Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of heparin therapy after subcutaneous injection of Common Brown Snake (Pseudonaja textilis) venom was studied in anaesthetised, mechanically ventilated dogs. Intravenous heparin (100 U/kg), administered fifteen minutes after envenomation, neither prevented nor hastened the recovery from cardiovascular depression and coagulopathy observed after venom administration. Heparin therapy is not recommended for the treatment of established human envenomation.
 ...
PMID:The efficacy of heparin in the treatment of common brown snake (Pseudonaja textilis) envenomation. 160 38

Heparin blocks the phorbol ester-induced progression of nontransformed cells through the G0/G1 phase (Wright, T.C., L.A. Pukac, J.J. Castellot, M.J. Karnovsky, R.A. Levine, H.-Y. Kim-Park, and J. Campisi. 1989. Proc. Natl. Acad. Sci. USA. 86: 3199-3203) or G1 to S phase (Reilly, C. F., M. S. Kindy, K. E. Brown, R. D. Rosenberg, and G. E Sonenshein. 1989. J. Biol. Chem. 264:6990-6995) of the cell cycle. Cell cycle arrest was associated with decreased levels of stage-specific mRNAs suggesting transcriptional regulation of cell growth. In the present report, we show that heparin selectively repressed TPA-inducible AP-1-mediated gene expression. Heparin-induced trans-repression was observed in primary vascular smooth muscle cells, as well as in the transformed HeLa cell line and in nondifferentiated F9 teratocarcinoma cells. Inhibition of AP-1-mediated trans-activation occurred with heparin and pentosan polysulfate but not with chondroitin sulfate A or C. Heparin-binding peptides or heparitinase I addition to nuclear lysates of heparin-treated cells allowed enhanced recovery of endogenous AP-1-specific DNA binding activity. We propose a model in which nuclear glycosaminoglycans play a trans-regulatory role in altering the patterns of inducible gene expression.
 ...
PMID:Trans-repressor activity of nuclear glycosaminoglycans on Fos and Jun/AP-1 oncoprotein-mediated transcription. 173 Jul 47

This study investigated the reaction of heparin cofactor II (HCII) with stimulated polymorphonuclear leukocytes (PMN). We have expanded upon previous studies showing that HCII can be degraded by stimulated PMN (Sie, P., Dupouy, D., Dol, F., and Boneu, B., Thromb. Res. 47, 657-664, 1987), and that chemotactic activity is produced when HCII is partially proteolyzed with purified leukocyte elastase or cathepsin G (Hoffman, M., Pratt, C.W., Brown, R.L., and Church, F.C., Blood, 73, 1682-1695, 1989). We found that HCII was proteolyzed by stimulated PMN, generating peptides with chemotactic activity. Both proteolysis and generation of chemotactic activity were inhibited by a specific leukocyte elastase inhibitor and by more general proteinase inhibitors. Leukocyte elastase activity was lost upon addition of either inhibitor. Heparin and dermatan sulfate altered the pattern of proteolysis. Our results suggest that HCII may be involved not only in functions related to thrombin inhibition but also in regulating acute inflammation.
 ...
PMID:Production of chemotactic peptides by neutrophil degradation of heparin cofactor II. 230 Sep 26

Heparin compounds are a complex mixture of mucopolysaccharides that, in addition to their anticoagulant properties, have immunosuppressive activities and affect the reparative aspects of the response to arterial injury. Heparin inhibits smooth muscle cell migration and proliferation and can alter the accumulation of the components of the extracellular matrix after arterial injury. Heparin also interacts specifically with the endothelium. Our hypothesis was that if heparin compounds do affect the immune system, coagulation, smooth muscle cell proliferation, and the endothelium, then heparin combined with cyclosporine should improve allograft survival, reduce rejection, and prevent accelerated graft coronary disease. Low molecular-weight heparins are derived from the larger molecular-weight unfractionated heparin. We chose to use low molecular-weight heparins because of their longer half-life, better bioavailability, and decreased incidence of induced thrombocytopenia and bleeding. With a rat intraabdominal heterotopic model of heart transplantation (Lewis-Brown Norway to Lewis), low molecular-weight heparin in combination with a low dose of cyclosporine (0.5 mg/kg/day) significantly improved allograft survival compared to controls and either low molecular-weight heparin or cyclosporine alone. Histologically, smooth muscle cells are an important cellular component of the lesions of accelerated graft coronary disease. In comparison to animals treated with cyclosporine alone (2 mg/kg/day), the addition of low molecular-weight heparin to cyclosporine (2 mg/kg/day) reduced the frequency and the severity of accelerated graft coronary disease and the extent of parenchymal rejection.
 ...
PMID:A reduction in accelerated graft coronary disease and an improvement in cardiac allograft survival using low molecular weight heparin in combination with cyclosporine. 839 35