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| 1 | 2019新型冠状病毒基因组特征和流行病学:病毒起源和受体结合的意义显示文摘研究者对来自9例新型冠状病毒肺炎住院患者的支气管肺泡灌洗液样本和培养的分离株进行了下一代测序。从这些个体中获得了严重急性呼吸综合征-冠状病毒2(severe acute respiratory syndrome-coronavirus 2,SARS-CoV-2)的完整和部分基因组序列。利用Sanger测序连接病毒重叠群以获得全长基因组,cDNA末端快速扩增确定终端区。对这些SARSCoV-2基因组和其他冠状病毒基因组进行了系统进化分析,以确定该病毒的进化史并有助于推断其可能的起源。 | 刘青(译) 刘莉(审校) Lu R Zhao X Li J Niu P Yang B Wu H Wang W Song H Huang B Zhu N Bi Y Ma X Zhan F Wang L Hu T Zhou H Hu Z Zhou W Zhao L Chen J Meng Y Wang J Lin Y Yuan J Xie Z Ma J Liu WJ Wang D Xu W Holmes EC Gao GF Wu G Chen W Shi W Tan W | 2020 | 中华高血压杂志2020，28，3： | 516 |
| 2 | The Global Boundary Stratotype Section and Point (GSSP) for the base of the Hirnantian Stage (the uppermost of the Ordovician System)显示文摘 | Xu Chen Jiayu Rong Junxuan Fan Renbin Zhan Charles E. Mitchell David A. T. Harper Michael J. Melchin Ping'an Peng Stan C. Finney Xiaofeng Wang | 2006 | Episodes2006，29，3： | 61 |
| 3 | Mechanism of the December 2015 Catastrophic Landslide at the Shenzhen Landfill and Controlling Geotechnical Risks of Urbanization显示文摘 | Yueping Yin Bin Li Wenpei Wang Liangtong Zhan Qiang Xue Yang Gao Nan Zhang Hongqi Chen Tiankui Liu Aiguo Li | 2016 | Engineering2016，2，2： | 64 |
| 4 | Current status of severe fever with thrombocytopenia syndrome in China显示文摘Severe fever with thrombocytopenia syndrome(SFTS) is an emerging infectious disease caused by SFTS virus(SFTSV). SFTSV is associated with a high mortality rate and has been reported in China, South Korea and Japan. SFTSV undergoes rapid changes owing to evolution, gene mutations, and reassortment between different strains of SFTSV. In this review, we summarize the recent cases and general properties of SFTS, focusing on the epidemiology, genetic diversity,clinical features, and diagnostics of SFTSV in China. From 2010 to October 2016, SFTS cases were reported in 23 provinces of China, with increased numbers yearly. Infection and death cases are mainly found in central China, where the Haemaphysalis longicornis ticks are spread. The national average mortality rate of SFTS infection was 5.3%, with higher risk to elder people. The main epidemic period was from May to July, with a peak in May. Thus, SFTS reminds a significant public health problem, and development of prophylactic vaccines and effective antiviral drugs will be highly needed. | Jianbo Zhan Qin Wang Jing Cheng Bing Hu Jing Li Faxian Zhan Yi Song Deyin Guo | 2017 | Virologica Sinica2017，32，1： | 71 |
| 5 | Evidence of crustal ‘channel flow’ in the eastern margin of Tibetan Plateau from MT measurements显示文摘Magnetotelluric (MT) survey has been carried out in the eastern margin of the Tibetan Plateau and its neighboring Shimian-Leshan area, Sichuan Province. Analysis of this MT data reveals that the electric structure of the Tibetan Plateau differ much from that of the Sichuan block. In general, the electric re-sistivity of crust beneath the Sichuan block in the east is larger than that of the eastern margin of the Tibetan Plateau in the west. The crust of the plateau is divided into upper, middle, and lower layers. The middle crust is a low resistivity layer with minimum down to 3―10 Ωm about 10―15 km thick. It pre-sumably contains partial melt and/or salt-bearing fluids with low viscosity, prone to deform and flow, producing a 'channel flow' under the southeastward squeeze of the eastern Tibetan Plateau. This low-resistivity layer makes the upper crust decoupled mechanically from the lower crust. In the brittle upper crust, faults are dominated by left-lateral strike-slip and thrust motions, leading to surface rising and shallow earthquakes. The low-resistivity layer also cut the Xianshuihe-Anninghe fault zone into two sections vertically. In this region, the thicknesses of upper, middle, and lower crust vary laterally, pro-ducing a transitional zone in the eastern margin of the Tibetan Plateau characterized by thicker crust and higher elevation in the west and thinner crust and lower elevation in the east. | ZHAO GuoZe CHEN XiaoBin WANG LiFeng WANG JiJun TANG Ji WAN ZhanSheng ZHANG JiHong ZHAN Yan XIAO QiBin | 2008 | Chinese Science Bulletin2008，53，12： | 57 |
| 6 | Mapping wetland changes in China between 1978 and 2008显示文摘Four wetland maps for all China have been produced,based on Landsat and CBERS-02B remote sensing data between 1978 and 2008 (1978,1990,2000 and 2008).These maps were mainly developed by manual interpretation and validated by substantial field investigation in 2009.Based on these maps,we analyzed the 2008 wetland distribution in China and discussed wetland changes and their drivers over the past 30 years.(i) There were about 324097 km 2 of wetlands in 2008,for which inland marshes or swamps were the most common wetland type (35%),with lakes (26%) second.Most of the wetlands were in Heilongjiang,Inner Mongolia,Qinghai and Tibet,occupying about 55% of the national wetland area.(ii) From 1978 to 2008,China's wetland area continually and significantly decreased,by about 33% based on changes in the wetland map.This was in sharp contrast to the increase in artificial wetlands,which increased by about 122%.Inland marshes accounted for the main loss of total wetlands from 1978 to 2000.From 2000 through 2008,riverine and lacustrine wetlands constituted the main wetland loss.Fortunately however,the rate of wetland loss decreased from 5523 to 831 km 2 /a.(iii) The change ratio of lost natural wetlands (including inland and coastal wetlands) to non-wetlands has decreased slightly over the past 30 years.From 1978 to 1990,nearly all natural wetlands (98%) lost were transformed into non-wetlands.However,the ratio declined to 86% from 1990 to 2000,and to 77% from 2000 to 2008.(iv) All Chinese provinces were divided into three groups according to patterns of wetland changes,which could relate to the driving forces of such changes.Tibet was completely different from other provinces,as it was one representative example in which there was a net wetland increase,because of global warming and decreased human activity since 1990.Increased economic development caused considerable wetland loss in most eastern provinces,and artificial wetlands increased. | NIU ZhenGuo ZHANG HaiYing WANG XianWei YAO WenBo ZHOU DeMin ZHAO KuiYi ZHAO Hui LI NaNa HUANG HuaBing LI CongCong YANG Jun LIU CaiXia LIU Shuang WANG Lin LI Zhan YANG ZhenZhong QIAO Fei ZHENG YaoMin CHEN YanLei SHENG YongWei GAO XiaoHong ZHU WeiHong WANG WenQing WANG Hong WENG YongLing ZHUANG DaFang LIU JiYuan LUO ZhiCai CHENG Xiao GUO ZiQi GONG Peng | 2012 | Chinese Science Bulletin2012，57，22： | 51 |
