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1.

001-es BibID:BIBFORM009063
Első szerző:Alvarez, Julio
Cím:ATP/UTP activate cation-permeable channels with TRPC3/7 properties in rat cardiomyocytes / Alvarez, J., Coulombe, A., Cazorla, O., Ugur, M., Rauzier, J. M., Magyar, J., Mathieu, E. L., Boulay, G., Souto, R., Bideaux, P., Salazar, G., Rassendren, F., Lacampagne, A., Fauconnier, J., Vassort, G.
Dátum:2008
ISSN:0363-6135 (Print)
Megjegyzések:Extracellular purines and pyrimidines have major effects on cardiac rhythm and contraction. ATP/UTP are released during various physiopathological conditions, such as ischemia, and despite degradation by ectonucleotidases, their interstitial concentrations can markedly increase, a fact that is clearly associated with arrhythmia. In the present whole cell patch-clamp analysis on ventricular cardiomyocytes isolated from various mammalian species, ATP and UTP elicited a sustained, nonselective cationic current, I(ATP). UDP was ineffective, whereas 2'(3')-O-(4-benzoylbenzoyl)-ATP was active, suggesting that P2Y(2) receptors are involved. I(ATP) resulted from the binding of ATP(4-) to P2Y(2) purinoceptors. I(ATP) was maintained after ATP removal in the presence of guanosine 5'-[gamma-thio]triphosphate and was inhibited by U-73122, a PLC inhibitor. Single-channel openings are rather infrequent under basal conditions. ATP markedly increased opening probability, an effect prevented by U-73122. Two main conductance levels of 14 and 23 pS were easily distinguished. Similarly, in fura-2-loaded cardiomyocytes, Mn(2+) quenching and Ba(2+) influx were significant only in the presence of ATP or UTP. Adult rat ventricular cardiomyocytes expressed transient receptor potential channel TRPC1, -3, -4, and -7 mRNA and the TRPC3 and TRPC7 proteins that coimmunoprecipitated. Finally, the anti-TRPC3 antibody added to the patch pipette solution inhibited I(ATP). In conclusion, activation of P2Y(2) receptors, via a G protein and stimulation of PLCbeta, induces the opening of heteromeric TRPC3/7 channels, leading to a sustained, nonspecific cationic current. Such a depolarizing current could induce cell automaticity and trigger the arrhythmic events during an early infarct when ATP/UTP release occurs. These results emphasize a new, potentially deleterious role of TRPC channel activation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Adenosine Triphosphate
Animals
Arrhythmias, Cardiac
Cell Membrane Permeability
Disease Models, Animal
Dogs
Estrenes
Humans
Male
Membrane Potentials
Mice
Mice, Knockout
Myocardial Infarction
Myocytes, Cardiac
Patch-Clamp Techniques
Phosphodiesterase Inhibitors
Phospholipase C beta
Pyrrolidinones
Rats
Rats, Wistar
Receptors, Purinergic P2
Signal Transduction
TRPC Cation Channels
Uridine Triphosphate
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology. - 295 (2008), p. H21-H28. -
További szerzők:Coulombe, Alaine Cazorla, Olivier Ugur, Mehmet Rauzier, Jean-Michel Magyar János (1961-) (élettanász) Mathieu, Eve-Lyne Boulay, Guylain Souto, Rafael Bideaux, Patrice Salazar, Guillermo Rassendren, Francois Lacampagne, Alain Fauconnier, Jérémy Vassort, Guy
Internet cím:DOI
elektronikus változat
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2.

001-es BibID:BIBFORM090884
Első szerző:Anker, Markus S.
Cím:ESC Heart Failure increases its impact factor / Anker Markus S., Papp Zoltán, Földes Gábor, von Haehling Stephan
Dátum:2020
ISSN:2055-5822
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:ESC heart failure. - 7 : 6 (2020), p. 3421-3426. -
További szerzők:Papp Zoltán (1965-) (kardiológus, élettanász) Földes Gábor Haehling, Stephan von
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3.

