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| 1 | Mettl3-/Mettl14-mediated mRNA N6-methyladenosine modulates murine spermatogenesis显示文摘精子发生在双 spermatogonial 干细胞(SSC ) 哪个生产 haploid 精子期间是一个区别过程。这个高度专业化的过程精确在 transcriptional, posttranscriptional,和翻译层次被控制。这里,我们报导那 N 6-methyladenosine (m 6 一) ,调整基因表示的一个 epitranscriptomic 标记,在精子发生期间起必要作用。我们现在的全面 m 6 从五个发展阶段的老鼠 spermatogenic 房间的 mRNA methylomes:无差别的 spermatogonia,类型 A 1 spermatogonia, preleptotene spermatocytes, pachytene/diplotene spermatocytes,和圆 spermatids。m 6 有 Vasa-Cre 的 RNA methyltransferase Mettl3 或 Mettl14 引起 m 6 SSC 的 A 和弄空。m 6 为 SSC 增长 / 区别被要求的抄本的一个弄空 dysregulates 翻译。在有 Stra8-GFPCre 的先进细菌房间的 Mettl3 和 Mettl14 的联合删除破坏精子形式,而有在先进细菌房间的 Mettl3 或 Mettl14 的单个删除的老鼠显示出正常精子发生。从双异种老鼠展览的 spermatids 损害了为精子形式是必要的 haploid 特定的基因的翻译。这研究加亮 mRNA m 6 在 germline 开发的修正,潜在地保证在精子发生的不同阶段协调了翻译。 | Zhen Lin Phillip J Hsu Xudong Xing Jianhuo Fang Zhike Lu Qin Zou Ke-Jia Zhang Xiao Zhang Yuchuan Zhou Teng Zhang Youcheng Zhang Wanlu Song Guifang Jia Xuerui Yang Chuan He Ming-Han Tong | 2017 | Cell Research2017，27，10： | 61 |
| 2 | Inhibitory effect of IGF-Ⅱ antisense RNA on malignant phenotype of hepatocellular carcinoma显示文摘INIRODUCTIONAccording to the therapeutic effect and strategy ofantisense RNA for hepatoccllular carcinoma(HCC),we have specifically synthesized partialcDNA of human insulin-like growth factor Ⅱ(IGF-Ⅱ)and constructed IGF-Ⅱ cDNA antisenseeukaryotic expression vector.The constructedvector was introduced into hepatoma cell lineSMMC-7721 to block the intrinsic IGF-Ⅱexpression.The biological behavior changes ofhepatoma cells were observed.All these | Dong Hua Yang Ming Qing Zhang Jiang Du Chong Xu Oiao Ming Liang Ji Fang Mao Han Rong Qin Zi Rong Fan Department of Gastroenterology,Zhujiang Hospital,the First Military Medical University,Guangzhou 510282,China Laboratory of Molecular Biology,Zhujiang Hospital,the First Military Medical University,Guangzhou,China Departrnent of Biochemistry,the Second Military Medical University,Shanghai,China | 2000 | World Journal of Gastroenterology2000，6，2： | 54 |
| 3 | PI3K/Akt signaling transduction pathway is involved in rat vascular smooth muscle cell proliferation induced by apelin-13显示文摘脉管的光滑的肌肉房间(VSMC ) 被将生物的活组织移植于培养基中培养方法从男 SpragueDawley 老鼠的胸的主动脉准备经由 3 kinase (PI3K )/Akt 发信号 transduction 小径由 apelin-13 导致了的 phosphoinositide 观察 VSMC 增长。PI3K, phospho-PI3K, phospho-Akt, ERK1/2, phospho-ERK1/2 和 cyclin D1 的表示被西方的污点分析检测。结果证明 apelin-13 在剂量依赖者和时间依赖者举止支持了 phospho-PI3K 和 phospho-Akt 的表示。PI3K 禁止者 LY294002 显著地减少了 phospho-PI3K, phospho-Akt, phospho-ERK1/2,和 cyclin D1 的表示由 apelin-13 导致了。Akt 禁止者 1701-1 显著地减少了 phospho-Akt, phospho-ERK1/2,和 cyclin D1 的表示由 apelin-13 刺激了。MTT 试金结果证明 PI3K 禁止者 LY294002 和 Akt 禁止者 1701-1 显著地禁止了 apelin-13 导致的 VSMC 增长。Apelin-13 通过表明 transduction 小径的 PI3K/Akt 支持了 VSMC 增长。 | Changhui Liu Tao Su Fang Li Lanfang Li Xuping Qin Weinan Pan Fen Feng Feng Chen Duanfang Liao Linxi Chen | 2010 | Acta Biochimica et Biophysica Sinica2010，42，6： | 41 |
| 4 | 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 |
| 5 | Anti-tumor activities of active ingredients in Compound Kushen Injection显示文摘Kushen (根值 Sophorae Flavescentis ) 在繁体中文药为肿瘤,发炎和另外的疾病的治疗有使用的长历史。复合 Kushen 注射(CKI ) 是从 Kushen 和 Baituling (根茎 Smilacis Glabrae ) 提取的自然混合物的混合物。CKI 的主要原则是 matrine (MT ) 和展出许多药理学活动的 oxymatrine (OMT ) ,包括反煽动性,反过敏,抗病毒, anti-fibrotic 和心血管的保护的效果。最近的证据证明这些混合物也产生反癌症行动,例如禁止癌症房间增长,导致房间周期拘捕,加速 apoptosis ,制止 angiogenesis ,导致房间区别,禁止癌症转移和侵略,逆行的 multidrug 抵抗,并且阻止或减少化疗--或导致放射疗法的毒性当与化学疗法的药结合了时。在这评论,我们在学习 MT, OMT 和 CKI 和他们的潜在的分子的目标的反癌症活动总结最近的进步,它为进一步的学习提供线索和参考书。 | Wei WANG Rong-li YOU Wen-jie QIN Li-na HAI Ming-jing FANG Guo-hua HUANG Rui-xia KANG Ming-hua LI Yu-feng QIAO Jian-wei LI An-ping LI | 2015 | Acta Pharmacologica Sinica2015，36，6： | 41 |
| 6 | Spatial differences and multi-mechanism of carbon footprint based on GWR model in provincial China显示文摘全球温暖是在世界后面的主要担心之一高速度的经济生长。怎么实现碳脚印和经济的协调发展将是世界的核心问题经济、社会的开发,以及在最近的年里的家和国外的研究的激烈的争论。基于精力消费,与自顶向下的生命周期途径和地理上加权的回归(GWR ) 综合模型,这篇论文在 2010 在省的中国分析了碳脚印的空间差别和多机制。第一,这研究用自顶向下的生命周期途径计算了每个省的碳脚印的数量并且发现在省的中国有碳脚印和人均的碳脚印的重要差别。有更高的碳脚印的省,主要在北中国定位了,有大经济规模;有更高人均的碳脚印的省主要在象北京,上海和充满精力的区域和重化学的底那样的中央城市里被散布。在 GIS 和空间分析模型(GWR 模型) 的帮助下,第二,这篇论文展开了经济规模的扩大是碳脚印的快速的生长的主要司机。人口和都市化的生长也充当了为碳脚印的增加支持因素。精力结构没为碳脚印的增加有可观的支持效果。改进精力效率是最重要的因素禁止成长的碳脚印。第三,开发低碳的经济和低碳的工业,以及倡导低碳的城市建设和改善的碳效率将是主要途径禁止碳脚印的快速的生长。中等控制经济规模和人口尺寸将也被要求减轻碳脚印。同时,低碳的城市的环境保护和建设将在都市化的过程唤起广泛的注意。 | WANG Shaojian FANG Chuanglin MA Haitao WANG Yang QIN Jing | 2014 | Journal of Geographical Sciences2014，24，4： | 40 |
| 7 | Polymorphism of p16INK4a gene and rare mutation of p15INK4b gene exon2 in primary hepatocarcinoma显示文摘INTRODUCTION Hepatocellular carcinoma(HCC)is the mostcommon cause of death from cancer in China.Themechanisms of hepatocarcinogenesis are not yetknown clearly,p16INK4a gene,the multiple tumorsuppressor gene 1(MTS1),encodes P16 protein,which acts as an inhibitor by binding directly toCDK4 and CDK6 and preventing its association | Yang Qin Bo Li Yong Shu Tan Zhi Lin Sun Feng Qiong Zuo Ze Fang Sun Institute of Biochemistry and Molecular Biology,West China University of Medical Sciences,Chengdu 610041,Sichuan Province,China Department of General Surgery,The First Affiliated Hospital,West China University of Medical Sciences,Chengdu 610041,Sichuan Province,China Department of Pathology,The First Affiliated Hospital,West China University of Medical Sciences,Chengdu 610041,Sichuan Province,China | 2000 | World Journal of Gastroenterology2000，6，3： | 30 |
| 8 | 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 |
| 9 | Multicenter case-control study of the risk factors for ulcerative colitis in China显示文摘AIM:To evaluate potential risk factors in the development of ulcerative colitis(UC) in China.METHODS:A total of 1308 patients with UC and 1308 age-matched and sex-matched controls were prospectively studied in China.The UC cases were collected from 17 hospitals in China from April 2007 to April 2010.Uniform questionnaires were designed to investigate risk factors including smoking,appendectomy,stress,socio-economic conditions,nonsteroidal antiinflammatory drugs(NSAIDs),oral contraceptives,diet,breastfeeding,infections and family sanitary conditions.Group comparisons by each factor were done using simple logistic regression analysis.Conditional logistic regression was used for multivariate analysis.RESULTS:By univariate analysis,the variables predictive of UC included feeling stress,light and heavy alcoholic drinking,spicy food,sugar consumption and infectious diarrhea,while heavy tea intake and tap water consumption were protective against UC.On multivariate analysis,the protective factor for UC was tap water consumption [odds ratios(OR) = 0.424,95%CI:0.302-0.594,P < 0.001];while the potential risk factors for UC were heavy sugar