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| 1 | MicroRNA-21 in the pathogenesis of acute kidney injury显示文摘Acute kidney injury(AKI),associated with significant mor-bidity and mortality,is widely known to involve epithelial apoptosis,excessive inflammation,and fibrosis in re-sponse to ischemia or reperfusion injury,which results in either chronic pathological changes or death.Therefore,it is imperative that investigations are conducted in order to fi nd effective,early diagnoses,and therapeutic targets needed to help prevent and treat AKI.However,the mech-anisms modulating the pathogenesis of AKI still remain largely undetermined.MicroRNAs(miRNAs),small non-coding RNA molecules,play an important role in several fundamental biological and pathological processes by a post transcriptional regulatory function of gene expres-sion.MicroRNA-21(miR-21)is a recently identifi ed,typi-cal miRNA that is functional as a regulator known to be involved in apoptosis as well as inflammatory and fi brotic signaling pathways in AKI.As a result,miR-21 is now considered a novel biomarker when diagnosing and treat-ing AKI.This article reviews the correlative literature and research progress regarding the roles of miR-21 in AKI. | Ya-Feng Li Ying Jing Jielu Hao Nathan C Frankfort Xiaoshuang Zhou Bing Shen Xinyan Liu Lihua Wang Rongshan Li | 2013 | Protein & Cell2013，4，11： | 18 |
| 2 | miR-182参与调节胶质母细胞瘤的凋亡、生长和分化(英文)显示文摘Glioblastoma multiforme(GBM)is a lethal,therapy-resistant brain cancer consisting of numerous tumor cell subpopulations,including stem-like glioma-initiating cells(GICs),which contribute to tumor recurrence following initial response to therapy.Here,we identified miR-182 as a regulator of apoptosis,growth,and differentiation programs whose expression level is correlated with GBM patient survival.Repression of Bcl2-like12(Bcl2L12),c-Met,and hypoxia-inducible factor 2α(HIF2A)is of central importance to miR-182 anti-tumor activity,as it results in enhanced therapy susceptibility,decreased GIC sphere size,expansion,and stemness in vitro.To evaluate the tumor-suppressive function of miR-182 in vivo,we synthesized miR-182-based spherical nucleic acids(182-SNAs);i.e.,gold nanoparticles covalently functionalized with mature miR-182 duplexes.Intravenously administered 182-SNAs penetrated the bloodbrain/blood-tumor barriers(BBB/BTB)in orthotopic GBM xenografts and selectively disseminated throughout extravascular glioma parenchyma,causing reduced tumor burden and increased animal survival.Our results indicate that harnessing the anti-tumor activities of miR-182 via safe and robust delivery of 182-SNAs represents a novel strategy for therapeutic intervention in GBM. | Kouri FM Hurley LA Daniel WL Day ES Hua Y Hao L Peng CY Merkel TJ Queisser MA Ritner C Zhang H James CD Sznajder JI Chin L Giljohann DA Kessler JA Peter ME Mirkin CA Stegh AH | 2015 | 中华神经外科疾病研究杂志2015，14，2： | 14 |
| 3 | 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 |
| 4 | Highly efficient derivation of ventricular cardiomyocytes from induced pluripotent stem cells with a distinct epigenetic signature显示文摘从 pluripotent 干细胞导出的 Cardiomyocytes 能在药测试,疾病建模和基于房间的治疗被使用。没有 procardiogenic 生长因素,然而,从 pluripotent 干细胞的 cardiomyogenesis 的效率通常是低的,产生 cardiomyocyte 人口是异构的。这里,我们证明导致的 pluripotent 干细胞( iPSCs )能从鼠科的室的 myocytes ( VM )被导出,并且与从各种各样的体的房间类型导出的 iPSCs 的另外的报告一致,自发地作为与遗传上匹配的胚胎的干细胞(转换字符)或 iPSCs 相比区分 cardiomyocytes 进跳动的显著地更高的倾向从尾巴尖端成纤维细胞导出的 导出VM 的 iPSCs ( ViPSCs )展览。惊人地,导出 ViPSC 的 cardiomyocytes 显示的多数室的显型。在 ViPSCs 的提高的室的 myogenesis 在区别的早阶段经由心血管的祖先的增加的数字被调停。以便从 ViPSCs 调查提高的室的 myogenesis 的机制,我们执行了全球基因表示和 DNA methylation 分析,它揭示了可以涉及在 pluripotent 干细胞指定 VM 命运的不同 epigenetic 签名。 | Huansheng Xu B Alexander Yi Hao Wu Christoph Bock Hongcang Gu Kathy O Lui Joo-Hye C Park Ying Shao Alyssa K Riley Ibrahim J Domian Erding Hu Robert Willette John Lepore Alexander Meissner Zhong Wang Kenneth R Chien | 2012 | Cell Research2012，22，1： | 7 |