001-es BibID:BIBFORM090864
035-os BibID:(Wos)000453600400009 (Scopus)85058704211
Első szerző:Anker, Markus S.
Cím:The new Heart Failure Association journal - ESC Heart Failure / Anker Markus S., von Haehling Stephan, Papp Zoltán, Anker Stefan D.
Dátum:2018
ISSN:1388-9842 1879-0844
Megjegyzések:ESC Heart Failure / Chichester : Heart Failure Association of the European Society of Cardiology, 2014
Tárgyszavak:Orvostudományok Elméleti orvostudományok recenzió, folyóirat-ismertetés
folyóiratcikk
Megjelenés:European Journal Of Heart Failure. - 20 : 12 (2018), p. 1657-1663. -
További szerzők:Haehling, Stephan von Papp Zoltán (1965-) (kardiológus, élettanász) Anker, Stefan D.
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4.

001-es BibID:BIBFORM082734
035-os BibID:(WoS)000504576700001 (Scopus)85077318693
Első szerző:Anker, Markus S.
Cím:ESC Heart Failure receives its first impact factor / Markus S. Anker, Stephan von Haehling, Zoltán Papp, Stefan D. Anker
Dátum:2019
ISSN:1388-9842 1879-0844
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:European Journal of Heart Failure. - 21 : 12 (2019), p. 1490-1503. -
További szerzők:Haehling, Stephan von Papp Zoltán (1965-) (kardiológus, élettanász) Anker, Stefan D.
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5.

001-es BibID:BIBFORM090855
Első szerző:Anker, Stefan D.
Cím:Research in acute and chronic heart failure is busier then ever worldwide and demands more publishing space: introducing, the sister journal of the European Journal of Heart Failure / Anker Stefan D., von Haehling Stephan, Papp Zoltán
Dátum:2014
ISSN:2055-5822
Tárgyszavak:Orvostudományok Elméleti orvostudományok levél
folyóiratcikk
Megjelenés:ESC heart failure. - 1 : 1 (2014), p. 1-3. -
További szerzők:von Haehling, Stephan Papp Zoltán (1965-) (kardiológus, élettanász)
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6.

001-es BibID:BIBFORM082735
Első szerző:Anker, Stefan D.
Cím:Open access efforts begin to bloom : ESC Heart Failure gets full attention and first impact factor / Stefan D. Anker, Stephan von Haehling, Zoltan Papp
Dátum:2019
ISSN:2055-5822
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:ESC heart failure. - 6 : 5 (2019), p. 903-908. -
További szerzők:Haehling, Stephan von Papp Zoltán (1965-) (kardiológus, élettanász)
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7.

001-es BibID:BIBFORM005623
Első szerző:Bagi Zsolt (orvos)
Cím:High intraluminal pressure via H2O2 upregulates arteriolar constrictions to angiotensin II by increasing the functional availability of AT1 receptors / Bagi, Z., Erdei, N., Koller, A.
Dátum:2008
ISSN:0363-6135 (Print)
Megjegyzések:Previously, we found that high intraluminal pressure leads to production of reactive oxygen species (ROS) and also upregulates several components of the renin-angiotensin system in the wall of small arteries. We hypothesized that acute exposure of arterioles to high intraluminal pressure in vitro via increasing ROS production enhances the functional availability of type 1 angiotensin II (Ang II) receptors (AT1 receptors), resulting in sustained constrictions. In arterioles ( approximately 180 mum) isolated from rat skeletal muscle, Ang II elicited dose-dependent constrictions, which decreased significantly by the second application [maximum (max.): from 59% +/- 4% to 26% +/- 5% at 10(-8) M; P < 0.05] in the presence of 80 mmHg of intraluminal pressure. In contrast, if the arterioles were exposed to high intraluminal pressure (160 mmHg for 30 min), Ang II-induced constrictions remained substantial on the second application (max.: 51% +/- 3% at 10(-8) M). In the presence of Tiron and polyethylene glycol (PEG)-catalase, known to reduce the level of superoxide anion and hydrogen peroxide (H(2)O(2)), second applications of Ang II evoked similarly reduced constrictions, even after high-pressure exposure (29% +/- 4% at 10(-8) M). Furthermore, when arterioles were exposed to H(2)O(2) (for 30 min, 10(-7) M, at normal 80 mmHg pressure), Ang II-induced constrictions remained substantial on second applications (59% +/- 5% at 10(-8) M). These findings suggest that high pressure, likely via inducing H(2)O(2) production, increases the functional availability of AT1 receptors and thus enhances Ang II-induced arteriolar constrictions. We propose that in hypertension-regardless of etiology-high intraluminal pressure, via oxidative stress, enhances the functional availability of AT1 receptors augmenting Ang II-induced constrictions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt/pharmacology
Angiotensin II
Animals
Antioxidants
Arterioles
Blood Pressure
Catalase
Hydrogen Peroxide
Hypertension
Male
Muscle
Oxidative Stress
Polyethylene Glycols
Rats
Rats, Wistar
Receptor
Up-Regulation
Vasoconstriction/drug effects
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology. - 295 : 2 (2008), p. H835-H841. -
További szerzők:Erdei Nóra (1979-) (orvos) Koller Ákos
Internet cím:elektronikus változat
elektronikus változat
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8.