consumption(OR = 1.632,95%CI:1.156-2.305,P < 0.001),spicy food(light intake:OR = 3.329,95%CI:2.282-4.857,P < 0.001;heavy intake:OR = 3.979,95%CI:2.700-5.863,P < 0.001),and often feeling stress(OR = 1.981,95%CI:1.447-2.711,P < 0.001).Other factors,such as smoking habit,appendectomy,breastfeeding,a history of measles,rural or urban residence,education,oral contraceptives,and NSAID use have not been found to have a significant association with the development of UC in the present study.CONCLUSION:Our study showed tap water consumption was a protective factor for UC,while spicy food,heavy sugar consumption and often feeling stress were risk factors for UC in this Chinese population. | Yu-Fang Wang Qin Ou-yang Bing Xia Li-Na Liu Fang Gu Kai-Fang Zhou Qiao Mei Rui-Hua Shi Zhi-Hua Ran Xiao-Di Wang Pin-Jin Hu Kai-Chun Wu Xin-Guang Liu Ying-Lei Miao Ying Han Xiao-Ping Wu Guo-Bing He Jie Zhong Guan-Jian Liu | 2013 | World Journal of Gastroenterology2013，19，11： | 24 |
| 10 | Blocking NF-kB nuclear translocation leads to p53-related autophagy activation and cell apoptosis显示文摘AIM: To investigate the anti-tumor effects of nuclear factor-κB (NF-κB) inhibitor SN50 and related mechanisms of SGC7901 human gastric carcinoma cells. METHODS: MTT assay was used to determine the cytotoxic effects of SN50 in gastric cancer cell line SGC7901. Hoechst 33258 staining was used to detect apoptosis morphological changes after SN50 treatment. Activation of autophagy was monitored with monodansylcadaverine (MDC) staining after SN50 treatment.Immunofluorescence staining was used to detect the expression of light chain 3 (LC3). Mitochondrial membrane potential was measured using the fluorescent probe JC-1. Western blotting analysis were used to determine the expression of proteins involved in apoptosis and autophagy including p53, p53 upregulated modulator of apoptosis (PUMA), damage-regulated autophagy modulator (DRAM), LC3 and Beclin 1. We detected the effects of p53-mediated autophagy activation on the apoptosis of SGC7901 cells with the p53 inhibitor pifithrin-α. RESULTS: The viability of SGC7901 cells was inhibited after SN50 treatment. Inductions in the expression of apoptotic protein p53 and PUMA as well as autophagic protein DRAM, LC3 and Beclin 1 were detected with Western blotting analysis. SN50-treated cells exhibited punctuate microtubule-associated protein 1 LC3 in immunoreactivity and MDC-labeled vesicles increased after treatment of SN50 by MDC staining. Collapse of mitochondrial membrane potential Δψ were detected for 6 to 24 h after SN50 treatment. SN50-induced increases in PUMA, DRAM, LC3 and Beclin 1 and cell death were blocked by the p53 specific inhibitor pifithrin-α. CONCLUSION: The anti-tumor activity of NF-κB inhibitors is associated with p53-mediated activation of autophagy. | Bao-Song Zhu Chun-Gen Xing Fang Lin xiao-Qing Fan Kui Zhao Zheng-Hong Qin | 2011 | World Journal of Gastroenterology2011，17，4： | 24 |
