Találati lista | Tudóstér

001-es BibID:	BIBFORM031969
Első szerző:	Szendrei Levente
Cím:	Mitochondrial gene expression and ventricular fibrillation in ischemic/reperfused nondiabetic and diabetic myocardium / Szendrei L., Turoczi T., Kovacs P., Vecsernyes M., Das D. K., Tosaki A.
Dátum:	2002
Megjegyzések:	We investigated the mitochondrial gene expression related to cardiac function and ventricular fibrillation (VF) in ischemic/reperfused nondiabetic and diabetic myocardium. To identify potentially more specific gene responses we performed subtractive screening, Northern blotting, and reverse transcription-polymerase chain reaction (RT-PCR) of mitochondrial genes expressed after 30 min ischemia followed by 120 min reperfusion in isolated rat hearts that showed VF or did not show VF. Cytochrome oxidase B subunit III (COXBIII) and ATP synthase subunit 6, studied and selected out of 40 mitochondrial genes by subtractive screening, showed an expression after 30 min ischemia (no VF was recorded) in both nondiabetic and diabetic subjects. Upon reperfusion, the down-regulation of these genes was only observed in fibrillated hearts. Such a reduction in signal intensity was not seen in nonfibrillated myocardium. In additional studies, nondiabetic and diabetic hearts, without the ischemia/reperfusion protocol, were subjected to electrical fibrillation, and a significant reduction in COXBIII and ATPS6 mRNA signal intensity was observed indicating that VF contributes to the down-regulation of these genes. Cardiac function (heart rate, coronary flow, aortic flow, left ventricular developed pressure) showed no correlation between the up- and down-regulation of these mitochondrial genes in both nondiabetic and diabetic ischemic/reperfused myocardium. Our data suggest that COXBIII and ATPS6 may play a critical role in arrhythmogenesis, and the stimulation of COXBIII and ATPS6 mRNA expression may prevent the development of VF in both nondiabetic and diabetic ischemic/reperfused myocardium
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Biochemical Pharmacology. - 63 : 3 (2002), p. 543-552. -
További szerzők:	Turóczi Tibor (1976-) (molekuláris biológus) Kovács Péter (1939-) (farmakológus) Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Das, Dipak Kumar Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
Borító:
Saját polcon:

001-es BibID:	BIBFORM041945
Első szerző:	Vecsernyés Miklós (gyógyszertechnológus, endokrinológus)
Cím:	The administration of a-melanocyte-stimulating hormone protects the ischemic/reperfused myocardium / Miklos Vecsernyes, Bela Juhasz, Peter Der, Reka Kocsan, Palma Feher, Ildiko Bacskay, Peter Kovacs, Arpad Tosaki
Dátum:	2003
ISSN:	0014-2999
Megjegyzések:	The contribution of alpha-melanocyte-stimulating hormone (alpha-MSH) treatment, an active fragment of adrenocorticotropic hormone (ACTH), to the recovery of postischemic cardiac function, infarct size, the incidence of reperfusion-induced ventricular fibrillation and apoptotic cell death was studied in ischemic/reperfused isolated rat hearts. Rats were subcutaneously injected with 40, 200 and 400 microg/kg of alpha-MSH, and 12 h later, hearts were isolated, perfused and subjected to 30 min of ischemia followed by 120 min of reperfusion. Thus, after 120 min of reperfusion, with the concentration of 200 microg/kg alpha-MSH, coronary flow, aortic flow and left ventricular developed pressure were significantly improved from their control values of 14.6+/-0.6 ml/min, 7.5+/-0.5 ml/min and 9.1+/-0.4 kPa to 20.2+/-0.4 ml/min (p<0.05), 31.5+/-0.9 ml/min (p<0.05) and 15.9+/-0.6 (p<0.05) kPa, respectively. With the doses of 40, 200 and 400 microg/kg of alpha-MSH, infarct size was reduced from its control value of 38+/-5% to 33+/-6% (NS), 17+/-3% (p<0.05) and 19+/-4% (p<0.05), respectively. The reduction in the incidence of reperfusion-induced ventricular fibrillation followed the same pattern. It is reasonable to assume that a reduction in infarct size, in the alpha-MSH-treated myocardium, resulted in a reduction as well in apoptotic cell death. Although we did not specifically study the exact mechanism(s) of alpha-MSH-afforded postischemic protection, we assume that this protection may be related to alpha-MSH-induced corticosterone release and corticosterone-induced de novo protein synthesis, which reflected in the recovery of postischemic cardiac function in isolated hearts. Thus, interventions that are able to increase plasma corticosterone or glucocorticoid release may prevent the development of ischemia/reperfusion-induced damage.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	European Journal of Pharmacology. - 470 : 3 (2003), p. 177-183. -
További szerzők:	Juhász Béla (1978-) (kísérletes farmakológus) Dér Péter Kocsán Réka (1979-) (gyógyszerész) Fehér Pálma (1976-) (gyógyszerész) Bácskay Ildikó (1969-) (gyógyszerész, gyógyszertechnológus) Kovács Péter (1939-) (farmakológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon: