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| 1 | 肌萎缩性侧索硬化蛋白激活小胶质细胞NLRP3炎性小体显示文摘小胶质细胞NLRP3炎性小体激活正在成为神经退行性变过程中神经炎症的关键因素。诸如β-淀粉样蛋白和α-突触核蛋白之类的致病性蛋白质聚集体触发小胶质NLRP3激活,从而导致半胱天冬酶-1激活和IL-1β的分泌。在小鼠肌萎缩性侧索硬化症(ALS)的SOD1G93A模型中,半胱天冬酶-1和IL-1β均促进疾病进展,提示小胶质NLRP3在该进程中发挥作用。然而先前的研究表明,SOD1G93A小鼠小胶质细胞不表达NLRP3,SOD1G93A蛋白在小胶质细胞中产生独立于NLRP3的IL-1β。本研究论证了使用Nlrp3-GFP基因敲入小鼠,在SOD1G93A小鼠中小胶质细胞表达NLRP3。本研究显示聚集和可溶性SOD1G93A均可激活小鼠原代小胶质细胞中的炎性小体,导致半胱天冬酶-1和IL-1β裂解,ASC斑点形成以及呈剂量和时间依赖性的IL-1β分泌。重要的是,SOD1G93A无法从缺乏Nlrp3的小胶质细胞或者用特异性NLRP3抑制剂MCC950预处理的小胶质细胞中诱导IL-1β分泌,从而证实NLRP3是介导SOD1诱导的小胶质细胞IL-1β分泌的关键炎症小体复合物。在TDP-43Q331K ALS小鼠模型中也观察到小胶质NLRP3上调,TDP-43野生型和突变蛋白亦可以NLRP3依赖性的方式激活小胶质炎性小体。从机制上讲,本研究确定了活性氧簇和ATP的生成是SOD1G93A介导的NLRP3激活所需的关键事件。总之,本研究的数据表明ALS小胶质细胞表达NLRP3,而病理ALS蛋白激活小胶质NLRP3炎性小体。因此,NLRP3抑制可能是阻止小胶质细胞神经炎症和ALS疾病进展的潜在治疗方法。 | Vandana Deora John D Lee Eduardo AAlbornoz Luke McAlary Cyril J Jagaraj Avril A B Robertson Julie D Atkin Matthew A Cooper Kate Schroder Justin J Yerbury Richard Gordon Trent MWoodruff 杜一星(编译) | 2020 | 神经损伤与功能重建2020，15，9： | 13 |
| 2 | 2型糖尿病患者采用血管紧张素转换酶抑制剂治疗后血清肌酐急性升高及其继续治疗对主要临床结局的影响显示文摘血管紧张素转换酶抑制剂开始治疗后血清肌酐急性升高≥30%时推荐停药。但血清肌酐升高后继续服药或停药对主要临床结局的长期影响仍不明确。在ADVANCE(糖尿病与血管疾病行动:培哚普利-吲达帕胺与达美康缓释片对照评估)试验中,11 140例糖尿病患者在6周活性导入期后随机采用培哚普利-吲达帕胺或安慰剂治疗。 | Ohkuma T Jun M Rodgers A Cooper ME Glasziou P Hamet P Harrap S Mancia G Marre M Neal B Perkovic V Poulter N Williams B Zoungas S Chalmers J Woodward M 赵狄 练桂丽 | 2019 | 中华高血压杂志2019，27，1： | 6 |
| 3 | Plecanatide-mediated activation of guanylate cyclase-C suppresses inflammation-induced colorectal carcinogenesis in Apc+/Min-FCCC mice显示文摘AIM To evaluate the effect of orally administered plecanatide on colorectal dysplasia in Apc^(+/Min-FCCC) mice with dextran sodium sulfate(DSS)-induced inflammation. METHODS Inflammation driven colorectal carcinogenesis was induced in Apc^(+/Min-FCCC) mice by administering DSS in their drinking water. Mice were fed a diet supplemented with plecanatide(0-20 ppm) and its effect on the multiplicity of histopathologically confirmed polypoid,flat and indeterminate dysplasia was evaluated. Plecanatide-mediated activation of guanylate cyclase-C(GC-C) signaling was assessed in colon tissues by measuring cyclic guanosine monophosphate(cG MP) by ELISA, protein kinase G-II and vasodilator stimulated phosphoprotein by immunoblotting. Ki-67, c-myc and cyclin D1 were used as markers of proliferation. Cellular levels and localization of b-catenin in colon tissues were assessed by immunoblotting and immunohistochemistry, respectively. Uroguanylin(UG) and GC-C transcript levels were measured by quantitative reverse transcription polymerase chain reaction(RT-PCR). A mouse cytokine array panel was used to detect cytokines in the supernatant of colon explant cultures. RESULTS Oral treatment of Apc^(+/Min-FCCC) mice with plecanatide produced a statistically significant reduction in the formation of inflammation-driven polypoid, flat and indeterminate dysplasias. This