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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 | Abnormal activation of the synuclein-gamma gene in hepatocellular carcinomas by epigenetic alteration.显示文摘 | Zhao W Liu H Liu W Wu Y Chen W Jiang B Zhou Y Xue R Luo C Wang L Jiang JD Liu J | 2006 | 中国生物学文摘2006，20，4： | 31 |
| 3 | Study of BESIII trigger efficiencies with the 2018 J/ψ data显示文摘Using a dedicated data sample taken in 2018 on the J/ψpeak,we perform a detailed study of the trigger efficiencies of the BESIII detector.The efficiencies are determined from three representative physics processes,namely Bhabha scattering,dimuon production and generic hadronic events with charged particles.The combined efficiency of all active triggers approaches 100%in most cases,with uncertainties small enough not to affect most physics analyses. | M.Ablikim M.N.Achasov P.Adlarson S.Ahmed M.Albrecht R.Aliberti A.Amoroso M.R.An Q.An X.H.Bai Y.Bai O.Bakina R.Baldini Ferroli I.Balossino Y.Ban K.Begzsuren N.Berger M.Bertani D.Bettoni F.Bianchi J.Bloms A.Bortone I.Boyko R.A.Briere H.Cai X.Cai A.Calcaterra G.F.Cao N.Cao S.A.Cetin J.F.Chang W.L.Chang G.Chelkov D.Y.Chen G.Chen H.S.Chen M.L.Chen S.J.Chen X.R.Chen Y.B.Chen Z.J Chen W.S.Cheng G.Cibinetto F.Cossio X.F.Cui H.L.Dai X.C.Dai A.Dbeyssi R.E.de Boer D.Dedovich Z.Y.Deng A.Denig I.Denysenko M.Destefanis F.De Mori Y.Ding C.Dong J.Dong L.Y.Dong M.Y.Dong X.Dong S.X.Du Y.L.Fan J.Fang S.S.Fang Y.Fang R.Farinelli L.Fava F.Feldbauer G.Felici C.Q.Feng J.H.Feng M.Fritsch C.D.Fu Y.Gao Y.Gao Y.Gao Y.G.Gao I.Garzia P.T.Ge C.Geng E.M.Gersabeck A Gilman K.Goetzen L.Gong W.X.Gong W.Gradl M.Greco L.M.Gu M.H.Gu S.Gu Y.T.Gu C.Y Guan A.Q.Guo L.B.Guo R.P.Guo Y.P.Guo A.Guskov T.T.Han W.Y.Han X.Q.Hao F.A.Harris H Hüsken K.L.He F.H.Heinsius C.H.Heinz T.Held Y.K.Heng C.Herold M.Himmelreich T.Holtmann Y.R.Hou Z.L.Hou H.M.Hu J.F.Hu T.Hu Y.Hu G.S.Huang L.Q.Huang X.T.Huang Y.P.Huang Z.Huang T.Hussain W.Ikegami Andersson W.Imoehl M.Irshad S.Jaeger S.Janchiv Q.Ji Q.P.Ji X.B.Ji X.L.Ji H.B.Jiang X.S.Jiang J.B.Jiao Z.Jiao S.Jin Y.Jin T.Johansson N.Kalantar-Nayestanaki X.S.Kang R.Kappert M.Kavatsyuk B.C.Ke I.K.Keshk A.Khoukaz P.Kiese R.Kiuchi R.Kliemt L.Koch O.B.Kolcu B.Kopf M.Kuemmel M.Kuessner A.Kupsc M.G.Kurth W.Kühn J.J.Lane J.S.Lange P.Larin A.Lavania L.Lavezzi Z.H.Lei H.Leithoff M.Lellmann T.Lenz C.Li C.H.Li Cheng Li D.M.Li F.Li G.Li H.Li H.Li H.B.Li H.J.Li J.L.Li J.Q.Li J.S.Li Ke Li L.K.Li Lei Li P.R.Li S.Y.Li W.D.Li W.G.Li X.H.Li X.L.Li Z.Y.Li H.Liang H.Liang H.Liang Y.F.Liang Y.T.Liang L.Z.Liao J.Libby C.X.Lin B.J.Liu C.X.Liu D.Liu F.H.Liu Fang Liu Feng Liu H.B.Liu H.M.Liu Huanhuan Liu