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001-es BibID:	BIBFORM010415
Első szerző:	Borbély Attila (kardiológus)
Cím:	Hypophosphorylation of the Stiff N2B titin isoform raises cardiomyocyte resting tension in failing human myocardium / Borbely, A., Falcao-Pires, I., van Heerebeek, L., Hamdani, N., Edes, I., Gavina, C., Leite-Moreira, A. F., Bronzwaer, J. G. F., Papp, Z., van der Velden, J., Stienen, G. J. M., Paulus, W. J.
Dátum:	2009
ISSN:	1524-4571 (Electronic)
Megjegyzések:	High diastolic stiffness of failing myocardium results from interstitial fibrosis and elevated resting tension (F(passive)) of cardiomyocytes. A shift in titin isoform expression from N2BA to N2B isoform, lower overall phosphorylation of titin, and a shift in titin phosphorylation from N2B to N2BA isoform can raise F(passive) of cardiomyocytes. In left ventricular biopsies of heart failure (HF) patients, aortic stenosis (AS) patients, and controls (CON), we therefore related F(passive) of isolated cardiomyocytes to expression of titin isoforms and to phosphorylation of titin and titin isoforms. Biopsies were procured by transvascular technique (44 HF, 3 CON), perioperatively (25 AS, 4 CON), or from explanted hearts (4 HF, 8 CON). None had coronary artery disease. Isolated, permeabilized cardiomyocytes were stretched to 2.2-microm sarcomere length to measure F(passive). Expression and phosphorylation of titin isoforms were analyzed using gel electrophoresis with ProQ Diamond and SYPRO Ruby stains and reported as ratio of titin (N2BA/N2B) or of phosphorylated titin (P-N2BA/P-N2B) isoforms. F(passive) was higher in HF (6.1+/-0.4 kN/m(2)) than in CON (2.3+/-0.3 kN/m(2); P<0.01) or in AS (2.2+/-0.2 kN/m(2); P<0.001). Titin isoform expression differed between HF (N2BA/N2B=0.73+/-0.06) and CON (N2BA/N2B=0.39+/-0.05; P<0.001) and was comparable in HF and AS (N2BA/N2B=0.59+/-0.06). Overall titin phosphorylation was also comparable in HF and AS, but relative phosphorylation of the stiff N2B titin isoform was significantly lower in HF (P-N2BA/P-N2B=0.77+/-0.05) than in AS (P-N2BA/P-N2B=0.54+/-0.05; P<0.01). Relative hypophosphorylation of the stiff N2B titin isoform is a novel mechanism responsible for raised F(passive) of human HF cardiomyocytes.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Aged Biopsy Elasticity Female Heart Failure Humans Male Middle Aged Muscle Proteins Myocardium Myocytes, Cardiac Phosphorylation Protein Isoforms Protein Kinases Sarcomeres
Megjelenés:	Circulation Research. - 104 : 6 (2009), p. 780-786. -
További szerzők:	Falcao-Pires, Ines Heerebeek, Loek, van Hamdani, Nazha Édes István (1952-) (kardiológus) Gavina, Cristina Leite-Moreira, Adelino F. Bronzwaer, Jean G. F. Papp Zoltán (1965-) (kardiológus, élettanász) Velden, Jolanda, van der Stienen, Ger J. M. Paulus, Walter J.
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001-es BibID:	BIBFORM090647
Első szerző:	Kiss Éva
Cím:	Thyroid Hormone-Induced Alterations in Phospholamban-Deficient Mouse Hearts / Kiss Eva, Brittsan Angie G., Edes Istvan, Grupp Ingrid L., Grupp Gunter, Kranias Evangelia G.
Dátum:	1998
ISSN:	0009-7330
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Circulation Research. - 83 : 6 (1998), p. 608-613. -
További szerzők:	Brittsan, Angie G. Édes István (1952-) (kardiológus) Grupp, Ingrid L. Grupp, Gunter Kranias, Evangelia G.
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001-es BibID:	BIBFORM018115
Első szerző:	Szerafin Tamás (szívsebész, mellkassebész)
Cím:	Increased cyclooxygenase-2 expression and prostaglandin-mediated dilation in coronary arterioles of patients with diabetes mellitus / Szerafin T., Erdei N., Fülöp T., Pasztor T. E., Edes I., Koller A., Bagi Z.
Dátum:	2006
ISSN:	0009-7330
Megjegyzések:	Based on findings of experimental models of diabetes mellitus (DM) showing increased expression of vascular cyclooxygenase-2 (COX-2), we hypothesized that in patients with DM changes in COX-2-dependent prostaglandin synthesis affect vasomotor responses of coronary arterioles. Arterioles were dissected from the right atrial appendages obtained at the time of cardiac surgery of patient with DM(+) or without documented diabetes DM(-). Isolated arterioles (89+/-15 microm in diameter) were cannulated and pressurized (at 80 mm Hg), and changes in diameter were measured with video microscopy. After spontaneous tone developed [DM(-): 32+/-7%; DM(+): 37+/-5%; P=NS], arteriolar responses to bradykinin were investigated. Dilations to bradykinin (0.1 nmol/L to 1 micromol/L) were significantly (P<0.05) greater in DM(+) than DM(-) patients (10 nmol/L: 77+/-10% versus 38+/-14%). In both groups, dilations were similar to the NO-donor, sodium nitroprusside. In arterioles of DM(+), but not those of DM(-), patients' bradykinin-induced dilations were reduced by the nonselective COX inhibitor indomethacin or by the selective COX-2 inhibitor NS-398 (DM(+) at 10 nmol/L: to 20+/-4% and 29+/-7%, respectively). Correspondingly, a marked COX-2 immunostaining was detected in coronary arterioles of DM(+), but not in those of DM(-) patients. We conclude that in coronary arterioles of diabetic patients bradykinin induces enhanced COX-2-derived prostaglandin-mediated dilation. These findings are the first to show that in humans diabetes mellitus increases COX-2 expression and dilator prostaglandin synthesis in coronary arterioles, which may serve to increase dilator capacity and maintain adequate perfusion of cardiac tissues.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Circulation Research. - 99 : 5 (2006), p. e12-e17. -
További szerzők:	Erdei Nóra (1979-) (orvos) Fülöp Tibor (1957-) (kardiológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Édes István (1952-) (kardiológus) Koller Ákos Bagi Zsolt (1974-) (orvos)
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