| 5 | Distinct regulatory mechanism of immunoglobulin gene transcription in epithelial cancer cells显示文摘The restriction of immunoglobulin(Ig)expression to B lymphocytes is well established.However,several reports have confirmed that the Ig gene can be expressed in many non-B cancer cells and/or some normal cells.Our aim is to determine whether the Ig gene promoter can be activated in non-B cancer cells and to identify the regulatory mechanism for Ig gene expression.Our results show that the Ig promoter of VH4-59 was activated in several non-B cancer cell lines.Moreover,two novel positive regulatory elements,an enhancer-like element at 2800 to 2610 bp and a copromoter-like element at 2610 to 2300 bp,were identified in two epithelial cancer cell lines,HeLa S3 and HT-29.The octamer element(59-ATGCAAAT-39)located in the Ig promoter,a crucial element for B-cell-derived Ig gene transcription,was also very important for non-B-cell-derived Ig gene transcription.More importantly,we confirmed that octamer-related protein-1(Oct-1),but not Oct-2,was a crucial transcriptional factor for Ig gene transcription due to its ability to bind to the octamer element of the Ig promoter in epithelial cancer cells.These results suggested the presence of a distinct regulatory mechanism for Ig gene expression in non-B cancer cells. | Xiaohui Zhu Lina Wu Li Zhang Peng Hao Shuai Zhang Jing Huang Jie Zheng Yinan Liu Wenjun Li Yingmei Zhang Chunyan Zhou Youhui Zhang C Cameron Yin Xiaoyan Qiu | 2010 | Cellular & Molecular Immunology2010，7，4： | 5 |
| 6 | 基于工作地点的分组干预对高血压控制的影响:一项随机临床研究显示文摘基于工作地点的干预可能为一种管理高血压的有效方法。但是目前缺少针对中国工作人群高血压控制情况的研究。本研究旨在评估基于工作地点的多组分别干预策略对改善血压控制的影响。研究设计及受试者:研究者在2013年1月至2014年12月于中国20个城区的60个工作地点进行了一系列高血压管理的随机临床试验。工作地点随机分为干预组(n=40)和对照组(n=20)。每个工作地点的受试者都需要完成一项横断面调查。 | 袁源(摘译) 叶鹏(审校) Wang Z Wang X Shen Y Li S Chen Z Zheng C Kang Y Jiang L Hao G Chang C Gao R | 2020 | 中华高血压杂志2020，28，6： | 3 |
| 7 | Novel role of STAT3 in microglia-dependent neuroinflammation after experimental subarachnoid haemorrhage显示文摘Background and purpose Signal transducer and activator of transcription 3(STAT3)may contribute to the proinflammation in the central nervous system diseases by modulating the microglial responses.Thus,this study was intended to investigate the effect of STAT3 on microglia-dependent neuroinflammation and functional outcome after experimental subarachnoid haemorrhage(SAH).Methods The SAH model was established by endovascular perforation in the mouse.Real-time PCR(RtPCR)and western blot were used to examine the dynamic STAT3 signalling pathway responses after SAH.To clarify the role of the STAT3 signalling pathway in the microglia-dependent neuroinflammation after SAH,the microglia-specific STAT3 knockout(KO)mice were generated by the Cre-LoxP system.The neurological functions were assessed by Catwalk and Morris water maze tests.Neuronal loss after SAH was determined by immunohistochemistry staining.Microglial polarisation status after STAT3 KO was then examined by RtPCR and immunofluorescence.Results The STAT3 and Janus kinase-signal transducer 2 activated immediately with the upregulation and phosphorylation after SAH.Downstream