| 11 | Ten cities cross-sectional questionnaire survey of children asthma and other allergies in China显示文摘Asthma,rhinitis and eczema(allergic or non-allergic)have increased throughout the world during the last decades,especially among children.Changes in the indoor environment are suspected to be important causes.China has experienced a dramatic change in indoor environmental exposures during the past two decades.However,such changes and their associations with children’s asthma and other health aspects have not been thoroughly studied.China,Children,Homes,Health(CCHH),Phase I,was a cross-sectional questionnaire survey of 48219 children 1–8 years old in 10 Chinese cities during 2010–2012.The questionnaire includes the International Study of Asthma and Allergies in Childhood(ISAAC)core health questions and additional questions regarding housing,life habits and outdoor environment.In health analyses,children aged 3–6 years old were included.The prevalences of doctor diagnosed asthma varied from 1.7%to 9.8%(mean 6.8%),a large increase from 0.91%in 1999 and 1.50%in2000.The prevalence of wheeze,rhinitis and atopic eczema(last 12 months)varied from 13.9%to 23.7%,24.0%to 50.8%and4.8%to 15.8%,respectively.Taiyuan had the lowest prevalences of all illnesses and Shanghai the highest,except for wheezewhere the highest value was for Urumqi.We found(1)no obvious association between disease prevalences and ambient PM10concentrations and(2)higher prevalences of disease in humid climates with hot summers and cold winters,but with no centrally heated buildings.Associations between the diseases and economic status as indexed by Gross Domestic Product(GDP)requires further study. | ZHANG YinPing LI BaiZhan HUANG Chen YANG Xu QIAN Hua DENG QiHong ZHAO ZhuoHui LI AnGui ZHAO JiaNing ZHANG Xin QU Fang HU Yu YANG Qin WANG Juan ZHANG Ming WANG Fang ZHENG XiaoHong LU Chan LIU ZhiJian SUN YueXia MO JinHan ZHAO YiLi LIU Wei WANG TingTing NORBCK Dan BORNEHAG Carl-Gustaf SUNDELL Jan | 2013 | Chinese Science Bulletin2013，58，34： | 22 |
| 12 | Collagen scaffolds modified with collagen-binding bFGF promotes the neural regeneration in a rat hemisected spinal cord injury model显示文摘Nerve conduit is one of strategies for spine cord injury(SCI)treatment.Recently,studies showed that biomaterials could guide the neurite growth and promote axon regeneration at the injury site.However,the scaffold by itself was difficult to meet the need of SCI functional recovery.The basic fibroblast growth factor(bFGF)administration significantly promotes functional recovery after organ injuries.Here,using a rat model of T9 hemisected SCI,we aimed at assessing the repair capacity of implantation of collagen scaffold(CS)modified by collagen binding bFGF(CBD-bFGF).The results showed that CS combined with CBD-bFGF treatment improved survival rates after the lateral hemisection SCI.The CS/CBD-bFGF group showed more significant improvements in motor than the simply CS-implanted and untreated control group,when evaluated by the 21-point Basso-Beattie-Bresnahan(BBB)score and footprint analysis.Both hematoxylin and eosin(H&E)and immunohistochemical staining of neurofilament(NF)and glial fibrillary acidic protein(GFAP)demonstrated that fibers were guided to grow through the implants.These findings indicated that administration of CS modified with CBD-bFGF could promote spinal cord regeneration and functional recovery. | SHI Qin GAO Wei HAN XingLong ZHU XueSong SUN Jie XIE Fang HOU XiangLin YANG HuiLin DAI JianWu CHEN Liang | 2014 | Science China(Life Sciences)2014，57，2： | 23 |
