@article{MTMT:32837575,
	title = {Purinergic signaling in thyroid disease},
	url = {https://m2.mtmt.hu/api/publication/32837575},
	author = {Le, Y. and Lu, D. and Xue, M.},
	doi = {10.1007/s11302-022-09858-2},
	journal-iso = {PURINERG SIGNAL},
	journal = {PURINERGIC SIGNALLING},
	volume = {19},
	unique-id = {32837575},
	issn = {1573-9538},
	abstract = {It is known that thyroid hormones play pivotal roles in a wide variety of pathological and physiological events. Thyroid diseases, mainly including hyperthyroidism, hypothyroidism, and thyroid cancer, are highly prevalent worldwide health problems and frequently associated with severe clinical manifestations. However, etiology of hyperthyroidism, hypothyroidism, and thyroid cancer is not fully understood. Purinergic signaling accounts for a complex network of receptors and extracellular enzymes responsible for the recognition and degradation of extracellular nucleotides and adenosine. It has been established that purinergic signaling modulates pathways in a wide range of physiopathological conditions including hypertension, diabetes, hepatic diseases, psychiatric and neurodegeneration, rheumatic immune diseases, and cancer. More recently, the purinergic system is found to exist in thyroid gland and play an important role in the pathophysiology of thyroid diseases. Therefore, throughout this review, we focus on elaborating the changes in purinergic receptors, extracellular enzymes, and extracellular nucleotides and adenosine in hyperthyroidism, hypothyroidism, and thyroid cancer. Profound understanding of the relationship between the purinergic signaling with thyroid diseases provides a promising research area for insights into the molecular basis of thyroid diseases and also develops new and exciting insights into the treatment of thyroid diseases, especially thyroid cancer. © 2022, The Author(s), under exclusive licence to Springer Nature B.V.},
	keywords = {hyperthyroidism; adenosine; HYPOTHYROIDISM; ATP; adenine nucleotides; purinergic receptors; thyroid cancer; Purinergic signaling},
	year = {2022},
	eissn = {1573-9546},
	pages = {221-227}
}

@article{MTMT:32193722,
	title = {A Body of Circumstantial Evidence for the Irreversible Ectonucleotidase Inhibitory Action of FSCPX, an Agent Known as a Selective Irreversible A1 Adenosine Receptor Antagonist So Far},
	url = {https://m2.mtmt.hu/api/publication/32193722},
	author = {Viczján, Gábor and Erdei, Tamás Dániel and Óvári, Ignác and Lampé, Nóra and Szekeres, Réka Mária and Bombicz, Mariann and Takács, Barbara and Szilágyi, Anna and Zsuga, Judit and Szilvássy, Zoltán and Juhász, Béla and Gesztelyi, Rudolf},
	doi = {10.3390/ijms22189831},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {22},
	unique-id = {32193722},
	issn = {1661-6596},
	abstract = {In previous studies using isolated, paced guinea pig left atria, we observed that FSCPX, known as a selective A(1) adenosine receptor antagonist, paradoxically increased the direct negative inotropic response to A(1) adenosine receptor agonists (determined using concentration/effect (E/c) curves) if NBTI, a nucleoside transport inhibitor, was present. Based on mathematical modeling, we hypothesized that FSCPX blunted the cardiac interstitial adenosine accumulation in response to nucleoside transport blockade, probably by inhibiting CD39 and/or CD73, which are the two main enzymes of the interstitial adenosine production in the heart. The goal of the present study was to test this hypothesis. In vitro CD39 and CD73 inhibitor assays were carried out; furthermore, E/c curves were constructed in isolated, paced rat and guinea pig left atria using adenosine, CHA and CPA (two A(1) adenosine receptor agonists), FSCPX, NBTI and NBMPR (two nucleoside transport inhibitors), and PSB-12379 (a CD73 inhibitor), measuring the contractile force. We found that FSCPX did not show any inhibitory effect during the in vitro enzyme assays. However, we successfully reproduced the paradox effect of FSCPX in the rat model, mimicked the "paradox" effect of FSCPX with PSB-12379, and demonstrated the lipophilia of FSCPX, which could explain the negative outcome of inhibitor assays with CD39 and CD73 dissolved in a water-based solution. Taken together, these three pieces of indirect evidence are strong enough to indicate that FSCPX possesses an additional action besides the A(1) adenosine receptor antagonism, which action may be the inhibition of an ectonucleotidase. Incidentally, we found that POM-1 inhibited CD73, in addition to CD39.},