factors and related mediators altered dynamically and accordingly.Microglial STAT3 deletion ameliorated the neurological impairment and alleviated the early neuronal loss after SAH.To investigate the underlying mechanism,we examined the microglial reaction after STAT3 KO.STAT3 deletion reversed the increase of microglia after SAH.Loss of STAT3 triggered the early morphological changes of microglia and primed microglia from M1 to M2 polarisation.Functionally,microglial STAT3 deletion suppressed the SAH-induced proinflammation and promoted the anti-inflammation in the early phase.Conclusions STAT3 is closely related to the microglial polarisation transition and modulation of microglia-dependent neuroinflammation.Microglial STAT3 deletion improved neurological function and neuronal survival probably through promoting M2 polarisation and anti-inflammatory responses after SAH.STAT3 may serve as a promising therapeutic target to alleviate early brain injury after SAH. | Zhiyuan Vera Zheng Junfan Chen Hao Lyu Sin Yu Erica Lam Gang Lu Wai Yee Chan George K C Wong | 2022 | Stroke & Vascular Neurology2022，7，1： | 3 |
| 8 | Tenecteplase Reperfusion therapy in Acute ischaemic Cerebrovascular Events-Ⅱ (TRACE Ⅱ): rationale and design显示文摘Background and purpose Tenecteplase(TNK)is a promising agent for treatment of acute ischaemic stroke(AIS).We hypothesised that recombinant human TNK tissue-type plasminogen activator(rhTNK-tPA)is non-inferior to rt-PA in achieving excellent functional outcome at 90 days,when administered within 4.5 hours of ischaemic stroke onset.Methods and design Tenecteplase Reperfusion therapy in Acute ischemic Cerebrovascular Events(TRACE)is a phase Ⅲ,multicentre,prospective,randomised,open-label,blinded-end point non-inferiority study.Patients eligible for intravenous thrombolysis therapy are randomised to rhTNK-tPA 0.25 mg/kg(single bolus)to a maximum of 25 mg or rt-PA 0.9 mg/kg(10%bolus+90%infusion/1 hour)to a maximum of 90 mg.Medications considered necessary for the patient’s health may be given at the discretion of the investigator during 90-day follow-up.Study outcomes The primary study outcome is excellent functional outcome defined as modified Rankin Scale(mRS)0–1 at 90 days.Secondary efficacy outcomes include favourable functional outcome defined as mRS≤2 at 90 days,ordinal distribution of mRS and major neurological improvement on the National Institutes of Health Stroke Scale.Safety outcomes are symptomatic intracranial haemorrhage within 36 hours and death from any cause.Discussion There is no completed registration study of TNK in AIS worldwide.TRACE Ⅱ strives to provide evidence for a new drug application for rhTNK-tPA in AIS within 4.5 hours through a well-designed and rigorously executed randomised trial in China. | Shuya Li Bruce C V Campbell Lee H Schwamm Marc Fisher Mark Parsons Hao Li Yuesong Pan Yongjun Wang | 2022 | Stroke & Vascular Neurology2022，7，1： | 2 |
| 9 | Numerical Simulation of the Generation of Axisymmetric Mode Jet Screech Tones显示文摘 | Hao Shen Tam C K W | 1998 | AIAA Journal1998，36，0： | 2 |
| 10 | Cancer Genome Scanning in Plasma: Detection of Tumor-Associated Copy Number Aberrations, Single-Nucleotide Variants, and Tumoral Heterogeneity by Massively Parallel Sequencing显示文摘 | Chan K C Allen Jiang Peiyong Zheng Yama W L Liao Gary J W Sun Hao Wong John Siu Shing Shun N Chan Wing C Chan Stephen L Chan Anthony T C Lai Paul B S Chiu Rossa W K Lo Y M D | 2013 | Clinical Chemistry2013，，1： | 2 |
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