| 7 | Effects of AT1 receptor antagonist,Iosartan,on rat hepatic fibrosis induced by CCl_4显示文摘AIM To investigate effect of losartan,an AT1receptor antagonist,on hepatic fibrosis induced byCCl;and to determine whether or not AT1receptors are expressed on hepatic stellate cells,METHODS AND RESULTS Fifty male Sprague-Dawley rats,weighing(180±20)g,wererandomized into five groups(control group,modelgroup,and three losartan treated groups),inwhich all rats were given the subcutaneousinjection of 40% CCl4(every 3 days for 6 weeks)except for rats of control group.Rats of losartan-treated groups were treated with losartan(20 mg/kg,10 mg/kg,5 mg/kg,daily gavage),After 6weeks liver tissue and serum samples of all ratswere examined.Serum hyaluronic acid(HA),procollagen typeⅢ(PCⅢ)were detected byradioimmunoassays,van Giesion collagen stainingwas used to evaluate the extracellular matrix of ratswith liver fibrosis.The expression of AT1receptors,transforming growth factor-beta(TGF-β),and alpha-smooth muscle actin(a-SMA)inliver tissue were determined byimmunohistochemical techniques.Compared withmodel group,serum ALT and AST of losartan-treated groups were significantly reduced(t=4.20,P<0.01 and t=4.57,P<0.01).Serum HAand PCⅢalso had significant differences(t=3.53,P<0.01 and t=2.20,P<0.05).Thedegree of fibrosis was improved by losartan and correlated with the expressions of AT1 receptors,TGF-β,and α-SMA in liver tissue.CONCLUSION AT1 receptor antagonist,losartan,could limit the progression of the hepatic fibrosisinduced by CCl4.The mechanism may be related tothe decrease in the expression of AT1 receptorsand TGF-β,ameliorating the injury of hepatocytes;activation of local renin-angiotensin system mightrelate to hepatic fibrosis;and during progressionof fibrosis,activated hepatic stellate cells mightexpress AT1 receptors. | Hong Shan Wei Ding Guo Li Han Ming Lu Yu Tao Zhan Zhi Rong Wang Xin Huang Jing Zhang Ji Lin Cheng Qin Fang Xu Department of Gastroenterology,Xinhua Hospital,Shanghai Second Medical University,Shanghai 200092,China | 2000 | World Journal of Gastroenterology2000，6，4： | 42 |
| 8 | Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice显示文摘最近的研究开始在心脏的肥大和机能障碍的致病揭示了 microRNAs (miRNAs ) 的关键角色。在这研究,我们测试了是否转变生长 factor-β(TGF-β) 调整 miRNA 在心脏的肥大和心失败(HF ) 的发展起了一个枢轴的作用。我们观察到 miR-27b 是在 cardiomyocyte 特定的 Smad4 猛烈老鼠的心的 upregulated,它开发了心脏的肥大。在 vitro,实验证明 miR-27b 表示能被 TGF-β 禁止; 1 并且它的 overexpression 支持了 hypertrophic 房间生长,当 miR-27b 抑制导致了 hypertrophic 房间的抑制时,生长由 phenylephrine (PE ) 引起了处理。而且,有 miR-27b 的 cardiomyocyte 特定的 overexpression 的转基因的老鼠的分析表明 miR-27b overexpression 是足够的导致心脏的肥大和机能障碍。我们验证了 peroxisome 激活 proliferator 的 receptor-γ(PPAR-γ) 作为在 cardiomyocyte 的 miR-27b 的一个直接目标。一致地, miR-27b 转基因的老鼠显著地显示了 PPAR-γ 的底层;比控制鼠标。而且,在用在一只 pressure-overload-induced 老鼠的特定的 antagomir 的 miR-27b 的 vivo silencing, HF 的模型增加了心脏的 PPAR-γ表示,稀释心脏的肥大和机能障碍。我们的学习的结果表明那 TGF-β 1-regulated miR-27b 涉及心脏的肥大的规定,并且为心脏病作为一个有效治疗学的目标验证 miR-27b。 | Jian Wang Yao Song Yan Zhang Han Xiao Qiang Sun Ning Hou Shuilong Guo Youliang Wang Kaiji Fan Dawei Zhan Lagabaiyila Zha Yang Cao Zhenhua Li Xuan Cheng Youyi Zhang Xiao Yang | 2012 | Cell Research2012，22，3： | 36 |