| 13 | The Chinese Society of Clinical Oncology(CSCO)clinical guidelines for the diagnosis and treatment of nasopharyngeal carcinoma显示文摘Nasopharyngeal carcinoma(NPC)is a malignant epithelial tumor originating in the nasopharynx and has a high incidence in Southeast Asia and North Africa.To develop these comprehensive guidelines for the diagnosis and management of NPC,the Chinese Society of Clinical Oncology(CSCO)arranged a multi-disciplinary team comprising of experts from all sub-specialties of NPC to write,discuss,and revise the guidelines.Based on the findings of evidencebased medicine in China and abroad,domestic experts have iteratively developed these guidelines to provide proper management of NPC.Overall,the guidelines describe the screening,clinical and pathological diagnosis,staging and risk assessment,therapies,and follow-up of NPC,which aim to improve the management of NPC. | Ling-Long Tang Yu-Pei Chen Chuan-Ben Chen Ming-Yuan Chen Nian-Yong Chen Xiao-Zhong Chen Xiao-Jing Du Wen-Feng Fang Mei Feng Jin Gao Fei Han Xia He Chao-Su Hu De-sheng Hu Guang-Yuan Hu Hao Jiang Wei Jiang Feng Jin Jin-Yi Lang Jin-Gao Li Shao-Jun Lin Xu Liu Qiu-Fang Liu Lin Ma Hai-Qiang Mai Ji-Yong Qin Liang-Fang Shen Ying Sun Pei-Guo Wang Ren-Sheng Wang Ruo-Zheng Wang Xiao-Shen Wang Ying Wang Hui Wu Yun-Fei Xia Shao-Wen Xiao Kun-Yu Yang Jun-Lin Yi Xiao-Dong Zhu Jun Ma | 2021 | Cancer Communications2021，41，11： | 22 |
| 14 | Mechanism of action of gypenosides on type 2 diabetes and non-alcoholic fatty liver disease in rats显示文摘AIM:To explore the mechanism of action of gypenosides(GPs)on type 2 diabetes mellitus and non-alcoholic fatty liver disease(T2DM-NAFLD)in rats.METHODS:Sixty rats were randomly divided into a healthy group,an untreated disease model group andGP-treatment groups.The study involved the evaluation of biochemical parameters,including serum aspartate transaminase(AST),alanine transferase(ALT),blood glucose(BG),triglycerides(TG)and total cholesterol(TC).Additionally,the protective effect of the treatments were confirmed histopathologically and the expression of TNF-αand NF-κB in the rat liver was analyzed using immunohistochemistry.The expression of proliferatoractivated receptor gamma(PPARγ)and cytochrome P450(CYP450)1A1 m RNA was determined by quantitative RTPCR.RESULTS:GP treatments at oral doses of 200,400,and800 mg/kg per day significantly decreased the levels of serum AST and ALT(P<0.05,P<0.01),especially at the dose of 800 mg/kg per day.To a similar extent,GP at800 mg/kg per day reduced the levels of BG(4.19±0.47,P<0.01),TG(80.08±10.05,P<0.01),TC(134.38±16.39,P<0.01)and serum insulin(42.01±5.04,P<0.01).The expression of TNF-αand NF-κB measured by immunohistochemistry was significantly reduced by GPs in a dose-dependent manner,and the expression of PPARγand CYP4501A1 m RNA,as measured using quantitative real-time PCR,were significantly down-regulated by GPs.Moreover,GPs decreased the infiltration of liver fats and reversed the histopathological changes in a dosedependent manner.CONCLUSION:This study suggests that GPs have a protective effect against T2DM-NAFLD by down-regulating the expression of TNF-αand NF-κB proteins,and PPARγand CYP4501A1 m RNAs. | Qin He Jin-Ke Li Fang Li Ru-Gui Li Guo-Qing Zhan Gang Li Wei-Xing Du Hua-Bing Tan | 2015 | World Journal of Gastroenterology2015，21，7： | 22 |
