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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:	BIBFORM023507
Első szerző:	Falcao-Pires, Ines
Cím:	Diabetes Mellitus Worsens Diastolic Left Ventricular Dysfunction in Aortic Stenosis Through Altered Myocardial Structure and Cardiomyocyte Stiffness / Falcao-Pires, I., Hamdani, N., Borbely, A., Gavina, C., Schalkwijk, C. G., van der Velden, J., van Heerebeek, L., Stienen, G. J. M., Niessen, H. W. M., Leite-Moreira, A. F., Paulus, W. J.
Dátum:	2011
ISSN:	0009-7322
Megjegyzések:	Aortic stenosis (AS) and diabetes mellitus (DM) are frequent comorbidities in aging populations. In heart failure, DM worsens diastolic left ventricular (LV) dysfunction, thereby adversely affecting symptoms and prognosis. Effects of DM on diastolic LV function were therefore assessed in aortic stenosis, and underlying myocardial mechanisms were identified. Methods and Results-Patients referred for aortic valve replacement were subdivided into patients with AS and no DM (AS; n=46) and patients with AS and DM (AS-DM; n=16). Preoperative Doppler echocardiography and hemodynamics were implemented with perioperative LV biopsies. Histomorphometry and immunohistochemistry quantified myocardial collagen volume fraction and myocardial advanced glycation end product deposition. Isolated cardiomyocytes were stretched to 2.2-gamma m sarcomere length to measure resting tension (Fpassive). Expression and phosphorylation of titin isoforms were analyzed with gel electrophoresis with ProQ Diamond and SYPRO Ruby stains. Reduced LV end-diastolic distensibility in AS-DM was evident from higher LV end-diastolic pressure (21±1 mm Hg for AS versus 28±4 mm Hg for AS-DM; P=0.04) at comparable LV end-diastolic volume index and attributed to higher myocardial collagen volume fraction (AS, 12.9±1.1% versus AS-DM, 18.2±2.6%; P<0.001), more advanced glycation end product deposition in arterioles, venules, and capillaries (AS, 14.4±2.1 score per 1 mm2 versus AS-DM, 31.4±6.1 score per 1 mm2; P=0.03), and higher Fpassive (AS, 3.5±1.7 kN/m2 versus AS-DM, 5.1±0.7 kN/m2; P=0.04). Significant hypophosphorylation of the stiff N2B titin isoform in AS-DM explained the higher Fpassive and normalization of Fpassive after in vitro treatment with protein kinase A. Conclusions-Worse diastolic LV dysfunction in AS-DM predisposes to heart failure and results from more myocardial fibrosis, more intramyocardial vascular advanced glycation end product deposition, and higher cardiomyocyte Fpassive, which was related to hypophosphorylation of the N2B titin isoform.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban aortic valve stenosis myocytes cardiac diabetes mellitus diastole fibrosis titin myofilamentary proteins
Megjelenés:	Circulation. - 124 : 10 (2011), p. 1151-1159. -
További szerzők:	Hamdani, Nazha Borbély Attila (1978-) (kardiológus) Gavina, Cristina Schalkwijk, Casper G. Velden, Jolanda, van der Heerebeek, Loek, van Stienen, Ger J. M. Niessen, Hans W. M. Leite-Moreira, Adelino F. Paulus, Walter J.
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001-es BibID:	BIBFORM030333
Első szerző:	Heerebeek, Loek, van
Cím:	Response to Letter Regarding Article, "Diastolic Stiffness of the Failing Diabetic Heart : Importance of Fibrosis, Advanced Glycation End Products, and Myocyte Resting Tension" / van Heerebeek L., Hamdani N., Handoko M. L., Falcao-Pires I., Musters R. J., Kupreishvili K., Ijsselmuiden A. J., Schalkwijk C. G., Bronzwaer J. G., Diamant M., Borbely A., van der Velden J., Stienen G. J. M., Laarman G. J., Niessen H. W., Paulus W. J.