| 9 | Deep structure beneath the southwestern section of the Longmenshan fault zone and seimogenetic context of the 4.20 Lushan M_S7.0 earthquake显示文摘Magnetotelluric measurements were carried out along two profiles across the middle and southwestern sections of the Longmenshan fault zone(LMSf)from 2009 to 2011,after the 2008 Wenchuan MW7.9 earthquake.The former profile crosses the Wenchuan event epicenter and the latter one crosses 2013 Lushan MS7.0 event epicenter.The data were analyzed using advanced processing techniques,including phase tensor and two-dimensional inversion methods,in order to obtain reliable 2-D profiles of the electrical structure in the vicinity of the two earthquakes.A comparison of the two profiles indicates both similarities and differences in the deep crustal structure of the LMSf.West of the southwestern section,a crustal high conductivity layer(HCL)is present at about 10 km depth below the Songpan-Garzêblock;this is about 10 km shallower than that under the middle section of the LMSf.A high resistivity body(HRB)is observed beneath the southwestern section,extending from the near surface to the top of upper mantle.It has a smaller size than the HRB observed below the middle section.In the middle section,there is a local area of decreased resistivity within the HRB but there is absence of this area.The 2013 Lushan earthquake occurred close to the eastern boundary of HRB and the Shuangshi-Dachuan fault,of which the seismogenic context has both common and different features in comparison with the 2008 Wenchuan event.On a large scale,the 2013 Lushan earthquake is associated with the HCL and deformation in the crust including HCL of the eastern Tibetan Plateau.In order to assess seismic risk,it is important to consider both the stress state and the detailed crustal structure in different parts of the LMSf. | ZHAN Yan ZHAO GuoZe UNSWORTH Martyn WANG LiFeng CHEN XiaoBin LI Tao XIAO QiBin WANG JiJun TANG Ji CAI JunTao WANG YanZhao | 2013 | Chinese Science Bulletin2013，58，28： | 39 |
| 10 | (-)-Epigallocatechin-3-gallate inhibits growth of gastric cancer by reducing VEGF production and angiogenesis显示文摘AIM: To investigate the effect of (-)-epigallocatechin- 3-gallate (EGCG) on growth of gastric cancer and its possible mechanism. METHODS: Heterotopic tumors were induced by subcutaneously injection of SGC-7901 cells in nude mice. Tumor growth was measured by calipers in two dimensions. Tumor angiogenesis was determined with tumor microvessel density (MVD) by immunohistology. Vascular endothelial growth factor (VEGF) protein level and activation of signal transducer and activator of transcription 3 (Stat3) were examined by Western blotting. VEGF mRNA expression was determined by RT-PCR and VEGF release in tumor culture medium by ELISA. VEGF-induced cell proliferation was studied by MTT assay, cell migration by gelatin modified Boyden chamber (Transwell) and in vitro angiogenesis by endothelial tube formation in Matrigel. RESULTS: Intraperitoneal injection of EGCG inhibited the growth of gastric cancer by 60.4%. MVD in tumor tissues treated with EGCG was markedly reduced. EGCG treatment reduced VEGF protein level in vitro and in vivo. Secretion and mRNA expression of VEGF in tumor cells were also suppressed by EGCG in a dose-dependent manner. This inhibitory effect was associated with reduced activation of Stat3, but EGCG treatment did not change the total Stat3 expression. EGCG also inhibited VEGF-induced endothelial cell proliferation, migration and tube formation. CONCLUSION: EGCG inhibits the growth of gastriccancer by reducing VEGF production and angiogenesis, and is a promising candidate for anti-angiogenic treatment of gastric cancer. | Bao-He Zhu, Wen-Hua Zhan, Zheng-Rong Li, Zhao Wang, Yu-Long He, Jun-Sheng Peng, Shi-Rong Cai, Jin-Ping Ma, Chang-Hua Zhang, Department of Gastrointestinal & Pancreatic Surgery, First Affiliated Hospital, Sun Yat-Sen University Gastric Center of Sun Yat-Sen University, Guangzhou 510080, Guangdong Province, China | 2007 | World Journal of Gastroenterology2007，13，8： | 30 |
