CCL

Összesen 9 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM101050
Első szerző:Balasubramanian, Priya
Cím:Obesity-induced cognitive impairment in older adults : a microvascular perspective / Balasubramanian Priya, Kiss Tamas, Tarantini Stefano, Nyúl-Tóth Ádám, Ahire Chetan, Yabluchanskiy Andriy, Csipo Tamas, Lipecz Agnes, Tabak Adam, Institoris Adam, Csiszar Anna, Ungvari Zoltan
Dátum:2021
ISSN:0363-6135
Megjegyzések:Over two-thirds of individuals aged 65 and older are obese or overweight in the United States. Epidemiological data show an association between the degree of adiposity and cognitive dysfunction in the elderly. In this review, the pathophysiological roles of microvascular mechanisms, including impaired endothelial function and neurovascular coupling responses, microvascular rarefaction, and blood-brain barrier disruption in the genesis of cognitive impairment in geriatric obesity are considered. The potential contribution of adipose-derived factors and fundamental cellular and molecular mechanisms of senescence to exacerbated obesity-induced cerebromicrovascular impairment and cognitive decline in aging are discussed.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 320 : 2 (2021), p. H740-H761. -
További szerzők:Kiss Tamás (1950-) (vegyész) Tarantini, Stefano Nyúl-Tóth Ádám Ahire, Chetan Yabluchanskiy, Andriy Csípő Tamás (1990-) Lipécz Ágnes Tabák Ádám Institóris Ádám Csiszár Anna Ungvári Zoltán
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM029129
Első szerző:Beleznai Tímea (orvos)
Cím:Arginase 1 contributes to diminished coronary arteriolar dilation in patients with diabetes / Beleznai T., Feher A., Spielvogel D., Lansman S. L., Bagi Z.
Dátum:2011
ISSN:0363-6135
Megjegyzések:Arginase 1, via competing with nitric oxide (NO) synthase for the substrate L-arginine, may interfere with NO-mediated vascular responses. We tested the hypothesis that arginase 1 contributes to coronary vasomotor dysfunction in patients with diabetes mellitus (DM). Coronary arterioles were dissected from the right atrial appendages of 41 consecutive patients with or without DM (the 2 groups suffered from similar comorbidities), and agonist-induced changes in diameter were measured with videomicroscopy. We found that the endothelium-dependent agonist ACh elicited a diminished vasodilation and caused constriction to the highest ACh concentration (0.1 mikroM) with a similar magnitude in patients with (18 ± 8%) and without (17 ± 9%) DM. Responses to ACh were not significantly affected by the inhibition of NO synthesis with N(G)-nitro-L-arginine methyl ester in either group. The NO donor sodium nitroprusside-dependent dilations were not different in patients with or without DM. Interestingly, we found that the presence of N(G)-hydroxy-L-arginine (10 mikroM), a selective inhibitor of arginase or application of L-arginine (3 mM), restored ACh-induced coronary dilations only in patients with DM (to 47 ± 6% and to 40 ± 19%, respectively) but not in subjects without DM. Correspondingly, the protein expression of arginase 1 was increased in coronary arterioles of patients with DM compared with subjects without diabetes. Moreover, using immunocytochemistry, we detected an abundant immunostaining of arginase 1 in coronary endothelial cells of patients with DM, which was colocalized with NO synthase. Collectively, we provided evidence for a distinct upregulation of arginase 1 in coronary arterioles of patients with DM, which contributes to a reduced NO production and consequently diminished vasodilation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 300 : 3 (2011), p. H777-H783. -
További szerzők:Fehér Attila (1982-) (orvos) Spielvogel, David Lansman, Steven L. Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:RE/08/004
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

3.