Huihui Liu J.B.Liu J.L.Liu J.Y.Liu K.Liu K.Y.Liu Ke Liu L.Liu M.H.Liu P.L.Liu Q.Liu Q.Liu S.B.Liu Shuai Liu T.Liu W.M.Liu X.Liu Y.Liu Y.B.Liu Z.A.Liu Z.Q.Liu X.C.Lou F.X.Lu H.J.Lu J.D.Lu J.G.Lu X.L.Lu Y.Lu Y.P.Lu C.L.Luo M.X.Luo b P.W.Luo T.Luo X.L.Luo S.Lusso X.R.Lyu F.C.Ma H.L.Ma L.L.Ma M.M.Ma Q.M.Ma R.Q.Ma R.T.Ma X.X.Ma X.Y.Ma F.E.Maas M.Maggiora S.Maldaner S.Malde Q.A.Malik A.Mangoni Y.J.Mao Z.P.Mao S.Marcello Z.X.Meng J.G.Messchendorp G.Mezzadri T.J.Min R.E.Mitchell X.H.Mo Y.J.Mo N.Yu.Muchnoi H.Muramatsu S.Nakhoul Y.Nefedov F.Nerling I.B.Nikolaev Z.Ning S.Nisar S.L.Olsen Q.Ouyang S.Pacetti X.Pan Y.Pan A.Pathak P.Patteri M.Pelizaeus H.P.Peng K.Peters J.Pettersson J.L.Ping R.G.Ping R.Poling V.Prasad H.Qi H.R.Qi K.H.Qi M.Qi T.Y.Qi T.Y.Qi S.Qian W.-B.Qian Z.Qian C.F.Qiao L.Q.Qin X.S.Qin Z.H.Qin J.F.Qiu S.Q.Qu K.H.Rashid K.Ravindran C.F.Redmer A.Rivetti V.Rodin M.Rolo G.Rong Ch.Rosner M.Rump H.S.Sang A.Sarantsev Y.Schelhaas C.Schnier K.Schoenning M.Scodeggio D.C.Shan W.Shan X.Y.Shan J.F.Shangguan M.Shao C.P.Shen P.X.Shen X.Y.Shen H.C.Shi R.S.Shi X.Shi X.D Shi W.M.Song Y.X.Song S.Sosio S.Spataro K.X.Su P.P.Su F.F.Sui G.X.Sun H.K.Sun J.F.Sun L.Sun S.S.Sun T.Sun W.Y.Sun X Sun Y.J.Sun Y.K.Sun Y.Z.Sun Z.T.Sun Y.H.Tan Y.X.Tan C.J.Tang G.Y.Tang J.Tang J.X.Teng V.Thoren I.Uman B.Wang C.W.Wang D.Y.Wang H.J.Wang H.P.Wang K.Wang L.L.Wang M.Wang M.Z.Wang Meng Wang W.Wang W.H.Wang W.P.Wang X.Wang X.F.Wang X.L.Wang Y.Wang Y.D.Wang Y.F.Wang Y.Q.Wang Y.Y.Wang Z.Wang Z.Y.Wang Ziyi Wang Zongyuan Wang D.H.Wei P.Weidenkaff F.Weidner S.P.Wen D.J.White U.Wiedner G.Wilkinson M.Wolke L.Wollenberg J.F.Wu L.H.Wu L.J.Wu X.Wu Z.Wu L.Xia H.Xiao S.Y.Xiao Z.J.Xiao X.H.Xie Y.G.Xie Y.H.Xie T.Y.Xing G.F.Xu Q.J.Xu W.Xu X.P.Xu F.Yan L.Yan W.B.Yan W.C.Yan Xu Yan H.J.Yang H.X.Yang L.Yang S.L.Yang Y.X.Yang Yifan Yang Zhi Yang M.Ye M.H.Ye J.H.Yin Z.Y.You B.X.Yu C.X.Yu G.Yu J.S.Yu T.Yu C.Z.Yuan L.Yuan X.Q.Yuan Y.Yuan Z.Y.Yuan C.X.Yue A.Yuncu A.A.Zafar Y.Zeng B.X.Zhang Guangyi Zhang H.Zhang H.H.Zhang H.Y.Zhang J.J.Zhang J.L.Zhang J.Q.Zhang J.W.Zhang J.Y.Zhang J.Z.Zhang Jianyu Zhang Jiawei Zhang L.Q.Zhang Lei Zhang S.Zhang S.F.Zhang Shulei Zhang X.D.Zhang X.Y.Zhang Y.Zhang Y.H.Zhang Y.T.Zhang Yan Zhang Yao Zhang Yi Zhang Z.H.Zhang Z.Y.Zhang G.Zhao J.Zhao J.Y.Zhao J.Z.Zhao Lei Zhao Ling Zhao M.G.Zhao Q.Zhao S.J.Zhao Y.B.Zhao Y.X.Zhao Z.G.Zhao A.Zhemchugov B.Zheng J.P.Zheng Y.Zheng Y.H.Zheng B.Zhong C.Zhong L.P.Zhou Q.Zhou X.Zhou X.K.Zhou X.R.Zhou A.N.Zhu J.Zhu K.Zhu K.J.Zhu S.H.Zhu T.J.Zhu W.J.Zhu W.J.Zhu Y.C.Zhu Z.A.Zhu B.S.Zou J.H.Zou | 2021 | Chinese Physics C2021，45，2： | 33 |
