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1.

001-es BibID:BIBFORM024618
Első szerző:Benkő Ilona (orvos, farmakológus)
Cím:Effect of myelopoietic and pleiotropic cytokines on colony formation by blast cells of children with acute lymphoblastic leukemia / Ilona Benkő, Péter Kovács, István Szegedi, Attila Megyeri, Attila Kiss, Erzsébet Balogh, Éva Oláh, János Kappelmayer, Csongor Kiss
Dátum:2001
ISSN:0028-1298
Megjegyzések:The aim of this study was to see whether pleiotropic or myeloid hematopoietic growth factors, which do not stimulate normal lymphoid cells, can induce proliferation of blast cells of the acute lymphoid leukemia (ALL) of childhood. Bone marrow cells of 13 children with untreated ALL (nine common ALL, two myeloid antigen positive ALL and two early T-cell ALL) formed colonies of leukemic blast cells in primary methylcellulose cultures. Spontaneous growth was observed in three of 13 cases, whereas phytohemagglutinin-stimulated leukocyte conditioned medium (PHA-LCM), a conventional source of various natural human cytokines, induced colony formation in ten of 13 cases. A similar rate of responsiveness was seen with recombinant human granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and stem cell factor (SCF); a combination of these three cytokines induced colony formation in all cases studied. The effect of these growth factors on colony formation seemed to be dose-dependent in some cases. Of the stimuli studied, GM-CSF induced the smallest number of colonies, whereas the effects of G-CSF, SCF and PHA-LCM were similar in this respect. Combination of cytokines proved to be even more efficient in inducing clonal proliferation of leukemic lymphoblasts. In double combinations, G-CSF and GM-CSF as well as G-CSF and SCF were able to potentiate each other's effects. Triple combination of these cytokines mediated the most potent growth stimulus. Our results demonstrate that myeloid and pleiotropic cytokines are able to stimulate clonal proliferation of pediatric leukemic lymphoblasts. This may present a potential hazard to children with ALL while on adjuvant therapy with hematopoietic growth factors. In vitro colony assays performed prior to or in parallel with the administration of hematopoietic growth factors to ALL patients may help to forecast their possible effects on leukemic cells in vivo.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedebergs Archives Of Pharmacology 363 : 5 (2001), p. 499-508. -
További szerzők:Kovács Péter (1939-) (farmakológus) Szegedi István (1969-) (hematológus, onkológus, nefrológus) Megyeri Attila (1968-) (orvos) Kiss Attila (1942-) (belgyógyász, haematológus) Balogh Erzsébet (1949-) (biológus, citogenetikus) Oláh Éva (1943-2019) (gyermekgyógyász, klinikai genetikus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Kiss Csongor (1956-) (hematológus, onkológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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2.

001-es BibID:BIBFORM042841
035-os BibID:PMID:23474828
Első szerző:Drimba László (farmakológus)
Cím:The role of acute hyperinsulinemia in the development of cardiac arrhythmias / László Drimba, Róbert Döbrönte, Csaba Hegedüs, Réka Sári, Yin Di, Joseph Németh, Zoltán Szilvássy, Barna Peitl
Dátum:2013
Megjegyzések:Patients with perturbed metabolic control are more prone to develop cardiac rhythm disturbances. The main purpose of the present preclinical study was to investigate the possible role of euglycemic hyperinsulinemia in development of cardiac arrhythmias. Euglycemic hyperinsulinemia was induced in conscious rabbits equipped with a right ventricular pacemaker electrode catheter by hyperinsulinemic euglycemic glucose clamp (HEGC) applying two different rates of insulin infusion (5 and 10 mIU/kg/min) and variable rate of glucose infusion to maintain euglycemia (5.5±0.5 mmol/l). The effect of hyperinsulinemia on cardiac electrophysiological parameters was continuously monitored by means of 12-lead surface ECG recording. Arrhythmia incidence was determined by means of programmed electrical stimulation (PES). The possible role of adrenergic activation was investigated by determination of plasma catecholamine levels and intravenous administration of a beta adrenergic blocking agent, metoprolol. All