001-es BibID:BIBFORM020103
Első szerző:Erdei Nóra (orvos)
Cím:High-fat diet-induced reduction in nitric oxide-dependent arteriolar dilation in rats: role of xanthine oxidase-derived superoxide anion / Nóra Erdei, Attila Tóth, Enikő T. Pásztor, Zoltán Papp, István Édes, Akos Koller, Zsolt Bagi
Dátum:2006
ISSN:0363-6135
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 291 : 5 (2006), p. H2107-H2115. -
További szerzők:Tóth Attila (1971-) (biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Koller Ákos Bagi Zsolt (1974-) (orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

4.

001-es BibID:BIBFORM002023
Első szerző:Erdei Nóra (orvos)
Cím:H2O2 increases production of constrictor prostaglandins in smooth muscle leading to enhanced arteriolar tone in Type 2 diabetic mice / Erdei N., Bagi Z., Edes I., Kaley G., Koller A.
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology. - 292 : 1 (2007), p. H649-H656. -
További szerzők:Édes István (1952-) (kardiológus) Kaley Gábor Koller Ákos Bagi Zsolt (1974-) (orvos)
Internet cím:elektronikus változat
DOI
Borító:

5.

001-es BibID:BIBFORM005634
Első szerző:Jebelovszki Éva
Cím:High-fat diet-induced obesity leads to increased NO sensitivity of rat coronary arterioles : role of soluble guanylate cyclase activation / Jebelovszki, E., Kiraly, C., Erdei, N., Feher, A., Pasztor, T. E., Rutkai, I., Forster, T., Edes, I., Koller, A., Bagi, Z.
Dátum:2008
ISSN:0363-6135 (Print)
Megjegyzések:The impact of obesity on nitric oxide (NO)-mediated coronary microvascular responses is poorly understood. Thus NO-mediated vasomotor responses were investigated in pressurized coronary arterioles ( approximately 100 microm) isolated from lean (on normal diet) and obese (fed with 60% of saturated fat) rats. We found that dilations to acetylcholine (ACh) were not significantly different in obese and lean rats (lean, 83 +/- 4%; and obese, 85 +/- 3% at 1 microM), yet the inhibition of NO synthesis with N(omega)-nitro-l-arginine methyl ester reduced ACh-induced dilations only in vessels of lean controls. The presence of the soluble guanylate cyclase (sGC) inhibitor oxadiazolo-quinoxaline (ODQ) elicited a similar reduction in ACh-induced dilations in the two groups of vessels (lean, 60 +/- 11%; and obese, 57 +/- 3%). Dilations to NO donors, sodium nitroprusside (SNP), and diethylenetriamine (DETA)-NONOate were enhanced in coronary arterioles of obese compared with lean control rats (lean, 63 +/- 6% and 51 +/- 5%; and obese, 78 +/- 5% and 70 +/- 5%, respectively, at 1 microM), whereas dilations to 8-bromo-cGMP were not different in the two groups. In the presence of ODQ, both SNP and DETA-NONOate-induced dilations were reduced to a similar level in lean and obese rats. Moreover, SNP-stimulated cGMP immunoreactivity in coronary arterioles and also cGMP levels in carotid arteries were enhanced in obese rats, whereas the protein expression of endothelial NOS and the sGC beta1-subunit were not different in the two groups. Collectively, these findings suggest that in coronary arterioles of obese rats, the increased activity of sGC leads to an enhanced sensitivity to NO, which may contribute to the maintenance of NO-mediated dilations and coronary perfusion in obesity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Acetylcholine
Adaptation, Physiological
Animals
Arterioles
Blotting, Western
Coronary Vessels
Cyclic GMP
Dietary Fats
Disease Models, Animal
Dose-Response Relationship, Drug
Enzyme Activation
Enzyme Inhibitors
Enzyme-Linked Immunosorbent Assay
Guanylate Cyclase
Immunohistochemistry
Male
NG-Nitroarginine Methyl Ester
Nitric Oxide
Nitric Oxide Donors
Nitric Oxide Synthase Type II
Nitroprusside
Nitroso Compounds
Obesity
Rats
Rats, Wistar
Receptors, Cytoplasmic and Nuclear
Vasodilation
Vasodilator Agents
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology. - 294 : 6 (2008), p. H2558-H2564. -
További szerzők:Király Csaba Erdei Nóra (1979-) (orvos) Fehér Attila (1982-) (orvos) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Rutkai Ibolya (1985-) (molekuláris biológus) Forster Tamás Édes István (1952-) (kardiológus) Koller Ákos Bagi Zsolt (1974-) (orvos)
Internet cím:elektronikus változat
elektronikus változat
DOI
Borító:

