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001-es BibID:	BIBFORM015066
035-os BibID:	(WOS)000297855700007 (Scopus)82455174750
Első szerző:	Galajda Zoltán (szívsebész, érsebész)
Cím:	Histamine and H1-Histamine receptors faster venous circulation / Zoltan Galajda, Jozsef Balla, A. Jozsef Szentmiklosi, Tamas Biro, Gabriella Czifra, Nora Dobrosi, Agnes Cseppento, Lajos Patonay, Tamas Roszer, Gyorgy Balla, Laurenciu M. Popescu, Istvan Lekli, Arpad Tosaki
Dátum:	2011
Megjegyzések:	The study has analysed the action of histamine in the rabbit venous system and evaluated its potential role in contraction during increased venous pressure. We have found that a great variety exists in histamine sensitivity and H1-histamine receptor expression in various types of rabbit veins. Veins of the extremities (saphenous vein, femoral vein, axillary vein) and abdomen (common iliac vein, inferior vena cava) responded to histamine by a prominent, concentration-dependent force generation, whereas great thoracic veins (subclavian vein, superior vena cavas, intrathoracic part of inferior vena cava) and a pelvic vein (external iliac vein) exhibited slight sensitivity to exogenous histamine. The lack of reactivity to histamine was not due to increased activity of nitric oxide synthase (NOS) or heme oxygenase-1. H1-histamine receptor expression of veins correlated well with the histamine-induced contractions. Voltage-dependent calcium channels mediated mainly the histamine-induced force generation of saphenous vein, whereas it did not act in the inferior vena cava. In contrast, the receptor-operated channels were not involved in this response in either vein. Tyrosine phosphorylation occurred markedly in response to histamine in the saphenous vein, but not in the inferior vena cava. Histamine induced a prominent p kinase activation in both vessels. Protein kinase C and mitogen-activated protein kinase (MAPK) were not implicated in the histamine-induced intracellular calcium sensitization. Importantly, transient clamping of the femoral vein in animals caused a short-term constriction, which was inhibited by H1-histamine receptor antagonist in vivo. Furthermore, a significantly greater histamine immunopositivity was detected in veins after stretching compared to the resting state. We conclude that histamine receptor density adapts to the actual requirements of the circulation, and histamine liberated by the venous wall during increased venous pressure contributes to the contraction of vessels, providing a force for the venous return.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Molekuláris Medicina
Megjelenés:	Journal of Cellular and Molecular Medicine. - 15 : 12 (2011), p. 2614-2623. -
További szerzők:	Balla József (1959-) (belgyógyász, nephrológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Bíró Tamás (1968-) (élettanász) Czifra Gabriella (1975-) (élettanász) Dobrosi Nóra (1981-) (molekuláris biológus) Cseppentő Ágnes (1953-) (orvos) Patonay Lajos (anatómus) Röszer Tamás (1979-) (orvos, biológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Popescu, Laurenciu M. Lekli István (1981-) (gyógyszerész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Vaszkuláris biológia K-72315 OTKA TÁMOP 4.2.2-08/1-2008-0007 TÁMOP ETT 586/2006 EGYÉB ETT 147/2009 EGYÉB K 75883 OTKA K 83478 OTKA MTA-DE-11003 EGYÉB
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM008845
Első szerző:	Józsa Tamás (gyermeksebész, urológus)
Cím:	Short-term adaptation of rat intestine to ileostomy : implication for pediatric practice / Józsa T., Magyar A., Cserni T., Szentmiklósi J. A., Erdélyi K., Kincses Z., Rákóczy G., Balla G., Roszer T.
