T. Nemkov

Biological and Genetic Determinants of Glycolysis: Phosphofructokinase Isoforms Boost Energy Status of Stored Red Blood Cells and Transfusion Outcomes

The paper identifies genetic polymorphisms and metabolite levels in stored red blood cells that correlate with hemolysis and transfusion outcomes.

Inflammation promotes aging-associated oncogenesis in the lung.

This study investigates how aging-related inflammation contributes to lung cancer development by analyzing gene expression data and using mouse models to assess the role of inflammation in oncogenesis.

Auxin Exposure Disrupts Feeding Behavior and Fatty Acid Metabolism in Adult Drosophila

This study shows auxin exposure affects adult Drosophila feeding behavior and fatty acid metabolism but not fecundity or progeny survival.

Metabolic Signatures of Performance in Elite World Tour Professional Cyclists

This study identifies metabolic signatures in elite cyclists during training and competition, revealing differences in metabolite profiles between exercise modes and race stages.

Proteolytic Activation of Human-specific Olduvai Domains by the Furin Protease

The paper shows human-specific Olduvai domains are cleaved by furin protease, suggesting they function as proproteins activated by this processing, linking their expansion to human brain evolution.

Traumatic Brain Injury Impairs Systemic Vascular Function Through Altered Lipid Metabolism and Disruption of Inward-Rectifier Potassium (Kir2.1) Channels

This study shows traumatic brain injury impairs vascular function by reducing Kir2.1 channel activity through PIP2 depletion caused by increased H2O2 and PLA2 activity.

Inflammation promotes tumor aggression by stimulating stromal cell-dependent collagen crosslinking and stromal stiffening

This study shows that inflammation promotes tumor aggression by stimulating stromal cell-dependent collagen crosslinking and stiffening, identifying lysyl hydroxylase two as a biomarker.

Targeting glutamine metabolism and redox state for leukemia therapy

This study shows that inhibiting glutaminase with CB-839 reduces glutathione and increases mitochondrial ROS in AML, leading to apoptosis, and that combining it with pro-oxidant drugs enhances cell death in AML and ALL.