Zobrazeno 1 - 10
of 61
pro vyhledávání: '"M. J. Broekman"'
Publikováno v:
Journal of Lipid Research, Vol 31, Iss 5, Pp 801-810 (1990)
Dietary marine n-3 polyunsaturated fatty acids have demonstrated an antiinflammatory potential in epidemiologic and intervention studies in humans. Proposed mechanisms, involving only leukocytes, fall short of explaining this potential completely. En
Externí odkaz:
https://doaj.org/article/d3145e738c6146a9b589ac2e89f0bb25
Publikováno v:
Journal of Lipid Research, Vol 30, Iss 12, Pp 1925-1932 (1989)
Albumin is a major determinant of eicosanoid formation, affecting autacoids important in cell-cell interactions. We delineated three mechanisms by which albumin controlled platelet eicosanoid formation: 1) Albumin diverted free arachidonate toward 12
Externí odkaz:
https://doaj.org/article/c202790560bb4412b02ac6d149720ece
Autor:
M J Broekman
Publikováno v:
Journal of Lipid Research, Vol 27, Iss 8, Pp 884-891 (1988)
Thrombin-induced changes in arachidonate content of platelet phospholipids were quantitated to establish the ultimate origins of this eicosanoid precursor. Fifteen seconds following thrombin addition (15 U/5 X 10(9) platelets), phosphatidylcholine lo
Externí odkaz:
https://doaj.org/article/3ff8a7f0c969457599040eddc19c67cf
Autor:
Richard B. Gayle, T. N. Alyonycheva, Aaron J. Marcus, M. A. Schoenborn, Charles R. Maliszewski, Joan H.F. Drosopoulos, M J Broekman, K. A. Schooley, L. B. Safier, Katherine A. Hajjar, David N. Posnett, Naziba Islam
Publikováno v:
Journal of Clinical Investigation. 99:1351-1360
We previously demonstrated that when platelets are in motion and in proximity to endothelial cells, they become unresponsive to agonists (Marcus, A.J., L.B. Safier, K.A. Hajjar, H.L. Ullman, N. Islam, M.J. Broekman, and A.M. Eiroa. 1991. J. Clin. Inv
Autor:
L. B. Safier, C von Schacky, W. E. Kaminski, Aaron J. Marcus, E. Jendraschak, M. J. Broekman, N Islam, J. H. Fliessbach, Katherine A. Hajjar, Roy L. Silverstein
Publikováno v:
Thrombosis and Haemostasis. 74:213-217
Platelet activation as a result of vascular injury provokes endothelial cells to respond in a manner which limits or reverses the occlusive consequences of platelet accumulation. If the agonistic forces are strong, platelet accumulation is irreversib
Autor:
M J Broekman, Jerold Brett, M C Oz, Hui Liao, Yoshifumi Naka, S Koga, Z. Taha, Aaron J. Marcus, Paul J. Cannon, David J. Pinsky
Publikováno v:
Journal of Clinical Investigation. 93:2291-2297
Nitric oxide (NO) is a novel biologic messenger with diverse effects but its role in organ transplantation remains poorly understood. Using a porphyrinic microsensor, the first direct measurements of coronary vascular and endocardial NO production we
Autor:
L B Safier, Justo Aznar, Aaron J. Marcus, N Islam, J. Valles, M T Santos, M J Broekman, H L Ullman
Publikováno v:
Journal of Clinical Investigation. 92:1357-1365
Unstimulated neutrophils inhibited activation and recruitment of thrombin- or collagen-stimulated platelets in an agonist-specific manner. This occurred under conditions of close physical cell-cell contact, although biochemical adhesion between the c
Autor:
N Islam, L B Safier, M J Broekman, Aaron J. Marcus, A M Eiroa, H L Ullman, Katherine A. Hajjar
Publikováno v:
Journal of Clinical Investigation. 88:1690-1696
We previously reported that platelets become unresponsive to agonists when stimulated in combined suspension with aspirin-treated human umbilical vein endothelial cells. Inhibition occurred concomitant with metabolism of platelet-derived endoperoxide
Publikováno v:
Blood. 78:1033-1040
To determine a role for endothelium-derived relaxing factor/nitric oxide (EDRF/NO) in regulation of human platelet reactivity by human endothelial cells (EC), we studied combined suspensions of human umbilical vein endothelial cells (HU-VEC, passage
Autor:
L B Safier, Justo Aznar, V Martinez-Sales, Maria-Teresa Santos, Juana Vallés, M J Broekman, Aaron J. Marcus, Manuel Portolés
Publikováno v:
Blood. 78:154-162
Erythrocytes promoted platelet reactivity in a plasma medium, as demonstrated in an in vitro system that independently evaluated the biochemistry of platelet activation and recruitment. The prothrombotic erythrocyte effects were metabolically regulat