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1.

001-es BibID:BIBFORM120388
Első szerző:Kecskeméti Valéria
Cím:Cardiac electrophysiological and vascular effects of fluoxetine / Kecskeméti V., Pacher P., Magyar J., Szigligeti P., Bányász T., Ungvári Z., Nánási P., Koller Á.
Dátum:1999
ISSN:0195-668X
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:European Heart Journal. - 20 : Abstract_Supplement (1999), p. 575. -
További szerzők:Pacher Pál Magyar János (1961-) (élettanász) Szigligeti Péter Bányász Tamás (1960-) (élettanász) Ungvári Zoltán Nánási Péter Pál (1956-) (élettanász) Koller Ákos
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2.

001-es BibID:BIBFORM120343
Első szerző:Kecskeméti Valéria
Cím:Cardiac electrophysiological effects of fluoxetine / V. Kecskemeti, J. Magyar, P. Szigligeti, T. Banyasz, Cs. Pankucsi, S. Korom, Z. Ungvari, P. P. Nanasi, P. Pacher
Dátum:1999
ISSN:0767-3981
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Fundamental & Clinical Pharmacology. - 13 : S1 (1999), p. 286s. -
További szerzők:Magyar János (1961-) (élettanász) Szigligeti Péter Bányász Tamás (1960-) (élettanász) Pankucsi Csaba (farmakológus) Korom S. Ungvári Zoltán Nánási Péter Pál (1956-) (élettanász) Pacher Pál
Pályázati támogatás:T019206
OTKA
T026577
OTKA
ETT-03505,098
Egyéb
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3.

001-es BibID:BIBFORM120530
Első szerző:Kecskeméti Valéria
Cím:Can the electrophysiological actions of antipsychoptic risperidone explain its cardiac side effects? / V. Kecskeméti, J. Magyar, T. Bányász, Z. S. Bagi, P. Pacher, N. Szentandrássy, L. Fülöp, P. P. Nánási
Dátum:2003
ISSN:1567-4215 1878-1314
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:European Journal of Heart Failure. - 2 : Suppl_1 (2003), p. 60-61. -
További szerzők:Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Bagi Z. S. Pacher Pál Szentandrássy Norbert (1976-) (élettanász) Fülöp L. (élettanász) Nánási Péter Pál (1956-) (élettanász)
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4.

001-es BibID:BIBFORM120244
Első szerző:Kecskeméti Valéria
Cím:Is the electrophysiological actions of psychotrop drugs responsible for their cardiac side effects? / Valeria Kecskeméti, J. Magyar, T. Bányász, N. Szentandrássy, P. Pacher, P. P. Nánási
Dátum:2006
ISSN:0022-2828
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Journal Of Molecular And Cellular Cardiology. - 40 : 6 (2006), p. 987-988. -
További szerzők:Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Pacher Pál Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:ETT 053/2003
Egyéb
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5.

001-es BibID:BIBFORM030340
035-os BibID:WOS:A1996VM24200008 PMID:8901455
Első szerző:Kecskeméti Valéria
Cím:Comparative study of cardiac electrophysiological effects of atrial natriuretic peptide / Valéria Kecskemeti, Pál Pacher, Csaba Pankucsi, Péter P. Nanasi
Dátum:1996
ISSN:0300-8177
Megjegyzések:The effects of atrial natriuretic peptide (ANP) on action potential characteristics were studied in various (human, rabbit, guineapig) atrial and guinea-pig right ventricular papillary muscles. ANP (1-100 nM) did not modify the resting membrane potential nor the maximum rate of depolarization phase (V-max). Up to 10 nM, ANP dose-dependently decreased the action potential amplitude both in guinea-pig atrial and ventricular muscles, but it did not affect this parameter in the other atrial preparations. ANP caused a dose-dependent, marked decrease of action potential duration (APD) in practically every cardiac preparation studied (exception of guinea-pig left atrium). The strongest effect on APD can be observed in human atrial and guinea-pig ventricular fibers. The K+ channel blocker 4-aminopyridine (1 mM) and the ATP-dependent K+ channel inhibitor glibenclamide (10 mu M) prevented the effect of ANP on APD in both ventricular atrial preparations. ANP prevented the appearance of isoprenaline (0.5 mu M) induced slow AP in K+ depolarized myocardium. The present data suggest that ANP may inhibit the slow inward Ca2+ channel activity and facilitate the K+ channel activity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Molecular and Cellular Biochemistry. - 160-161 (1996), p. 53-59. -
További szerzők:Pacher Pál Pankucsi Csaba (farmakológus) Nánási Péter Pál (1956-) (élettanász)
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6.

001-es BibID:BIBFORM009079
Első szerző:Lengyel Csaba (Szeged)
Cím:Role of slow delayed rectifier K+-current in QT prolongation in the alloxan-induced diabetic rabbit heart / Lengyel, C., Virag, L., Kovacs, P. P., Kristof, A., Pacher, P., Kocsis, E., Koltay, Z. M., Nanasi, P. P., Toth, M., Kecskemeti, V., Papp, J. G., Varro, A., Jost, N.
Dátum:2008
ISSN:1748-1716 (Electronic)
Megjegyzések:In diabetes mellitus, several cardiac electrophysiological parameters are known to be affected. In rodent experimental diabetes models, changes in these parameters were reported, but only limited relevant information is available in other species, having cardiac electrophysiological properties more resembling the human, including the rabbit. The present study was designed to analyse the effects of experimental type 1 diabetes on ventricular repolarization and the underlying transmembrane potassium currents in rabbit hearts. METHODS: Diabetes was induced by a single injection of alloxan (145 mg kg(-1) i.v.). After the development of diabetes (3 weeks), electrophysiological studies were performed using whole cell voltage clamp and ECG measurements. RESULTS: The QT(c) interval in diabetic rabbits was moderately but statistically significantly longer than measured in the control animals (155 +/- 1.8 ms vs. 145 +/- 2.8 ms, respectively, n = 9-10, P < 0.05). This QT(c)-lengthening effect of diabetes was accompanied by a significant reduction in the density of the slow delayed rectifier K(+) current, I(Ks) (from 1.48 +/- 0.35 to 0.86 +/- 0.17 pA pF(-1) at +50 mV, n = 19-21, P < 0.05) without changes in current kinetics. No differences were observed either in the density or in the kinetics of the inward rectifier K(+) current (I(K1)), the rapid delayed rectifier K(+) current (I(Kr)), the transient outward current (I(to)) and the L-type calcium current (I(CaL)) between the control and alloxan-treated rabbits. CONCLUSION: It is concluded that type 1 diabetes mellitus, although only moderately, lengthens ventricular repolarization. Diabetes attenuates the repolarization reserve by decreasing the density of I(Ks) current, and thereby may enhance the risk of sudden cardiac death.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Alloxan
Animals
Delayed Rectifier Potassium Channels
Diabetes Mellitus, Experimental
Electrocardiography
Heart
Heart Conduction System
Heart Ventricles
Long QT Syndrome
Male
Patch-Clamp Techniques
Rabbits
Megjelenés:Acta Physiologica (Oxford, England). - 192 : 3 (2008), p. 359-368. -
További szerzők:Virág László (élettanász Szeged) Kovacs Péter Pál (Szeged) Kristóf A. (Szeged) Pacher Pál Kocsis E. Koltay Zs. M. Nánási Péter Pál (1956-) (élettanász) Tóth M. Kecskeméti Valéria Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Jost Norbert
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7.