	keywords = {HEART; Guinea pig; atrium; A(1) adenosine receptor; ectonucleotidase; FSCPX; rat; NBTI; extracellular adenosine; POM-1; PSB-12379; NBMPR},
	year = {2021},
	eissn = {1422-0067},
	orcid-numbers = {Zsuga, Judit/0000-0002-5350-8188; Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:31012994,
	title = {Accuracy and Precision of the Receptorial Responsiveness Method (RRM) in the Quantification of A1 Adenosine Receptor Agonists},
	url = {https://m2.mtmt.hu/api/publication/31012994},
	author = {Vargáné Szabó, Adrienn Mónika and Viczján, Gábor and Erdei, Tamás Dániel and Simon, Ildiko and Kiss, Rita and Szentmiklósi, József András and Juhász, Béla and Papp, Csaba Sándor and Zsuga, Judit and Pinter, Akos and Szilvassy, Zoltan and Gesztelyi, Rudolf},
	doi = {10.3390/ijms20246264},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {20},
	unique-id = {31012994},
	issn = {1661-6596},
	year = {2019},
	eissn = {1422-0067},
	orcid-numbers = {Kiss, Rita/0000-0003-1208-366X; Zsuga, Judit/0000-0002-5350-8188; Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:3407995,
	title = {FSCPX, a Chemical Widely Used as an Irreversible A1 Adenosine Receptor Antagonist, Modifies the Effect of NBTI, a Nucleoside Transport Inhibitor, by Reducing the Interstitial Adenosine Level in the Guinea Pig Atrium},
	url = {https://m2.mtmt.hu/api/publication/3407995},
	author = {Erdei, Tamás Dániel and Vargáné Szabó, Adrienn Mónika and Lampé, Nóra and Szabo, K and Kiss, Rita and Zsuga, Judit and Papp, Csaba Sándor and Pintér, Ákos and Szentmiklósi, József András and Szilvassy, Z and Juhász, Béla and Gesztelyi, Rudolf},
	doi = {10.3390/molecules23092186},
	journal-iso = {MOLECULES},
	journal = {MOLECULES},
	volume = {23},
	unique-id = {3407995},
	issn = {1420-3049},
	year = {2018},
	eissn = {1420-3049},
	orcid-numbers = {Kiss, Rita/0000-0003-1208-366X; Zsuga, Judit/0000-0002-5350-8188; Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:3224927,
	title = {Methodical Challenges and a Possible Resolution in the Assessment of Receptor Reserve for Adenosine, an Agonist with Short Half-Life},
	url = {https://m2.mtmt.hu/api/publication/3224927},
	author = {Zsuga, Judit and Erdei, Tamás Dániel and Szabo, K and Lampé, Nóra and Papp, Csaba Sándor and Pintér, Ákos and Szentmiklósi, József András and Juhász, Béla and Szilvássy, Zoltán and Gesztelyi, Rudolf},
	doi = {10.3390/molecules22050839},
	journal-iso = {MOLECULES},
	journal = {MOLECULES},
	volume = {22},
	unique-id = {3224927},
	issn = {1420-3049},
	year = {2017},
	eissn = {1420-3049},
	orcid-numbers = {Zsuga, Judit/0000-0002-5350-8188; Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:24573133,
	title = {Adenosine A1 receptor activation modulates human equilibrative nucleoside transporter 1 (hENT1) activity via PKC-mediated phosphorylation of serine-281},
	url = {https://m2.mtmt.hu/api/publication/24573133},
	author = {Hughes, SJ and Cravetchi, X and Vilas, G and Hammond, JR},
	doi = {10.1016/j.cellsig.2015.02.023},
	journal-iso = {CELL SIGNAL},
	journal = {CELLULAR SIGNALLING},
	volume = {27},
	unique-id = {24573133},
	issn = {0898-6568},
	year = {2015},
	eissn = {1873-3913},
	pages = {1008-1018}
}

@article{MTMT:2883644,
	title = {The effect of adenosine deaminase inhibition on the A1 adenosinergic and M2 muscarinergic control of contractility in eu- and hyperthyroid guinea pig atria},
	url = {https://m2.mtmt.hu/api/publication/2883644},
	author = {Pák, Krisztián and Zsuga, Judit and Képes, Zita and Erdei, Tamás Dániel and Varga, Balázs and Juhász, Béla and Szentmiklósi, József András and Gesztelyi, Rudolf},
