Találati lista | Tudóstér

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)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM012831
Első szerző:	Kemény-Beke Ádám (szemész)
Cím:	Adenosine deaminase inhibition enhances the inotropic response mediated by A1 adenosine receptor in hyperthyroid guinea pig atrium / Kemény-Beke Á., Jakab A., Zsuga J., Vecsernyes M., Karsai D., Pasztor F., Grenczer M., Szentmiklósi J. A., Berta A., Gesztelyi R.
Dátum:	2007
ISSN:	1043-6618
Megjegyzések:	The aim of the present studywas to test the hypothesis that inhibition of adenosine deaminase(ADA) enhances the efficiency of signal-transduction of myocardial A1 adenosine receptors in hyperthyroidism. The inotropic response to N6-cyclopentyladenosine (CPA), a selective A1 adenosine receptor agonist resistant to ADA, was investigated in the absence or presence of erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA), an ADA and cGMP-stimulated 3 ,5 -cyclic nucleotide phosphodiesterase (PDE2) inhibitor, or of pentostatin (2 -deoxycoformycin; DCF), an exclusive ADA inhibitor, in left atria isolated from eu- or hyperthyroid guinea pigs. Both ADA inhibitors enhanced the effect of CPA only in hyperthyroid atria. EHNA significantly increased the Emax (mean±S.E.M.) from 83.8±1.2% to 93.4±1.2%, whileDCFsignificantly decreased the log EC50 from-7.5±0.07 to-7.83±0.07 in hyperthyroid samples. Conversely, EHNA also diminished the log EC50 (from -7.5±0.07 to -7.65±0.07) and DCF also raised the Emax (from 83.8±1.2% to 85.7±2%) in hyperthyroidism, but these changes were not significant. In conclusion,ADAinhibition moderately but significantly enhanced the efficiency ofA1 adenosine receptor signaling pathway in the hyperthyroid guinea pig atrium. This suggests that elevated intracellular adenosine level caused byADAinhibition may improve the suppressed responsiveness to A1 adenosine receptor agonists associated with the hyperthyroid state. Alternatively or in addition, the role of decreased concentration of adenosine degradation products cannot be excluded. Furthermore, in the case of EHNA, inhibition of PDE2 also appears to contribute to the enhanced A1 adenosine receptor signaling in the hyperthyroid guinea pig atrium.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Pharmacological Research 56 : 2 (2007), p. 124-131. -
További szerzők:	Jakab Anita Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Karsai Dénes Pásztor Fanni Grenczer Maria (1983-) (gyógyszerész) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Berta András (1955-) (szemész, gyermekszemész) Gesztelyi Rudolf (1969-) (kísérletes farmakológus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon: