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1.

001-es BibID:BIBFORM020522
Első szerző:Németh József (Pécs)
Cím:Decreased sensory neuropeptide release from trachea of rats with streptozotocin-induced diabetes / Joseph Nemeth, Zoltan Szilvassy, Martha Than, Gabor Oroszi, Reka Sari, Janos Szolcsanyi J.
Dátum:2000
Megjegyzések:We studied the release of somatostatin, calcitonin gene-related peptide (CGRP) and substance P in response to electrical field stimulation from isolated tracheas of rats following 4 weeks of streptozotocin (50 mg/kg i.v.)-induced diabetes. Field stimulation (40 V, 0.1 ms, 10 Hz for 120 s) increased the release of somatostatin, CGRP and substance P from the baseline 0.18+/-0.029, 0.17+/-0.027, and 1.77+/-0.086 to 0.51+/-0.022, 0.69+/-0.115, and 5.96+/-0.377 in control preparations and 0.31+/-0.081, 0.41+/-0.142, and 3.14+/-0.443 fmol/mg wet tissue weight in preparations from diabetic rats as measured by radioimmunoassay (control vs. diabetic P<0.01 for each). The results show a simultaneous decrease in release of the three sensory neuropeptides and an enhanced plasma somatostatin level in rats with streptozotocin-induced diabetes.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
neuropeptide release
trachea
streptozotocin-induced
streptozotocin-induced diabetes
Megjelenés:European Journal of Pharmacology. - 369 : 2 (1999), p. 221-224. -
További szerzők:Thán Márta Oroszi Gábor (Pécs) Sári Réka (farmakológus) Szolcsányi János (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM020464
Első szerző:Németh József (Pécs)
Cím:Impairment of neurogenic inflammatory and anti-inflammatory responses in diabetic rats / József Németh, Márta Thán, Réka Sári, Barna Peitl, Gábor Oroszi, Beatrix Farkas, János Szolcsányi, Zoltán Szilvássy
Dátum:1999
Megjegyzések:AbstractThe effect was studied of a primary (preconditioning) neurogenic inflammatory challenge induced by electrical stimulation of the peripheral stump of the sciatic nerve (20 V, 0.5 ms, 5 Hz, for 5 min) on neurogenic oedema (5 min later) induced by stimulation of the contralateral sciatic nerve. Plasma extravasation due to the second stimulation was decreased by 52.7+/-3.1% (P<0.01) in normal animals and by 29.7+/-2.2 and 18.1+/-1.5% with 50 mg/kg streptozotocin pretreatment i.v. 4 and 8 weeks previously, respectively. Subsequently, bilateral sciatic nerve stimulation increased baseline plasma somatostatin levels from 6.4+/-0.3, 11. 7+/-1.4, and 16.8+/-3.8 to 28.3+/-2.9 (P<0.01), 17.9+/-3.7, and 25. 1+/-1.7 pmol/l in normal, and 4- and 8-week diabetic animals, respectively. We conclude that experimental diabetes impairs the capability of a preconditioning neurogenic inflammatory episode to elicit a systemic anti-inflammatory effect. This is accompanied by a deficiency in elevation of the plasma somatostatin level in response to nerve stimulation, although the baseline plasma somatostatin level increases proportionally to the duration of experimental diabetes.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
neurogenic inflammatory
neurogenic inflammatory responses
anti-inflammatory
anti-inflammatory responses
Megjelenés:European Journal of Pharmacology. - 386 : 1 (1999), p. 83-88. -
További szerzők:Thán Márta Sári Réka (farmakológus) Peitl Barna (1972-) (orvos, farmakológus) Oroszi Gábor (Pécs) Farkas Beatrix Szolcsányi János (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM046502
Első szerző:Pálvölgyi Attila
Cím:Interplay between nitric oxide and VIP in CCK-8-induced phasic contractile activity in the rabbit sphincter of Oddi / Attila Pálvölgyi, Réka Sári, József Németh, Annamária Szabolcs, István Nagy, Péter Hegyi, János Lonovics, Zoltán Szilvássy
Dátum:2005
ISSN:1007-9327
Megjegyzések:AIM: The sphincter of Oddi (SO) plays an important role indelivery of bile into the duodenum. To establish whethervasoactive intestinal polypeptide (VIP) and nitric oxide (NO)were involved in phasic contractile activity of the rabbitSO stimulated by cholecystokinin-octapeptide (CCK-8).METHODS: Isolated SO muscle rings were cleaned of fatand mounted horizontally on two small L-shaped hooksone of which was connected to a force transducer for themeasurement of isometric tension. The experiments werecarried out in a thermostatically controlled (37?0.2 )organ bath (5 mL) containing Krebs solution. The organfluid was gassed with 95% O2 and 50 mL/L CO2 to keepthe pH at 7.40?0.05. Contractile responses to CCK-8(1 ?mol/L) were evaluated in the presence and absenceof NG-nitro-L-arginine (LNNA), an inhibitor of NO synthase(100 ?mol/L), and (p-chloro-D-Phe6-Leu17)-VIP (VIPa,30 ?mol/L), a VIP receptor antagonist.RESULTS: CCK-8 stimulated the phasic activity of the SO.NO synthase inhibition increased the frequency and amplitudeof contractions with a slight increase in developed tension.Pre-incubation with VIPa also attenuated this CCK-8 effect.The combined application of LNNA and VIPa abolishedthe phasic activity of the muscle rings with a marked increasein tension in response to CCK-8.CONCLUSION: VIP and NO together contribute to anincrease in phasic activity of SO.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Sphincter of Oddi
CCK
VIP
NO
LNNA
Megjelenés:World Journal of Gastroenterology. - 11 : 21 (2005), p. 3264-3266. -
További szerzők:Sári Réka (farmakológus) Németh József (Pécs) Szabolcs Annamária Nagy István Hegyi Péter Jenő (belgyógyász) Lonovics János (Szeged) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
Pályázati támogatás:3.2.2.-2004-07-0001/3.0
GVOP
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM020242
Első szerző:Peitl Barna (orvos, farmakológus)
Cím:Meal-induced enhancement in insulin sensitivity is not triggered by hyperinsulinemia in rats / Barna Peitl, Róbert Döbrönte, József Németh, Csaba Pankucsi, Réka Sári, Angelika Varga, Zoltán Szilvássy
Dátum:2009
Megjegyzések:Several reports confirmed the phenomenon of postprandial increase in whole-body insulin sensitivity. Although the initial step of this process is unknown, the pivotal role of postprandial hyperinsulinemia has strongly been suggested. The aim of the present study was to determine whether hyperinsulinemia per se induces insulin sensitization in healthy male Wistar rats. Rapid insulin sensitivity test (RIST) were performed in fasted, anesthetized rats before and during stable hyperinsulinemia achieved by hyperinsulinemic euglycemic glucose clamping (HEGC) with insulin infused either through the jugular vein (systemic HEGC) or into the portal circulation (portal HEGC) at a rate of 3 mU/(kg min). Insulin sensitivity expressed by the rapid insulin sensitivity (RIST) index (in milligrams per kilogram) was characterized by the total amount of glucose needed to maintain prestudy blood glucose level succeeding an intravenous bolus infusion of 50 mU/kg insulin over 5 minutes. In fasted animals, the RIST index was 37.4 +/- 3.1 mg/kg. When hyperinsulinemia mimicking the postprandial state was achieved by systemic HEGC, the RIST index (39.7 +/- 10.6 mg/kg) showed no significant changes as compared with the pre-HEGC values. Hyperinsulinemia achieved by portal insulin infusion also failed to modify the RIST index (35.7 +/- 4.3 mg/kg). The results demonstrate that acute hyperinsulinemia, no matter how induced, does not yield any sensitization to the hypoglycemic effect of insulin.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
insulin
insulin sensitivity
hyperinsulinemia
Megjelenés:Metabolism: Clinical and Experimental. - 58 : 3 (2009), p. 328-332. -
További szerzők:Döbrönte Róbert Németh József (Pécs) Pankucsi Csaba (farmakológus) Sári Réka (farmakológus) Varga Angelika (1977-) (biológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
Pályázati támogatás:HO7-BEL 74162
Egyéb
K75965
OTKA
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