	doi = {10.1007/s00210-015-1121-6},
	journal-iso = {N-S ARCH PHARMACOL},
	journal = {NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY},
	volume = {388},
	unique-id = {2883644},
	issn = {0028-1298},
	year = {2015},
	eissn = {1432-1912},
	pages = {853-868},
	orcid-numbers = {Zsuga, Judit/0000-0002-5350-8188; Képes, Zita/0000-0003-2889-8521; Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:2441369,
	title = {Approximation of A1 adenosine receptor reserve appertaining to the direct negative inotropic effect of adenosine in hyperthyroid guinea pig left atria},
	url = {https://m2.mtmt.hu/api/publication/2441369},
	author = {Pák, Krisztián and Papp, Csaba Sándor and Galajda, Z and Szerafin, Tamás and Varga, Balázs and Juhász, Béla and Haines, David and Szentmiklósi, József András and Tósaki, Árpád and Gesztelyi, Rudolf},
	doi = {10.4149/gpb_2013079},
	journal-iso = {GEN PHYSIOL BIOPHYS},
	journal = {GENERAL PHYSIOLOGY AND BIOPHYSICS},
	volume = {33},
	unique-id = {2441369},
	issn = {0231-5882},
	keywords = {Myocardial Contraction; Animals; Male; ARTICLE; Guinea Pigs; controlled study; HEART; Dose-Response Relationship, Drug; nonhuman; animal tissue; animal model; animal experiment; concentration response; Ischemic Preconditioning; hyperthyroidism; adenosine; receptor upregulation; intracellular space; heart protection; thyroxine; Cardiovascular mortality; adenosine A1 receptor; thyroid hormones; inotropism; Heart Atria; heart left atrium; euthyroidism; atrium; heart atrium contractility; Receptorial responsiveness method; Receptor reserve; Inotropy; Receptor, Adenosine A1; Hartley guinea pig; A1 adenosine receptor},
	year = {2014},
	eissn = {1338-4325},
	pages = {177-188},
	orcid-numbers = {Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:25422883,
	title = {Új lehetőség farmakológiai agonisták receptorközeli koncentrációjának becslésére: a receptoriális válaszkészség módszer (RRM)},
	url = {https://m2.mtmt.hu/api/publication/25422883},
	author = {Pák, Krisztián and Kiss, Z and Erdei, Tamás Dániel and Képes, Zita and Gesztelyi, Rudolf},
	journal-iso = {ACTA PHARM HUNG},
	journal = {ACTA PHARMACEUTICA HUNGARICA},
	volume = {84},
	unique-id = {25422883},
	issn = {0001-6659},
	abstract = {Cardiovascular disease is the biggest challenge in terms of life expectancy in developed countries. Adenosine contributes to the adaptation of the heart to ischemia and hypoxia, because adenosine, in addition to its metabolite role in the nucleic acid metabolism, is the endogenous agonist of the ubiquitous adenosine receptor family. Adenosine receptor activation is beneficial in most cases, it improves the balance between energy supply and consumption, reduces injury caused by stressors and inhibits the unfavorable tissue remodeling. Pharmacological manipulation of cardioprotective effects evoked by adenosine is an important, although to date not sufficiently utilized endeavor that may have therapeutic and preventive implications in cardiovascular diseases. As the ligand binding site of adenosine receptors is accessible from the extracellular space, it is especially important to know the adenosine concentration of the interstitial fluid ([Ado]ISF). However, in the functioning heart, [Ado]ISF values range in an extremely wide interval, spanning from nano- to micromolar concentrations, as estimated by the commonly used methods. Our recently developed procedure, the receptorial responsiveness method (RRM), may resolve this problem in certain cases. RRM enables quantification of an acute increase in the concentration of a pharmacological agonist, uniquely in the microenvironment of the receptors of the given agonist. As a limitation, concentration of agonists with short half-life (just like adenosine) at their receptors can only be quantified with the equieffective concentration of a stable agonist exerting the same action. In a previous study using RRM, inhibition of the transmembrane nucleoside transport in the euthyroid guinea pig atrium produced an increase in [Ado]ISF that was equieffective with 18.8 ± 3 nM CPA (N6-cyclopentyladenosine, a stable, selective A1 adenosine receptor agonist). This finding is consistent with observations of others, i.e., in the normoxic heart, adenosine flow is directed into the cell interior, and thus transport blockade elevates the extracellular adenosine level. In turn, nucleoside transport inhibition in the hyperthyroid guinea pig atrium caused a rise in [Ado]ISF equieffective with 46.5 ± 13.7 nM CPA. In sum, our work team was the first to demonstrate that adenosine transport in the hyperthyroid atrium has the same direction but is more intense as/than that in the euthyroid one.},
	keywords = {atrium; RRM; Heart.; interstitial adenosine concentration},
	year = {2014},
	eissn = {1587-1495},
	pages = {38-52},
	orcid-numbers = {Képes, Zita/0000-0003-2889-8521; Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:2360355,
	title = {The guinea pig atrial A1 adenosine receptor reserve for the direct negative inotropic effect of adenosine},
	url = {https://m2.mtmt.hu/api/publication/2360355},
	author = {Kiss, Zsuzsanna Mária and Pák, Krisztián and Zsuga, Judit and Juhász, Béla and Varga, Balázs and Szentmiklósi, József András and Haines, David and Tósaki, Árpád and Gesztelyi, Rudolf},
	doi = {10.4149/gpb_2013041},
	journal-iso = {GEN PHYSIOL BIOPHYS},
	journal = {GENERAL PHYSIOLOGY AND BIOPHYSICS},
	volume = {32},
	unique-id = {2360355},
	issn = {0231-5882},
	year = {2013},
	eissn = {1338-4325},
	pages = {325-335},
	orcid-numbers = {Zsuga, Judit/0000-0002-5350-8188; Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@mastersthesis{MTMT:25250675,
	title = {Az A1 adenozin receptor tiroxinnal szembeni érzékenységének és a direkt negatív inotróp hatáshoz tartozó receptor rezervjének meghatározása tengerimalac pitvaron},
	url = {https://m2.mtmt.hu/api/publication/25250675},
	author = {Kiss, Zsuzsanna Mária},
	unique-id = {25250675},
	abstract = {Első vizsgálati modellünk eredményei szerint a tengerimalac pitvari A1 receptor CPX (szelektív, ortoszterikus A1 receptor antagonista) iránti affinitása hyperthyreosisban kismértékben csökken az euthyreoid állapothoz képest. A kötőhely affinitáscsökkenése hozzájárulhat az A1 receptor mediálta folyamatok jól ismert gyengüléséhez hyperthyreoid állapotban, a mérték alapján azonban valószínű, hogy ez a mechanizmus csak részben felelős a jelenségért. Azt is megállapítottuk, hogy a CPX nem csak az eu-, hanem a hyperthyreoid pitvari A1 receptoron is tisztán kompetitív antagonista. Második vizsgálati modell kísérletei során azt kaptuk, hogy az irreverzibilis A1 receptor antagonista FSCPX (10 µM 45 percig, majd 75 perc mosás) nem csökkentette olyan mértékben a működőképes A1 receptorok számát, ami miatt szignifikánsan csökkenne a vizsgált A1 receptor full agonisták (NECA, CPA, CHA és adenozin) által kiváltott direkt negatív inotróp hatás maximuma tengerimalac bal pitvaron. Ezzel összhangban a stabil, szintetikus A1 receptor full agonisták (NECA, CPA, CHA) esetén a közel maximális direkt negatív inotróp hatáshoz tartozó A1 receptor rezervre igen nagy, 80-92% közötti értékeket kaptunk. Ezek a receptor rezerv értékek nagyobbak voltak minden korábbi irodalmi adatnál, ami az A1 receptor mediálta egyéb hatásokra vonatkozott tengerimalac pitvaron. Az élő szövetben bomlékony és gyorsan kompartmentalizálódó adenozin esetében az A1 receptor rezerv kvantifikálása nem sikerült, sőt az adenozin E/c görbék paradox módon viselkedtek NBTI (az adenozin intracelluláris eliminációját kivédő nukleozid transzport gátló) jelenlétében. Az NBTI miatt torzult adenozin E/c görbék matematikai korrekciója után azonban kiderült, hogy az adenozin direkt negatív inotróp hatására vonatkozó A1 receptor rezerv a szintetikus agonistákéhoz hasonlóan nagy. Ezek az eredményeink arra utalnak, hogy a pitvari kontraktilitás igen érzékeny az A1 receptor stimulációjára, ami miatt számítani kell a pitvari kontrakciós erő csökkenésére parciális A1 receptor agonisták és A1 receptor enhancer-ek esetében is, mint lehetséges mellékhatásra. 