| 4 | 体内腺相关病毒-常间回文重复序列丛集及其相关蛋白9介导的基因编辑可改善家族性高胆固醇血症的动脉粥样硬化显示文摘低密度脂蛋白受体(low-density lipoprotein receptor,Ldlr)基因突变是家族性高胆固醇血症的主要原因之一,可导致动脉粥样硬化,并具有很高的终生心血管病风险。常间回文重复序列丛集(clustered regularly interspaced short palindromic repeats,CRISPR)/CRISPR相关蛋白9(CRISPR-related protein 9,Cas9)系统是基因编辑纠正基因突变从而改善疾病的有效工具。该研究的目的是通过腺相关病毒(adeno-associated virus,AAV)携带的CRISPR/Cas9系统进行体内体细胞基因编辑,以确定其能否在小鼠模型中治疗由Ldlr突变体引起的家族性高胆固醇血症。 | 刘青(译) 叶鹏(审校) Zhao H Li Y He L Pu W Yu W Li Y Wu YT Xu C Wei Y Ding Q Song BL Huang H Zhou B | 2020 | 中华高血压杂志2020，28，3： | 22 |
| 5 | Nicotine attenuates beta-amyloid-induced neurotoxicity by regulating metal homeostasis.显示文摘 | Zhang J Liu Q Chen Q Liu NQ Li FL Lu ZB Qin C Zhu H Huang YY He W Zhao BL | 2006 | 中国生物学文摘2006，20，9： | 17 |
| 6 | An ABA-mimicking ligand that reduces water loss and promotes drought resistance in plants显示文摘Abscisic 酸(骆驼毛的织物) 是最重要的荷尔蒙让植物抵抗干旱和另外的不能生活的压力。骆驼毛的织物直接绑在骆驼毛的织物受体的 PYR/PYL 家庭,导致类型 2C 磷酸酶(PP2C ) 和下游的骆驼毛的织物发信号的激活的抑制。骆驼毛的织物由小分子发信号的干预能帮助植物克服象干旱,寒冷和土壤咸度那样的不能生活的压力,这被想象。然而,由植物酶的化学不稳定性和快速的分解代谢限制骆驼毛的织物本身的实际申请。这里,我们报导一件小分子骆驼毛的织物的鉴定模仿(AM1 ) 那充当骆驼毛的织物受体的家庭的多重成员的有势力使活跃之物。在 Arabidopsis, AM1 激活高度类似于由骆驼毛的织物导致了那的一个基因网络。有 AM1 的处理禁止种子萌芽,阻止叶水损失,并且支持干旱抵抗。我们与 PYL2 骆驼毛的织物受体和 HAB1 PP2C 在建筑群解决了 AM1 的水晶结构,它表明 AM1 调停交往的 gate-latch-lock 网络,在骆驼毛的织物界限 receptor/PP2C 建筑群被保存的一个结构的特征。一起,这些结果证明一件单个小分子骆驼毛的织物模仿能激活多重骆驼毛的织物受体并且保护植物免受水损失和干旱应力的伤害。而且, AM1 复杂水晶结构为设计 ABA-mimicking 小分子的下一代提供一个结构的基础。 | Minjie Cao Xue Liu Yan Zhang Xiaoqian Xue X EdwardZhou Karsten Melcher Pan Gao Fuxing Wang Liang Zeng Yang Zhao Pan Deng Dafang Zhong Jian-Kang Zhu H Eric Xu Yong Xu | 2013 | Cell Research2013，23，8： | 17 |
| 7 | Arrhythmogenic mechanisms in ryanodine receptor channelopathies显示文摘Ryanodine receptors(Ry Rs) are the calcium release channels of sarcoplasmic reticulum(SR) that provide the majority of calcium ions(Ca2+) necessary to induce contraction of cardiac and skeletal muscle cells.In their intracellular environment,Ry R channels are regulated by a variety of cytosolic and luminal factors so that their output signal(Ca2+) induces finely-graded cell contraction without igniting cellular processes that may lead to aberrant electrical activity(ventricular arrhythmias) or cellular remodeling.The importance of Ry R dysfunction has been recently highlighted with the demonstration that point mutations in RYR2,the gene encoding for the cardiac isoform of the Ry R(Ry R2),are associated with catecholaminergic polymorphic ventricular tachycardia(CPVT),an arrhythmogenic syndrome characterized by the development of adrenergically-mediated ventricular tachycardia in individuals with an apparently normal heart.Here we summarize the state of the field in regards to the main arrhythmogenic mechanisms