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1.

001-es BibID:BIBFORM023040
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Ferriporphyrins and endothelium : a 2-edged sword-promotion of oxidation and induction of cytoprotectants / Balla, J., Balla, G., Jeney, V., Kakuk, G., Jacob, H. S., Vercellotti, G. M.
Dátum:2000
ISSN:0006-4971
Megjegyzések:Heme arginate infusions blunt the symptoms of patients with acute intermittent porphyria without evidence of the vascular or thrombotic side effects reported for hematin, To provide a rationale for heme arginate's safety, the present study examined the effects of various ferriporphyrins to sensitize human endothelial cells to free radical injury and to induce heme oxygenase and ferritin expression. Heme arginate, unlike hematin, did not amplify oxidant-induced cytotoxicity mediated by hydrogen peroxide (5.3 +/- 2.4 versus 62.3 +/- 5.3% Cr-51 release, P < .0001) or by activated neutrophils (14.4 +/- 2.9 versus 41.1 +/- 6.0%, P < .0001), Nevertheless, heme arginate efficiently entered endothelial cells similarly to hematin, since both markedly induced heme oxygenase mRNA (more than 20-fold increase) and enzyme activity. Even with efficient permeation, endothelial cell ferritin content was only minimally increased by heme arginate compared with a 10-fold induction by hematin; presumably less free iron was derived from heme arginate despite up-regulation of heme oxygenase, Hematin is potentially vasculopathic by its marked catalysis of oxidation of low-density lipoprotein (LDL) to endothelial-toxic moieties, Heme arginate was significantly less catalytic. Heme arginate-conditioned LDL was less than half as cytotoxic to endothelial cells as hematin-conditioned LDL (P < .004), It is concluded that heme arginate may be less vasculotoxic than hematin since it is an effective heme oxygenase gene regulator but a less efficient free radical catalyst.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Blood. - 95 : 11 (2000), p. 3442-3450. -
További szerzők:Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Jeney Viktória (1971-) (vegyész, kémia tanár) Kakuk György (1938-2018) (belgyógyász) Jacob, Harry S. Vercellotti, Gregory M.
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2.

001-es BibID:BIBFORM035233
Első szerző:Cermak, Jaroslav
Cím:C-reactive protein induces human peripheral blood monocytes to synthesize tissue factor / Cermak Jaroslav, Key Nigel S., Bach Ronald R., Balla Jozsef, Jacob Harry S., Vercellotti Gregory M.
Dátum:1993
ISSN:0006-4971
Megjegyzések:The acute inflammatory response is frequently accompanied by serious thrombotic events. We show that C-reactive protein (CRP), an acute-phase reactant that markedly increases its serum concentration in response to inflammatory stimuli, induced monocytes to express tissue factor (TF), a potent procoagulant. Purified human CRP in concentrations commonly achieved in vivo during inflammation (10 to 100 micrograms/mL) induced a 75-fold increase in TF procoagulant activity (PCA) of human peripheral blood mononuclear cells (PBM), with a parallel increase in TF antigen levels. CRP-induced PCA was completely blocked by a monoclonal antibody against human TF but not by irrelevant murine IgG. Dot blot analysis showed a significant increase of TF mRNA after 4 hours of incubation with CRP, followed by a peak of PCA within 6 and 8 hours. Actinomycin D and cycloheximide blocked CRP-stimulated PCA, suggesting that de novo TF protein synthesis was required. Endotoxin (LPS) contamination of CRP was excluded as the mediator of TF synthesis because: (1) CRP was Limulus assay negative; (2) induction of TF PCA by CRP was not blocked by Polymyxin B, in contrast to LPS-induced PCA; (3) antihuman CRP IgG inhibited CRP-induced PCA, but not LPS-induced PCA; (4) CRP was able to stimulate TF production in LPS-pretreated PBM refractory to additional LPS stimulation; and, (5) unlike LPS, CRP was incapable of inducing TF in human umbilical vein endothelial cells. We suggest that CRP-mediated TF production in monocytes may contribute to the development of disseminated intravascular coagulation and thrombosis in inflammatory states.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Blood. - 82 : 2 (1993), p. 513-520. -
További szerzők:Key, Nigel S. Bach, Ronald R. Balla József (1959-) (belgyógyász, nephrológus) Jacob, Harry S. Vercellotti, Gregory M.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM023038
Első szerző:Jeney Viktória (vegyész, kémia tanár)
Cím:Pro-oxidant and cytotoxic effects of circulating heme / Jeney V., Balla J., Yachie A., Varga Zs., Vercellotti G. M., Eaton J. W., Balla G.
Dátum:2002
ISSN:0006-4971
Megjegyzések:Numerous pathologies may involve toxic side effects of free heme and hemederived iron. Deficiency of the hemecatabolizing enzyme, heme oxygenase-1 (HO-1), in both a human patient and transgenic knockout mice leads to an abundance of circulating heme and damage to vascular endothelium. Although heme can be directly cytotoxic, the present investigations examine the possibility that hemoglobin-derived heme and iron might be indirectly toxic through the generation of oxidized forms of low-density lipoprotein (LDL). In support, hemoglobin in plasma, when oxidized to methemoglobin by oxidants such as leukocyte-derived reactive oxygen, causes oxidative modification of LDL. Heme, released from methemogiobin, catalyzes the oxidation of LDL, which in turn induces endothelial cytolysis primarily caused by lipid hydroperoxides. Exposure of endothelium to sublethal concentrations of this oxidized LDL leads to induction of both HO-1 and ferritin. Similar endothelial cytotoxicity was caused by LDL isolated from plasma of an HO-1-deficient child. Spectral analysis of the child's plasma revealed a substantial oxidation of plasma hemoglobin to methemoglobin. Iron accumulated in the HO-1-deficient child's LDL and several independent assays revealed oxidative modification of the LDL. We conclude that hemoglobin, when oxidized in plasma, can be. indirectly cytotoxic through the generation of oxidized LDL by released heme and that, in response, the intracellular defense-HO-1 and ferritin-Is induced. These results may be relevant to a variety of disorders-such as renal failure associated with intravascular hemolysis, hemorrhagic injury to the central nervous system, and, perhaps, atherogenesis-in which hemoglobin-derived heme may promote the formation of fatty acid hydroperoxides.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Blood. - 100 : 3 (2002), p. 879-887. -
További szerzők:Balla József (1959-) (belgyógyász, nephrológus) Yachie, Akihiro Varga Zsuzsa (1951-) (biokémikus, nephrológus) Vercellotti, Gregory M. Eaton, John W. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus)
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4.

