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1.

001-es BibID:BIBFORM042635
Első szerző:Fürjes Gergely
Cím:Thrittene radioimmunoassay : description and application of a novel method / G. Fürjes, G. K. Tóth, B. Peitl, R. Pórszász, B. Lelesz, R. Sári, A. Tóth, Z. Szilvássy, J. Németh
Dátum:2012
Megjegyzések:In the present paper the development andapplication of a novel thrittene radioimmunoassay (RIA)are described. 125I-labeling of Tyr(0)-thrittene was performedby the iodogen-method and the mono-iodinatedpeptide, as RIA tracer, was separated by reversed-phasehigh performance liquid chromatography (HPLC). TheRIA results show that the antiserum used in the radioimmunoassayturned to be C-terminal specific, without significantaffinity to other members of the somatostatinpeptide hormone family. Detection limit of the assay was0.2 fmol/ml. This highly specific and sensitive thritteneRIA was used to investigate the distribution of thrittene inthe rat gastrointestinal tract and other tissue samples. Differentareas of the gastrointestinal tract and other tissueswere removed from rats and after extraction the sampleswere processed for thrittene radioimmunoassay. Highestconcentrations were found in the duodenum samplesfollowed by jejunum and ileum, however, all the examinedtissues contained highly enough thrittene for themeasurement.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény hazai lapban
Megjelenés:Journal of Radioanalytical and Nuclear Chemistry. - 292 : 1 (2012), p. 113-118. -
További szerzők:Tóth Gábor K. Peitl Barna (1972-) (orvos, farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Lelesz Beáta (1989-) (molekuláris biológus) Sári Réka (farmakológus) Tóth Attila (1971-) (biológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Németh József (1954-) (vegyész, analitikus)
Pályázati támogatás:75965
OTKA
Internet cím:DOI
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2.

001-es BibID:BIBFORM020441
Első szerző:Sári Réka (farmakológus)
Cím:Impairment by lovastatin of neural relaxation of the rabbit sphincter of Oddi / Reka Sari, Jozsef Nemeth, Robert Porszasz, Peter Horvath, Ingolf E. Blasig, Peter Ferdinandy, Istvan Nagy, Janos Lonovics, Zoltan Szilvassy
Dátum:2001
Megjegyzések:AbstractWe sought whether inhibition of cholesterol biosynthesis by lovastatin influenced the nitrergic relaxation response of the sphincter of Oddi. Rabbit sphincters of Oddi rings were tested for changes in isometric tension in response to field stimulation in the presence of 4 microM guanethidine and 1 microM atropine. Tissue samples were then analyzed for cAMP and cGMP content by radioimmunoassay for nitric oxide concentration by electron spin resonance and for vasoactive intestinal peptide and calcitonin gene-related peptide (CGRP) release by radioimmunoassay. Membrane G(salpha) protein was determined by Western blot analysis. Field stimulation relaxed the preparations with an increase in nitric oxide, cAMP and cGMP concentrations at increased calcitonin gene-related peptide and vasoactive intestinal polypeptide (VIP) release. Preparations from rabbits pre-treated with lovastatin (5 mg/kg/day intragastrically, over 5 days) contracted under the same conditions with an attenuated cGMP-increase at preserved increase in NO content and neuropeptide release. The relaxation was recaptured combining lovastatin with farnesol (1 mg/kg intravenously, twice a day for 5 days). The field stimulation-induced increase in cyclic nucleotides was also restored. Lovastatin decreased membrane G(salpha) protein content, which was re-normalized by farnesol. Farnesol treatment reinstates neurogenic relaxation of the sphincter of Oddi deteriorated by lovastatin possibly by normalizing G-protein coupling.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Impairment by lovastatin
lovastatin
neural relaxation
Megjelenés:European Journal of Pharmacology. - 432 : 1 (2001), p. 91-97. -
További szerzők:Németh József (Pécs) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Horváth Péter Blasig, Ingolf E. Ferdinándy Péter Nagy István (orvos) Lonovics János (Szeged) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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DOI
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3.

001-es BibID:BIBFORM020340
Első szerző:Sári Réka (farmakológus)
Cím:Cyclic GMP-mediated activation of a glibenclamide-sensitive mechanism in the rabbit sphincter of Oddi / Reka Sari, Barna Peitl, Peter Kovacs, Janos Lonovics, Attila Palvolgyi, Peter Hegyi, Istvan Nagy, Jozsef Nemeth, Zoltan Szilvassy, Robert Porszasz
Dátum:2004
Megjegyzések:AbstractWe investigated whether glibenclamide-sensitive potassium channels are involved in cyclic GMP (cGMP)-mediated relaxation of the rabbit Oddi's sphincter. Changes in isometric tension were measured in the presence of atropine (1 microM) and guanethidine (4 microM). Concentration-response curves for nitroglycerin, vasoactive intestinal polypeptide (VIP), and sodium nitroprusside (SNP) were shifted to the right in the presence of (p-chloro-D-Phe6, Leu17)-VIP (VIPa), a VIP receptor antagonist. Glibenclamide (1 microM) attenuated the relaxations to VIP, nitroglycerin, or 8-bromo cGMP. In the presence of tetrodotoxin (TTX), glibenclamide attenuated relaxations to VIP without effect on those to nitroglycerin. Furthermore, nitroglycerin increased both cAMP and cGMP concentrations, however, it failed to increase the tissue cAMP concentration in the presence of TTX. VIPa also blocked the increase in content of either cyclic nucleotide. VIP increased cAMP with a TTX-sensitive increase in cGMP content. 8-Bromo cGMP (1 microM) significantly increased the tissue cAMP content. This was blocked by either TTX or VIPa (both 1 microM). We conclude that ATP-sensitive potassium channel (KATP) activation contributes to cGMP-mediated relaxation of the Oddi's sphincter of the rabbit. Activation of KATP results from a cyclic AMP-mediated process due to cGMP-dependent VIP release from neurons.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Cyclic GMP
GMP-Mediated Activation
Glibenclamide-Sensitive
Megjelenés:Digestive Diseases and Sciences. - 49 : 3 (2004), p. 514-520. -
További szerzők:Peitl Barna (1972-) (orvos, farmakológus) Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Lonovics János (Szeged) Pálvölgyi Attila Hegyi Péter Jenő (belgyógyász) Nagy István (orvos) Németh József (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus)
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4.

001-es BibID:BIBFORM020269
Első szerző:Szilvássy Judit (fül- orr- gégész)
Cím:Neurogenic insulin resistance in guinea-pigs with cisplatin-induced neuropathy / Judit Szilvássy, István Sziklai, Réka Sári, József Németh, Barna Peitl, Robert Porszasz, János Lonovics, Zoltán Szilvássy
Dátum:2006
Megjegyzések:The aim of the present work was to study whether neurotoxicity produced by cisplatin modified tissue insulin sensitivity in guinea-pigs. One week after selective sensory denervation of the anterior hepatic plexus by means of perineurial 2% capsaicin treatment, hyperinsulinaemic euglycaemic glucose clamp were performed to estimate insulin sensitivity in male guinea-pigs. The guinea-pigs underwent regional sensory denervation of the anterior hepatic plexus exhibited insulin resistance, whereas systemic capsaicin desensitization increased insulin sensitivity. Intraportal administration of L-nitro-arginine methyl ester (L-NAME decreased, whereas capsaicin increased insulin sensitivity. Neither atropine nor acetylcholine produced any significant effect. In animals with preceding regional capsaicin desensitization, none of the pharmacological maneuvers modified the resulting insulin resistant state. Cisplatin pretreatment induced sensory neuropathy and decreased insulin sensitivity. Insulin sensitivity did not change after either regional or systemic capsaicin desensitization in the cisplatin-treated animals. CGRP(8-37), a nonselective calcitonin gene-related peptide (CGRP) antagonist (50 microg/kg i.v.), significantly increased insulin sensitivity in normal animals but only a tendency to insulin sensitization was seen after cisplatin treatment. Cisplatin treatment, similar to regional capsaicin desensitization of the anterior hepatic plexus, produced a significant decrease in insulin-stimulated uptake of 2-deoxy-D [L-14C] glucose in cardiac and gastrocnemius muscle with no effect on percentage suppression of endogenous glucose production by hyperinsulinaemia. We conclude that the majority of cisplatin-induced insulin resistance is related to functional deterioration of the hepatic insulin sensitizing substance (HISS) mechanism.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
neurogenic insulin
insulin resistance
cisplatin-induced
neuropathy
Megjelenés:European Journal of Pharmacology. - 531 : 1-3 (2006), p. 217-225. -
További szerzők:Sziklai István (1954-) (fül-orr-gégész) Sári Réka (farmakológus) Németh József (1954-) (vegyész, analitikus) Peitl Barna (1972-) (orvos, farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Lonovics János (Szeged) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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