| 11 | The regulatory role of AT 1 receptor on activated HSCs in hepat,c fibrogenesis,effects of RAS inhibitors on hepatic fibrosis induced by CCl_4显示文摘AIM To assess the effect of ACE inhibitor andAng Ⅱ type Ⅰ(AT1)receptor antagonist inpreventing hepatic fibrosis caused by CCl4administration in rats;to investigate whether ornot there are expression of AT 1 receptors onhepatic stellate cells;and to observe the effectof Ang Ⅱ on proliferation and ECM synthesis ofcultured HSCs.METHODS Studies were conducted in maleSprague-Dawley rats.Except for thehepatofibrotic model group and the controlgroup,in three treated groups,either enalapril(5 mg/kg),or Iosartan(10 mg/kg),or enalapril+Iosartan were given to the fibrotic rats bydaily gavage,and saline vehicle was given tomodel and normal control rats.After 6 weeks,liver fibrosis was assessed directly by hepaticmorphometric analysis,which has beenconsidered the gold standard for thequantification of fibrosis.The expressions of AT1 receptors and(α-mooth muscle actin,α-SMA)in liver tissue or isolated hepatic stellate cells(HSCs)were detected by immunohistochemicaltechniques.The effect of Ang Ⅱ on HSCproliferation was determined by MTT method.Effect of Ang Ⅱ on collagen synthesis of HSCswas determined by 3H-proline incorporation.RESULTS Contrasted to the fibrosis in rats ofthe model group,groups of rats treated with either enalapril or Iosartan,or a combination oftwo drugs showed a limited expansion of theinterstitium(4.23±3.70 vs 11.22±4.79,P<0.05),but no difference was observedamong three treated groups(5.38±3.43,4.96±2.96,4.23±2.70,P>0.05).Expression of AT 1receptors was found in fibrotic interstitium offibrotic rats,whereas in normal control rats theywere limited to vasculature only to a very slightdegree.AT 1 receptors were also expressed onactivated HSCs in the culture.At concentrationsfrom 10-9to 10-5mol/L,Ang Ⅱ stimulated HSCproliferation in culture in a dose-dependentmanner.Increasing Ang Ⅱ concentrationsproduced corresponding increases in 3H-prolineincorporation.Differences among groups were significant.CONCLUSION Angiotensin-converting enzyme inhibitors and AT I blocker may slow the progression of hepatic fibrosis; activated HSCs express AT 1 receptors, and Ang Ⅱ can stimulate the proliferation and collagen synthesis of HSCs in a dose-dependent manner; and activation of RAS may be related to hepatic fibrogenesis induced by CCI4. | Hong Shan Wei Han Ming Lu Ding Guo Li Yu Tao Zhan Zhi Rong Wang Xin Huang Ji Lin Cheng Qin Fang Xu Department of Gastroenterology,Xinhua Hospital,Shanghai Second Medical University,Shanghai 200092,China | 2000 | World Journal of Gastroenterology2000，6，6： | 27 |
