Zoltán Maróti

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The Col4A3, Col4A4 and Col4A5 collagen type IV genes are found to be mutated in Col IV nephropathy. In males with a mutation in the Col4A5 gene (X-linked Alport syndrome: XL-AS), progressive renal disease always develops. Female carriers with a mutation in the Col4A5 gene can develop thin basement membrane nephropathy (TBMN). Males and females who carry 1(More)
The relationship between renal disease progression and genetic polymorphism of enzymes influencing endothelial function remains incompletely understood. We genotyped three cohorts of elderly Hungarian patients: 245 patients with end-stage renal disease (ESRD) on chronic hemodialysis (HD), 88 patients with mild chronic kidney disease (CKD), and 200 healthy(More)
Oxidative stress plays an important role in the cardiovascular complications in end-stage renal disease (ESRD) patients on long-term hemodialysis (HD). Heme oxygenase-1 (HO-1) inhibits inflammatory events and protects against oxidative stress and endothelial injury. Therefore, we followed the effects of single HD sessions on HO-1 expression. A competitive(More)
Newborns are exposed to mechanical and oxidative stress during labor and to relative hyperoxia thereafter during the course of adaptation to the extrauterine conditions. Part of the adaptation mechanism is the rapid degradation of fetal hemoglobin and the oxidation of its heme moiety by heme oxygenases (HOs). Heme oxygenase-1 enzyme (HO-1) is the inducible(More)
Alport syndrome (AS) is an inherited type IV collagen nephropathies characterized by microscopic hematuria during early childhood, the development of proteinuria and progression to end-stage renal disease. Since choosing the right therapy, even before the onset of proteinuria, can delay the onset of end-stage renal failure and improve life expectancy, the(More)
Oxidative stress is known to play an important role in the pathogenesis of certain severe illnesses in preterm infants. The enzyme heme oxygenase-1 (HO-1) participates in cytoprotection against oxygen radical injury. We have previously described the role of HO-1 in physiologic adaptation by demonstrating the induction of HO-1 in healthy mature neonates and(More)
Osteogenesis imperfecta (OI) tarda dominant type is caused by mutations in the type I collagen genes, COL1A1 and COL1A2. The essence of our haplotype analysis of osteogenesis imperfecta (OI) was to get information about the value of 8 short tandem repeat (STR) markers for the segregation of COL1A1 and COL1A2 genes on the 12 OI pedigrees and to delimit the(More)
AIM Oxidative stress, observed in the asthmatic airways, is not localized only to the bronchial system. It would be a great advantage to monitor the oxidative stress markers from blood especially in childhood asthma following the inflammation. Our aim was to measure the levels of antioxidants and the oxidatively damaged biomolecules. We were also interested(More)
We carried out whole-exome ultra-high throughput sequencing in brain samples of suicide victims who had suffered from major depressive disorder and control subjects who had died from other causes. This study aimed to reveal the selective accumulation of rare variants in the coding and the UTR sequences within the genes of suicide victims. We also analysed(More)
Autosomal, dominantly inherited spinocerebellar ataxias (SCAs) are a continuously expanding, clinically and genetically heterogeneous group of neurological disorders. Prevalence of the autosomal dominant cerebellar ataxias (ADCAs) is estimated to be approximately 1–5:100,000 population [1, 2]. The main neurological symptoms are gait and limb ataxia and(More)