001-es BibID:BIBFORM030258
035-os BibID:WOS:000181565400020
Első szerző:Magyar János (élettanász)
Cím:Differential effects of fluoxetine enantiomers in mammalian neural and cardiac tissues / János Magyar, Zoltán Rusznák, Csaba Harasztosi, Ágnes Körtvély, Pál Pacher, Tamás Bányász, Csaba Pankucsi, László Kovács, Géza Szűcs, Péter P. Nánási, Valéria Kecskeméti
Dátum:2003
ISSN:1107-3756
Megjegyzések:Racemic fluoxetine is a widely used SSRI antidepressant compound having also anticonvulsant effect. In addition, it was shown that it blocked several types of voltage gated ion channels including neural and cardiac calcium channels. In the present study the effects of enantiomers of fluoxetine (R(-)-fluoxetine and S(+)-fluoxetine) were compared on neuronal and cardiac voltage-gated Ca2+ channels using the whole cell configuration of patch clamp techniques, and the anticonvulsant action of these enantiomers was also evaluated in a mouse epilepsy model. In isolated pyramidal neurons of the dorsal cochlear nucleus of the rat the effect of fluoxetine (S(+), R(-) and racemic) was studied on the Ca2+ channels by measuring peak Ba2+ current during ramp depolarizations. All forms of fluoxetine reduced the Ba2+ current of the pyramidal cells in a concentration-dependent manner, with a K, value of 22.3 +/- 3.6 muM for racemic fluoxetine. This value of K, was higher by one order of magnitude than found in cardiac myocytes with fluoxetine enantiomers (2.4 +/- 0.1 and 2.8 +/- 0.2 muM). Difference between the effects of the two enantiomers on neuronal Ba2+, current was observed only at 5 muM concentration: R(-)-fluoxetine inhibited 28 +/- 3% of the peak current, while S(+)-fluoxetine reduced the current by 18 +/- 2% (n=13, P<0.05). In voltage clamped canine ventricular cardiomyocytes both enantiomers of fluoxetine caused a reversible concentration-dependent block of the peak Ca2+ current measured at 0 mV. Significant differences between the two enantiomers in this blocking effect was observed at low concentrations only: S(+)-fluoxetine caused a higher degree of block than R(-)-fluoxetine (56.3 +/- 2.2% versus 49.1 +/- 2.2% and 95.5 +/- 0.9% versus 84.5 +/- 3.1% block with 3 and 10 &mu;M S(+) and R(-)-fluoxetine, respectively, P<0.05, n=5). Studied in current clamp mode, micromolar concentrations of fluoxetine shortened action potential duration of isolated ventricular cells, while higher concentrations also suppressed maximum velocity of depolarization and action potential amplitude. This shortening effect was significantly greater in the case of S(+) than R(-)-fluoxetine at 1 and 3 muM concentrations, whereas no differences in their effects on depolarization were observed. In pentylenetetrazole-induced mouse epilepsy model fluoxetine pretreatment significantly increased the 60 min survival rate, survival duration and seizure latency. These effects were more pronounced with the R(-) than the S(+) enantiomer. The results indicate that fluoxetine exerts much stronger suppressive effect on cardiac than neuronal calcium channels. At micromolar concentrations (between 1 and 10 muM) R(-)-fluoxetine is more effective than the S(+) enantiomer on neuronal, while less effective on cardiac calcium channels. The stronger anticonvulsant effect of the R(-) enantiomer may, at least partially, be explained by these differences. Used as an antidepressant or anticonvulsant drug, less severe cardiac side-effects are anticipated with the R(-) enantiomer.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:International Journal of Molecular Medicine. - 11 : 4 (2003), p. 535-542. -
További szerzők:Rusznák Zoltán (1965-) (élettanász) Harasztosi Csaba Körtvély Ágnes Pacher Pál Bányász Tamás (1960-) (élettanász) Pankucsi Csaba (farmakológus) Kovács László (1939-) (élettanász) Szűcs Géza (1948-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Kecskeméti Valéria
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8.

001-es BibID:BIBFORM030256
035-os BibID:WOS:000178499200009
Első szerző:Magyar János (élettanász)
Cím:Electrophysiological effects of risperidone in mammalian cardiac cells / János Magyar, Tamás Bányász, Zsolt Bagi, Pál Pacher, Norbert Szentandrássy, László Fülöp, Valéria Kecskeméti, Péter P. Nánási
Dátum:2002
ISSN:0028-1298
Megjegyzések:In this study, the effects of risperidone, the widely used antipsychotic drug, on isolated canine ventricular myocytes and guinea-pig papillary muscles were analyzed using conventional microelectrode and whole cell voltage-clamp techniques. Risperidone concentration-dependently lengthened action potential duration in guinea-pig papillary muscles (EC50=0.29 +/- 0.02 muM) and single canine ventricular myocytes (EC50=0.48 +/- 0.14 muM). This effect was reversible, showed reverse rate dependence, and it was most prominent on the terminal portion of repolarization. No significant effect of risperidone on the resting membrane potential, action potential amplitude or maximum rate of depolarization was observed. In voltage-clamped canine ventricular myocytes risperidone caused concentration-dependent block of the rapid component of the delayed rectifier K+ current (1(Kr)), measured as outward current tails at -40 mV with an IC50 of 0.92 +/- 0.26 muM. Suppression of I-Kr was not associated with changes in activation or deactivation kinetics. High concentration of risperidone (10 muM) suppressed also the slow component of the delayed rectifier K+ current (I-Ks) by 9.6 +/- 1.5% at +50 mV. These effects of risperidone developed rapidly and were readily reversible. Risperidone had no significant effect on the amplitude of other K+ currents (I-K1 and I-to). The inhibition of cardiac I-Kr current by risperidone may explain the cardiac side-effects observed occasionally with the drug. Our results suggest that risperidone displays class III antiarrhythmic properties, and as such, may produce QTc prolongation, especially in patients with long QT syndrome. Therefore, in psychotic patients having also cardiac disorders, ECG control may be suggested during risperidone therapy.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedebergs Archives of Pharmacology. - 366 : 4 (2002), p. 350-356. -
További szerzők:Bányász Tamás (1960-) (élettanász) Bagi Zsolt (1974-) (orvos) Pacher Pál Szentandrássy Norbert (1976-) (élettanász) Fülöp László (1976-) (kardiológus) Kecskeméti Valéria Nánási Péter Pál (1956-) (élettanász)
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9.

