يعرض 1 - 20 نتائج من 60 نتيجة بحث عن '"Kelley, William J"', وقت الاستعلام: 0.56s تنقيح النتائج
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    المساهمون: National Institutes of Health, National Heart, Lung, and Blood Institute, National Institute of General Medical Sciences, American Heart Association

    المصدر: Science Advances ; volume 7, issue 17 ; ISSN 2375-2548

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    المساهمون: National Science Foundation Graduate Research Fellowship Program, University of Michigan’s Postdoctoral Fellowship, NIH

    المصدر: Acta Biomaterialia ; volume 79, page 283-293 ; ISSN 1742-7061

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    وصف الملف: application/pdf

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    مصطلحات موضوعية: Rheumatology, Health Sciences

    وصف الملف: application/pdf

    Relation: Sule, Gautam; Kelley, William J.; Gockman, Kelsey; Yalavarthi, Srilakshmi; Vreede, Andrew P.; Banka, Alison L.; Bockenstedt, Paula L.; Eniola‐adefeso, Omolola; Knight, Jason S. (2020). "Increased Adhesive Potential of Antiphospholipid Syndrome Neutrophils Mediated by β2 Integrin Macâ 1." Arthritis & Rheumatology 72(1): 114-124.; https://hdl.handle.net/2027.42/153125; Arthritis & Rheumatology; Fadlon E, Vordermeier S, Pearson TC, Mireâ Sluis AR, Dumonde DC, Phillips J, et al. Blood polymorphonuclear leukocytes from the majority of sickle cell patients in the crisis phase of the disease show enhanced adhesion to vascular endothelium and increased expression of CD64. Blood 1998; 91: 266 â 74.; Libby P, Lichtman AH, Hansson GK. Immune effector mechanisms implicated in atherosclerosis: from mice to humans. Immunity 2013; 38: 1092 â 104.; Doring Y, Drechsler M, Soehnlein O, Weber C. Neutrophils in atherosclerosis: from mice to man. Arterioscler Thromb Vasc Biol 2015; 35: 288 â 95.; Jickling GC, Liu D, Ander BP, Stamova B, Zhan X, Sharp FR. Targeting neutrophils in ischemic stroke: translational insights from experimental studies. J Cereb Blood Flow Metab 2015; 35: 888 â 901.; Meisel SR, Shapiro H, Radnay J, Neuman Y, Khaskia AR, Gruener N, et al. Increased expression of neutrophil and monocyte adhesion molecules LFAâ 1 and Macâ 1 and their ligand ICAMâ 1 and VLAâ 4 throughout the acute phase of myocardial infarction: possible implications for leukocyte aggregation and microvascular plugging. J Am Coll Cardiol 1998; 31: 120 â 5.; Han L, Shen X, Pan L, Lin S, Liu X, Deng Y, et al. Aminobenzoic acid hydrazide, a myeloperoxidase inhibitor, alters the adhesive properties of neutrophils isolated from acute myocardial infarction patients. Heart Vessels 2012; 27: 468 â 74.; Tsai NW, Chang WN, Shaw CF, Jan CR, Huang CR, Chen SD, et al. The value of leukocyte adhesion molecules in patients after ischemic stroke. J Neurol 2009; 256: 1296 â 302.; Zapponi KC, Mazetto BM, Bittar LF, Barnabé A, Santiagoâ Bassora FD, De Paula EV, et al. Increased adhesive properties of neutrophils and inflammatory markers in venous thromboembolism patients with residual vein occlusion and high Dâ dimer levels. Thromb Res 2014; 133: 736 â 42.; Lard LR, Mul FP, de Haas M, Roos D, Duits AJ. Neutrophil activation in sickle cell disease. J Leukoc Biol 1999; 66: 411 â 5.; Stocks SC, Ruchaudâ Sparagano MH, Kerr MA, Grunert F, Haslett C, Dransfield I. CD66: role in the regulation of neutrophil effector function. Eur J Immunol 1996; 26: 2924 â 32.; Skubitz KM, Campbell KD, Skubitz AP. CD66a, CD66b, CD66c, and CD66d each independently stimulate neutrophils. J Leukoc Biol 