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VERES, Balázs

VERES, Balázs

PhD, med. habil

associate professor , head of department

Department of Biochemistry and Medical Chemistry

Telefon: 31674

Supervisor of the following TDK topics

Supervisor: VERES, Balázs

Co-supervisor: KÁLMÁN, Nikoletta

 

Sepsis is one of the leading causes of death in intensive care units affecting more than 18 million people worldwide. Although precise mechanisms by which sepsis leads to multiple organ dysfunction are unknown, growing evidence suggests that blocking the main inflammatory signaling pathways might be a strategy to control the pathophysiology of sepsis. Nuclear factor-κB (NF-κB) as one of the most important inflammatory transcription factors plays a crucial role in regulation of uncontrollable inflammatory processes leading to sepsis. Naturally abundant biomolecules with significant anti-inflammatory effect (e.g. polyphenols) are in the limelight of our studies. We focus on the effect of these biomolecules on enzymes and adaptor proteins in signaling pathway between the cell surface TLR4 receptor and the NF-κB transcription factor.

Supervisor: VERES, Balázs

Co-supervisor: Dr. ANTUS, Csenge

 

Sepsis is one of the leading causes of death in intensive care units affecting more than 18 million people worldwide. Although precise mechanisms by which sepsis leads to multiple organ dysfunction are unknown, growing evidence suggests that blocking the main inflammatory signaling pathways might be a strategy to control the pathophysiology of sepsis. Nuclear factor-κB (NF-κB) as one of the most important inflammatory transcription factors plays a crucial role in regulation of uncontrollable inflammatory processes leading to sepsis. A number of enzymes and adaptor proteins play important role in signaling pathway between the cell surface TLR4 receptor and the NF-κB transcription factor, localized in the nucleus, thereby our studies focusing on these molecules.

Supervisor: ERŐS, Krisztián

Co-supervisor: Dr. VERES, Balázs

A redox imbalance characterizes the pathomechanisms of various diseases. Here, we aim to assess the importance of emerging oxidative stress in the liver tissue during microbial infection. For this purpose, we use new generation sequencing (NGS) data originating from bacterial lipopolysaccharide (LPS) exposed wild type, Cyclophylin D knock-out -a key regulator of the mitochondrial permeability transition pore- and an antioxidant compound, TEMPOL pre-treated mice model. The primary focus is laid on the network-based modelling and analysis of LPS-induced gene expression alterations, and hypotheses testing on the role of oxidative stress in sepsis-related tissue damage and organ dysfunction.