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001-es BibID:	BIBFORM068608
035-os BibID:	(cikkazonosító)9795271 (WOS)000402835500001 (Scopus)85021663462
Első szerző:	Hudák Renáta
Cím:	The phosphatase inhibitor calyculin-A impairs clot retraction, platelet activation and thrombin generation / Hudák Renáta, Vincze János, Csernoch László, Bekéné Debreceni Ildikó, Oláh Tamás, Erdődi Ferenc, Kenneth J. Clemetson, Kappelmayer János
Dátum:	2017
ISSN:	2314-6133 2314-6141
Megjegyzések:	The aim of this study was to investigate the effect of the serine/threonine protein phosphatase inhibitor, calyculin-A (CLA) on clot formation and on the procoagulant activity of human platelets. Platelet rich plasma (PRP) samples were preincubated with buffer or CLA and subsequently platelets were activated by the protease-activated receptor 1 (PAR-1) activator, thrombin-receptor activating peptide (TRAP). Clot retraction was detected by observing clot morphology up to 1 hour, phosphatidylserine (PS)-expression was studied by flow cytometry and thrombin generation was measured by a fluorimetric assay. For the intracellular Ca2+ assay, platelets were loaded with calcium-indicator dyes and the measurements were carried out using a ratiometric method with real-time confocal microscopy. CLA preincubation inhibited clot retraction, PS-expression and thrombin formation. TRAP activation elicited Ca2+ response and PS-expression in a subset of platelets. The activated PRP displayed significantly faster and enhanced thrombin generation compared to non-activated samples. CLA pretreatment abrogated PS-exposure and clot retraction also in TRAP-activated samples. As a consequence of the inhibitory effect on calcium elevation and PS-expression, CLA significantly downregulated thrombin generation in PRP. Our results show that CLA-pretreatment may be a useful tool to investigate platelet activation mechanisms that contribute to clot formation and thrombin generation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk phosphatases calyculin-A phosphatidylserine thrombin generation
Megjelenés:	Biomed Research International. - 2017 (2017), p. 1-10. -
További szerzők:	Vincze János (1988-) (orvos) Csernoch László (1961-) (élettanász) Bekéné Debreceni Ildikó (1970-) (biológus) Oláh Tamás (1983-) (élettanász) Erdődi Ferenc (1953-) (biokémikus) Clemetson, Kenneth J. Kappelmayer János (1960-) (laboratóriumi szakorvos)
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM054351
Első szerző:	Kappelmayer János (laboratóriumi szakorvos)
Cím:	Distinct effects of Re- and S-forms of LPS on modulating platelet activation / J. Kappelmayer, I. Beke Debreceni, A. Vida, P. Antal-Szalmás, K. J. Clemetson, B. Nagy Jr.
Dátum:	2013
ISSN:	1538-7933
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Journal of Thrombosis and Haemostasis. - 11 : 4 (2013), p. 775-778. -
További szerzők:	Bekéné Debreceni Ildikó (1970-) (biológus) Vida András (1979-) (molekuláris biológus, genetikus) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos) Clemetson, Kenneth J. Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM028396
Első szerző:	Nagy Béla Jr. (labordiagnosztikai szakorvos)
Cím:	Potential therapeutic targeting of platelet-mediated cellular interactions in atherosclerosis and inflammation / B. Nagy Jr., K. Miszti-Blasius, A. Kerényi, K. J. Clemetson, J. Kappelmayer
Dátum:	2012
ISSN:	0929-8673
Megjegyzések:	Cellular interactions among platelets, leukocytes and endothelial cells are considered as a major cause of inflammation and atherosclerosis in many diseases. Via exposed surface receptors and released soluble substances, activated platelets play a crucial role in the initiation of inflammatory processes, resulting in endothelial injury and leading to formation of atherosclerotic plaque with possible thrombotic complications. Classic anti-platelet treatments (e.g. cyclooxygenase inhibitor or ADP-receptor antagonist) have favorable effects in patients with vascular diseases, but they also have several limitations such as increased bleeding risk or non-responsiveness. Thus, the need and opportunities for developing novel therapeutic inhibitors for platelet-mediated events are obvious. Animal and (pre)clinical human studies have suggested that some recently produced specific antagonists of P-selectin from α-granules, as well as its main ligand/receptor P-selectin Glycoprotein Ligand-1, the two major platelet chemokines CXCL4 and CCL5, as well as CD40L, may be considered potential new candidates in the treatment of atherogenesis and inflammation. In this review, we summarize the pathophysiological roles of these effectors in platelet activation and acute or chronic inflammation, and discuss the latest findings on promising antagonistic agents in basic and clinical studies in the prevention of platelet-mediated cellular interaction.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Molekuláris Medicina atherosclerosis CD40L chemokine endothelial cell inflammation leukocyte platelet P-selectin
Megjelenés:	Current Medicinal Chemistry. - 19 : 4 (2012), p. 518-531. -
További szerzők:	Miszti-Blasius Kornél (1977-) (laboratóriumi szakorvos) Kerényi Adrienne (1970-) (laboratóriumi szakorvos) Clemetson, Kenneth J. Kappelmayer János (1960-) (laboratóriumi szakorvos)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Celluláris hematológia - immunológia OTKA T75199 OTKA
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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