1996; 60: 106 â 17.; Skubitz KM, Skubitz AP. Two new synthetic peptides from the Nâ domain of CEACAM1 (CD66a) stimulate neutrophil adhesion to endothelial cells. Biopolymers 2011; 96: 25 â 31.; Skubitz KM, Skubitz AP. Interdependency of CEACAMâ 1, â 3, â 6, and â 8 induced human neutrophil adhesion to endothelial cells. J Transl Med 2008; 6: 78.; Ludewig P, Sedlacik J, Gelderblom M, Bernreuther C, Korkusuz Y, Wagener C, et al. Carcinoembryonic antigenâ related cell adhesion molecule 1 inhibits MMPâ 9â mediated bloodâ brainâ barrier breakdown in a mouse model for ischemic stroke. Circ Res 2013; 113: 1013 â 22.; Sobey CG, Drummond GR. CEACAM1: an adhesion molecule that limits bloodâ brain barrier damage by neutrophils after stroke [editorial]. Circ Res 2013; 113: 952 â 3.; Wong C, Liu Y, Yip J, Chand R, Wee JL, Oates L, et al. CEACAM1 negatively regulates plateletâ collagen interactions and thrombus growth in vitro and in vivo. Blood 2009; 113: 1818 â 28.; Khan SQ, Khan I, Gupta V. CD11b activity modulates pathogenesis of lupus nephritis. Front Med (Lausanne) 2018; 5: 52.; Rosetti F, Mayadas TN. The many faces of Macâ 1 in autoimmune disease. Immunol Rev 2016; 269: 175 â 93.; Tang T, Rosenkranz A, Assmann KJ, Goodman MJ, Gutierrezâ Ramos JC, Carroll MC, et al. A role for Macâ 1 (CDIIb/CD18) in immune complexâ stimulated neutrophil function in vivo: Macâ 1 deficiency abrogates sustained Fcγ receptorâ dependent neutrophil adhesion and complementâ dependent proteinuria in acute glomerulonephritis. J Exp Med 1997; 186: 1853 â 63.; Kevil CG, Hicks MJ, He X, Zhang J, Ballantyne CM, Raman C, et al. Loss of LFAâ 1, but not Macâ 1, protects MRL/MpJâ Fas(lpr) mice from autoimmune disease. Am J Pathol 2004; 165: 609 â 16.; Wolf D, Antoâ Michel N, Blankenbach H, Wiedemann A, Buscher K, Hohmann JD, et al. A ligandâ specific blockade of the integrin Macâ 1 selectively targets pathologic inflammation while maintaining protective hostâ defense. Nat Commun 2018; 9: 525.; Maiguel D, Faridi MH, Wei C, Kuwano Y, Balla KM, Hernandez D, et al. Small moleculeâ mediated activation of the integrin CD11b/CD18 reduces inflammatory disease. Sci Signal 2011; 4: ra57.; Faridi MH, Khan SQ, Zhao W, Lee HW, Altintas MM, Zhang K, et al. CD11b activation suppresses TLRâ dependent inflammation and autoimmunity in systemic lupus erythematosus. J Clin Invest 2017; 127: 1271 â 83.; Miyakis S, Lockshin MD, Atsumi T, Branch DW, Brey RL, Cervera R, et al. International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost 2006; 4: 295 â 306.; Garcia D, Erkan D. Diagnosis and management of the antiphospholipid syndrome. N Engl J Med 2018; 378: 2010 â 21.; Abreu MM, Danowski A, Wahl DG, Amigo MC, Tektonidou M, Pacheco MS, et al. The relevance of â nonâ criteriaâ clinical manifestations of antiphospholipid syndrome: 14th International Congress on Antiphospholipid Antibodies Technical Task Force report on antiphospholipid syndrome clinical features. Autoimmun Rev 2015; 14: 401 â 14.; Rao AN, Kazzaz NM, Knight JS. Do neutrophil extracellular traps contribute to the heightened risk of thrombosis in inflammatory diseases? World J Cardiol 2015; 7: 829 â 42.; Yalavarthi S, Gould TJ, Rao AN, Mazza LF, Morris AE, Núñezâ à lvarez C, et al. Release of neutrophil extracellular traps by neutrophils stimulated with antiphospholipid antibodies: a newly identified mechanism of thrombosis in the antiphospholipid syndrome. Arthritis Rheumatol 2015; 67: 2990 â 3003.; Leffler J, Stojanovich L, Shoenfeld Y, Bogdanovic G, Hesselstrand R, Blom AM. Degradation