triggered by Ry R2 channels harboring mutations linked to CPVT.Most CPVT mutations characterized to date endow Ry R2 channels with a gain of function,resulting in hyperactive channels that release Ca2+ spontaneously,especially during diastole.The spontaneous Ca2+ release is extruded by the electrogenic Na+/Ca2+ exchanger,which depolarizes the external membrane(delayed afterdepolarization or DAD) and may trigger untimely action potentials.However,a rare set of CPVT mutations yield Ry R2 channels that are intrinsically hypo-active and hypo-responsive to stimuli,and it is unclear whether these channels release Ca2+ spontaneously during diastole.We discuss novel cellular mechanisms that appear more suitable to explain ventricular arrhythmias due to Ry R2 loss-of-function mutations. | ZHAO Yan-Ting VALDIVIA Carmen R. GURROLA Georgina B. HERNNDEZ Jonathan J. VALDIVIA Héctor H. | 2015 | Science China(Life Sciences)2015，58，1： | 14 |
| 8 | Structural shifts of mucosa-associated lactobacilli and Clostridium leptum subgroup in patients with ulcerative colitis显示文摘 | Zhang ML Liu BY Zhang Y Wei H Lei YF Zhao LP | 2007 | 中国生物学文摘2007，21，8： | 14 |
| 9 | 健康成人动脉粥样硬化斑块易感性和血栓形成的生物标志物变化与极端空气污染水平相关:北京AIRCHD研究显示文摘空气污染与心血管事件恶化的病理生理机制尚不完全清楚。该文探讨环境空气污染是否可以触发易损斑块.通过全身炎症途径促进血栓形成。方法:在北京AIRCHD研究中.2014-2016年间对73名健康成年人[年龄(23.3±5.4)岁]进行了随访。研究者使用线性混合效应模型评估了空气污染物与动脉粥样硬化斑块易损性、血栓形成和炎症相关生物标志物之间的关系,并使用中介效应分析(mediation analyses)探讨涉及的生物学途径。通过受试者工作特征(receiver operating characteristic,ROC)曲线分析评估每种生物标记物预测环境空气污染暴露的能力。 | 刘青 叶鹏 Xu H Wang T Liu S Brook RD Feng B Zhao Q Song X Yi T Chen J Zhang Y Wang Y Zheng L Rajagopalan S Li J Huang W | 2019 | 中华高血压杂志2019，27，4： | 13 |
| 10 | Immune responses against SARS-coronavirus nucleocapsid protein induced by DNA vaccine显示文摘 | Zhao P Cao J Zhao LJ Ke JS Pan W Ren H Yu JG Qi ZT | 2005 | 第二军医大学学报2005，26，10： | 12 |
| 11 | Bone tissue engineering via nanostructured calcium phosphate biomaterials and stem cells显示文摘Tissue engineering is promising to meet the increasing need for bone regeneration. Nanostructured calcium phosphate(CaP) biomaterials/scaffolds are of special interest as they share chemical/crystallographic similarities to inorganic components of bone. Three applications of nano-CaP are discussed in this review:nanostructured calcium phosphate cement(CPC); nano-CaP composites; and nano-CaP coatings. The interactions between stem cells and nano-CaP are highlighted, including cell attachment, orientation/morphology, differentiation and in vivo bone regeneration. Several trends can be seen:(i) nano-CaP biomaterials support stem cell attachment/proliferation and induce osteogenic differentiation, in some cases