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1.

001-es BibID:BIBFORM046615
Első szerző:Agarwal, Anupam
Cím:Induction of heme oxygenase in toxic renal injury : a protective role in cisplatin nephrotoxicity in the rat / Anupam Agarwal, József Balla, Jawed Alam, Anthony J. Croatt, Karl A. Nath
Dátum:1995
ISSN:0085-2538
Megjegyzések:Cellular content of heme is regulated by heme oxygenase, the rate limiting enzyme in the degradation of heme. Induction of heme oxygenase is a protective response in an in vivo model of heme protein mediated renal injury, the glycerol model of acute renal failure. In addition to heme, heme oxygenase is induced by diverse forms of oxidative stress, the functional significance of which is currently unknown. We examined whether heme oxygenase is induced, and the functional significance of such induction, in two in vivo models of oxidant-induced toxic nephropathy, namely, cisplatin and gentamicin nephropathies; nephrotoxicity in these models is not dependent on the delivery of a burden of heme proteins to the kidney as occurs in the glycerol model. We demonstrate induction of heme oxygenase mRNA and protein in the kidney as early as 6 and 12 hours after a single dose of cisplatin (6 mg/kg i.v.). Pretreatment with tin protoporphyrin, a competitive inhibitor of heme oxygenase, led to higher serum creatinine values on days 3 through 5 and lower inulin clearances on day 5; tin protoporphyrin also exacerbated renal injury in this model. Renal hemodynamics studied at day 2 after cisplatin demonstrate reduced renal blood flow rates, increased renal vascular resistance and increased fractional excretion of sodium in rats treated with tin protoporphyrin. Tin protoporphyrin alone had no significant effect on serum creatinine and renal hemodynamics in rats with intact, disease-free kidneys. We confirmed that tin protoporphyrin prevented the increase in heme oxygenase activity induced by cisplatin. Induction of heme oxygenase by cisplatin was associated with increased kidney heme content and ferritin content.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Kidney International. - 48 : 4 (1995), p. 1298-1307. -
További szerzők:Balla József (1959-) (belgyógyász, nephrológus) Alam, Jawed Croatt, Anthony J. Nath, Karl
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2.

001-es BibID:BIBFORM059550
Első szerző:Bolisetty, Subhashini
Cím:Macrophage and epithelial cell H-ferritin expression regulates renal inflammation / Subhashini Bolisetty, Abolfazl Zarjou, Travis D. Hull, Amie M. Traylor, Anjana Perianayagam, Reny Joseph, Ahmed I. Kamal, Paolo Arosio, Miguel P. Soares, Viktoria Jeney, Jozsef Balla, James F. George, Anupam Agarwal
Dátum:2015
ISSN:0085-2538
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
acute kidney injury
ferritin
fibrosis
inflammation
macrophage polarization
Megjelenés:Kidney International. - 88 : 1 (2015), p. 95-108. -
További szerzők:Zarjou, Abolfazl (1979-) (kutató orvos) Hull, Travis D. Traylor, Amie M. Perianayagam, Anjana Joseph, Reny Kamal, Ahmed I. Arosio, Paolo Soares, Miguel P. Jeney Viktória (1971-) (vegyész, kémia tanár) Balla József (1959-) (belgyógyász, nephrológus) George, James F. Agarwal, Anupam
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3.

001-es BibID:BIBFORM040437
035-os BibID:PMID:11169001 WOS:000166798700029
Első szerző:Galli, Francesco
Cím:Vitamin E, lipid profile, and peroxidation in hemodialysis patients / Galli F., Varga Z., Balla J., Ferraro B., Canestrari F., Floridi A., Kakuk G., Buoncristiani U.
Dátum:2001
ISSN:0085-2538
Megjegyzések:Hypertriglyceridemia, lipid peroxidation, and abnormalities of the plasma fatty acid (PUFA) profile may be important risk factors for the atherosclerotic cardiovascular disease in hemodialysis (HD) patients. METHODS: We investigated how these factors are affected by vitamin E supplementation carried out by oral administration (clinical study 1) and dialysis with vitamin E-modified dialyzers (clinical study 2). RESULTS: In the HD patients, conditions of relative vitamin E deficiency were observed [lowered vitamin E/triglyceride (TG) ratio] in the presence of high levels of thiobarbituric acid reactants (TBARs) and decreased levels of the polyunsaturated fraction of PUFAs paired with an increased amount of monounsaturated ones (MUFA). In both studies, vitamin E supplementation significantly increased the levels of vitamin E in the plasma without affecting TG levels and provided a partial correction of TBAR levels. Of note was the relative increase in the PUFA fraction, which gave solid proof of an anti(per)oxidant effect of vitamin E supplementation in HD patients. Vitamin E supplementation was also observed to increase plasma levels of reduced glutathione and NOx (NO2 + NO3). CONCLUSION: The results suggest that vitamin E supplementation may be an effective accessory therapy to combat oxidative stress-lowering lipid peroxidation in HD patients.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Kidney International. Supplement 59 : Suppl. 78 (2001), p. S148-S154. -
További szerzők:Varga Z. Balla József (1959-) (belgyógyász, nephrológus) Ferraro, B. Canestrari, F. Floridi, A. Kakuk György (1938-2018) (belgyógyász) Buoncristiani, U.
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4.