| 12 | The prognostic value of preoperative serum levels of CEA,CA19-9 and CA72-4 in patients with colorectal cancer显示文摘INTRODUCTIONCarcinoembryonic antigen ( CEA) , originally described by Gold and Freedman [1] in 1965, is now an acknowledged member of immunoglobulin superfamily[2],with a role as an intracellular adhesion molecule[3].Carbohydrate antigen 19-9(CA19-9), obtained with a monoclonal antibody produced by immunizing a monoclonal antibody produced by immunizing a mouse with a colonic cancer cell line in 1979[4],is a ligand for E-selectin that plays an important role in the addhesion of cancer cells to endothelial cells [5,6]. | Chao Xu Zheng~1 Wen Hua Zhan~1 Ji Zong Zhao~2 Dong Zheng~3 Dong Ping Wang~1 Yu Long He~1 Zhang Qing Zheng~1 ~1Department of General Surgery,~2Laboratory of Surgery,~3Department of Medicine,First Affiliated Hospital,Sun Yat-Sen University of Medical Sciences,Guangzhou 510080,Guangdong Province,ChinaDr.Chao Xu Zheng now working as a surgeon and lecturer in the Department of General Surgery,First Affiliated Hospital,Sun Yat-Sen University of Medical Sciences,who is a Ph.D.student,having 7 papers published. | 2001 | World Journal of Gastroenterology2001，7，3： | 25 |
| 13 | Telomerase activity in gastric cancer and its clinical implications显示文摘INTRODUCTIONThedevelopmentofcarcinomaresultsfrommultipleindependentgeneticchangesthatactivateprotooncogenesorinactivatetheac... | ZHAN Wen Hua, MA Jin Ping, PENG Jun Sheng, GAO Jing Song, CAI Shi Rong, WANG Jian Ping, ZHENG Zhang Qing and WANG Lei | 1999 | World Journal of Gastroenterology1999，5，4： | 25 |
| 14 | Serum leptin and soluble leptin receptor in non-alcoholic fatty liver disease显示文摘AIM: To determine the role of leptin system in non-al- coholic fatty liver disease (NAFLD) development by deli- neating the changes in serum levels of leptin and soluble leptin receptor (sOB-R). METHODS: Blood samples were collected from 30 consecutive patients with liver-biopsy-proven NAFLD and 30 patients with cholecystolithiasis (stationary phase) as controls. Serum leptin levels were determined by radio- immunoassay and concentration of sOB-R was measured by ELISA. Body mass index (BMI) was calculated for all subjects, and serum insulin, C-peptide, and lipoprotein levels were also detected. RESULTS: Mean serum leptin level and BMI in the NAFLD group were significantly higher than in the con- trols (both P < 0.001), but mean sOB-R level was lower in the NAFLD group when compared to the controls. Both men and women in the NAFLD group had higher mean serum leptin levels and lower sOB-R levels than did the men and women in the control group (all P < 0.001). The- re was a significant negative correlation between serum leptin and sOB-R levels (r = -0.725, P < 0.001). Multiva- riate analysis showed that the percentage of hepatocyte steatosis, sex, BMI, and homeostasis model assessment of insulin resistance (HOMA IR) were independently rela- ted to serum leptin levels. CONCLUSION: Elevated serum leptin seems to be afeature of steatosis, and serum leptin seems to increase as hepatocyte steatosis develops. An enhanced release of leptin is accompanied by an decrease in sOB-R con- centration, which suggests higher resistance of periphe- ral tissues towards the action of leptin. | Xiao-Dong Huang Yan Fan Hen Zhang Ping Wang Jing Ping Yuan Ming-Jie Li Xi-Yan Zhan | 2008 | World Journal of Gastroenterology2008，14，18： | 26 |