001-es BibID:BIBFORM006864
Első szerző:Mohás Márton
Cím:Serum total LDH activity and LDH-2 isozyme in nephrotic syndrome / Mohas, M., Szigeti, N., Marko, L., Molnar, G. A., Cseh, J., Laczy, B., Tamasko, M., Balla, J., Kappelmayer, J., Wagner, L., Wagner, Z., Csiky, B., Nagy, J., Wittmann, I.
Dátum:2008
Megjegyzések:Proteinuria, hypoproteinaemia, hypoalbuminaemia and oedema are major characteristics of nephrotic syndrome. Aims of this study were to detect serum total LDH activity and its isozymes in nephrotic syndrome. METHODS: In a cross-sectional study, clinical parameters were compared in three cohorts, namely kidney patients with or without nephrotic syndrome and hypoalbuminaemic controls (NEPHR, NON-NEPHR, CONTR, respectively). RESULTS: Serum total LDH activity in the NEPHR group was increased compared with the NON-NEPHR and CONTR groups (p < 0.001) and correlated with serum total protein (r = -0.549, p < 0.001), serum albumin (r = -0.596, p < 0.001), proteinuria (r = 0.456, p < 0.001) and serum total cholesterol (r = 0.523, p < 0.001). LDH isozyme pattern was analysed in three subgroups of the patients. Serum LDH-2 activity was higher in the NEPHR subgroup compared with the NON-NEPHR and CONTR subgroups (p < 0.001). Serum LDH-2 activity correlated with serum total protein (r = -0.665, p < 0.001), serum albumin (r = -0.615, p < 0.001), proteinuria (r = 0.694, p < 0.001), and serum total cholesterol (r = 0.723, p < 0.001). Linear regression analysis revealed that serum total protein proved to be an independent predictor of serum total LDH activity, while serum total protein and proteinuria were predictors of LDH-2. CONCLUSIONS: These findings suggest that serum total LDH activity might be a marker of the activity of the nephrotic syndrome.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Adult
Aged
Biological Markers/blood
Cohort Studies
Cross-Sectional Studies
Enzyme Activation/physiology
Female
Humans
Male
Middle Aged
Retrospective Studies
Megjelenés:Kidney and Blood Pressure Research. - 31 : 1 (2008), p. 47-54. -
További szerzők:Szigeti Nóra Markó Lajos Molnár Gergő Attila Cseh Judit Laczy Boglárka Tamaskó Mónika Balla József (1959-) (belgyógyász, nephrológus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Wagner László Wagner Zoltán Csiky Botond Nagy Judit (kutató) Wittmann István
Internet cím:elektronikus változat
elektronikus változat
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5.