Dátum:	2009
ISSN:	0894-1939
Megjegyzések:	Surgical neonates with complex intestinal conditions, such as enterocolitis, midgut volvulus with bowel loss and multiple atresias, often require temporary stomas. Little is known on the postsurgical response of the altered gut segments, although adaptation is an important consideration in neonatal postoperative care, particularly after stoma closure. MATERIALS AND METHODS: Rats underwent bowel resection at a point 15 cm proximal to the ileocecal valve, and a split ileostomy was performed. On the 6th postoperative day the mucosal thickness was calculated with Soft Imaging System Analysis Pro, the rate of proliferation was measured following Ki67 immunohistochemistry and the apoptotic index was determined on sections stained with ApopTag Plus. The intestinal motor activity was recorded on isolated gut segments. Neuronal nitric oxide synthase (nNOS) expression and distribution was examined with NADPH-diaphorase histochemistry and Western blot analysis. RESULTS: An increased wet weight of the mucosa and a pronounced mucosal thickening were observed in the proximal functional bowel segment. Enterocyte proliferation rate was increased significantly, while the apoptotic index remained unchanged in the epithelial layer. The dilation of the gut lumen resulted in a morphological change in the nitrergic myenteric network with an overexpression of nNOS. As a consequence of the surgical procedure, the functional proximal gut segment showed strong and frequent contraction waves, with an enhanced responsiveness to cholinergic stimuli. CONCLUSIONS: The dilated functional bowel segment was characterized by hyperplasic changes in the mucosa and stronger mechanical activity with overproduction of nNOS. Although early restoration of intestinal continuity is recommended, our observations on adaptive changes may partly explain intestinal motility disorders after early stoma closure, suggesting the need for a careful approach to a redo-laparotomy.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk rat intestine to ileostomy ileostomy short bowel syndrome intestinal adaptation neonate gastrointestinal nervous system egyetemen (Magyarországon) készült közlemény
Megjelenés:	Journal of Investigative Surgery. - 22 : 4 (2009), p. 292-300. -
További szerzők:	Magyar Ágnes (1979-) (gyermeksebész) Cserni Tamás (1967-) (gyermeksebész) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Erdélyi Katalin (1978-) (molekuláris biológus, biokémikus) Kincses Zsolt (1961-) (orvos) Rákóczy György Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Röszer Tamás (1979-) (orvos, biológus)
Internet cím:	elektronikus változat DOI
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001-es BibID:	BIBFORM012889
Első szerző:	Nagy Emőke (neonatológus, gyermekgyógyász)
Cím:	Red cells, hemoglobin, heme, iron, and atherogenesis / Emőke Nagy, John W. Eaton, Viktória Jeney, Miguel P. Soares, Zsuzsa Varga, Zoltán Galajda, József Szentmiklósi, Gábor Méhes, Tamás Csonka, Ann Smith, Gregory M. Vercellotti, György Balla, József Balla
Dátum:	2010
Megjegyzések:	We investigated whether red cell infiltration of atheromatous lesions promotes the later stages of atherosclerosis. METHODS AND RESULTS: We find that oxidation of ferro (FeII) hemoglobin in ruptured advanced lesions occurs generating ferri (FeIII) hemoglobin and via more extensive oxidation ferrylhemoglobin (FeIII/FeIV=O). The protein oxidation marker dityrosine accumulates in complicated lesions, accompanied by the formation of cross-linked hemoglobin, a hallmark of ferrylhemoglobin. Exposure of normal red cells to lipids derived from atheromatous lesions causes hemolysis and oxidation of liberated hemoglobin. In the interactions between hemoglobin and atheroma lipids, hemoglobin and heme promote further lipid oxidation and subsequently endothelial reactions such as upregulation of heme oxygenase-1 and cytotoxicity to endothelium. Oxidative scission of heme leads to release of iron and a feed-forward process of iron-driven plaque lipid oxidation. The inhibition of heme release from globin by haptoglobin and sequestration of heme by hemopexin suppress hemoglobin-mediated oxidation of lipids of atheromatous lesions and attenuate endothelial cytotoxicity. CONCLUSIONS: The interior of advanced atheromatous lesions is a prooxidant environment in which erythrocytes lyse, hemoglobin is oxidized to ferri- and ferrylhemoglobin, and released heme and iron promote further oxidation of lipids. These events amplify the endothelial cell cytotoxicity of plaque components.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban Red cells, hemoglobin egyetemen (Magyarországon) készült közlemény
Megjelenés:	Arteriosclerosis, Thrombosis, and Vascular Biology 30 : 7 (2010), p. 1347-1353. -
További szerzők:	Eaton, John W. Jeney Viktória (1971-) (vegyész, kémia tanár) Soares, Miguel P. Varga Zsuzsa (1951-) (biokémikus, nephrológus) Galajda Zoltán (1962-) (szívsebész, érsebész) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Méhes Gábor (1966-) (patológus) Csonka Tamás (1984-) (pathológus) Smith, Ann Vercellotti, Gregory M. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:	OTKA-K75883 OTKA
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat elektronikus változat DOI
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