of the measurements were performed during the steady-state period of HEGC and subsequent to metoprolol administration. Both 5 and 10 mIU/kg/min insulin infusion prolonged significantly QTend, QTc, and Tpeak-Tend intervals. The incidence of ventricular arrhythmias generated by PES was increased significantly by euglycemic hyperinsulinemia and exhibited linear relationship to plasma levels of insulin. No alteration on plasma catecholamine levels could be observed; however, metoprolol treatment restored the prolonged QTend, QTc, and Tpeak-Tend intervals and significantly reduced the hyperinsulinemia-induced increase of arrhythmia incidence. Euglycemic hyperinsulinemia can exert proarrhythmic effect presumably due to the enhancement of transmural dispersion of repolarization. Metoprolol treatment may be of benefit in hyperinsulinemia associated with increased incidence of cardiac arrhythmias.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedeberg's Archives of Pharmacology. - 386 : 5 (2013), p. 435-444. -
További szerzők:Döbrönte Róbert Hegedűs Csaba (1983-) (Molekuláris biológus, Cera-Med Kft. Debrecen) Sári Réka (farmakológus) Di, Yin Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
Pályázati támogatás:GOP-1.2.1-08-2009-0023
Egyéb
NKFP_07-A2-2008-0260
Egyéb
GOP-1.1.2-07/1-2008-0004
Egyéb
TÁMOP-4.2.2.-08/1-2008-0014
TÁMOP
OM-00174/2008
Egyéb
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
GOP-1.1.1-07/1- 2008-0032
Egyéb
OTKA-75965
OTKA
Internet cím:DOI
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3.

001-es BibID:BIBFORM061365
Első szerző:Kovács Diána Klára (Molekuláris biológus)
Cím:Meal-induced insulin sensitization is preserved after acute olanzapine administration in female Sprague-Dawley rats / Diána Kovács, Csaba Hegedűs, Rita Kiss, Réka Sári, József Németh, Zoltán Szilvássy, Barna Peitl
Dátum:2015
ISSN:0028-1298
Megjegyzések:Olanzapine, an atypical antipsychotic, can acutely induce fasting insulin resistance, but we do not know whether it is able to modulate the meal-induced insulin sensitization (MIS). Two main experimental groups (control and olanzapine-treated) were created with two subgroups (fasted and re-fed) within each. After oral vehicle/olanzapine administration, the first meal size and duration and the total amount of consumed food was recorded in conscious rats. Then, under anaesthesia, the carotid artery and jugular vein was prepared and cannulated to obtain samples for blood glucose and hormone determination as well as for insulin/glucose infusion, respectively. Basal insulin sensitivity and MIS was determined by homeostasis model assessment (HOMA) calculation and by rapid insulin sensitivity test, respectively. In fasted animals, olanzapine increased blood glucose and plasma insulin and reduced basal insulin sensitivity, but it failed to modify other hormone levels. Postprandial leptin and glucose-dependent insulinotropic polypeptide (GIP) levels increased, and ghrelin level decreased significantly (p?<?0.05) both in vehicle- and olanzapine-treated groups, but plasma insulin increased only in vehicle-treated animals. Furthermore, decrement in ghrelin level was attenuated in olanzapine-treated animals compared to controls. There was no significant change in the first meal size and duration or in the total amount of food consumed. Olanzapine had no effect on the MIS. We demonstrated that olanzapine can induce insulin resistance without weight gain in healthy rats. Furthermore, the MIS was preserved after acute olanzapine treatment. The blunted postprandial ghrelin and insulin response could contribute to the effect of olanzapine on feeding behaviour. Pharmacological induction of MIS may improve the olanzapine-induced insulin resistance.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Olanzapine
Insulin sensitivity
Satiety
Ghrelin
Gut hormones
Megjelenés:Naunyn-Schmiedebergs Archives Of Pharmacology. - 388 : 5 (2015), p. 525-530. -
További szerzők:Hegedűs Csaba (1983-) (Molekuláris biológus, Cera-Med Kft. Debrecen) Kiss Rita (1974-) (laboratóriumi diagnosztika szakorvos) Sári Réka (farmakológus) Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
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DOI
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4.