even without osteogenic supplements;(ii) the influence of nano-CaP surface patterns on cell alignment is not prominent due to non-uniform distribution of nano-crystals;(iii) nano-CaP can achieve better bone regeneration than conventional CaP biomaterials;(iv) combining stem cells with nano-CaP accelerates bone regeneration, the effect of which can be further enhanced by growth factors; and(v) cell microencapsulation in nano-CaP scaffolds is promising for bone tissue engineering. These understandings would help researchers to further uncover the underlying mechanisms and interactions in nano-CaP stem cell constructs in vitro and in vivo, tailor nano-CaP composite construct design and stem cell type selection to enhance cell function and bone regeneration, and translate laboratory findings to clinical treatments. | Ping Wang Liang Zhao Jason Liu Michael D Weir Xuedong Zhou Hockin H K Xu | 2014 | Bone Research2014，2，3： | 11 |
| 12 | Transcriptomic landscape regulated by the 14 types of bone morphogenetic proteins(BMPs)in lineage commitment and differentiation of mesenchymal stem cells(MSCs)显示文摘Mesenchymal stem cells(MSCs)are ubiquitously-existing multipotent progenitors that can self-renew and differentiate into multiple lineages including osteocytes,chondrocytes,adipocytes,tenocytes and myocytes.MSCs represent one of the most commonly-used adult progenitors and serve as excellent progenitor cell models for investigating lineagespecific differentiation regulated by various cellular signaling pathways,such as bone morphogenetic proteins(BMPs).As members of TGFb superfamily,BMPs play diverse and important roles in development and adult tissues.At least 14 BMPs have been identified in mammals.Different BMPs exert distinct but overlapping biological functions.Through a comprehensive analysis of 14 BMPs in MSCs,we demonstrated that BMP9 is one of the most potent BMPs in inducing osteogenic differentiation of MSCs.Nonetheless,a global mechanistic view of BMP signaling in regulating the proliferation and differentiation of MSCs remains to be fully elucidated.Here,we conducted a comprehensive transcriptomic profiling in the MSCs stimulated by 14 types of BMPs.Hierarchical clustering analysis classifies 14 BMPs into three subclusters:an osteo/chondrogenic/adipogenic cluster,a tenogenic cluster,and BMP3 cluster.We also demonstrate that six BMPs(e.g.,BMP2,BMP3,BMP4,BMP7,BMP8,and BMP9)can induce ISmads effectively,while BMP2,BMP3,BMP4,BMP7,and BMP11 up-regulate Smad-independent MAP kinase pathway.Furthermore,we show that many BMPs can upregulate the expression of the signal mediators of Wnt,Notch and PI3K/AKT/mTOR