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70篇 您的检索式:作者名="MANES L"
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1Human fetal mesenchymal stem cells differentiate into brown and white adipocytes: a role for ERRα in human UCP1 expression显示文摘我们调查了胎儿的间充质的干细胞(fMSCs ) 的能力区分进棕色、白的 adipocytes 并且比较了很多标记基因和关键规章的因素的表示。我们证明关键 adipocyte 管理者和标记的表示在另外的人、鼠科的 adipocyte 模型在区别期间类似于那,包括 PPAR 纬 2 和 FABP4 的正式就职。尤其是,我们发现 preadipocyte 标记, Pref-1,当这个过程继续,显著地在区别然后衰落早被导致,当他们承诺 adipogenic 系,建议 fMSCs 首先获得 preadipocyte 特征,在他们进成熟 adipocytes 的区别以前。在 adipogenic 正式就职以后,某干细胞孤立区分了进类似于棕色的 adipocytes 和其它进白 adipocytes 的房间。一个的详细调查孤立证明新奇棕色的胖决定的因素 PRDM16 在区别前后两个都被表示。重要地,展出的这些房间提高了基础 UCP-1 表示,它依赖于孤儿的活动原子受体犯错伪,加亮一个新奇角色为犯错在人的棕色的脂肪的伪。因此 fMSCs 代表一在 vitro 有用为人的 adipogenesis 当模特儿,并且提供机会在对 adipocyte 系的承诺以前学习阶段。他们也提供无价的卓见进人的棕色的脂肪的特征。Daniel L Morganstein Pensee Wu Meritxell R Mane Nick M Fisk Roger White Malcolm G Parker 2010Cell Research2010,20,4:5
2A meta-analysis of randomized controlled trials in pulmonary arterial hypertension显示文摘Galie N Manes A Negro L 2009Eur HeartJ2009,30,4:1
3The contributions of lesion laterality and lesion volume to decision-making impairment follwing frontal lobe damage显示文摘Clark L Manes F Antoun N 2003Neuropsychologia2003,41,11:1
4Amera-nanalysis of randomized controlled trials in polmonary hypertension显示文摘Galie N Manes A Negro L 2009Eur Heart J2009,30,:1
5Electrostatic fiber spinning from polymer melts: Ⅰ experimental observations on fiber formation and properties显示文摘Larro L Manely J 1996Modern Plastics1996,73,4:1
6Mammalian alkaline phosphatases are allosteric enzymes 显示文摘HOYLAERTS M F MANES T MILAN J L 1997J Biol Chem1997,272,22:1
7Primary pulmonary hypertension; insights into pathogenesis from epidemiology 显示文摘Galie N Manes A Uguccioni L 1998Chest1998,114,3:1
8Adeno-associated virus is associated with a lower risk of high-grade neoplasia显示文摘Coker A L Liu Y Mane M 2001Exp Mol Pathol2001,70,:1
9Squamous papilloma of the esophagus long term follow up显示文摘MOSCA S MANES G MONACOR et a l 2001J Gastroenterol Hepatol2001,16,8:1
10查看详情显示文摘Matthews D L Campbell E M Ceglio N M Hermes G Kauffman R Koppel L Lee R Manes K Rupert V Slivinsky W Turner R Ze F 0,,:1
11Rapamycin antagonizes TNF induction of VCAM-1 on endothelial cells by inhibiting m TORC2显示文摘Wang C Qin L Manes TD 2014J Exp Med2014,211,3:1
12Not all arrestins are created equal: Therapeutic implications of the functional diversity of the β-arrestins in the heart显示文摘The two ubiquitous, outside the retina, G protein-coupled receptor(GPCR)adapter proteins, β-arrestin-1 and-2(also known as arrestin-2 and-3,respectively), have three major functions in cells: GPCR desensitization, i.e.,receptor decoupling from G-proteins; GPCR internalization via clathrin-coated pits; and signal transduction independently of or in parallel to G-proteins. Bothβ-arrestins are expressed in the heart and regulate a large number of cardiac GPCRs. The latter constitute the single most commonly targeted receptor class by Food and Drug Administration-approved cardiovascular drugs, with about onethird of all currently used in the clinic medications affecting GPCR function.Since β-arrestin-1 and-2 play important roles in signaling and function of several GPCRs, in particular of adrenergic receptors and angiotensin II type 1 receptors,in cardiac myocytes, they have been a major focus of cardiac biology research in recent years. Perhaps the most significant realization coming out of their studies is that these two GPCR adapter proteins, initially thought of as functionally interchangeable, actually exert diametrically opposite effects in the mammalian myocardium. Specifically, the most abundant of the two β-arrestin-1 exerts overall detrimental effects on the heart, such as negative inotropy and promotion of adverse remodeling post-myocardial infarction(MI). In contrast, β-arrestin-2 is overall beneficial for the myocardium, as it has anti-apoptotic and antiinflammatory effects that result in attenuation of post-MI adverse remodeling,while promoting cardiac contractile function. Thus, design of novel cardiac GPCRligands that preferentially activate β-arrestin-2 over β-arrestin-1 has the potential of generating novel cardiovascular therapeutics for heart failure and other heart diseases.Anastasios Lymperopoulos Shelby L Wertz Celina M Pollard Victoria L Desimine Jennifer Maning Katie A McCrink 2019World Journal of Cardiology2019,11,2:1
13Molecular mechanism of uncompetitive inhibition of human placental and germ-cell alkaline phosphatase显示文摘HOYLAERTS M F MANES T MILLAN J L 1992Biochem J1992,286,:1
14Impaired Endothelial Repair Capacity of Early Endothelial Progenitor Cells in Prehypertension: Relation to Endothelial Dysfunction显示文摘Giovanna Giannotti Carola Doerries Pavani S. Mocharla Maja F. Mueller Ferdinand H. Bahlmann Tibor Horvàth Hong Jiang Sajoscha A. Sorrentino Nora Steenken Costantina Manes Mario Marzilli K. Lenhard Rudolph Thomas F. Lüscher Helmut Drexler Ulf Landmesser 2010Hypertension2010,,6:1
15Penile fracture-experience in 56cases显示文摘Koifman L Cavalcanti A G Manes C H 2003Int Braz J Urol2003,29,1:1
16Effect of sulfated beta- cyclodextrin, a water soluble cycloamylose, on the promotion and/ or inhibition of angiogenesis 显示文摘Strauss L Fuenzalida M manes J 2002Pathol Oncol Res2002,8,1:1
17Effective connectivity among the working memory regions during preparation for and during performance of the n-back task显示文摘MANELIS A REDE L M 2014Frontiers in Human Neuroscience2014,8,:1
18Seminoma-derived Nagao isozyme is encoded by a germ-cell alkaline phosphatase gene 显示文摘Millan J L Manes T 1988Proc Natl Acad Sci USA1988,85,:1
19Kinetic characterization of hypophosphatasia mutations with physiological substrates显示文摘Di Mauro S Manes T Hessle L 2002J Bone Miner Res2002,17,8:1
20A meta-analysis of randomized con- trolled trails in pulmonary arterial hypertension 显示文摘Galii N Manes A Negro L 2009Eur Heart J2009,30,4:1
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