anti-carcinogenic activity of plecanatide was accompanied by activation of cG MP/GC-C signaling mediated inhibition of Wnt/b-catenin signaling and reduced proliferation. Plecanatide also decreased secretion of pro-inflammatory cytokines(IL-6, IL-1 TNF), chemokines(MIP-1, IP-10) and growth factors(GCSF and GMCSF) from colon explants derived from mice with acute DSS-induced inflammation. The effect of plecanatidemediated inhibition of inflammation/dysplasia on endogenous expression of UG and GC-C transcripts was measured in intestinal tissues. Although GC-C expression was not altered appreciably, a statistically significant increase in the level of UG transcripts was detected in the proximal small intestine and colon, potentially due to a reduction in intestinal inflammation and/or neoplasia. Taken together, these results suggest that reductions in endogenous UG, accompanied by dysregulation in GC-C signaling, may be an early event in inflammation-promoted colorectal neoplasia; an event that can potentially be ameliorated by prophylactic intervention with plecanatide.CONCLUSION This study provides the first evidence that orally administered plecanatide reduces the multiplicity of inflammation-driven colonic dysplasia in mice, demonstrating the utility for developing GC-C agonists as chemopreventive agents. | Wen-Chi L Chang Shet Masih Anusha Thadi Viren Patwa Apoorva Joshi Harry S Cooper Vaseem A Palejwala Margie L Clapper Kunwar Shailubhai | 2017 | World Journal of Gastrointestinal Pharmacology and Therapeutics2017，8，1： | 5 |
| 4 | 中年成人平均动脉压的体位改变与动脉硬度的关系:Framingham心脏研究显示文摘Torjesen A, Cooper LL, Rong J, Larson MG, Hamburg NM, Levy D, Benjamin EJ, Vasan RS, Mitchell GF. Relations of arterial stiffness with postural change in mean arterial pressure in middle-aged adults:the Framingham heart study. Hyperten- sion,2017,69(4) :685-690.站立位血压稳定调节受损可导致不良结果,包括跌倒、晕厥和定向障碍。平均动脉压(meanarterialpressure,MAP)通常在站立位时增加,然而,站立位MAP增加不足或减少可能导致脑灌注减少。已有研究报道,在动脉硬度增加的老年人中存在体位性低血压,年轻至中年人MAP的体位性改变与动脉硬度的相关性尚未阐明。该研究分析了Framingham心脏研究第3代队列中的受试者3205人(女性1693人,占53%)的直立性血压反应和全面血液动力学数据。 | Torjesen A Cooper LL Rong J Larson MG Hamburg NM Levy D Benjamin EJ Vasan RS Mitchell GF 刘莉 叶鹏 | 2017 | 中华高血压杂志2017，25，3： | 5 |
| 5 | 中国南方人A型行为问卷测查结果的分析显示文摘本文采用张伯源主持编制的A型行为问卷对中国南方13,808名正常成人进行测查,其中男性7943例,女性5865例。结果表明:我国南方人较北方人行为节凑慢、竞争性强;南方人男性与女性A型行为特征无明显差异,与北方人测查结果一致;不同年龄组的A型行为特征与北方人测查结果相同:即:45~>25~>35~>55~>15~>65岁以上组;不同职业组的A型行为特征是:商业>科技>干部>工人,与北方人测查结果存在一定差异;不同地区(省)间存在较大差异。 | Guo Huimin et al, Thesurvey cooperative group of the question paper on Chinese Southerners’type A bebavior pattern | 1995 | 中国临床心理学杂志1995，3，4： | 4 |
| 6 | 难治性疼痛和高血压在急性B型主动脉夹层中的重要性:国际急性主动脉夹层登记的意见显示文摘急性B型主动脉夹层患者,可表现出对药物治疗无效的反复、难治性疼痛和(或)难治性高血压,当出现这些症状时有时可作为介入治疗的指征。研究者利用国际急性主动脉夹层登记(international registry of a-cute aortic dissection,IRAD)的资料调查难治性疼痛和(或)难治性高血压对急性B型主动脉夹层患者临床转归的影响。 | 张玲玉 叶鹏 Trimarchi S Eagle KA Nienaber CA Pyeritz RE Jonker FH Suzuki T O'Gara PT Hutchinson SJ Rampoldi V Grassi V Bossone E Muhs BE Evangelista A Tsai TT Froehlich JB Cooper JV Montgomery D Mein-hardt G Myrmel T Upchurch GR Sundt TM Issel-bacher EM | 2010 | 中华高血压杂志2010，18，12： | 4 |
| 7 | Nat Genet:单基因突变导致过敏性皮炎的发生显示文摘最近,研究者们鉴定出了一类导致神经性皮炎发生的关键基因突变:CARDll。来自美国NIH过敏与传染病研究所的研究者们通过对四个没有血缘关系的患病家庭进行分析,发现了这一导致疾病产生的基因、 | Chi A Ma, Yuan Zhang, Michael A Weinreich, Jonathan J Lyons, Celeste G Nelson, Thomas DiMaggio, Kelly D Stone, Joshua D Milner Jeffrey R Stinson, Elisa Ruffo, Batsukh Dorjbal, Swadhinya Arjunaraja, Kelsey Voss, Andrew L Snow Jordan K Abbott, Pia J Hauk, Paul R Reynolds, Erwin W Gelfand Elisa Ruffo Salomé Glauzy, Natsuko Yamakawa, Eric Meffre Jennifer Stoddard, Julie Niemela, Sergio D Rosenzweig Yu Zhang, Helen F Matthews Joshua J McElwee Nina Jones Alejandro Palma, Matías Oleastro, Emma Prieto, Andrea R Bernasconi, Geronimo Dubra, Silvia Danielian, Jonathan Zaiat, Marcelo A Marti Brian Kim Megan A Cooper Neil Romberg | 2017 | 现代生物医学进展2017，17，27： | 3 |
| 8 | Do age-associated changes of voltage-gated sodium channel isoforms expressed in the mammalian heart predispose the elderly to atrial fibrillation?显示文摘Atrial fibrillation(AF)is the most common cardiac arrhythmia worldwide.The prevalence of the disease increases with age,strongly implying an age-related process underlying the pathology.At a time when people are living longer than ever before,an exponential increase in disease prevalence is predicted worldwide.Hence unraveling the underlying mechanics of the disease is paramount for the development of innovative treatment and prevention strategies.The role of voltage-gated sodium channels is fundamental in cardiac electrophysiology and may provide novel insights into the arrhythmogenesis of AF.Na_v1.5 is the predominant cardiac isoform,responsible for the action potential upstroke.Recent studies have demonstrated that Na_v1.8(an isoform predominantly expressed within the peripheral nervous system)is responsible for cellular arrhythmogenesis through the enhancement of pro-arrhythmogenic currents.Animal studies have shown a decline in Na_v1.5 leading to a diminished action potential upstroke during phase 0.Furthermore,the study of human tissue demonstrates an inverse expression of sodium channel isoforms;reduction of Na_v1.5 and increase of Na_v1.8 in both heart failure and ventricular hypertrophy.This strongly suggests that the expression of voltage-gated sodium channels play a crucial role in the development of arrhythmias in the diseased heart.Targeting aberrant sodium currents has led to novel therapeutic approaches in tackling AF and continues to be an area of emerging research.This review will explore how voltage-gated sodium channels may predispose the elderly heart to AF through the examination of laboratory and clinical based evidence. | Emmanuel Isaac Stephanie M Cooper Sandra A Jones Mahmoud Loubani | 2020 | World Journal of Cardiology2020，12，4： | 3 |