001-es BibID:BIBFORM029096
Első szerző:Bak István (vegyész, analitikus, farmakológus)
Cím:Cardioprotective mechanisms of Prunus cerasus (sour cherry) seed extract against ischemia-reperfusion-induced damage in isolated rat hearts / Bak I., Lekli I., Juhasz B., Nagy N., Varga E., Varadi J., Gesztelyi R., Szabo G., Szendrei L., Bacskay I., Vecsernyes M., Antal M., Fesus L., Boucher F., de Leiris J., Tosaki A.
Dátum:2006
Megjegyzések:The effects of kernel extract obtained from sour cherry (Prunus cerasus) seed on the postischemic cardiac recovery were studied in isolated working rat hearts. Rats were treated with various daily doses of the extract for 14 days, and hearts were then isolated and subjected to 30 min of global ischemia followed by 120 min of reperfusion. The incidence of ventricular fibrillation (VF) and tachycardia (VT) fell from their control values of 92% and 100% to 50% (not significant) and 58% (not significant), 17% (P<0.05), and 25% (P<0.05) with the doses of 10 mg/kg and 30 mg/kg of the extract, respectively. Lower concentrations of the extract (1 and 5 mg/kg) failed to significantly reduce the incidence of VF and VT during reperfusion. Sour cherry seed kernel extract (10 and 30 mg/kg) significantly improved the postischemic recovery of cardiac function (coronary flow, aortic flow, and left ventricular developed pressure) during reperfusion. We have also demonstrated that the extract-induced protection in cardiac function significantly reflected in a reduction of infarct size. Immunohistochemistry indicates that a reduction in caspase-3 activity and apoptotic cells by the extract, beside other potential action mechanisms of proanthocyanidin, trans-resveratrol, and flavonoid components of the extract, could be responsible for the cardioprotection in ischemic-reperfused myocardium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology 291 : 3 (2006), p. H1329-H1336. -
További szerzők:Lekli István (1981-) (gyógyszerész) Juhász Béla (1978-) (kísérletes farmakológus) Nagy Norbert (1977-) (kísérletes farmakológus) Varga Edit (gyógyszerész) Váradi Judit (1973-) (gyógyszerész, gyógyszertechnológus) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Szabó Gergő Szendrei Levente Bácskay Ildikó (1969-) (gyógyszerész, gyógyszertechnológus) Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Antal Miklós (1951-) (orvos, anatómus) Fésüs László (1947-) (orvos biokémikus) Boucher, Francois de Leiris, Joel Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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9.

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
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10.

