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001-es BibID:BIBFORM020272
Első szerző:Djazayeri, Katayoun
Cím:Effect of rosiglitazone, an insulin sensitizer, on myelotoxicity caused by repeated doses of 5-fluorouracil / Katayoun Djazayeria, Zoltán Szilvássy, Klára Benkő, Bernadett Rózsa, Boglárka Szabó, A. József Szentmiklósi, Ilona Benkő
Dátum:2006
ISSN:1043-6618
Megjegyzések:AbstractHaematopoietic colony-stimulating factors are used frequently to moderate myelotoxicity, but administration of granulocyte-colony-stimulating factor (G-CSF) prior to chemotherapy actually may worsen the toxic effects on bone marrow. This is important in the design of clinical cancer treatment protocols. Previously, we found that rosiglitazone may protect granulocyte-macrophage progenitor cells (CFU-GM) against damage caused by a single dose of 5-fluorouracil (5-FU). Our new studies are designed to evaluate whether rosiglitazone has similar beneficial effects on bone marrow preservation when administered concurrently with repeated, daily doses of 5-FU while restricting regeneration time. Myelotoxicity characterized by the decrease in cellularity, frequency of granulocyte-macrophage progenitor cells and CFU-GM content of femoral bone marrow in mice. Five-day oral rosiglitazone pre-treatment decreased the susceptibility of granulocyte-macrophage progenitors to 5-FU damage. Significantly, more CFU-GM cells survived after the single intraperitoneal dose of 5-FU (100 mg kg(-1)). The increased frequency of CFU-GM cells with their intensive proliferation allowed faster restoration of the damaged CFU-GM compartment than was seen in the case of repeated daily administration of the cytostatic drug (25 or 50 mg kg(-1)) together with rosiglitazone for 7 consecutive days. The expansion of the CFU-GM compartment was 3 times and 50 times greater in the combined-treated mice than in their counterparts treated with repeated doses of 5-FU alone, although differences in absolute neutrophil counts were not significant. In conclusion, our results indicated that rosiglitazone has protective effects on bone marrow progenitor cells even after daily 5-FU treatment but further studies are warranted to evaluate the optimal treatment schedules.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
rosiglitazone
myelotoxicity
5-fluorouracil
Megjelenés:Pharmacological Research. - 53 : 2 (2006), p. 156-161. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Benkő Klára Rózsa Bernadett (1981-) (molekuláris biológus) Szabó Boglárka Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Benkő Ilona (1954-) (orvos, farmakológus)
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DOI
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2.

001-es BibID:BIBFORM020523
Első szerző:Ferdinándy Péter
Cím:Cardioprotective effect of enantiomers of cicletanine (BN50417, BN50418) in ischaemic/reperfused isolated working rat hearts : interaction with glibenclamide / P. Ferdinandy, Z. Szilvássy, T. Csont, M. Koltai, M. T. Droy-lefaix
Dátum:2000
ISSN:1043-6618
Megjegyzések:AbstractIn the present study, interaction of the ATP-sensitive K+-channel blocker glibenclamide with enantiomers of the antihypertensive drug, cicletanine, was studied on ischaemic myocardial function, lactate-dehydrogenase (LDH) release, and early reperfusion-induced ventricular fibrillation (VF). Isolated working rat hearts subjected to 10-min coronary artery occlusion followed by 2-min reperfusion were perfused with 1.5x10(-5)-6.0x10(-5)M D-cicletanine[+] (BN50417) and L-cicletanine[-] (BN50418), respectively. Their interaction with 10(-7) M glibenclamide was also studied. The most effective concentration of BN50418 (3x10(-5) M) increased ischaemic aortic flow (AF) from its non-treated control value of 20.3+/-1.16 to 30.3+/-2.6 ml min-1(P<0.01), decreased left ventricular end-diastolic pressure (LVEDP) from 1.81+/-0.05 to 0.97+/-0.08 kPa (P<0.001), attenuated ischaemia-induced increase in LDH leakage from 164+/-41 to 14.8+/-20 mU min-1g-1 wet wt. (P<0.01) at the 10th-min of coronary occlusion, and reduced VF upon reperfusion. Glibenclamide did not considerably affect cardiac performance, however, it inhibited the anti-ischaemic but not the antiarrhythmic effect of BN50418. BN50417 (3x10(-5) M) tended to improve ischaemic AF to 24.2+/-1.1 ml min-1, and significantly attenuated ischaemia-induced increase in LVEDP to 1.3+/-0.08 kPa (P<0.01), relative increase in LDH release to 29.4+/-44 mU min-1g-1(P<0.05), and alleviated reperfusion-induced VF. Glibenclamide abolished the anti-ischaemic and antiarrhythmic effect of BN50417. The cardioprotective effect of both enantiomers of cicletanine involves a glibenclamide-sensitive mechanism, however, the antiarrhythmic effect of BN50418 is not glibenclamide sensitive. BN50418 is the more potent enantiomer of cicletanine in terms of its cardioprotective effect.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
cardioprotective effect
enantiomers of cicletanine
enantiomers
cicletanine
BN50417
BN50418
glibenclamide
Megjelenés:Pharmacological Research. - 39 : 3 (1999), p. 225-231. -
További szerzők:Csont Tamás Koltai M. Droy-Lefaix, Marie-Thérèse Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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3.