001-es BibID:BIBFORM048029
Első szerző:Miszti-Blasius Kornél (laboratóriumi szakorvos)
Cím:P-selectin glycoprotein ligand-1 deficiency augments G-CSF induced myeloid cell mobilization / Kornél Miszti-Blasius, Szabolcs Felszeghy, Csongor Kiss, Ilona Benkő, Krisztina Géresi, Attila Megyeri, Zsuzsanna Hevessy, János Kappelmayer
Dátum:2014
Megjegyzések:The effect of G-CSF was investigated in P-selectin Glycoprotein Ligand-1 (PSGL-1) deficient (PSGL-1-/-) and wild-type (PSGL-1+/+) mice to establish the role of this mucin in myeloid cell mobilization. G-CSF activates tissue proteases that cleave adhesion molecules, thus enhances the mobilization of myeloid cells and haematopoietic stem cells. Cytopenia was induced with a single dose of cyclophosphamide. In PSGL-1-/- animals, we observed a delayed extravasation of mature myeloid cells from the peripheral vessels into the tissue compartments and their faster mobilization from the bone marrow. Subsequently, animals received G-CSF twice a day for four days. Neutrophil and monocyte counts increased upon completion of G-CSF treatment and both values were significantly higher in PSGL-1-/- mice; 47.7 G/L vs. 28.3 G/L for neutrophils and 4.1 G/L vs. 2.0 G/L for monocytes. The ratio of atypical myeloid cells was also elevated. Analyzing the causes of the above differences, we identified a 4-fold increase in the colony forming unit (CFU-GM) counts of the peripheral blood in PSGL-1-/- mice, compared to wild type animals. A significantly elevated number of CFU-GM was detected also in the femurs of PSGL-1-/- mice, 4 and 5 days after cyclophosphamide treatment and these values paralleled with the elevation of CD34+/CD117+ stem cell counts in the peripheral blood. Our data suggest, that in the absence of PSGL-1, G-CSF was more potent in elevating absolute myeloid cell numbers by acting on cell release from the bone marrow, maturation from circulating precursor cells in the peripheral blood and prolonged retainment in the circulation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
P-selectin glycoprotein ligand-1
G-CSF
Myeloid cells
Colony-forming units
Stem cells
Mobilization
Megjelenés:Naunyn-Schmiedeberg's Archives of Pharmacology. - 387 : 2 (2014), p. 109-118. -
További szerzők:Felszeghy Szabolcs Béla (1972-) (fogorvos, anatómus, kötőszövetbiológus) Kiss Csongor (1956-) (hematológus, onkológus) Benkő Ilona (1954-) (orvos, farmakológus) Géresi Krisztina (1985-) (molekuláris biológus) Megyeri Attila (1968-) (orvos) Hevessy Zsuzsanna (1966-) (laboratóriumi szakorvos) Kappelmayer János (1960-) (laboratóriumi szakorvos)
Pályázati támogatás:TÁMOP 4.2.4. A/2-11-1-2012-0001
TÁMOP
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5.

001-es BibID:BIBFORM020267
Első szerző:Peitl Barna (orvos, farmakológus)
Cím:Insulin sensitization induced by oral cicletanine in conscious rabbits / Peitl B., Németh J., Pankucsi C., Szilvássy Z.