001-es BibID:BIBFORM030332
035-os BibID:WOS:000080469500003
Első szerző:Pacher Pál
Cím:Speculations on difference between tricyclic and selective serotonin reuptake inhibitor antidepressants on their cardiac effects : Is there any? / Pal Pacher, Zoltan Ungvari, Peter P. Nanasi, Susanna Furst, Valeria Kecskemeti
Dátum:1999
ISSN:0929-8673
Megjegyzések:The cardiovascular effects and toxicity of tricyclic antidepressants (TCAs) have been well documented in medical literature. The most common manifestation of such effects is slowing of intraventricular conduction, manifested by prolonged PR, QRS and QT intervals on the standard electrocardiogram (ECG) and postural hypotension. In contrast to TCAs; selective serotonin reuptake inhibitors (SSRIs), including fluoxetine and citalopram, are considered to cause less effect on cardiac impulse conduction. In addition, these compounds induced significantly less anticholinergic, antihistaminergic and cardiotoxic side-effects than TCAs. However, there is an increasing number of case reports on dysrhythmias, like atrial fibrillation or bradycardia and syncope associated with fluoxetine and another SSRI treatment and overdose. Although such reports have not been common, they do raise concerns. In cardiac tissues isolated from canine, rabbit, rat and guinea pig hearts we have found that fluoxetine and citalopram inhibited cardiac Na+ and Ca2+ channels. These direct cardiac electrophysiological effects were similar to those of observed for tricyclic antidepressants clomipramine and imipramine. The inhibition of cardiac Ca2+ and Na+ channels by fluoxetine may explain most cardiac side-effects observed occasionally with the drug and mild but significant bradycardia reported during chronic treatment. Our results suggest that fluoxetine and citalopram may have antiarrhythmic (class I + IV type), as well as proarrhythmic properties (due to impairment of atrioventricular or intraventricular conduction and shortening of repolarization). Taking all these into consideration, in depressed patients having also severe cardiac disorders, ECG control may be suggested during fluoxetine and probable another SSRI therapy. The primary goal of this review is to compare these direct cardiac effects of fluoxetine and citalopram to those of previously reported for TCAs. This paper also summarizes the recently observed effects of fluoxetine apparently not related to the blockage of 5-HT transporter based on literature.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current Medicinal Chemistry. - 6 : 6 (1999), p. 469-480. -
További szerzők:Ungvári Zoltán Nánási Péter Pál (1956-) (élettanász) Furst, Susanna Kecskeméti Valéria
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10.

001-es BibID:BIBFORM030273
Első szerző:Pacher Pál
Cím:Electrophysiological changes in rat ventricular and atrial myocardium at different stages of experimental diabetes / P. Pacher, Z. Ungvari, P. P. Nanasi, V. Kecskemeti
Dátum:1999
ISSN:0001-6772
Megjegyzések:Action potential configuration in ventricular and atrial myocardium, as well as rate-dependent changes in ventricular action potential duration (APD) were studied and compared in healthy and diabetic rats. Diabetes was induced by a single injection of streptozotocin (STZ, 65 mg kg(-1) i.v.). Conventional microelectrode techniques were applied to record action potentials after the establishment of diabetes (2, 6, 10 and 18 weeks after STZ-treatment). Untreated age-matched animals were used as controls. Both depolarization and repolarization were significantly retarded following STZ-treatment. However, the time course of development of diabetic changes in atrial and ventricular myocardium was different. APD was significantly lengthened from week 2 of diabetes in ventricular; but only from week 6 in atrial preparations. In atrial myocardium. lengthening of APD was more pronounced at early rather than late phases of repolarization.,The maximum rate of depolarization (V-max) was significantly reduced from the 6th week of diabetes in both preparations. No differences were observed in action potential amplitude (except at week 18) and in the resting membrane potential in diabetic rats. Diabetic ventricular preparations showed a positive APD-frequency relationship at any level of repolarization. in contrast to control muscles, where APD(25) and APD(50) values lengthened. But APD(75) and APD(90) values were not changed significantly with increase in the pacing frequency. The results indicate that development of diabetic alterations are not fully identical in atrial and ventricular myocardium of the rat, probably owing to differences in density and kinetics of ionic currents responsible for atrial and ventricular action potentials.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Acta Physiologica Scandinavica. - 166 : 1 (1999), p. 7-13. -
További szerzők:Ungvári Zoltán Nánási Péter Pál (1956-) (élettanász) Kecskeméti Valéria
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11.

