Zobrazeno 1 - 10
of 91
pro vyhledávání: '"H B, Hechtman"'
Autor:
J. M. Klausner, S. Abu-Abid, J. S. Alexander, R. Hanshke-Mineau, G. Goldman, N. Morel, C. R. Valeri, D. Shepro, H. B. Hechtman
Publikováno v:
Mediators of Inflammation, Vol 3, Iss 2, Pp 149-153 (1994)
The study tests the role of thromboxane in modulating microvascular permeability in vitro. Cultured monolayers of bovine aortic endothelial cells were challenged with the thromboxane (Tx) mimic U46619. This led to disassembly of actin microfilaments,
Externí odkaz:
https://doaj.org/article/55e98f69a4634e508b7d2591ae691b2d
Publikováno v:
The Journal of Immunology. 149:1723-1728
We examined the role of C activation in ischemia reperfusion injury by inhibiting C activation in a rat model of mesenteric arterial occlusion. In anesthetized rats, 60 min of mesenteric arterial occlusion was followed by 3 h of reperfusion. PBS alon
Publikováno v:
The Journal of Immunology. 145:1906-1911
Neutrophils and eicosanoid chemoattractants are centrally involved with ischemia-reperfusion (I/R) injury. The CD 18 complex of adhesive glycoproteins, readily up-regulated by chemoattractants in vitro, is required for polymorphonuclear leukocyte (PM
Publikováno v:
The Annals of thoracic surgery. 72(5)
Shed nonwashed blood and shed washed red blood cells (RBC) are being used as alternatives to allogeneic liquid-preserved RBC for patients during thoracic and cardiovascular surgical procedures.Mongrel dogs were bled a volume of blood into the abdomin
Publikováno v:
Journal of cellular biochemistry. 75(1)
Vascular pathologies induced by ischemia/reperfusion involve the production of reactive oxygen species (ROS) that in part cause tissue injury. The production of ROS that occurs upon reperfusion activates specific second messenger pathways. In diabeti
Publikováno v:
Surgery. 126(2)
The dependence of intestinal ischemia-reperfusion injury on the classical complement pathway has been shown with the complement antagonist (sCR1) and complement-specific knockout mice. Using C5 deficient mice, we show that the membrane attack complex
Publikováno v:
Journal of cellular biochemistry. 68(4)
Hypoxia/reoxygenation injury to cultured endothelial cells results in cytoskeletal rearrangement and second messenger activation related to increased monolayer junctional permeability. Cytoskeletal rearrangement by reactive oxygen species may be rela
Publikováno v:
Journal of cellular physiology. 172(3)
Hypoxia/reoxygenation injury in vitro causes endothelial cell cytoskeletal rearrangement that is related to increased monolayer permeability. Nonmuscle filamin (ABP-280) promotes orthogonal branching of F-actin and links microfilaments to membrane gl
Publikováno v:
Journal of cellular biochemistry. 62(3)
Endothelial cell (EC) cytoskeletal proteins are one of the earliest primary targets of second messenger cascades generated in response to inflammatory agonists. Actin binding proteins, by modulating actin gelation-solation state and membrane-cytoskel