001-es BibID:BIBFORM049053
Első szerző:P. Szabó Réka (orvos)
Cím:Prognosis of Dialysed Patients after Kidney Transplant Failure / Réka P. Szabó, Nóra Klenk, József Balla, László Asztalos, László Szabó, Zoltán Vokó
Dátum:2013
ISSN:1420-4096
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Kidney & Blood Pressure Research 37 : 2-3 (2013), p. 151-157. -
További szerzők:Klenk Nóra (1967-) (belgyógyász, nefrológus) Balla József (1959-) (belgyógyász, nephrológus) Asztalos László (1951-) (sebész) Szabó László Vokó Zoltán (1968-) (epidemiológus)
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6.

001-es BibID:BIBFORM081967
Első szerző:Udvardy Miklós (belgyógyász, haematológus)
Cím:Toward Optimised Intrapulmonary and Systhemic Hemostatic Interventions in Diffuse Alveolar Hemorrhage, a Single Center Experience / Miklos Udvardy, Anna Selmeczi, Miklos Egyed, Attila Szucs, Arpad Illes, Lajos Gergely, Joseph Balla, Janos Matyus
Dátum:2015
ISSN:0006-4971
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Blood. - 126 : 23 (2015), p. 4686. -
További szerzők:Selmeczi Anna (1982-) (orvos) Egyed Miklós Szűcs Attila (belgyógyász) Illés Árpád (1959-) (belgyógyász, haematológus, onkológus) Gergely Lajos (1965-) (belgyógyász, haematológus) Balla József (1959-) (belgyógyász, nephrológus) Mátyus János (1957-) (belgyógyász, nephrológus)
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7.

001-es BibID:BIBFORM040452
035-os BibID:PMID:8087243
Első szerző:Vercellotti, Gregory M.
Cím:Heme and the vasculature : an oxidative hazard that induces antioxidant defenses in the endothelium / Gregory M. Vercellotti, György Balla, József Balla, Karl Nath, John W. Eaton, Harry S. Jacob
Dátum:1994
ISSN:1073-1199
Megjegyzések:Heme proteins transport oxygen and facilitate redox reactions. Heme, however, may be dangerous, especially when free in biologic systems. For example, iron released from hemoglobin-derived heme can catalyze oxidative injury to neuronal cell membranes and may be a factor in post-traumatic damage to the central nervous system. We have shown that heme catalyzes the oxidation of low density lipoproteins which can damage vascular endothelial cells. The endothelium is susceptible to damage by oxidants generated by activated phagocytes, and this has been invoked as an important mechanism in a number of pathologies including the Adulte Respiratory Distress Syndrome (ARDS), acute tubular necrosis, reperfusion injury and atherosclerosis. Because of its highly hydrophobic nature, heme readily intercalates into endothelial membranes and potentiates oxidant-mediated damage. This injury is dependent on the iron content of heme and is completely blocked when concomitant hemopexin is added. Ferrohemoglobin, when added to cultured endothelial cells, is without deleterious effects, but if oxidized to ferrihemoglobin (methemoglobin), it greatly amplifies oxidant damage. Methemoglobin, but not ferrohemoglobin, releases its hemes which can then be incorporated into endothelial cells. Cultured endothelial cells, when exposed to methemoglobin but not ferrohemoglobin, cytochrome c or metmyoglobin, potentiate this oxidant injury. Stabilization of the methemoglobin by cyanide, haptoglobin or capture of the heme by hemopexin abrogates this effect. Paradoxically, more prolonged exposure of endothelium to heme or methemoglobin renders them remarkably resistant to oxidant challenge. Endothelium defends itself from heme by induction of the heme degrading enzyme heme oxygenase and the concomitant production of large amounts of the iron binding protein ferritin.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Artificial Cells, Blood Substitutes, and Immobilization Biotechnology 22 : 2 (1994), p. 207-213. -
További szerzők:Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus) Nath, Karl Eaton, John W. Jacob, Harry S.
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