| 15 | circRNA_0046366 inhibits hepatocellular steatosis by normalization of PPAR signaling显示文摘AIM To investigate micro(mi)R-34 a-antagonizing circular(circ)RNA that underlies hepatocellular steatosis.METHODS The effect of circ RNA on mi R-34 a was recognized by the mi RNA response element(MRE), and validated by the dual-luciferase reporter assay. Its association with hepatocellular steatosis was investigated in Hep G2-based hepatocellular steatosis induced by free fatty acids(FFAs; 2:1 oleate:palmitate) stimulation. After normalization of the steatosis-related circRNA by expression vector, analysis of mi R-34 a activity,peroxisome proliferator-activated receptor(PPAR)α level, and expression of downstream genes were carried out so as to reveal its impact on the mi R-34 a/PPARα regulatory system. Both triglyceride(TG) assessment and cytopathological manifestations uncovered the role of circRNA in miR-34 a-dependent hepatosteatogenesis.RESULTS Bioinformatic and functional analysis verified circRNA_0046366 to antagonize the activity of mi R-34 a via MRE-based complementation. In contrast to its lowered level during FFA-induced hepatocellular steatosis, circ RNA_0046366 up-regulation abolished the mi R-34 a-dependent inhibition of PPARα that played a critical role in metabolic signaling pathways. PPARα restoration exerted transcriptional improvement to multiple genes responsible for lipid metabolism. TGspecific lipolytic genes [carnitine palmitoyltransferase 1 A(CPT1 A) and solute-carrier family 27 A(SLC27 A)] among these showed significant increase in their expression levels. The circ RNA_0046366-related rebalancing of lipid homeostasis led to dramatic reduction of TG content, and resulted in the ameliorated phenotype of hepatocellular steatosis.CONCLUSION Dysregulation of circ RNA_0046366/mi R-34 a/PPARα signaling may be a novel epigenetic mechanism underlying hepatocellular steatosis. circ RNA_0046366 serves as a potential target for the treatment of hepatic steatosis. | Xing-Ya Guo Fang Sun Jian-Neng Chen Yu-Qin Wang Qin Pan Jian-Gao Fan | 2018 | World Journal of Gastroenterology2018，24，3： | 21 |
| 16 | 14-3-3 mediates apeHn-13-induced enhancement of adhesion of monocytes to human umbilical vein endothelial cells显示文摘调查 apelin-13 是否导致了 THP-1 单核白血球(MC ) 对经由表明 transduction 小径和潜在的小说的 14-3-3 的 ECV304 人的脐的静脉 endothelial 房间(HUVEC ) 的粘附生理的功能和 apelin-APJ 的发信号的 transduction 小径, HUVEC ECV304 在 DMEM 和 MC THP-1 是有教养的在 RPMI 1640 是有教养的中等。单核白血球粘附和脉管的房间粘附 molecule-1 (VCAM-1 ) 和 14-3-3 的表示与单核白血球粘附试金和西方的污点分析被测量。数据证明 apelin-13 在一个集中依赖者和时间依赖者举止增加了 MC 的粘附到 HUVEC,它分别地在 1 M 和 12 h 到达了他们的山峰。同样, apelin-13 导致了 HUVEC 粘附分子的表示,在一个集中依赖者和时间依赖者举止, VCAM-1 分别地在 1 M 和 12 h 到达了他们的山峰。Apelin-13 在一个集中依赖者和时间依赖者举止导致了 14-3-3 的表示,它分别地在 1 M 和 5 min 到达了他们的山峰。而且,有势力 14-3-3 禁止者 difopein 显著地减少了 14-3-3 的表示,在 apelin-13 的 VCAM-1 刺激了 HUVEC,并且 difopein 显著地在对 HUVEC 的 MC 粘附的正式就职上禁止了 apelin-13 的效果。这些数据建议 14-3-3 调停了到由 Apelin-13 的 HUVEC 的 MC 的粘附的正式就职。 | Xin Li Xianhui Zhang Fang Li Linxi Chen Lanfang Li Xuping Qin Jing Gao Tao Su Yixin Zeng Duanfang Liao | 2010 | Acta Biochimica et Biophysica Sinica2010，42，6： | 21 |
| 17 | Fibrinogen-like protein 2/fibroleukin prothrombinase contributes to tumor hypercoagulability via IL-2 and IFN-γ显示文摘AIM: To examine the role of Fibrinogen-like protein 2 (fgl2)/fibroleukin in tumor development. Fgl2 has been reported to play a vital role in the pathogenesis in MHV-3 (mouse hepatitis virus) induced fulminant and severe hepatitis,spontaneous abortion,allo-and xeno-graft rejection by mediating 'immune coagulation'. METHODS: Tumor tissues from 133 patients with six types of distinct cancers and the animal tumor tissues from human hepatocellular