		The main finding of our first study is that affinity of the guinea pig atrial A1 receptor towards CPX, a selective, orthosteric A1 receptor antagonist, moderately decreases in hyperthyroidism as compared to the euthyroid state. The reduced affinity of the binding site may contribute to the well-known decrease of A1 receptor mediated actions in hyperthyroidism (although it is probable that this mechanism is only in part responsible for the phenomenon). In addition, we found that CPX is a pure competitive antagonist for the hyperthyroid and not only for the euthyroid atrial A1 receptor. Results of our second study show that FSCPX, an irreversible A1 receptor antagonist (used in 10 µM for 45 min, followed by 75 min wash-out), failed to decrease the number of operable A1 receptors in an extent that would be sufficient to significantly reduce the maximum of the direct negative inotropic effect of NECA, CPA, CHA and adenosine, four A1 receptor full agonists, in guinea pig left atria. Accordingly, A1 receptor reserve has been found to be considerably great, ranging between 80-92% for the near maximal direct negative inotropic effect evoked by NECA, CPA and CHA, three stable synthetic A1 receptor full agonists. These receptor reserve values are higher than all historical values determined for any other A1 receptor mediated effect in the guinea pig atrium. Quantification of A1 receptor reserve failed for adenosine, a compound that is eliminated and compartmentalizes rapidly in the living tissues. Moreover, adenosine E/c curves generated in the presence of NBTI, a nucleoside transport inhibitor preventing the intracellular elimination of adenosine, seemed to behave paradoxically. However, after the mathematical correction of adenosine E/c curves biased by NBTI, it turned out that A1 receptor reserve for the direct negative inotropic effect of adenosine is similarly great as that of the synthetic agonists. These results indicate that atrial contractility is very sensitive to the stimulation of A1 receptors. Thus, a decrease in the contractile force of atria, as a possible side effect, should be considered even in the case of partial A1 receptor agonists and A1 receptor enhancers.},
	year = {2013}
}

@article{MTMT:2128687,
	title = {Thyroid hormones decrease the affinity of 8-cyclopentyl-1,3-dipropylxanthine (CPX), a competitive antagonist, for the guinea pig atrial A1 adenosine receptor},
	url = {https://m2.mtmt.hu/api/publication/2128687},
	author = {Gesztelyi, Rudolf and Kiss, Z and Zsuga, Judit and Pák, Krisztián and Papp, Csaba Sándor and Galajda, Zoltán and Branzaniuc, K and Szentmiklósi, József András and Tósaki, Árpád},
	doi = {10.4149/gpb_2012_043},
	journal-iso = {GEN PHYSIOL BIOPHYS},
	journal = {GENERAL PHYSIOLOGY AND BIOPHYSICS},
	volume = {31},
	unique-id = {2128687},
	issn = {0231-5882},
	year = {2012},
	eissn = {1338-4325},
	pages = {389-400},
	orcid-numbers = {Gesztelyi, Rudolf/0000-0001-7911-055X; Zsuga, Judit/0000-0002-5350-8188}
}

@mastersthesis{MTMT:23119512,
	title = {A receptoriális válaszkészség módszer (RRM) hasznosíthatósága és megbízhatósága, különös tekintettel az agonisták és a biológiai rendszer tulajdonságainak befolyására},
	url = {https://m2.mtmt.hu/api/publication/23119512},
	author = {Grenczer, M},