pathways.While the reported transcriptomic changes need to be further validated,our expression profiling represents the first-of-its-kind to interrogate a comprehensive transcriptomic landscape regulated by the 14 types of BMPs in MSCs. | Linghuan Zhang Qing Luo Yi Shu Zongyue Zeng Bo Huang Yixiao Feng Bo Zhang Xi Wang Yan Lei Zhenyu Ye Ling Zhao Daigui Cao Lijuan Yang Xian Chen Bin Liu William Wagstaff Russell R*Reid Hue H*Luu Rex C*Haydon Michael J*Lee Jennifer Moriatis Wolf Zhou Fu Tong-Chuan He Quan Kang | 2019 | Genes & Diseases2019，6，3： | 11 |
| 13 | 烟酰胺磷酸核糖基转移酶促进肺血管重塑,是肺动脉高压的治疗靶点显示文摘肺动脉高压(pulmonary arterial hypertension,PAH)是一种严重的进行性疾病,其标志之一是肺血管重塑。烟酰胺磷酸核糖基转移酶(nicotinamide phosphoribosyl transferase,NAMPT)是调节细胞内烟酰胺腺嘌呤二核苷酸水平、细胞氧化还原状态,调节组蛋白脱乙酰酶,促进细胞增殖和抑制凋亡的一种细胞酶。研究人员假设NAMPT可促进肺血管重塑, | Chen J Sysol JR Singla S Zhao S Yamamura A Valdez-Jasso D Abbasi T Shioura KM Sahni S Reddy V Sridhar A Gao H Torres J Camp SM Tang H Ye SQ Comhair S Dweik R Hassoun P Yuan JX Garcia JG Machado RF 刘莉 叶鹏 | 2017 | 中华高血压杂志2017，25，2： | 10 |
| 14 | A unique sequence in the N-terminal regulatory region controls the nuclear localization of KLF8 by cooperating with the C-terminal zinc-fingers显示文摘Kr 眉 p 像像素的因素 8 (KLF8 ) 抄写因素在房间周期前进起一个关键作用, oncogenic 转变,对间充质的转变和侵略上皮。然而,它的原子本地化信号(NLS ) 没被识别。有另外的 KLF monopartite NLS (mNLS ) 和 C2H2 锌手指(ZF ) 的 KLF8 份额,哪个被显示了是为一些另外的 KLF 的 NLS。在这份报告,用指导 PCR 的 mutagenesis 和 immunofluorescent 显微镜学,我们显示出 mNLSs,任何单个 ZF 的删除,或变化的那混乱 Zn2+ 有约束力或联系 DNA 主题没影响 KLF8 的原子本地化。删除 > 然而,从 C 终点的 1.5 ZF 引起了 KLF8 的细胞质的累积。令人惊讶地,氨基酸(aa ) 的删除 151-200 区域几乎从原子核消除了 KLF8。有 PKC 禁止者的 S165A, K171E 或 K171R 变化,或处理导致了部分细胞质的累积。Co-immunoprecipitation 证明 KLF8 与 importin- 交往了,这个相互作用要求了 ZF 主题。aa 1-150 或 201-261 区域的删除独自没改变原子本地化。BrdU 加入和 cyclin D1 倡导者酶试金作为野类型的 KLF8 证明在原子本地化的 KLF8 异种有缺陷者不能支持 DNA 合成或 cyclin D1 倡导者激活。一起拿,这些结果建议 KLF8 有二 NLS,一包围 S165 和 K171 并且另外的是二双人脚踏车 ZF,它为 KLF8 原子本地化和它的细胞的功能的规定是批评的。 | Tina S Mehta Heng Lu Xianhui Wang Alison M Urvalek Kim-Hang H Nguyen Farah Monzur Jojo D Hammond Jameson Q Ma Jihe Zhao | 2009 | Cell Research2009，19，9： | 10 |
| 15 | Parkinson's disease in China: prevalence in Beijing, Xian, and Shanghai.显示文摘 | Zhang ZX Roman GC Hong Z Wu CB Qu QM Huang JB Zhou B Geng ZP Wu JX Wen HB Zhao H Zahner GE | 2006 | 中国生物学文摘2006，20，8： | 9 |
| 16 | 膳食中钠(盐)与血压的关系及其他膳食因素可能的调节作用显示文摘现有资料表明,膳食钠(盐)与血压直接相关。以往大多数研究结果来自缺乏膳食数据的研究;因此,这种钠-血压关系是否受其他膳食因素调节尚不清楚。国际宏量/微量营养素和血压研究(international study on macro/micronutrients and blood pressure,INTERMAP)结果显示,在控制多种非膳食因素情况下,年龄40~59岁的男性和女性4680人(中国、日本、英国和美国的17个人口样本)的血压与24h尿钠排泄和尿钠/钾直接相关。 | 刘莉 叶鹏 Stamler J Chan Q Daviglus ML Dyer AR Van Horn L Garside DB Miura K Wu Y Ueshima H Zhao L Elliott P INTERMAP Research Group | 2018 | 中华高血压杂志2018，26，4： | 8 |