001-es BibID:BIBFORM040446
035-os BibID:PMID:7723246
Első szerző:Nath, Karl
Cím:Heme protein-mediated renal injury : a protective role for 21-aminosteroids in vitro and in vivo / Karl A. Nath, József Balla, Anthony J. Croatt, Gregory M. Vercellotti
Dátum:1995
ISSN:0085-2538
Megjegyzések:21-aminosteroids ("lazaroids") have recently excited much interest by virtue of their ability to inhibit lipid peroxidation in vitro and to protect against neural injury in vivo. We tested the effect of these compounds in models of heme protein-mediated renal injury in vitro and in vivo. We devised an in vitro model of heme protein-induced toxicity in which renal epithelial cells were exposed to heme proteins for one hour, after which they were subjected to glutathione depletion by 1-chloro-2,4-dinitrobenzene (CDNB). This model was associated with more than a threefold increase in lipid peroxidation (as measured by thiobarbituric acid reactive substances, TBARS) and a marked reduction in cellular glutathione content. In this model, 21-aminosteroids virtually prevented cytotoxicity as measured by the 51-chromium release assay, and significantly reduced TBARS in a dose-dependent manner. Catalase was partially protective in this model, thereby indicating hydrogen peroxide-dependent toxicity. While pursuing mechanisms accounting for enhanced cellular generation of hydrogen peroxide, we uncovered the first direct evidence that the heme prosthetic group per se directly stimulates cellular generation of hydrogen peroxide; complementing these findings is the remarkable efficacy of 21-aminosteroids in protecting against cytotoxicity induced by hydrogen peroxide. We also tested the capacity of 21-aminosteroids to protect against heme protein-mediated renal injury in vivo. Prior administration of 21-aminosteroids attenuated reductions in GFR and renal blood flow rates following the systemic infusion of methemoglobin in normal rats. 21-aminosteroids also attenuated renal injury observed over three successive days in the glycerol model of heme protein-mediated injury when this model was induced at a higher dose of glycerol (8 ml/kg body wt) but not at a lower dose (5 ml/kg body wt). We conclude that 21-aminosteroids protect against heme protein-mediated renal injury in vitro and in vivo. We suggest that these compounds are potentially useful in such clinical conditions as rhabdomyolysis, intravascular hemolysis and renal injury associated with hemoglobin-based red blood cell substitutes.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Kidney International 47 : 2 (1995), p. 592-602. -
További szerzők:Balla József (1959-) (belgyógyász, nephrológus) Croatt, Anthony J. Vercellotti, Gregory M.
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5.

001-es BibID:BIBFORM040761
Első szerző:Újhelyi László (belgyógyász)
Cím:Response to p-Cresol for better or worse: But what are we measuring? / L. Ujhelyi, Gy. Balla, V. Jeney, Z. Varga, E. Nagy, G. M. Vercellotti, A. Agarwal, J. W. Eaton, J. Balla
Dátum:2006
ISSN:0085-2538
Tárgyszavak:Orvostudományok Klinikai orvostudományok szerkesztői levél
egyetemen (Magyarországon) készült közlemény
Megjelenés:Kidney International. - 70 : 1 (2006), p. 232-233. -
További szerzők:Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Jeney Viktória (1971-) (vegyész, kémia tanár) Varga Z. Nagy E. Vercellotti, Gregory M. Agarwal, Anupam Eaton, John W. Balla József (1959-) (belgyógyász, nephrológus)
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6.