001-es BibID:BIBFORM030272
Első szerző:Pacher Pál
Cím:Post-partum prolongation of the atrial repolarization in rabbit / P. Pacher, Z. Ungvari, P. P. Nanasi, I. Mucha, V. Kecskemeti, Gy. Losonczy
Dátum:1999
ISSN:0001-6772
Megjegyzések:Female sexual steroids are known to modify the expression of various K+ channels and thus they can alter cardiac repolarization. In the present work, using conventional microelectrode techniques, action potential characteristics were studied in atrial myocardium isolated from virgin, late pregnant, early (1-3 days) post-partum and late (2-3 weeks) post-partum rabbits. No changes in action potential configuration were observed during pregnancy. However, the duration, overshoot and amplitude of action potentials were significantly increased in the early (1-3 days) post-partum period. Resting potential and maximum rate of depolarization remained unchanged. The observed changes were transient, normal action potential characteristics were obtained at weeks 2-3 post-partum. 4-aminopyridine (1 mmol L-1). caused a marked lengthening of action potential duration in all preparations obtained from non-pregnant and pregnant rabbits, whereas this 4-aminopyridine-induced prolongation was moderate in those preparations excised from the hearts of early post-partum animals. Action potential configuration was not affected by pinacidil (10 mu mol L-1) or glibenclamide (5 mu mol L-1) in non-pregnant or pregnant animals. In preparations obtained from early post-partum rabbits, pinacidil significantly shortened action potential duration, which was reverted by glibenclamide. The lengthening of action potential duration together with the decreased sensitivity to 4-aminopyridine observed in early post-partum animals may probably be caused by reduction of the transient outward K+ current at this stage. The results also suggest that electrophysiological alterations in the early post-partum period may probably be more pronounced than those associated with pregnancy itself.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Acta Physiologica Scandinavica. - 166 : 1 (1999), p. 1-5. -
További szerzők:Ungvári Zoltán Nánási Péter Pál (1956-) (élettanász) Mucha, I. Kecskeméti Valéria Losonczy György
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12.

001-es BibID:BIBFORM030271
Első szerző:Pacher Pál
Cím:Cardiac electrophysiological effects of citalopram in guinea pig papillary muscle comparison with clomipramine / Pál Pacher, Zsolt Bagi, Zoltán Lako-Futo, Zoltán Ungvari, Péter P. Nanasi, Valéria Kecskemeti
Dátum:2000
ISSN:0306-3623
Megjegyzések:The effect of citalopram, a selective serotonin reuptake inhibitor (SSRI) antidepressant, was studied on cardiac action potential configuration and compared with that of the tricyclic antidepressant (TCA) clomipramine. Conventional microelectrode techniques were used in right ventricular papillary muscle preparations of the guinea pig. Citalopram caused a concentration-dependent (10-100 mu M) shortening of action potential duration (APD), depression of plateau and overshoot potential, and reduction of maximum velocity of depolarization (V-max). No significant changes in resting membrane potential were observed. Similar results were obtained with clomipramine; however, reduction of V-max and overshoot was more pronounced with clomipramine, whereas citalopram caused relatively greater shortening of APD. Effects of both drugs were partly reversible. The results indicate that the SSRI antidepressant citalopram, similarly to TCA compounds, alters cardiac action potential configuration in guinea pig ventricular muscle, probably owing to inhibition of cardiac Na+ and Ca2+ channels. Differences in cardiac side effects of the two drugs may be related to their different actions on cardiac action potential configuration. (C) 2000 Elsevier Science inc. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:General Pharmacology. - 34 : 1 (2000), p. 17-23. -
További szerzők:Bagi Zsolt (1974-) (orvos) Lakó-Futó Zoltán Ungvári Zoltán Nánási Péter Pál (1956-) (élettanász) Kecskeméti Valéria
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