	unique-id = {23119512},
	year = {2011}
}

@article{MTMT:1395017,
	title = {Effect of asymmetry of concentration-response curves on the results obtained by the receptorial responsiveness method (RRM). an in silico study},
	url = {https://m2.mtmt.hu/api/publication/1395017},
	author = {Grenczer, Mária and Zsuga, Judit and Majoros, László and Pintér, Ákos and Kemény-Beke, Ádám and Juhász, Béla and Tósaki, Árpád and Gesztelyi, Rudolf},
	doi = {10.1139/Y10-089},
	journal-iso = {CAN J PHYSIOL PHARM},
	journal = {CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY},
	volume = {88},
	unique-id = {1395017},
	issn = {0008-4212},
	year = {2010},
	eissn = {1205-7541},
	pages = {1074-1083},
	orcid-numbers = {Zsuga, Judit/0000-0002-5350-8188; Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:1395027,
	title = {The influence of affinity, efficacy, and slope factor on the estimates obtained by the receptorial responsiveness method (RRM). a computer simulation study},
	url = {https://m2.mtmt.hu/api/publication/1395027},
	author = {Grenczer, Mária and Pintér, Ákos and Zsuga, Judit and Kemény-Beke, Ádám and Juhász, Béla and Szodoray, P and Tósaki, Árpád and Gesztelyi, Rudolf},
	doi = {10.1139/Y10-078},
	journal-iso = {CAN J PHYSIOL PHARM},
	journal = {CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY},
	volume = {88},
	unique-id = {1395027},
	issn = {0008-4212},
	year = {2010},
	eissn = {1205-7541},
	pages = {1061-1073},
	orcid-numbers = {Zsuga, Judit/0000-0002-5350-8188; Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@inbook{MTMT:1254050,
	title = {Some useful methods for the detection of redox signaling in various organs},
	url = {https://m2.mtmt.hu/api/publication/1254050},
	author = {Juhász, Béla and Gesztelyi, Rudolf and Tósaki, Árpád},
	booktitle = {Methods in Redox Signaling},
	unique-id = {1254050},
	year = {2010},
	pages = {163-171},
	orcid-numbers = {Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:2057566,
	title = {Az aszimmetrikus dimetil-arginin (adma) mint kapocs az inzulinrezisztencia és az atherosclerosis között [Asymmetric dimethil-arginine (ADMA) as a link between insulin resistance and atherosclerosis]},
	url = {https://m2.mtmt.hu/api/publication/2057566},
	author = {Zsuga, Judit},
	journal-iso = {IDEGGYOGY SZEMLE},
	journal = {IDEGGYOGYASZATI SZEMLE / CLINICAL NEUROSCIENCE},
	volume = {61},
	unique-id = {2057566},
	issn = {0019-1442},
	year = {2008},
	eissn = {2498-6208},
	pages = {183-192},
	orcid-numbers = {Zsuga, Judit/0000-0002-5350-8188}
}

@article{MTMT:1191395,
	title = {Adenosine deaminase inhibition enhances the inotropic response mediated by A(1) adenosine receptor in hyperthyroid guinea pig atrium},
	url = {https://m2.mtmt.hu/api/publication/1191395},
	author = {Kemény-Beke, Ádám and Jakab, A and Zsuga, Judit and Vecsernyés, Miklós and Karsai, D and Pasztor, F and Grenczer, Mária and Szentmiklósi, József András and Berta, András and Gesztelyi, Rudolf},
	doi = {10.1016/j.phrs.2007.04.017},
	journal-iso = {PHARMACOL RES},
	journal = {PHARMACOLOGICAL RESEARCH},
	volume = {56},
	unique-id = {1191395},
	issn = {1043-6618},
	year = {2007},
	eissn = {1096-1186},
	pages = {124-131},
	orcid-numbers = {Zsuga, Judit/0000-0002-5350-8188; Gesztelyi, Rudolf/0000-0001-7911-055X}
}