Publications by authors named "Mustafa A Atik"

Article Synopsis
  • Effector memory T cells without CCR7 promote inflammation in autoimmune diseases like multiple sclerosis and rheumatoid arthritis, making them significant therapeutic targets.
  • The Kv1.3 potassium channel regulates the activation of these T cells, and blocking it can reduce inflammation associated with these conditions.
  • The peptide HsTX1[R14A], derived from scorpion venom and modified for better performance (PEG-HsTX1[R14A]), effectively inhibits Kv1.3 and has shown promise in reducing inflammation in arthritis models, with improved longevity in the bloodstream compared to its non-PEGylated version.
View Article and Find Full Text PDF

Allergic asthma is a chronic inflammatory disease of the airways. Of the different lower airway-infiltrating immune cells that participate in asthma, T lymphocytes that produce Th2 cytokines play important roles in pathogenesis. These T cells are mainly fully differentiated CCR7(-) effector memory T (TEM) cells.

View Article and Find Full Text PDF
Article Synopsis
  • Asthma is a complex disease with various overlapping types, and researchers are studying biomarkers to help define these types and guide treatment.
  • Periostin, a protein linked to TH2-driven asthma, is highlighted as a key biomarker that can indicate airway inflammation and predict how well patients respond to treatments like inhaled corticosteroids and biologic therapies.
  • While the initial research on periostin's effectiveness is encouraging, more studies are needed to validate these results and explore additional uses for the biomarker in clinical practice.
View Article and Find Full Text PDF

Background: Hyponatremia after traumatic brain injury (TBI) may influence neurological function and treatment. A causal relationship between elevated serum concentrations of Type B natriuretic peptide (BNP) and hyponatremia has been implied after subarachnoid hemorrhage and other neurosurgical disorders, although the source of BNP has not been identified. We evaluated if hyponatremia and increased BNP occur after TBI and if BNP is produced/released by the brain within 24 h after injury.

View Article and Find Full Text PDF