001-es BibID:BIBFORM041935
Első szerző:Bányász Tamás (élettanász)
Cím:Profile of L-type Ca(2+) current and Na(+)/Ca(2+) exchange current during cardiac action potential in ventricular myocytes / Tamas Banyasz, Balazs Horvath, Zhong Jian, Leighton T. Izu, Ye Chen-Izu
Dátum:2012
ISSN:1547-5271
Megjegyzések:OBJECTIVE: The L-type Ca(2+) current (I(Ca,L)) and the Na(+)/Ca(2+) exchange current (I(NCX)) are major inward currents that shape the cardiac action potential (AP). Previously, the profile of these currents during the AP was determined from voltage-clamp experiments that used Ca(2+) buffer. In this study, we aimed to obtain direct experimental measurement of these currents during cardiac AP with Ca(2+) cycling. METHOD: A newly developed AP-clamp sequential dissection method was used to record ionic currents in guinea pig ventricular myocytes under a triad of conditions: using the cell's own AP as the voltage command, using internal and external solutions that mimic the cell's ionic composition, and, importantly, not using any exogenous Ca(2+) buffer. RESULTS: The nifedipine-sensitive current (I(NIFE)), which is composed of I(Ca,L) and I(NCX), revealed hitherto unreported features during the AP with Ca(2+) cycling in the cell. We identified 2 peaks in the current profile followed by a long residual current extending beyond the AP, coinciding with a residual depolarization. The second peak and the residual current become apparent only when Ca(2+) is not buffered. Pharmacological dissection of I(NIFE) by using SEA0400 shows that I(Ca,L) is dominant during phases 1 and 2 whereas I(NCX) contributes significantly to the inward current during phases 3 and 4 of the AP. CONCLUSION: These data provide the first direct experimental visualization of I(Ca,L) and I(NCX) during cardiac the AP and Ca(2+) cycle. The residual current reported here can serve as a potential substrate for afterdepolarizations when increased under pathologic conditions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Heart Rhythm. - 9 : 1 (2012), p. 134-142. -
További szerzők:Horváth Balázs (1981-) (élettanász) Jian, Zhong Izu, Leighton T. Chen-Izu, Ye
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11.

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
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12.

001-es BibID:BIBFORM095042
035-os BibID:(WoS)000755462300001 (Scopus)85142845979
Első szerző:Blöndal, Mai
Cím:Comparison of management and outcomes of ST-segment elevation myocardial infarction patients in Estonia, Hungary, Norway and Sweden according to national ongoing registries / Mai Blöndal, Tiia Ainla, Jaan Eha, Piret Lõiveke, Toomas Marandi, Aet Saar, Gudrun Veldre, Robert Edfors, Christian Lewinter, Tomas Jernberg, Jarle Jortveit, Sigrun Halvorsen, Dávid Becker, Zoltán Csanádi, Tamas Ferenci, Péter Andréka, András Jánosi
Dátum:2022
ISSN:2058-5225 2058-1742
Megjegyzések:Aims Describe the characteristics, management and outcomes of hospitalized ST-segment elevation myocardial infarction (STEMI) patients according to national ongoing myocardial infarction registries in Estonia, Hungary, Norway, and Sweden. Methods and results Country-level aggregated data was used to study baseline characteristics, use of in-hospital procedures, medications at discharge, in-hospital complications, 30-day and 1-year mortality for all patients admitted with STEMI during 2014-2017 using data from EMIR (Estonia; n = 4584), HUMIR (Hungary; n = 23 685), NORMI (Norway; n = 12 414, data for 2013?2016), and SWEDEHEART (Sweden; n = 23 342). Estonia and Hungary had a higher proportion of women, patients with hypertension, diabetes, and peripheral artery disease compared to Norway and Sweden. Rates of reperfusion varied from 75.7% in Estonia to 84.0% in Sweden. Rates of recommendation of discharge medications were generally high and similar. However, Estonia demonstrated the lowest rates of dual antiplatelet therapy (78.1%) and statins (86.5%). Norway had the lowest rates of beta-blockers (80.5%) and angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers (61.5%). The 30-day mortality rates ranged between 9.9% and 13.4% remaining lowest in Sweden. One-year mortality rates ranged from 14.8% in Sweden and 16.0% in Norway to 20.6% in Hungary and 21.1% in Estonia. Age-adjusted lethality rates were highest for Hungary and lowest for Sweden. Conclusion This inter-country comparison of data from four national ongoing European registries provides new insights into the risk factors, management and outcomes of patients with STEMI. There are several possible reasons for the findings, including coverage of the registries and variability of baseline-characteristics' definitions that need to be further explored.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
ST-segment elevation myocardial infarction
Registry study
Real-world evidence
Mortality
Megjelenés:European Heart Journal - Quality of Care and Clinical Outcomes. - 8 : 3 (2022), p. 307-314. -
További szerzők:Ainla, Tiia Eha, Jaan Lõiveke, Piret Marandi, Toomas Saar, Aet Veldre, Gudrun Edfors, Robert Lewinter, Christian Jernberg, Tomas Jortveit, Jarle Halvorsen, Sigrun Becker Dávid Csanádi Zoltán (1960-) (kardiológus) Ferenci Tamás Andréka Péter Jánosi András
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