carcinoma (HCC) model on nude mice (established from high metastasis HCC cell line MHCC97LM6) were obtained. RESULTS: Hfgl2 was detected in tumor tissues from 127 out of 133 patients as well as tumor tissues collected from human HCC nude mice. Hfgl2 was highly expressed both in cancer cells and interstitial inflammatory cells including macrophages,NK cells,and CD8+ T lymphocytes and vascular endothelial cells. Hfgl2 mRNA was localized in cells that expressed hfgl2 protein. Fibrin (nogen) co-localization with hfgl2 expression was determined by dual immunohistochemical staining. In vitro,IL-2 and IFN-γ increased hfgl2 mRNA by 10-100 folds and protein expression in both THP-1 and HUVEC cell lines. One-stage clotting assays demonstrated that THP-1 and HUVEC cells expressing hfgl2 had increased procoagulant activity following cytokines stimulation. CONCLUSION: The hfg12 contributes to the hypercoagulability in cancer and may induce tumor angiogenesis and metastasis via cytokine induction. | Kai Su Fang Chen Wei-Ming Yan Qi-Li Zeng Li Xu Dong Xi Bin Pi Xiao-Ping Luo Qin Ning | 2008 | World Journal of Gastroenterology2008，14，39： | 20 |
| 18 | TRANSFORMING GROWTH FACTOR-β1 AND SMAD4 SIGNALING PATHWAY DOWN-REGULATES RENAL EXTRACELLULAR MATRIX DEGRADATION IN DIABETIC RATS显示文摘Objective To investigate the role of transforming growth factor-β1(TGF-β1)/Smad4 pathway in development of renal fibrosis in streptozotocin(STZ)-induced diabetic nephropathy(DN) rats and explore its possible mechanism.Methods Male Wistar rats weighing 180-220 g were divided into 5 groups:group A(normal control),group B [diabetes mellitus(DM) 2 weeks],group C(DM 4 weeks),group D(DM 8 weeks),and group E(DM 16 weeks).Except for the normal control group,other groups were induced DM by single injection of STZ(55 mg/kg) respectively.Blood glucose level,serum creatinine,and 24-hour urine protein were examined.Expressions of TGF-β1 and Smad4 protein and mRNA in kidney were detected using immunohistochemical technique,Western blot,and real-time PCR.mRNA expressions of stromelysin-1(MMP-3),tissue inhibitor of metalloproteinase-1(TIMP-1),and collagen Ⅲ in kidney were also detected by real-time PCR..Results The levels of blood glucose,serum creatinine,and 24-hour urine protein in rats of group B,C,D,and E were higher than those of the control group.With the progression of renal fibrosis,the expressions of TGF-β1 and Smad4 protein and mRNA in kidney of diabetic rats elevated.In addition,the renal MMP-3 mRNA expression diminished in diabetic rats,while TIMP-1 and collagen Ⅲ mRNA increased.Conclusions In STZ-induced diabetic rats,the TGF-β1/Smad4 appears to play an important role in renal fibrosis of DN.The increased expression of TGF-β1 and Smad4 might result in the transcriptional regulation of downstream target genes of TGF-β1/Smad4 pathway,which contributes to the progression of renal fibrosis in diabetic rats. | Qin Yang Ru-jia Xie Ting Yang Li Fang Bing Han Guo-zhong Zhang Ming-liang Cheng | 2007 | Chinese Medical Sciences Journal2007，22，4： | 19 |