Dátum:2006
Megjegyzések:The endogenous insulin sensitizing machinery termed the hepatic insulin sensitizing substance (HISS) mechanism has been shown to be nitrergic and linked to sensory fibers in the anterior hepatic plexus. We studied whether this mechanism could pharmacologically be exploited by cicletanine, a cGMP-PDE inhibitor antihypertensive drug, in conscious rabbits. Whole body insulin sensitivity and peripheral glucose uptake were determined by hyperinsulinaemic euglycaemic glucose clamping, and cardiac radiolabelled deoxyglucose (DOG) uptake in neurogenic, achieved by perineurial capsaicin treatment of the anterior hepatic plexus through defunctionalization of hepatic sensory fibers, and metabolic, induced by dietary hypercholesterolemia, insulin resistance models after single oral doses of cicletanine (3, 10 and 30 mg kg(-1)) or rosiglitazone (3 mg kg(-1)). The effect of cicletanine on cardiac and vascular tissue NO, cGMP, cAMP was measured by means of spin trapping technique and radioimmunoassay, respectively. Insulin sensitivity and peripheral DOG uptake were significantly increased by 10 and 30 mg kg(-1) cicletanine in both healthy and hypercholesterolaemic rabbits, but not in those with neurogenic insulin resistance. Rosiglitazone had no effect in healthy and neurogenic insulin resistant rabbits although it improved insulin sensitivity in hypercholesterolemic animals. The 10 mg kg(-1) cicletanine dose induced no change in either cardiac or vascular tissue NO, cGMP or cAMP concentrations. Nevertheless, at a dose of 30 mg kg(-1) producing an insulin sensitizing effect of approximately the same amplitude as seen with 10 mg kg(-1), the drug significantly increased tissue NO and cGMP concentrations. Oral cicletanine attains its insulin sensitizing effect at doses lower than those necessary to activate the NO-cGMP pathway in the cardiovascular system. This metabolic effect requires functional integrity of hepatic sensory nerves.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
insulin
cicletanine
Megjelenés:Naunyn-Schmiedeberg's archives of pharmacology. - 373 : 6 (2006), p. 429-439. -
További szerzők:Németh József (1954-) (vegyész, analitikus) Pankucsi Csaba (farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
Pályázati támogatás:T043467
OTKA
T046244
OTKA
D45922
OTKA
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DOI
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6.

001-es BibID:BIBFORM009644
Első szerző:Szentmiklósi József András (farmakológus, klinikai laboratóriumi szakorvos)
Cím:Adenosine receptors mediate both contractile and relaxant effects of adenosine in main pulmonary artery of guinea pigs / Szentmiklósi A. J., Ujfalusi A., Cseppentő Á., Kovács P., Szabó J. Zs.
Dátum:1995
Megjegyzések:In guinea pig main pulmonary artery precontracted with noradrenaline, adenosine exerted an initial phasic contraction followed by a tonic contraction and a slow relaxation. After selective blockade by 1,3-dipropyl-8-cyclopentylxanthine (DPCPX: 10 nM) of A1 receptors, adenosine only elicited a rapid relaxation. This initial response was characterized by use of adenosine (AR) and its analogues N6-cyclopentyl-adenosine (CPA), R-N6-phenylisopropyladenosine (R-PIA), 2-chloroadenosine (CADO), 5'-N-ethyl-carboxamidoadenosine(NECA), N6-2-(4-aminophenyl) ethyl adenosine (APNEA) and 2-p-((carboxyethyl)-phenethylamino)-5'-carboxamidoadenosine (CGS 21 680). The order of potency of the adenosine analogues for purine-induced phasic contraction was CPA > R-PIA > NECA = APNEA > AR > CGS 21 680 suggesting the involvement of activation of A1 type adenosine receptors in the contraction phase. DPCPX antagonized the CPA-induced contraction with a pA2 = 9.27 +/- 0.26, but the Schild plot slope parameter was significantly lower than unity (0.58 +/- 0.09). In contrast, in electrically driven guinea pig atrial myocardium (a tissue reported to possess A1 receptors), the DPCPX-CPA antagonism was purely competitive (pA2 = 8.95 +/- 0.06; slope = 0.93 +/- 0.06). In the presence of 300 nM DPCPX, the rank order of potency for the purine-induced fast relaxation was NECA > CADO = AR > CGS 21 680 = R-PIA > CPA. The NECA- and adenosine-induced relaxation was influenced neither by 300 nM CP 66713 (an antagonist at A2a receptors), nor by endothelial removal and inhibition of nitric oxide synthase (100 microM NG-nitro-L-arginine: L-NOARG)
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedeberg's Archives of Pharmacology. - 351 : 4 (1995), p. 417-425. -
További szerzők:Ujfalusi Anikó (1968-) (gyermekorvos, laboratóriumi szakorvos) Cseppentő Ágnes (1953-) (orvos) Kovács Péter (1939-) (farmakológus) Szabó Judit Zsuzsanna (farmakológus, klinikai laboratóriumi szakorvos)
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