| 17 | 钠-葡萄糖共转运蛋白-2抑制剂或胰高血糖素样肽-1受体激动剂治疗成人2型糖尿病:临床实践指南显示文摘临床问题对于存在不同心血管风险及肾脏结局的2型糖尿病患者,在原有生活方式干预和/或其他降糖药物的基础上加用钠-葡萄糖共转运蛋白2(SGLT-2)抑制剂和胰高血糖素样肽1(GLP-1)受体激动剂的获益及风险是什么?现行做法几十年来,2型糖尿病的治疗决策都以控制血糖为主导。SGLT-2抑制剂和GLP-1受体激动剂在传统观念中常被用于二甲双胍治疗后血糖仍控制不佳的患者。目前这一现状已经发生了改变,这得益于多项临床研究结果。研究显示SGLT-2抑制剂和GLP-1受体激动剂拥有独立于药物降糖作用之外的对于动脉粥样硬化性心血管病(CVD)和慢性肾脏病(CKD)的获益。建议本指南阐述了针对不同风险分层的成人2型糖尿病患者使用SGLT-2抑制剂或GLP-1受体激动剂的建议。•伴有3种或更少的心血管风险因素且不存在CVD或CKD:不建议启动SGLT-2抑制剂或GLP-1受体激动剂治疗。(推荐等级:弱)•伴有3种以上心血管风险因素且不存在CVD或CKD:建议启动SGLT-2抑制剂治疗,不建议启动GLP-1受体激动剂治疗。(推荐等级:弱)•已经存在CVD或CKD:建议启动SGLT-2抑制剂治疗和GLP-1受体激动剂治疗。(推荐等级:弱)•已经存在CVD和CKD:建议启动SGLT-2抑制剂治疗(推荐等级:强)和GLP-1受体激动剂治疗。(推荐等级:弱)•对于那些想要进一步降低CVD和CKD结局风险的患者:推荐优先启用SGLT-2抑制剂治疗而非GLP-1受体激动剂治疗。(推荐等级:弱)这项指南是如何制订的一个由患者、临床医生和方法学家共同组成的国际小组提出了这些推荐意见。这些推荐意见基于可信度较高的指南的标准,并使用GRADE分级方法进行评估。该小组采用了息者个体化的观点。证据一项关于获益与风险的系统综述和网络meta分析(764项随机对照研究,包括421346例参与者)发现SGLT-2抑制剂和GLP-1受体激动剂可以降低总体死亡率、心肌梗死发生率、终末期肾病或肾衰竭的发生率(中等至高等质量的证据)。在不同的亚组中这些药物对卒中、因心力衰竭所致住院和其他主要不良事件有不同的影响。药物绝对获益的程度因患者个体风险的不同有很大的差异。(例如,对于接受了超过5年药物治疗的1000例患者,在最低风险人群中死亡人数减少了5人,在最高风险人群中死亡人数减少了48人)。一项关于预后的综述确认了14种风险预测模型,其中一种(RECODe)在证据总结中报告了大部分基线风险评估数据,小组利用该模型以支持风险分层的建议。考虑到患者的价值观及个体差异,指南推荐的支撑证据包括一项对已发表论文的系统综述、一项患者焦点小组研究、一项临床问题总结,以及一项指南调查。指南解读我们依据不同的CVD和CKD风险水平,综合考虑获益、风险和其他因素的平衡,以及每一个风险组别的实际问题,来对推荐意见进行分层。本指南强烈建议CVD和CKD患者使用SGLT-2抑制剂治疗,这说明专家组认为其具有显著的获益。而对于其他成人2型糖尿病患者,推荐等级较弱,这说明专家组想要在获益、风险及治疗花费上取得一个更好的平衡。临床医生通过该指南可以使用可靠的风险计算模型,如RECODe,来明确其患者的个体心血管和肾脏疾病风险。医患交互式总结临床证据和制订决策有助于患者知晓治疗选择,包括进行共同决策。2型糖尿病人群(全球患病率不断增长1-2)正面临着不断增加的心血管疾病、肾脏病和其他并发症的风险3。数十年来,2型糖尿病的管理始终以控制血糖及糖化血红蛋白(HbA1c)为治疗目标4-5,但是,最近的高质量随机对照研究已经对这种以血糖为中心的治疗模式发起了挑战。研究结果显示,强化血糖控制未必会降低大血管不良事件,它还可能带来不利影响监管机构现在要求新型糖尿病药物必须证明其具有心血管和肾脏获益才能获得批准。对两类新药--钠-葡萄糖共转运蛋白2(SGLT-2)抑制剂和胰高血糖素样肽1(GLP-1)受体激动剂(见框图1)的临床试验结果显示,在现有治疗方案(常规治疗)之上加用这些药物,对死亡、心肌梗死、卒中、心力衰竭和肾脏的结局(如进展为终末期肾病)都有获益8-12。 | Sheyu Li Per Olav Vandvik Lyubov Lytvyn Gordon H Guyatt Suetonia C Palmer Rene Rodriguez-Gutierrez Farid Foroutan Thomas Agoritsas Reed A C Siemieniuk Michael Walsh Lawrie Frere David J Tunnicliffe Evi V Nagler Veena Manja Bjφrn Olav Asvold Vivekanand Jha Mieke Vermandere Karim Gariani Qian Zhao Yan Ren Emma Jane Cartwright Patrick Gee Alan Wickes Linda Fems Robin Wright Ling Li Qiukui Hao Reem A Mustafa 无 郭鹤鸣(译) | 2021 | 英国医学杂志中文版2021，24，9： | 7 |
| 18 | Destabilization of strigolactone receptor DWARF14 by binding of ligand and E3-1igase signaling effector DWARF3显示文摘 | Li-Hua Zhao X Edward Zhou Wei Yi Zhongshan Wu Yue Liu Yanyong Kang Li Hou Parker W de Waal Suling Li Yi Jiang Adrian Scaffidi Gavin R Flematti Steven M Smith Vinh Q Lam Patrick R Griffin YonghongWang Jiayang Li Karsten Melcher H Eric Xu | 2015 | Cell Research2015，25，11： | 7 |
