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001-es BibID:	BIBFORM005578
Első szerző:	Katkó Mónika (biológus)
Cím:	Relationship between serum nickel and homocysteine concentration in hemodialysis patients / Katkó Mónika, Kiss Ildikó, Kárpáti István, Kádár András, Mátyus János, Csongrádi Éva, Posta József, Paragh György, Balla József, Kovács Béla, Varga Zsuzsa
Dátum:	2008
Megjegyzések:	Severe hyperhomocysteinemia (HHC) is associated with atherosclerosis. In hemodialysis (HD) patients, one of the main causes of death is cardiovascular disease. In animals, trace elements such as cobalt, copper, iron, and nickel ameliorated vitamin B-12 deficiency-induced HHC. However, correlations between plasma total homocysteine (tHcy) and trace elements in HD patients have not been investigated. Therefore, tHcy, folate, vitamin B-12, trace elements (cobalt, copper, iron, and nickel), and some laboratory parameters such as serum total protein, albumin, transferrin, ferritin, C-reactive protein (CRP), and interleukin-6 concentrations were determined in 122 hemodialysis patients. When patients were divided into groups according to their tHcy, we found no significant differences in concentrations of cobalt, copper, and total protein, while nickel was higher, and folate, vitamin B-12, and iron were lower in patients with lower than higher tHcy. In univariate regression analysis, tHcy negatively correlated with concentrations of folate (r=-0.302, p < 0.006), vitamin B-12 (r=-0.347, p < 0.0001), nickel (r=-0.289, p < 0.006), and CRP (r=-0.230, p < 0.02) and positively with serum albumin (r=0.316, p < 0.0004) and hemoglobin (r=0.329, p < 0.0001) values. No relationship between tHcy and serum concentrations of cobalt, copper, iron, or other laboratory parameters was found in HD patients. The effect of cobalt and nickel on homocysteine production was assessed in human peripheral mononuclear cells (PBMCs). Nickel but not cobalt at concentrations found in HD patients significantly inhibited homocysteine, cysteine, and S-adenosylhomocysteine production in human PBMCs. These results suggest that nickel might also be involved in the regulation of the methionine-folate cycle in humans, as was demonstrated in animal experiments.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Biological Trace Element Research. - 124 : 3 (2008), p. 195-205. -
További szerzők:	Kiss Ildikó (1980-) Kárpáti István (1955-) (belgyógyász, nephrológus) Kádár András (1977-) (belgyógyász) Mátyus János (1957-) (belgyógyász, nephrológus) Csongrádi Éva (1969-) (szakorvos) Posta József (1948-) (vegyész, analitikus) Paragh György (1953-) (belgyógyász) Balla József (1959-) (belgyógyász, nephrológus) Kovács Béla (1963-) (okleveles vegyész, angol szakfordító) Varga Zsuzsa (1951-) (biokémikus, nephrológus)
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001-es BibID:	BIBFORM083275
035-os BibID:	(cikkazonosító)1584 (WoS)000509956400001 (Scopus)85078738706
Első szerző:	Nagy Annamária
Cím:	Zinc Inhibits HIF-Prolyl Hydroxylase Inhibitor-Aggravated VSMC Calcification Induced by High Phosphate / Annamária Nagy, Dávid Pethő, Tamás Gáll, Erzsébet Zavaczki, Mónika Nyitrai, József Posta, Abolfazl Zarjou, Anupam Agarwal, György Balla, József Balla
Dátum:	2020
ISSN:	1664-042X
Megjegyzések:	Vascular calcification is a life-threatening clinical condition in chronic kidney disease (CKD) and is associated with reduced zinc serum levels. Anemia is another frequent complication of CKD. Hypoxia-inducible factor (HIF) stabilizers, also known as HIF prolyl hydroxylase inhibitors (PHI), are promising candidates to treat CKD-associated anemia by increasing erythropoietin synthesis. Recent evidence suggests that HIFs play a pivotal role in vascular calcification. Our study explored feasible impacts of HIF PHI on phosphate (Pi)-induced calcification of vascular smooth muscle cells (VSMCs) and tested whether zinc might inhibit this mineralization process. Treatment of VSMCs with PHI aggravated Pi-induced calcium deposition and Pi uptake. PHI promoted Pi-induced loss of smooth muscle cell markers (ACTA-2, MYH11, SM22?) and enhanced osteochondrogenic gene expression (Msx-2, BMP-2, Sp7) triggering osteochondrogenic phenotypic switch of VSMCs. These effects of PHI paralleled with increased pyruvate dehydrogenase kinase 4 (PDK4) expression, decreased Runx2 Ser451 phosphorylation, and reduced cell viability. Zinc inhibited Pi-induced mineralization of VSMCs in a dose-dependent manner and also attenuated the pro-calcification effect of PHI in Pi-induced mineralization. Zinc inhibited osteochondrogenic phenotypic switch of VSMCs reflected by lowering Pi uptake, decreasing the expressions of Msx-2, BMP-2, and Sp7 as well as the loss of smooth muscle cell-specific markers. Zinc preserved phosphorylation state of Runx2 Ser451, decreased PDK4 level, and restored cell viability. PHI alone reduced the expression of smooth muscle markers without inducing mineralization, which was also inhibited by zinc. In addition, we observed a significantly lower serum zinc level in CKD as well as in patients undergoing carotid endarterectomy compared to healthy individuals. Conclusion - PHI promoted the loss of smooth muscle markers and augmented Pi-induced osteochondrogenic phenotypic switch leading to VSMCs calcification. This mineralization process was attenuated by zinc. Enhanced vascular calcification is a potential risk factor during PHI therapy in CKD which necessitates the strict follow up of vascular calcification and zinc supplementation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk vascular calcification, PHI
