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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: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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3.

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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4.

001-es BibID:BIBFORM049053
Első szerző:P. Szabó Réka (belgyógyász, nephrológus)
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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5.

001-es BibID:BIBFORM133215
035-os BibID:(scopus)105007521568 (wos)001528713000001
Első szerző:Setayesh, Tahereh
Cím:A novel mouse model of hemoglobin SC disease reveals mechanisms underlying beneficial effects of hydroxyurea / Setayesh T., Chi M., Oestreicher Z., Sakabe M., Seu K., Zhu Z., Kaur H., Tijani A., Xin M., Shova A., Greis K. D., Townes T. M., Balla J., VandenHeuvel K., Hu Yueh-Chiang, Malik P.
Dátum:2025
ISSN:0006-4971
Megjegyzések:Sickle cell hemoglobin C (HbSC) disease results from compound heterozygosity of hemoglobin S (HbS) and hemoglobin C (HbC), comprising 30% of sickle cell disease (SCD). HbC induces red blood cell (RBC) dehydration/xerocytosis, which promotes sickling. HbSC-SCD causes significant morbidity despite being milder than homozygous HbSS-SCD. Current research/treatment strategies have focused on HbSS-SCD, whereas patients with HbSC are deprived of disease-modifying/transformative therapies because of lack of preclinical models. We generated HbSC mice, which resemble human HbSC-SCD: HbSC erythrocytes showed marked xerocytosis. Anemia, hemolysis, inflammation, and organ damage were milder than HbSS mice but hypoxia/reperfusion injury was similar. Retinopathy developed at higher frequency than HbSS mice (66.7% vs 16.7%; P < .05), as in patients with HbSC-SCD. Although HbSC RBCs sickled at lower oxygen tension than HbSS RBCs, they did not completely recover deformability after hypoxia/reoxygenation. Using the HbSC mice, we studied the mechanism by which hydroxyurea causes significant clinical benefit in patients with HbSC-SCD, despite minimal/modest increases in fetal Hb (HbF). We found hydroxyurea had distinct non-HbF and HbF effects. Hydroxyurea did not increase HbF in adult HbSC/HbSS mice but reduced RBC reactive oxygen species, ferryl Hb, and Heinz-body formation, thereby reducing membrane damage; however, RBC hydration was unaffected. When given to unborn pups before ?-globin expression was switched off, and continued postnatally, we could induce HbF in both HbSC and HbSS mice (higher HbF in HbSS vs HbSC mice). Minimal increases in HbF (?1%) improved HbSC RBC hydration. Peak HbF levels of 7% in HbSC mice abrogated sickling. Overall, this HbSC model will help bridge the knowledge gap in mechanistic/therapeutic studies in this neglected disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Red Cells
Hemoglobin
Iron
Erythropoiesis
Sickle Cell Disease
Megjelenés:Blood. - 146 : 1 (2025), p. 13-28. -
További szerzők:Chi, Mengna Oestreicher, Zachery Sakabe, Masahide Seu, Katie Zhu, Zhenqi Kaur, Harsimran Tijani, Anifat Xin, Mei Shova, Amy Greis, Kenneth D. Townes, Tim M. Balla József (1959-) (belgyógyász, nephrológus) VandenHeuvel, Katherine Hu, Yueh-Chiang Malik, Punam
Pályázati támogatás:TKP2021-EGA-18
Egyéb
NKFIH ADVANCED 149734
Egyéb
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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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