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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Intézményi repozitóriumban (DEA) tárolt változat
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6.

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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7.

001-es BibID:BIBFORM020568
Első szerző:Szilvássy Zoltán (belgyógyász, farmakológus, klinikai farmakológus)
Cím:Improvement of nitrergic relaxation by farnesol of the sphincter of Oddi from hypercholesterolaemic rabbits / Zoltan Szilvassy, Reka Sari, Jozsef Nemeth, Istvan Nagy, Sandor Csati, Janos Lonovics
Dátum:1998
Megjegyzések:AbstractField stimulation relaxed the rabbit sphincter of Oddi muscle rings after incubation with atropine (1 microM) and guanethidine (4 microM) with a threefold increase in tissue cyclic cGMP content, a response previously shown to be essentially nitrergic. Preparations from hypercholesterolaemic rabbits (1.5% dietary cholesterol load over 8 weeks increasing serum total cholesterol from pre-diet 1.4+/-0.3 to 22.6+/-3.8 mmol/l) exhibited contractions with no change in cyclic GMP content under the same conditions. The nitrergic relaxation was recaptured with a twofold increase in tissue cyclic GMP content in preparations from hypercholesterolaemic rabbits undergone a treatment with 30 microM/kg farnesol i.v. twice a day over the last 3 days of the dietary period. We conclude that farnesol treatment restores nitrergic relaxation of the sphincter of Oddi in hypercholesterolaemia.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
nitrergic relaxation
farnesol
hypercholesterolaemic
Megjelenés:European Journal of Pharmacology. - 353 : 1 (1998), p. 75-78. -
További szerzők:Sári Réka (farmakológus) Németh József (Pécs) Nagy István Csáti Sándor Lonovics János (Szeged)
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