001-es BibID:BIBFORM020518
Első szerző:Oroszi Gábor (Pécs)
Cím:Interplay between nitric oxide and CGRP by capsaicin in isolated guinea-pig heart / Gabor Oroszi, Zoltan Szilvassy, Joseph Nemeth, Arpad Tosaki, Janos Szolcsanyi
Dátum:1999
ISSN:1043-6618
Megjegyzések:AbstractCapsaicin at a concentration of 10(-7)m induced a significant increase in heart rate and increased coronary flow in isolated Langendorff-perfused guinea-pig hearts. This effect was completely blocked by 30 microm of N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase. Additional incubation with 3 m m L-Arg antagonized the inhibitory effect of L-NAME. In the presence of 1 microm of a human calcitonin gene-related peptide fragment (hCGRP 8-37), a CGRP-receptor antagonist, L-Arg was without effect. We conclude that a capsaicin-induced increase in coronary flow and heart rate is dependent from an interplay between CGRP and NO in guinea-pig hearts. 1999 Academic Press.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
nitric oxide
CGRP
capsaicin
Megjelenés:Pharmacological Research 40 : 2 (1999), p. 125-128. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Németh József (Pécs) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Szolcsányi János (Pécs)
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4.

001-es BibID:BIBFORM020575
Első szerző:Sári Réka (farmakológus)
Cím:Cross tolerance between nitroglycerin and neural relaxation of the rabbit sphincter of Oddi / Réka Sári, Zoltán Szilvássy, Ildikó Jakab, István Nagy, János Lonovics
Dátum:1998
ISSN:1043-6618
Megjegyzések:Szegedi Tudományegyetem - Belgyógyászati Klinika
We studied whether non-adrenergic, non-cholinergic (NANC) relaxation of the rabbit sphincter of Oddi was influenced by tolerance to nitroglycerin (NG)in vitro. Sphincter of Oddi (SO) muscle rings precontracted with EC50concentrations of cholecystokinin octapeptide (CCK8) were exposed to cumulative increases in NG concentrations and tested for relaxation by measurement of isometric tension. A separate group of six rings was subjected to a preceding exposure to 275 mnitroglycerin over 60 min to inducein vitrotolerance to nitroglycerin. The rings (both tolerant and non-tolerant) were subjected to electrical field stimulation (FS: 50 V, 0.1 ms, 20 Hz, 3 and 10 stimuli). The rings were then preincubated with NANC solution: phentolamine, oxprenolol and atropine (all 1 m) for 20 min and FS was applied again. FS was repeated after additional incubation withNG-nitro-l-arginine methyl ester (l-NAME), an inhibitor of NO synthase (30 m) and after a successive incubation with 3 mml-arginine (20 min). Maximum contractions produced by CCK8 in `tolerant' and 'non-tolerant' sphincters were 29.9±5.8 and 28.3±5.2 mN, respectively. The sensitivity to CCK8 also was not different between the two groups with EC50(-log M) values of 8.5±0.2 and 8.3±0.1, respectively. FS evoked twitchlike contraction followed by relaxation in the ampullary SO in both `tolerant' and `non-tolerant' preparations. Incubation in NANC solution resulted in monophasic relaxations in response to FS in non-tolerant sphincters but not in tolerant ones.l-NAME (30 m) reversed NANC relaxation in non-tolerant muscle rings whereas it failed to modify NANC contractions in the tolerant preparations.l-arginine (3 mm) reversed the inhibitory effect ofl-NAME on NANC relaxation in the `non-tolerant' rings and it was without effect on FS-induced contractions in the `tolerant' SO. As measured by radioimmunoassay, tolerance to NG was without any significant effect on tissue content of both cyclic adenosine 3:5 monophosphate (cAMP) and cyclic guanosine 3:5 monophosphate (cGMP). FS significantly increased tissue cAMP and cGMP content in 'non-tolerant' preparations. FS failed to increase the level of either cyclic nucleotide in `tolerant' tissue. We conclude that NANC relaxation of the ampullary part of the rabbit SO is significantly impaired in the state of tolerance to NG`in vitro'.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
cross tolerance
nitroglycerin
neural relaxation
Megjelenés:Pharmacological Research. - 37 : 6 (1998), p. 505-512. -
További szerzők:Jakab Ildikó (farmakológus) Nagy István Lonovics János (Szeged) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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5.

001-es BibID:BIBFORM046507
Első szerző:Szilvássy Zoltán (belgyógyász, farmakológus, klinikai farmakológus)
Cím:Glibenclamide sensitivity of neural relaxation of the rabbit sphincter of oddi / Zoltan Szilvassy, Janos Lonovics, Ildiko Jakab, Istvan Nagy
Dátum:1997
ISSN:1043-6618
Megjegyzések:In this article we studied whether the nitrergic relaxation of the rabbit sphincter wassensitive to glibenclamide. Field stimulation relaxed the sphincter of Oddi rings afterincubation with atropine 1 mM. and guanethidine 4 mM. with threefold and fourfoldincreases in tissue guanosine 39:59-cyclic monophosphate and adenosine 39:59-cyclicmonophosphate contents, respectively. These changes were blocked by 30 mM NG-nitro-L-arginine methyl ester. Glibenclamide 0.1]10 mM. attenuated the field stimulation-inducedrelaxation and completely abolished the relaxation produced by 0.1 mM cromakalim. Weconclude that nitrergic relaxation of the rabbit sphincter of Oddi comprises a mechanismsensitive to glibenclamide.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
nitric oxide NO
glibenclamide
field stimulation
cyclic nucleotides
sphincter of Oddi
Megjelenés:Pharmacological Research. - 36 : 2 (1997), p. 129-133. -
További szerzők:Lonovics János (Szeged) Jakab Ildikó (farmakológus) Nagy István
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