Zobrazeno 1 - 10
of 44
pro vyhledávání: '"L B Safier"'
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
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
Publikováno v:
Circulation. 95:63-68
Background Aspirin effectively reduces the incidence of secondary vascular occlusive events in only 25% of patients. Low-dose aspirin as currently used blocks platelet production of prothrombotic thromboxane A 2 and allows endothelial synthesis of an
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:
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
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
Autor:
J. Valles, Aaron J. Marcus, A M Eiroa, M J Broekman, N Islam, L B Safier, M T Santos, H L Ullman, Justo Aznar
Publikováno v:
Journal of Clinical Investigation. 87:571-580
Erythrocytes are known to influence hemostasis. Bleeding times are prolonged in anemia and corrected by normalizing the hematocrit. We now demonstrate that intact erythrocytes modulate biochemical and functional responsiveness of activated platelets.
Autor:
M. J. Broekman, H. L. Ullman, S Fischer, C von Schacky, L. B. Safier, Aaron J. Marcus, N. Islam
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
Autor:
A J, Marcus, L B, Safier, M J, Broekman, N, Islam, J H, Fliessbach, K A, Hajjar, W E, Kaminski, E, Jendraschak, R L, Silverstein, C, von Schacky
Publikováno v:
Thrombosis and haemostasis. 74(1)
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