| 19 | Expression of co-stimulator 4-1BB molecule in hepatocellular carcinoma and adjacent non-tumor liver tissue,and its possible role in tumor immunity显示文摘AIM:To investigate the expression of 4-1BB molecule in hepatocellular carcinoma (HCC) and its adjacent tissues.METHODS:Reverse transcription-polymerase chain reaction (RT-PCR) was used to determine the gene expression of 4-1BB in hepatocarcinoma and its adjacent tissues,and peripheral blood mononuclear cells (PBMCs) from both HCC and health control groups.Flow cytometry was used to analyse the phenotypes of T cell subsets from the blood of HCC patients and healthy volunteers,and further to determine whether 4-1BB molecules were also expressed on the surface of CD4+ and CD8+ T cells. The localization of 4-1BB proteins on tumor infiltrating T cells was determined by direct immunofluorescence cytochemical staining and detected by confocal microscopy.RESULTS:4-1BB mRNA, which was not detectable in normal liver,was found in 19 liver tissues adjacent to tumor edge(<1.0cm).Low expression of 4-1BB mRNA was shown in 8 tumor tissues and 6 liver tissues located within 1 to 5cm away from tumor edge. In PBMCs, 4-1BB mRNA was almost not detected. Percentage of CD4^+, CD8^+ and CD3^+/CD25^+ T cells, as well as ratio of CD4 to CD8 revealed no difference between groups (P>0.05,respectively),while a significant lower percentage of CD3^+ T cell was found in HCC group as compared to healthy control group (P<0.05).However, 4-1BB molecules were almost not found on the surface of CD4+ and CD8+ T cells in HCC and healthy control group.Double-staining of 4-1BB^+/CD4^+ and 4-1BB^+/CD8^+ immunofluorescence on tumor infiltrating T cells was detected in 13 liver tissues adjacent to tumor edge (<1.0cm) by confocal microscopy.CONCLUSION: Although HCC may escape from immune attack by weak immunogenicity or downregulated expression of MHC-1 molecules on the tumor cell surface,tumor infiltrating T cells can be activated via other costimulatory signal pathways to exert a limited antitumor effect on local microenvironment. The present study also implicates that modulating 4-1BB/4-1BBL costimulatory pathway may be an effective immunotherapy strategy to augment the host response. | Wan, YL Zheng, SS Zhao, ZC Li, MW Jia, CK Zhang, H | 2004 | World Journal of Gastroenterology2004，10，2： | 6 |
| 20 | Mutation analysis of autosomal dominant polycystic kidney disease genes in Han Chinese显示文摘 | Zhang S Mei C Zhang D Dai B Tang B Sun T Zhao H Zhou Y Li L Wu Y Wang W Shen X Song J | 2005 | 第二军医大学学报2005，26，8： | 6 |
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