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001-es BibID:BIBFORM015074
Első szerző:Borbély Attila (kardiológus)
Cím:Cardiomyocyte Stiffness in Diastolic Heart Failure / Borbély A., van der Velden J., Papp Z., Bronzwaer J. G. F., Edes I., Stienen G. J. M., Paulus W. J.
Dátum:2005
ISSN:0009-7322
Megjegyzések:Heart failure with preserved left ventricular (LV) ejection fraction (EF) is increasingly recognized and usually referred to as diastolic heart failure (DHF). Its pathogenetic mechanism remains unclear, partly because of a lack of myocardial biopsy material. Endomyocardial biopsy samples obtained from DHF patients were therefore analyzed for collagen volume fraction (CVF) and sarcomeric protein composition and compared with control samples. Single cardiomyocytes were isolated from these biopsy samples to assess cellular contractile performance.METHODS AND RESULTS: DHF patients (n=12) had an LVEF of 71+/-11%, an LV end-diastolic pressure (LVEDP) of 28+/-4 mm Hg, and no significant coronary artery stenoses. DHF patients had higher CVFs (7.5+/-4.0%, P<0.05) than did controls (n=8, 3.8+/-2.0%), and no conspicuous changes in sarcomeric protein composition were detected. Cardiomyocytes, mechanically isolated and treated with Triton X-100 to remove all membranes, were stretched to a sarcomere length of 2.2 microm and activated with solutions containing varying [Ca2+]. Compared with cardiomyocytes of controls, cardiomyocytes of DHF patients developed a similar total isometric force at maximal [Ca2+], but their resting tension (F(passive)) in the absence of Ca2+ was almost twice as high (6.6+/-3.0 versus 3.5+/-1.7 kN/m2, P<0.001). F(passive) and CVF combined yielded stronger correlations with LVEDP than did either alone. Administration of protein kinase A (PKA) to DHF cardiomyocytes lowered F(passive) to control values.CONCLUSIONS: DHF patients had stiffer cardiomyocytes, as evident from a higher F(passive) at the same sarcomere length. Together with CVF, F(passive) determined in vivo diastolic LV dysfunction. Correction of this high F(passive) by PKA suggests that reduced phosphorylation of sarcomeric proteins is involved in DHF.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation. - 111 : 6 (2005), p. 774-781. -
További szerzők:Velden, Jolanda, van der Papp Zoltán (1965-) (kardiológus, élettanász) Bronzwaer, Jean G. F. Édes István (1952-) (kardiológus) Stienen, Ger J. M. Paulus, Walter J.
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2.

001-es BibID:BIBFORM010417
Első szerző:Borbély Attila (kardiológus)
Cím:Transcriptional and posttranslational modifications of titin : implications for diastole / Borbely, A., van Heerebeek, L., Paulus, W. J.
Dátum:2009
ISSN:1524-4571 (Electronic)
Tárgyszavak:Orvostudományok Klinikai orvostudományok szerkesztőségi anyag
Alternative Splicing
Animals
Cyclic AMP-Dependent Protein Kinases
Cyclic GMP-Dependent Protein Kinases
Diabetes Complications
Diacetyl
derivatives
Diastole
Elasticity
Extracellular Matrix
Gelsolin
Heart Failure, Diastolic
Humans
Mice
Muscle Proteins
Myocytes, Cardiac
Phosphorylation
Protein Isoforms
Protein Kinases
Protein Processing, Post-Translational
Rats
Sarcomeres
Triiodothyronine
Ventricular Remodeling
Megjelenés:Circulation Research. - 104 : 1 (2009), p. 12-14. -
További szerzők:Heerebeek, Loek, van Paulus, Walter J.
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3.

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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4.

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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5.

001-es BibID:BIBFORM014721
Első szerző:Heerebeek, Loek, van
Cím:Myocardial Structure and Function Differ in Systolic and Diastolic Heart Failure / van Heerebeek L., Borbély A., Niessen H. W. M., Bronzwaer J. G. F., van der Velden J., Stienen G. J., Linke W. A., Laarman G. J., Paulus W. J.
Dátum:2006
ISSN:0009-7322
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation. - 113 : 16 (2006), p. 1966-1973. -
További szerzők:Borbély Attila (1978-) (kardiológus) Niessen, Hans W. M. Bronzwaer, Jean G. F. Velden, Jolanda, van der Stienen, Ger J. M. Linke, Wolfgang A. Laarman, Gerrit J. Paulus, Walter J.
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6.

001-es BibID:BIBFORM015744
Első szerző:Papp Zoltán (kardiológus, élettanász)
Cím:Troponin I Degradation and Myocardial Stunning / Papp Zoltán, Barta Judit, Ger J. M. Stienen
Dátum:2001
ISSN:0009-7322
Megjegyzések:Nem létezik
Tárgyszavak:Orvostudományok Elméleti orvostudományok szerkesztői levél
Megjelenés:Circulation. - 104 : 25 (2001), p. e157. -
További szerzők:Barta Judit (1975-) (kardiológus) Stienen, Ger J. M.
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7.

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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