| 15 | Magnetic resonance susceptibility weighted imaging in detecting intracranial calcification and hemorrhage显示文摘背景计算断层摄影术(CT ) 在检测 intracranial 石灰化比平淡的磁性的回声成像(MRI ) 好。试图估计在 intracranial 石灰化和 hemorrhage.Methods 的察觉和区别的加权的成像(SWI ) 在这研究注册了的先生危险性的价值的这研究是包括 CT 表明的石灰化的 13 个盒子和 intracerebral 出血的 22 个盒子的 35 个病人。在所有这些题目使用的先生序列包括了轴的 T1WI, T2WI 和 SWI。SWI 上的石灰化和出血的阶段移动(PS ) 被计算,他们的信号在改正的阶段图象上展示被比较。在检测 intracranial 石灰化和出血的 T1WI, T2WI 和 SWI 的敏感是为头部的石灰化的 SWI 的察觉率是的分析 statistically.Results 98.2% ,比 T1 Wl 和 T2WI 的显著地高。它不与 CT 的显著地不同(P > 0.05 ) 。在不同阶段有 49 出血性的损害检测 n SWI, 30 在 T2WI 上并且 18 在 T1WI 上。石灰化和出血的平均 PS 是在检测的 +0.734han 常规 MRI 微出血, SWI 可以在区分与石灰化或出血联系的服的疾病起一个重要作用。 | ZHU Wen-zhen QI Jian-pin ZHAN Chuan-jia SHU Hong-ge ZHANG Lin WANG Cheng-yuan XIA Li-ming HU Jun-wu FENG Ding-yi | 2008 | Chinese Medical Journal2008，，20： | 26 |
| 16 | Two mechanical methods for thromboembolism prophylaxis after gynaecological pelvic surgery: a prospective, randomised study显示文摘 | GAO Jie ZHANG Zhen-yu LI Zhan LIU Chong-dong ZHAN Yu-xin QIAO Bao-li SANG Cui-qin GUO Shu-li WANG Shu-zhen JIANG Ying ZHAO Na | 2012 | Chinese Medical Journal2012，，23： | 25 |
| 17 | Management Recommendations on Sleep Disturbance o Patients with Parkinson's Disease显示文摘INTRODUCTION Sleep disturbance is one of the most common nonmotor symptoms in Parkinson's disease (PD).Sleep disturbance affects 40-98% of PD patients in the world. In China, the prevalence of PD patients with sleep disturbance ranges from 47.66% to 89.10%. Sleep disturbance usually has adverse impact on the quality of life of PD patients. Apossible pathogenesis of PD with sleep disturbance include thalamocortical pathway degeneration and changes of neurotransmitter systems. The etiology of sleep disturbance is multifactorial,involving degeneration of areas regulating sleep,sleep structure affected by drugs,sleep disturbance induced by drug,and sleep fragmentation by multiple factors. | Chun-Feng Liu Tao Wang Shu-Qin Zhan De-Qin Geng Jian Wang Jun Liu Hui-Fang Shang Li-Juan Wang Piu Chan Hai-Bo Chen Sheng-Di Chen Yu-Ping Wang Zhong-Xin Zhao K Ray Chaudhuri | 2018 | Chinese Medical Journal2018，，24： | 26 |
| 18 | Overexpression of Aurora-A kinase promotes tumor cell proliferation and inhibits apoptosis in esophageal squamous cell carcinoma cell line显示文摘曙光 A kinase, serine/threonine 蛋白质 kinase,是潜在的 oncogene。扩大并且在人的肿瘤的几种类型在曙光 A 的表示上被发现了,包括的食道的有鳞的房间癌(ESCC ) 。在表示曙光 A 上的房间对导致 cisplatin 的 apoptosis 更抵抗,这被表明了。然而,调停的分子的机制这些效果仍然保持大部分未知。在这份报告,我们证明在通过在人的 ESCC KYSE150 的 pEGFP-Aurora-A 的稳定的 transfection 的曙光 A 的表示上,房间显著地支持了房间增长并且禁止了 cisplatin- 或紫外导致照耀的 apoptosis。caspase-3 并且 poly 的劈开(自动数据处理核糖) 在在表示房间上的曙光 A 的聚合酶(PARP ) 实质地在 cisplatin 或紫外处理以后被减少。而且,我们发现有 siRNA 的内长的曙光 A kinase 的那 silencing 实质地提高了敏感到导致 cisplatin 或在人的 ESCC EC9706 房间的紫外导致 apoptosis。在平行,在曙光 A 的表示上 potently 起来调整了 Bcl-2 的表示。而且,由废除的 siRNA 的 Bcl-2 击倒 Aurora-A 禁止 apoptosis 上的效果。总起来说,这些数据提供证据在支持房间增长并且禁止 apoptosis 的表示上的那曙光 A,建议是的新奇机制仔细与恶意的显型和 ESCC 房间的反癌症药抵抗有关。 | Xiao Xia Wang Rong Liu Shun Qian Jin Fei Yue Fan Qi Min Zhan | 2006 | Cell Research2006，16，4： | 24 |
| 19 | Laparoscopic splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension显示文摘Since the first laparoscopic splenectomy(LS)was reported in 1991,LS has become the gold standard for the removal of normal to moderately enlarged spleens in benign conditions.Compared with open splenectomy,fewer postsurgical complications and better postoperative recovery have been observed,but LS is contraindicated for hypersplenism secondary to liver cirrhosis in many institutions owing to technical difficulties associated with splenomegaly,well-developed collateral circulation,and increased risk of bleeding.With the improvements of laparoscopic technique,the concept is changing.This article aims to give an overview of the latest development in laparoscopic splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension.Despite a lack of randomized controlled trial,the publications obtained have shown that with meticulous surgical techniques and advanced instruments,LS is a technically feasible,safe,and effective procedure for hypersplenism secondary to cirrhosis and portal hypertension and contributes to decreased blood loss,shorter hospital stay,and less impairment of liver function.It is recommended that the dilated short gastric vessels and other enlarged collateral circulation surrounding the spleen be divided with the LigaSure vessel sealing equipment,and the splenic artery and vein be transected en bloc with the application of the endovascular stapler.To support the clinical evidence,further randomized controlled trials about this topic are necessary. | Xiao-Li Zhan Yun Ji Yue-Dong Wang | 2014 | World Journal of Gastroenterology2014，20，19： | 24 |
| 20 | Impaired PI3K/Akt signal pathway and hepatocellular injury in high-fat fed rats显示文摘AIM:To determine whether mitochondrial dysfunction resulting from high-fat diet is related to impairment of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt,also known as PKB) pathway. METHODS:Rat models of nonalcoholic fatty liver were established by high-fat diet feeding. The expression of total and phosphorylated P13K and Akt proteins in hepatocytes was determined by Western blotting. Degree of fat accumulation in liver was measured by hepatic triglyceride. Mitochondrial number and size were determined using quantitative morphometric analysis under transmission electron microscope. The permeability of the outer mitochondrial membrane was assessed by determining the potential gradient across this membrane.RESULTS:After Wistar rats were fed with high-fat diet for 16 wk,their hepatocytes displayed an accumulation of fat (103.1 ± 12.6 vs 421.5 ± 19.7,P < 0.01),deformed mitochondria (9.0% ± 4.3% vs 83.0% ± 10.9%,P < 0.05),and a reduction in the mitochondrial membrane potential (389.385% ± 18.612% vs 249.121% ± 13.526%,P < 0.05). In addition,the expression of the phosphorylated P13K and Akt proteins in hepatocytes was reduced,as was the expression of the anti-apoptotic protein Bcl-2,while expression of the pro-apoptotic protein caspase-3 was increased. When animals were treated with pharmacological inhibitors of P13K or Akt,instead of high-fat diet,a similar pattern of hepatocellular fat accumulation,mitochondrial impairment,and change in the levels of PI3K,Akt,Bcl-2 was observed. CONCLUSION:High-fat diet appears to inhibit the PI3K/Akt signaling pathway,which may lead to hepa-tocellular injury through activation of the mitochondrial membrane pathway of apoptosis. | Ji-Wu Han,Department of Gastroenterology,The 4th Hospital of Harbin Medical University,Harbin 150001,Heilongjiang Province,China Xiao-Rong Zhan,Xin-Yu Li,Bing Xia,Yue-Ying Wang,Jing Zhang,Department of Endocrinology,First Hospital of Harbin Medical University,Harbin 150001,Heilongjiang Province,China Bao-Xin Li,Department of Pharmacology,State Key Laboratory of Biomedicine and Pharmacology,Harbin Medical University,Harbin 150001,Heilongjiang Province,China | 2010 | World Journal of Gastroenterology2010，16，48： | 22 |
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