Dátum:	2008
ISSN:	0009-7322
Tárgyszavak:	Orvostudományok Elméleti orvostudományok levél
Megjelenés:	Circulation. - 117 (2008), p. e484. -
További szerzők:	Hamdani, Nazha Handoko, Martin Louis Falcao-Pires, Ines Musters, René J. Kupreishvili, Koba Ijsselmuiden, Alexander J. J. Schalkwijk, Casper G. Bronzwaer, Jean G. F. Diamant, Michaela Borbély Attila (1978-) (kardiológus) Velden, Jolanda, van der Stienen, Ger J. M. Laarman, Gerrit J. Niessen, Hans W. M. Paulus, Walter J.
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001-es BibID:	BIBFORM005642
Első szerző:	Heerebeek, Loek, van
Cím:	Diastolic stiffness of the failing diabetic heart : importance of fibrosis, advanced glycation end products, and myocyte resting tension / van Heerebeek, L., Hamdani, N., Handoko, M. L., Falcao-Pires, I., Musters, R. J., Kupreishvili, K., Ijsselmuiden, A. J. J., Schalkwijk, C. G., Bronzwaer, J. G. F., Diamant, M., Borbely, A., van der Velden, J., Stienen, G. J. M., Laarman, G. J., Niessen, H. W. M., Paulus, W. J.
Dátum:	2008
ISSN:	1524-4539 (Electronic)
Megjegyzések:	Excessive diastolic left ventricular stiffness is an important contributor to heart failure in patients with diabetes mellitus. Diabetes is presumed to increase stiffness through myocardial deposition of collagen and advanced glycation end products (AGEs). Cardiomyocyte resting tension also elevates stiffness, especially in heart failure with normal left ventricular ejection fraction (LVEF). The contribution to diastolic stiffness of fibrosis, AGEs, and cardiomyocyte resting tension was assessed in diabetic heart failure patients with normal or reduced LVEF. METHODS AND RESULTS: Left ventricular endomyocardial biopsy samples were procured in 28 patients with normal LVEF and 36 patients with reduced LVEF, all without coronary artery disease. Sixteen patients with normal LVEF and 10 with reduced LVEF had diabetes mellitus. Biopsy samples were used for quantification of collagen and AGEs and for isolation of cardiomyocytes to measure resting tension. Diabetic heart failure patients had higher diastolic left ventricular stiffness irrespective of LVEF. Diabetes mellitus increased the myocardial collagen volume fraction only in patients with reduced LVEF (from 14.6+/-1.0% to 22.4+/-2.2%, P<0.001) and increased cardiomyocyte resting tension only in patients with normal LVEF (from 5.1+/-0.7 to 8.5+/-0.9 kN/m2, P=0.006). Diabetes increased myocardial AGE deposition in patients with reduced LVEF (from 8.8+/-2.5 to 24.1+/-3.8 score/mm2; P=0.005) and less so in patients with normal LVEF (from 8.2+/-2.5 to 15.7+/-2.7 score/mm2, P=NS). CONCLUSIONS: Mechanisms responsible for the increased diastolic stiffness of the diabetic heart differ in heart failure with reduced and normal LVEF: Fibrosis and AGEs are more important when LVEF is reduced, whereas cardiomyocyte resting tension is more important when LVEF is normal.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Case-Control Studies Diabetes Complications/ physiopathology Diabetes Mellitus/physiopathology Diastole Female Fibrosis Glycosylation End Products, Advanced Heart Failure/etiology/ pathology Heart Ventricles/pathology Humans Male Middle Aged Muscle Tonus Myocytes, Cardiac/ physiology Stroke Volume
Megjelenés:	Circulation. - 117 : 1 (2008), p. 43-51. -
További szerzők:	Hamdani, Nazha Handoko, Martin Louis Falcao-Pires, Ines Musters, René J. Kupreishvili, Koba Ijsselmuiden, Alexander J. J. Schalkwijk, Casper G. Bronzwaer, Jean G. F. Diamant, Michaela Borbély Attila (1978-) (kardiológus) Velden, Jolanda, van der Stienen, Ger J. M. Laarman, Gerrit J. Niessen, Hans W. M. Paulus, Walter J.
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