Megjelenés:	Frontiers in Physiology. - 10 (2020), p. 1-15. -
További szerzők:	Pethő Dávid Gáll Tamás (1982-) (molekuláris biológus, mikrobiológus) Zavaczki Erzsébet (1983-) (biotechnológus) Nyitrai Mónika Posta József (1948-) (vegyész, analitikus) Zarjou, Abolfazl (1979-) (kutató orvos) Agarwal, Anupam Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:	OTKA-112333 OTKA K132828 OTKA GINOP-2.3.2-15-2016-00043 GINOP EFOP-3.6.2-16-2017-00006 EFOP EFOP-3.6.3-VEKOP16-2017-00009 EFOP ED-18-1-2019-0028 Egyéb
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001-es BibID:	BIBFORM086144
Első szerző:	Posta Niké
Cím:	Hemoglobin oxidation generates globin-derived peptides in atherosclerotic lesions and intraventricular hemorrhage of the brain, provoking endothelial dysfunction / Niké Posta, Éva Csősz, Melinda Oros, Dávid Pethő, László Potor, Gergő Kalló, Zoltán Hendrik, Katalin Éva Sikura, Gábor Méhes, Csaba Tóth, József Posta, György Balla, József Balla
Dátum:	2020
ISSN:	0023-6837
Megjegyzések:	The lysis of red blood cells was shown to occur in human ruptured atherosclerotic lesions and intraventricular hemorrhage (IVH) of the brain. Liberated cell-free hemoglobin was found to undergo oxidation in both pathologies. We hypothesize that hemoglobin-derived peptides are generated during hemoglobin oxidation both in complicated atherosclerotic lesions and IVH of the brain, triggering endothelial cell dysfunction. Oxidized hemoglobin and its products were followed with spectrophotometry, LC?MS/MS analysis and detection of the cross-linking of globin chains in complicated atherosclerotic lesions of the human carotid artery and the hemorrhaged cerebrospinal liquid of preterm infants. The vascular pathophysiologic role of oxidized hemoglobin and the resultant peptides was assessed by measuring endothelial integrity, the activation of endothelial cells and the induction of proinflammatory genes. Peptide fragments of hemoglobin (VNVDEVGGEALGRLLVVYPWTQR, LLVVYPWTQR, MFLSFPTTK, VGAHAGEYGAELERMFLSFPTTK, and FLASVSTVLTSKYR) were identified in ruptured atherosclerotic lesions and in IVH of the human brain. Fragments resulting from the oxidation of hemoglobin were accompanied by the accumulation of ferryl hemoglobin. Similar to complicated atherosclerotic lesions of the human carotid artery, a high level of oxidized and cross-linked hemoglobin was observed in the cerebrospinal fluid after IVH. Haptoglobin inhibited hemoglobin fragmentation provoked by peroxide. The resultant peptides failed to bind haptoglobin or albumin. Peptides derived from hemoglobin oxidation and ferryl hemoglobin induced intercellular gap formation, decreased junctional resistance in the endothelium, and enhanced monocyte adhesion to endothelial cells. Enhanced expression of TNF and the activation of NLRP3 and CASP1 followed by the increased generation of IL-1? and nuclear translocation of the NF-?? transcription factor occurred in response to hemoglobin-derived peptides, and ferryl hemoglobin in endothelium was upregulated in both pathologies. We conclude that the oxidation of hemoglobin in complicated atherosclerotic lesions and intraventricular hemorrhage of the brain generates peptide fragments and ferryl hemoglobin with the potential to trigger endothelial cell dysfunction.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Laboratory Investigation. - 100 : 7 (2020), p. 986-1002. -
További szerzők:	Csősz Éva (1977-) (biokémikus, molekuláris biológus) Oros Melinda (1975-) (molekuláris biológus) Pethő Dávid Potor László Kalló Gergő (1989-) (molekuláris biológus) Hendrik Zoltán (1986-) (orvos) Sikura Katalin Éva (1985-) (biológus) Méhes Gábor (1966-) (patológus) Tóth Csaba (1968-) (sebész, érsebész) Posta József (1948-) (vegyész, analitikus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:	OTKA-K-132828 OTKA EFOP-3.6.3-VEKOP-16- 2017-00009 EFOP GINOP-2.3.2-15-2016-00043 GINOP EFOP-3.6.2-16- 2017-00006 GINOP
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001-es BibID:	BIBFORM027839
Első szerző:	Varga Zsuzsa (biokémikus, nephrológus)
Cím:	Nickel affects methionine cycle by a concentration dependent manner and resulted in decreased homocysteine and S-adenosylhomocysteine concentration in vitro and in vivo / Zsuzsa Varga, Istvan Karpati, Sandor Biro, Janos Matyus, Laszlo Ujhelyi, Lajos Papp, Jozsef Posta, Gyorgy Paragh, Jozsef Balla
Dátum:	2006
ISSN:	0931-0509
Tárgyszavak:	Természettudományok Biológiai tudományok idézhető absztrakt Transplantation Urology & Nephrology
Megjelenés:	Nephrology Dialysis Transplantation. Supplement. - 21 : 4 (2006), p. 189. -
További szerzők:	Kárpáti István (1955-) (belgyógyász, nephrológus) Biró Sándor (1949-) (molekuláris genetikus) Mátyus János (1957-) (belgyógyász, nephrológus) Újhelyi László (1956-) (belgyógyász) Pap Lajos (1929-) (vegyész, analitikus) Posta József (1948-) (vegyész, analitikus) Paragh György (1953-) (belgyógyász) Balla József (1959-) (belgyógyász, nephrológus)
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