6.

001-es BibID:BIBFORM099988
Első szerző:Koller Ákos
Cím:Nitric oxide and H2O2 contribute to reactive dilation of isolated coronary arterioles / Koller Akos, Bagi Zsolt
Dátum:2004
ISSN:0363-6135
Megjegyzések:The role of metabolic factors derived from cardiac muscle in the development of reactive hyperemia after brief occlusions of the coronary circulation seems to be well established. However, the contribution of occlusion-induced changes in hemodynamic forces to eliciting reactive hyperemia is less known. We hypothesized that in isolated coronary arterioles changes in intraluminal pressure and flow, during and after release of occlusion (O/R), themselves via activating intrinsic mechanosensitive mechanisms, elicit release of vasoactive factors resulting in reactive dilations. Thus in isolated coronary arterioles (diameter: 88 +/- 8 microm) changes in diameter to changes in pressure or pressure plus flow (P+F) during and after a brief period (30, 60, and 120 s) of O/R of cannulating tube were measured by videomicroscopy. In response to both types of O/R, diameter first decreased, then, subsequently increased during occlusions. When only pressure was changed (from 80-10-80 mmHg), after release of occlusion, peak dilations increased as a function of the duration of occlusions. After flow was established (30 microl/min), O/R elicited changes in both pressure and flow (from 80-10-80 mmHg and from 0 to 30 microl/min). In these conditions, after the release of occlusions, not only the peak but also the duration of reactive dilation increased significantly as a function of the length of occlusions. The dilations during, and peak dilations after occlusions both in pressure and P+F protocols were significantly reduced by the inhibition of NO synthase with Nomega-nitro-L-arginine-methyl-ester (L-NAME) or by endothelium removal, whereas duration of postocclusion dilations were reduced by L-NAME or by endothelium removal only in P+F protocols. Furthermore, in both protocols, catalase significantly reduced the peak but not the duration of reactive dilations. Thus, mechanosensitive mechanisms that are sensitive to deformation, pressure, stretch, and wall shear stress elicit release of NO and H2O2, resulting in reactive dilation of isolated coronary arterioles.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 287 : 6 (2004), p. H2461-H2467. -
További szerzők:Bagi Zsolt (1974-) (orvos)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

001-es BibID:BIBFORM064197
Első szerző:Kovács Árpád (kardiológus)
Cím:Renin overexpression leads to increased titin-based stiffness contributing to diastolic dysfunction in hypertensive mRen2 rats / Árpád Kovács, Gábor Á. Fülöp, Andrea Kovács, Tamás Csípő, Beáta Bódi, Dániel Priksz, Béla Juhász, Lívia Beke, Zoltán Hendrik, Gábor Méhes, Henk L. Granzier, István Édes, Miklós Fagyas, Zoltán Papp, Judit Barta, Attila Tóth
Dátum:2016
ISSN:0363-6135
Megjegyzések:Hypertension (HTN) is a major risk factor for heart failure. We investigated the influence of HTN on cardiac contraction and relaxation in transgenic renin overexpressing rats (carrying mouse Ren-2 renin gene, mRen2, n = 6). Blood pressure (BP) was measured. Cardiac contractility was characterized by echocardiography, cellular force measurements, and biochemical assays were applied to reveal molecular mechanisms. Sprague-Dawley (SD) rats (n = 6) were used as controls. Transgenic rats had higher circulating renin activity and lower cardiac angiotensin-converting enzyme two levels. Systolic BP was elevated in mRen2 rats (235.11 ? 5.32 vs. 127.03 ? 7.56 mmHg in SD, P < 0.05), resulting in increased left ventricular (LV) weight/body weight ratio (4.05 ? 0.09 vs. 2.77 ? 0.08 mg/g in SD, P < 0.05). Transgenic renin expression had no effect on the systolic parameters, such as LV ejection fraction, cardiomyocyte Ca(2+)-activated force, and Ca(2+) sensitivity of force production. In contrast, diastolic dysfunction was observed in mRen2 compared with SD rats: early and late LV diastolic filling ratio (E/A) was lower (1.14 ? 0.04 vs. 1.87 ? 0.08, P < 0.05), LV isovolumetric relaxation time was longer (43.85 ? 0.89 vs. 28.55 ? 1.33 ms, P < 0.05), cardiomyocyte passive tension was higher (1.74 ? 0.06 vs. 1.28 ? 0.18 kN/m(2), P < 0.05), and lung weight/body weight ratio was increased (6.47 ? 0.24 vs. 5.78 ? 0.19 mg/g, P < 0.05), as was left atrial weight/body weight ratio (0.21 ? 0.03 vs. 0.14 ? 0.03 mg/g, P < 0.05). Hyperphosphorylation of titin at Ser-12742 within the PEVK domain and a twofold overexpression of protein kinase C-? in mRen2 rats were detected. Our data suggest a link between the activation of renin-angiotensin-aldosterone system and increased titin-based stiffness through phosphorylation of titin's PEVK element, contributing to diastolic dysfunction.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
hypertension
passive stiffness
renin-angiotensin-aldosterone system
RAAS
diastolic dysfunction
titin phosphorylation
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 310 : 11 (2016), p. H1671-H1682. -
További szerzők:Fülöp Gábor Áron (1988-) (általános orvos) Kovács Andrea (1974-) (neurológus) Csípő Tamás (1990-) Bódi Beáta (1989-) (molekuláris biológus) Priksz Dániel (1989-) (farmakológus) Juhász Béla (1978-) (kísérletes farmakológus) Beke Lívia Hendrik Zoltán (1986-) (orvos) Méhes Gábor (1966-) (patológus) Granzier, Henk L. Édes István (1952-) (kardiológus) Fagyas Miklós (1984-) (orvos) Papp Zoltán (1965-) (kardiológus, élettanász) Barta Judit (1975-) (kardiológus) Tóth Attila (1971-) (biológus)
Pályázati támogatás:PD116212
OTKA
K109083
OTKA
K116940
OTKA
MEDIA
FP7
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

8.

001-es BibID:BIBFORM020693
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:The role of peroxiredoxins in ischemia-reperfusion-induced cardiac damage / Árpád Tósaki, István Édes
Dátum:2006
ISSN:0363-6135
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology-Heart And Circulatory Physiology. - 291 : 6 (2006), p. H2586-H2587. -
További szerzők:Édes István (1952-) (kardiológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Szerző által megadott URL
Borító:

9.

001-es BibID:BIBFORM002143
Első szerző:Tóth Erika
Cím:Contribution of polyol pathway to arteriolar dysfunction in hyperglycemia : role of oxidative stress, reduced NO, and enhanced PGH(2)/TXA(2) mediation / Toth E., Racz A., Toth J., Kaminski P. M., Wolin M. S., Bagi Z., Koller A.
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Heart and circulatory physiology. - 293 : 5 (2007), p. H3096-H3104. -
További szerzők:Rácz Anita Tóth János Kaminski, Pawel M. Wolin, Michael S. Koller Ákos Bagi Zsolt (1974-) (orvos)
Internet cím:elektronikus változat
DOI
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.