups.After intra-gastric administration of puerarin(500 mg/kg/day for 4 weeks),levels of SOD and malondialdehyde(MDA) were determined in serum and retina.mRNA and protein expression levels of RAGE and VEGF in retinas were determined by real-lime polymerase chain reaction(RT-PCR)(mRNA) and Western blot analysis(protein levels).Results:There was significantly lower SOD activity and significantly higher MDA in serum and retinas of the DM group compared with the two other groups(P<0.05).After treatment with puerarin,SOD activity increased and MDA content decreased in this group(P<0.05).mRNA and protein expression levels of RACE and VECF in the DM group were significantly higher than those of the other groups (P<0.05),and decreased after puerarin treatment(P<0.05).Conclusions:Puerarin is able to enhance SOD activity,and inhibit RAGE and VEGF expressions in retinas of STZ-induced early diabetic ruts. | Fang Chen Hong-Quan Zhang Jun Zhu Kai-Yang Liu Hong Cheng Guo-Li Li Shan Xu Wei-Hong Lv Zheng-Gao Xie | 2012 | Asian Pacific Journal of Tropical Medicine2012，5，11： | 16 |
| 19 | Recurrent gain-of-function USP8 mutations in Cushing's disease显示文摘库欣的疾病,引起过量皮质醇生产的也已知的同样促肾上腺皮质的荷尔蒙(ACTH )-secreting 垂体腺瘤(舞步) ,占多达 85%corticotrophin 依赖的库欣的症候群盒子。然而,在这疾病的基因改变是不清楚的。这里,我们执行了从 12 秘密 ACTH 舞步导出并且匹配血样品的 DNA 定序的 whole-exome,它在候选人基因揭示了体的变化的三种类型, USP8 (编码 ubiquitin 特定的朊酶 8 ) ,专门在 exon 14 在 12 秘密 ACTH 舞步中的 8 个。我们进一步评估了体的 USP8 变化在另外由定序的 Sanger 的 258 舞步。进一步定序指向在 108 秘密 ACTH 舞步(62.04%) 中的 67 个识别了 USP8 变体的 17 种类型的一个总数。然而,任何一个都没在舞步的另外的类型这些变化被检测(n = 150 ) 。这些变化在 USP8 的 14-3-3 绑定主题以内聚集并且破坏在 USP8 和 14-3-3 蛋白质之间的相互作用,导致保护 EGFR 免受 lysosomal 降级的伤害的一个提高的能力。因此,有 EGFR 表示,提高的 EGFR 蛋白质丰富和 mRNA 表示的更高的发生 POMC 铺平的变异的 USP8 显示的舞步,它编码 ACTH 的先锋。有变异的 USP8 的舞步在尺寸是显著地更小的并且比野类型的舞步有更高的 ACTH 生产。在里面通过手术 resected 主要变异 USP8 的肿瘤房间, USP8 击倒或堵住的 EGFR 有效地稀释 ACTH 分泌物。一起拿,体的 gain-of-function USP8 变化是普通的并且在库欣的疾病贡献 ACTH 生产过剩。USP8 或 EGFR 的抑制为对待变异 USP8 的 corticotrophin 腺瘤是有希望的。我们的学习在库欣的疾病加亮潜在地功能的变异的基因并且提供卓见进这疾病的治疗学。 | Zeng-Yi Ma Zhi-Jian Song Jian-Hua Chen Yong-Fei Wang Shi-Qi Li Liang-Fu Zhou Ying Mao Yi-Ming Li Rong-Gui Hu Zhao-Yun Zhang Hong-Ying Ye Ming Shen Xue-Fei Shou Zhi-Qiang Li Hong Peng Qing-Zhong Wang Dai-Zhan Zhou Xiao-Lan Qin Jue Ji Jie Zheng Hong Chen Yin Wang Dao-Ying Geng Wei-Jun Tang Chao-Wei Fu Zhi-Feng Shi Yi-Chao Zhang Zhao Ye Wen-Qiang He Qi-Lin Zhang Qi-Sheng Tang Rong Xie Jia-Wei Shen Zu-Jia Wen Juan Zhou Tao Wang Shan Huang Hui-Jia Qiu Ni-Dan Qiao Yi Zhang Li Pan Wei-Min Bao Ying-Chao Liu Chuan-Xin Huang Yong-Yong Shi Yao Zhao | 2015 | Cell Research2015，25，3： | 16 |
| 20 | Lymphocyte Subsets and Sister-chromatid Exchanges in the Students Exposed to Formaldehyde Vapor显示文摘The present report evaluates the effects of formaldehyde (FA) exposure on peripheral lymphocytes by using heth genetic and immunological parameters. Twenty-three non-smoking students in the study had inhalation exposure to 0.508 ±0. 299 mg/m3 of FA for a Period of 8 weeks (3h × 3 times each week) during anatomy classes. As for composition of lymphocyte subsets after FA exposare,significant increase was found in the percentage of CD19(B cells), while sighficant decrease was observed in CD3(total T cells), CD4(T helper-inducer cells), and CD8(T cytotoxic-suppressior cells) with a P<0 .01. Increase in the ratio of T-helper-inducer cells to T-cytotoxic-suppressor cells (T4 / T8) was also observed with statistical sighcance after exposure (P < 0.001). In the meanwhile,no significant difference (P > 0 .05) was reported between lymphocyte prolifendion rate and sisterchromatid exchange (SCE) at the exposure level and duration. It is suggested that the lymphocyte subsets may be most susceptible to the effects of FA, though a single immunological endpoint is rarely related with pathophysiological interpretation. | YING CHEN-JIANG YE XIAO-LEI XIE HONG YAN WEN-SHENG ZHAO MEI-YING XIA TONG AND YIN SHU-YI.(Department of Environmental Health, Tongji Medical University, Wuhan 430030, China Department of Public Health, Wenzhou Medical College, Wenzhou 317400, China Department of Anatomy,Tongji Medical University, Wuhan 430030, China) | 1999 | Biomedical and Environmental Sciences1999，12，2： | 15 |
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