001-es BibID:BIBFORM023028
Első szerző:Újhelyi László (belgyógyász)
Cím:Hemodialysis reduces inhibitory effect of plasma ultrafiltrate on LDL oxidation and subsequent endothelial reactions / L. Ujhelyi, G. Balla, V. Jeney, Z. Varga, E. Nagy, G. M. Vercellotti, A. Agarwal, J. W. Eaton, J. Balla
Dátum:2006
ISSN:0085-2538
Megjegyzések:Oxidative modification of low-density lipoprotein (LDL) and its deleterious effect on endothelium is implicated in the pathogenesis of atherosclerosis. Endothelium responds to such an insult by upregulating the synthesis of heme oxygenase-1 (HO-1) and ferritin. Endothelial cell damage and dysfunction have been observed in patients with chronic kidney disease (CKD) on maintenance hemodialysis (HD). We studied the effect of low-molecular-weight components of uremic plasma on LDL oxidation and LDL-oxidation-provoked endothelial cell reactions, such as the induction of cytotoxicity and the upregulation of cell-protective HO-1 and ferritin. Plasma ultrafiltrate (molecular weight < 5000 Da) from CKD patients on HD or when treated conservatively exhibited a pronounced inhibition on heme-mediated oxidative modification of LDL. Endothelial cell cytotoxicity provoked by LDL oxidation was also attenuated by plasma ultrafiltrate from CKD patients. During HD treatment, a dramatic drop occurred in the retardation of oxidative reactions, and a loss of endothelial cytoprotection exerted by plasma ultrafiltrate was noted. The upregulation of HO-1 and ferritin in response to oxidative stress of LDL was blunted by uremic plasma ultrafiltrate that was released by the end of HD. The decreased antioxidant capacity of ultrafiltrate after HD occurred as a consequence of the intradialytic removal of L-ascorbic acid, uric acid, bilirubin, 3-indoxyl sulfate, indoxyl-beta-D-glucuronide, p-cresol, and phenol. Intradialytic removal of L-ascorbic acid, uric acid, bilirubin, 3-indoxyl sulfate, indoxyl-beta-D-glucuronide, p-cresol, and phenol increases the risk of LDL oxidation and subsequent endothelial cell damage, which underlines the importance of activation of cytoprotective HO-1 and ferritin in endothelium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Kidney International. - 69 : 1 (2006), p. 144-151. -
További szerzők:Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Jeney Viktória (1971-) (vegyész, kémia tanár) Varga Zoltán (orvos) Nagy Emőke (neonatológus, gyermekgyógyász) Vercellotti, Gregory M. Agarwal, Anupam Eaton, John W. Balla József (1959-) (belgyógyász, nephrológus)
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7.

001-es BibID:BIBFORM020460
Első szerző:Zavaczki Erzsébet (biotechnológus)
Cím:Hydrogen sulfide inhibits the calcification and osteoblastic differentation of vascular smooth muscle cells / Erzsebet Zavaczki, Viktoria Jeney, Anupam Agarwal, Abolfazl Zarjou, Melinda Oros, Monika Katko, Zsuzsa Varga, Gyorgy Balla, Jozsef Balla
Dátum:2011
ISSN:0085-2538
Megjegyzések:Osteoblastic differentiation of vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of vascular calcification. Hydrogen sulfide (H2S) is a gas endogenously produced by cystathionine gamma-lyase in VSMC. Here we determined whether H2S plays a role in phosphate-induced osteoblastic transformation and mineralization of VSMC. Hydrogen sulfide was found to inhibit calcium deposition in the extracellular matrix and to suppress the induction of the genes involved in osteoblastic transformation of VSMC: alkaline phosphatase, osteocalcin, and Cbfa1. Moreover, phosphate uptake and phosphate-triggered upregulation of the sodium-dependent phosphate cotransporter (Pit-1) were also prevented by H2S. Reduction of endogenous production of H2S by inhibition of cystathionine gamma-lyase activity resulted in increased osteoblastic transformation and mineralization. Low plasma levels of H2S, associated with decreased cystathionine gamma-lyase enzyme activity, were found in patients with chronic kidney disease receiving hemodialysis. Thus, H2S is a potent inhibitor of phosphate-induced calcification and osteoblastic differentiation of VSMC. This mechanism might contribute to accelerated vascular calcification in chronic kidney disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Kidney International. - 80 : 7 (2011), p. 731-739. -
További szerzők:Jeney Viktória (1971-) (vegyész, kémia tanár) Agarwal, Anupam Zarjou, Abolfazl (1979-) (kutató orvos) Oros Melinda (1975-) (molekuláris biológus) Katkó Mónika (1980-) (biológus) Varga Zsuzsa (1951-) (biokémikus, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A hem-stressz és a hemoxigenáz-ferritin-ferroxidáz rendszerek szerepe az erek szöveti kalcifikációjában
OTKA-K75883
OTKA
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