of neutrophil extracellular traps is decreased in patients with antiphospholipid syndrome. Clin Exp Rheumatol 2014; 32: 66 â 70.; Meng H, Yalavarthi S, Kanthi Y, Mazza LF, Elfline MA, Luke CE, et al. In vivo role of neutrophil extracellular traps in antiphospholipid antibodyâ mediated venous thrombosis. Arthritis Rheumatol 2017; 69: 655 â 67.; Ali RA, Gandhi AA, Meng H, Yalavarthi S, Vreede AP, Estes SK, et al. Adenosine receptor agonism protects against NETosis and thrombosis in antiphospholipid syndrome. Nat Commun 2019; 10: 1916.; Knight JS, Meng H, Coit P, Yalavarthi S, Sule G, Gandhi AA, et al. Activated signature of antiphospholipid syndrome neutrophils reveals potential therapeutic target. JCI Insight 2017; 2: 93897.; Pierangeli SS, Vegaâ Ostertag ME, Raschi E, Liu X, Romayâ Penabad Z, De Micheli V, et al. Tollâ like receptor and antiphospholipid mediated thrombosis: in vivo studies. Ann Rheum Dis 2007; 66: 1327 â 33.; Pierangeli SS, Coldenâ Stanfield M, Liu X, Barker JH, Anderson GL, Harris EN. Antiphospholipid antibodies from antiphospholipid syndrome patients activate endothelial cells in vitro and in vivo. Circulation 1999; 99: 1997 â 2002.; Pierangeli SS, Espinola RG, Liu X, Harris EN. Thrombogenic effects of antiphospholipid antibodies are mediated by intercellular cell adhesion moleculeâ 1, vascular cell adhesion moleculeâ 1, and Pâ selectin. Circ Res 2001; 88: 245 â 50.; Espinola RG, Liu X, Coldenâ Stanfield M, Hall J, Harris EN, Pierangeli SS. Eâ selectin mediates pathogenic effects of antiphospholipid antibodies. J Thromb Haemost 2003; 1: 843 â 8.; Ramesh S, Morrell CN, Tarango C, Thomas GD, Yuhanna IS, Girardi G, et al. Antiphospholipid antibodies promote leukocyteâ endothelial cell adhesion and thrombosis in mice by antagonizing eNOS via β2GPI and apoER2. J Clin Invest 2011; 121: 120 â 31.; Simantov R, LaSala JM, Lo SK, Gharavi AE, Sammaritano LR, Salmon JE, et al. Activation of cultured vascular endothelial cells by antiphospholipid antibodies. J Clin Invest 1995; 96: 2211 â 9.; Del Papa N, Guidali L, Sala A, Buccellati C, Khamashta MA, Ichikawa K, et al. Endothelial cells as target for antiphospholipid antibodies. Human polyclonal and monoclonal antiâ β 2 â glycoprotein I antibodies react in vitro with endothelial cells through adherent β 2 â glycoprotein I and induce endothelial activation. Arthritis Rheum 1997; 40: 551 â 61.; Dunoyerâ Geindre S, de Moerloose P, Galveâ de Rochemonteix B, Reber G, Kruithof EK. NF kB is an essential intermediate in the activation of endothelial cells by antiâ β(2)â glycoprotein 1 antibodies. Thromb Haemost 2002; 88: 851 â 7.; Vegaâ Ostertag M, Casper K, Swerlick R, Ferrara D, Harris EN, Pierangeli SS. Involvement of p38 MAPK in the upâ regulation of tissue factor on endothelial cells by antiphospholipid antibodies. Arthritis Rheum 2005; 52: 1545 â 54.; Allen KL, Hamik A, Jain MK, McCrae KR. Endothelial cell activation by antiphospholipid antibodies is modulated by Kruppelâ like transcription factors. Blood 2011; 117: 6383 â 91.; Hochberg MC, for the Diagnostic and Therapeutic Criteria Committee of the American College of Rheumatology. Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus [letter]. 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    المساهمون: University of Michigan, National Heart, Lung, and Blood Institute, Division of Graduate Education

    المصدر: ACS Biomaterials Science & Engineering ; volume 5, issue 12, page 6530-6540 ; ISSN 2373-9878 2373-9878

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