| 19 | Atomic spin gyroscope based on 129Xe-Cs comagnetometer显示文摘Atomic spin gyroscope (ASG) based on comagnetometer is a high sensitive and compact gyroscope for future inertial navigation applications. The start-up time was several hours of the demonstrated ASGs based on 3He-K or21 Ne-Rb-K comagnetometer, and only a few inertial navigation applications allow such a long time for preparation. We report the demonstration of an ASG based on 129Xe-Cs comagnetometer, which decreases the start-up time to 10 minutes and decreases the operation temperature by 40% as well. By operating this ASG in spin exchange relaxation free regime, a sensitivity of 7×10 -5 °/(s Hz1/2) was achieved. | FANG JianCheng QIN Jie WAN ShuangAi CHEN Yao LI RuJie | 2013 | Chinese Science Bulletin2013，58，13： | 19 |
| 20 | Clinical and laboratory survey of 65 Chinese patients with Leigh syndrome显示文摘Background Leigh syndrome is an inherited neurodegenerative disease that emerges in infancy and childhood and presents with a clinically heterogeneous variety of neuromuscular and non-neuromuscular disorders. It can result from the inheritance of mutations in either nuclear or mitochondrial DNA. In the current study, we performed a retrospective study in 65 patients in order to investigate the clinical and genetic characteristics of Leigh syndrome in Chinese patients. Methods Sixty-five unrelated cases (35 men and 30 women) who were hospitalized in the past 12 years were reviewed. Diagnosis was based on both the clinical presentation and the characteristic neuropathologic findings of bilateral symmetric necrotizing lesions in the basal ganglia and brain stem as detected using cranial computed tomography (CT) scan or magnetic resonance imaging (MRI). The differential diagnosis of organic acidurias and fatty acid ?-oxidation defects were performed. Specific point mutations and deletions in mitochondrial DNA (T8993G, T8993C, T9176C, A8344G, A3243G) were screened by PCR-restriction analysis and Southern blot. The SURF1 gene was sequenced. Skeletal muscle biopsies were performed in 17 (26.2%) of the patients. The diagnosis was confirmed by autopsy in 6 (9.2%) patients. Results The patients had various forms of metabolic encephalomyopathy. Fifty-nine (90.8%) of the patients had the typical neuroradiological features of Leigh syndrome, including symmetrical necrotizing lesions scattered within the basal ganglia, thalamus and brain stem. Twenty (30.8%) patients were confirmed by genetic, biochemical analysis and autopsy. Specific point mutations in mitochondrial DNA were found in 5 cases (7.7%). Of these, the A8344G mutation was detected in 2 patients. The T8993G, T8993C, and A3243G point mutations were identified in 3 other patients, respectively. SURF1 mutations associated with cytochrome c oxidase deficiency were identified in 8 (12.3%) families by DNA sequencing. A G604C mutation was identified in 6 (9.2%) patients. The genotypes of 52 patients remained unknown. Conclusions Leigh syndrome presents as a diverse array of clinical features and can result from specific mutations in nuclear or mitochondrial DNA. In this study, SURF1 mutations associated with cytochrome c oxidase deficiency were identified in 8 (12.3%) out of 65 patients with Leigh syndrome. It indicates that SURF1 mutations might be a common cause of Leigh syndrome in China. The etiology of Leigh syndrome in Chinese patients represents a persistent challenge to clinicians. | YANG Yan-ling SUN Fang ZHANG Yao QIAN Ning YUAN Yun WANG Zhao-xia QI Yu XIAO Jiang-xi WANG Xiao-ying QI Zhao-yue ZHANG Yue-hua JIANG Yu-wu BAO Xin-hua QIN Jiong WU Xi-ru | 2006 | Chinese Medical Journal2006，，5： | 17 |
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