| 9 | Global land cover mapping from MODIS: algorithms and early results显示文摘 | M.A Friedl D.K McIver J.C.F Hodges X.Y Zhang D Muchoney A.H Strahler C.E Woodcock S Gopal A Schneider A Cooper A Baccini F Gao C Schaaf | 2002 | Remote Sensing of Environment2002，，1： | 2 |
| 10 | Some models for estimating technical and scale inefficiency in data envelopment analysis显示文摘 | BANKER R D CHARMES A COOPER W W | 1984 | Management Science1984，32，： | 2 |
| 11 | The safety of tenofovir disoproxil fumarate for the treatment of HIV infection in adults: the first 4 years显示文摘 | Mark R Nelson Christine Katlama Julio S Montaner David A Cooper Brian Gazzard Bonaventura Clotet Adriano Lazzarin Knud Schewe Joep Lange Christina Wyatt Sue Curtis Shan-Shan Chen Stephen Smith Norbert Bischofberger James F Rooney | 2007 | AIDS2007，，10： | 2 |
| 12 | 【特刊综述】雄激素和前列腺疾病显示文摘越来越多的文献认同睾酮治疗在性腺机能低下患者中具有促合成代谢作用。而关于老年男性使用外源性雄激素的风险和其对前列腺潜在副作用的研究数据仍然匮乏。老年和性腺机能低下男性接受睾酮治疗是否会加重下尿路症状或加剧、揭露,甚至刺激前列腺癌发展,这一问题使采用睾酮治疗的热情有所减缓,与此同时前列腺疾病被视作睾酮治疗的相对禁忌。雄激素对于前列腺的发育和维护是必要的。无论如何,流行病学研究并没有一致地发现内源性血清雄激素浓度与前列腺疾病风险之间存在正相关。虽然最新研究显示5α还原酶抑制剂降低了患低级别前列腺癌的风险,说明抑制雄激素代谢有利于前列腺健康,但是对于高级别前列腺癌并没有类似作用,因此对这些药物化学预防的真正临床效益提出了质疑。鉴于缺乏大样本随机试验,很难了解如何最好地研究雄激素和前列腺疾病发展之间的关系。越来越多研究质疑雄激素在血清中的变化与其在前列腺激素环境中的变化有类似效应或者改变腺体内雄激素的调节过程。需要长期的干预性研究来真正证实雄激素对前列腺组织和疾病风险的操控。然而,现有数据认为恢复血清雄激素至生理水平并不会触发前列腺疾病。 | Lori A Cooper Stephanie T Page | 2014 | Asian Journal of Andrology2014，16，2： | 2 |
| 13 | Obesity in adults with Down syndrome: a ease-control study显示文摘 | Melville C A Cooper S A Grother C W | 2005 | Journal of Intellectual Disability Research2005，49，2： | 1 |
| 14 | Cuticle-degrading enzymes of entomopathogenic fungi :Regulation of productionof chitinolytic enzymes显示文摘 | STLEGER RJ COOPER R M CHARNLEY A K | 1986 | Gen Microbio1986，132，： | 1 |
| 15 | More objectives tools for the integration of postural comfort in automobile seat design显示文摘 | Judic J M Cooper J A Truchot P | 1993 | SAE Paper 9301131993，，： | 1 |
| 16 | Tall fescue genomic SSR markers:development and transferability across multiple grass species 显示文摘 | SAHA M C COOPER J D ROUF MIAN M A | 2006 | Theor Appl Genet2006，113，： | 1 |
| 17 | Foundation of data envelopment analysis for Pareto-Koopmans efficient empirical production functions 显示文摘 | Charnes A Cooper W W Golany B | 1985 | Journal of Econometrics1985，，1： | 1 |
| 18 | Avian adipose lipoprotein lipase: cDNA sequence and reciprocal regulation of mRNA levels in adipose and heart显示文摘 | Cooper D A Stein J C Strieleman P J | 1989 | Biochim Biophys Acta1989，1008，1： | 1 |
| 19 | Measuring the efficiency of decision making units显示文摘 | Charnes A Cooper W W Rhodes E | 1978 | European Journal of Operational Research1978，2，6： | 1 |
| 20 | The influence of electron irradiation on electron holography of focused ion beam milled GaAs p-n junctions 显示文摘 | Cooper D Twitchett-Harrison A C Midgley P A | 2007 | J Appl Phys2007，101，09： | 1 |
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