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Simvastatin preserves the ischemic-reperfused myocardium in normocholesterolemic rat hearts.
TLDR
Evidence is provided that HMG-CoA reductase inhibitors are potent and effective cardioprotective agents that inhibit leukocyte-endothelial cell interactions and preserve cardiac contractile function and coronary perfusion after myocardial ischemia and reperfusion. Expand
Peroxynitrite inhibits leukocyte-endothelial cell interactions and protects against ischemia-reperfusion injury in rats.
TLDR
It is suggested that the inhibition of P-selectin expression by peroxynitrite is a key mechanism of the modulatory actions of ONOO- on leukocyte-endothelial cell interactions and exert cytoprotective effects in myocardial ischemia-reperfusion injury. Expand
Synergism between platelets and neutrophils in provoking cardiac dysfunction after ischemia and reperfusion: role of selectins.
TLDR
Evidence is provided that platelets and neutrophils act synergistically in provoking postreperfusion cardiac dysfunction and that this may be largely due to cell-to-cell interactions mediated by P-selectin, which may help explain the reperfusion injury phenomenon. Expand
Recombinant soluble P-selectin glycoprotein ligand-1 protects against myocardial ischemic reperfusion injury in cats.
TLDR
The results demonstrate that the administration of a recombinant soluble PSGL-1 reduces myocardial reperfusion injury and preserves vascular endothelial function, which is largely the result of reduced PMN-endothelial cell interactions. Expand
Cardioprotective effects of a novel proteasome inhibitor following ischemia and reperfusion in the isolated perfused rat heart.
TLDR
Evidence is provided that PS-519 is a potent and effective cardioprotective agent that inhibits P-selectin leukocyte-endothelial cell interactions and preserves cardiac contractile function and coronary perfusion following myocardial ischemia and reperfusion. Expand
The role of bacteria in the pathogenesis of inflammatory bowel disease.
TLDR
The response to antitumor necrosis factor treatments suggests that, if relevant at all, MAP is not acting as a conventional pathogen, but there is increased colonization by MAP in CD, and there is evidence that it could have an indirect effect mediated by the suppression of macrophage function. Expand
P‐selectin is up‐regulated in vital organs during murine traumatic shock
TLDR
The findings suggest that severe trauma results in up‐regulation of P‐selectin at the transcriptional level, which is partly controlled by an NF‐κB‐responsive element in the region of the P‐ selectin promoter. Expand
TIME COURSE OF ENDOTHELIAL DYSFUNCTION AND NEUTROPHIL ADHERENCE AND INFILTRATION DURING MURINE TRAUMATIC SHOCK
TLDR
It is suggested that endothelial dysfunction resulting in reduced NO release occurs in the early phase of murine traumatic shock, and that this phenomenon is followed by a time-dependent increase in adhesivity of neutrophils to the vascular endothelium leading to a progressive accumulation of PMNs in injured tissues (e.g., intestine). Expand
Effects of defibrotide on leukocyte-endothelial cell interaction in the rat mesenteric vascular bed: role of P-selectin.
TLDR
The present study confirms the crucial role exerted by nitric oxide in attenuating leukocytes-endothelial cell interaction during various pathophysiological conditions and in vivo administration of defibrotide can reduce leukocyte rolling and adherence in the mesenteric rat microvasculature by attenuating P-selectin expression. Expand
Effects of a metalloproteinase that truncates P-selectin glycoprotein ligand on neutrophil-induced cardiac dysfunction in ischemia/reperfusion.
TLDR
Results provide evidence that neutrophils provoke post-reperfusion cardiac dysfunction, and that this may be largely due to P-selectin-induced adherence of neutrophil to the endothelium. Expand
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