uridine diphosphate/hemorrhage

BACKGROUND Despite ongoing advances in treatment, thousands of patients still die annually from complications due to hemorrhagic shock, a condition causing dramatic physiologic and metabolic changes as cells switch to anaerobic metabolism in response to oxygen deprivation. As the shift from aerobic

A patient with blood type A had acute myelomonocytic leukemia; his red cells (RBCs) typed as O and his serum had anti-B. RBC membranes were isolated from the patient as well as from controls with group A and O red cells. The membranes were incubated with uridine diphosphate (UDP)-N-acetyl-D-14C

In vitro studies have demonstrated that curcumin is a substrate for uridine diphosphate glucuronosyltransferase (UGTs), with a putative ability to both induce expression and inhibit function, highlighting the potential for interaction with some drugs. Therefore, we sought to evaluate the effect of

An early and rapid response to severe injury or trauma is the development of hyperglycemia, which has long been thought to be an essential survival response by providing fuel for vital organ systems and facilitating mobilization of interstitial fluid reserves by increasing osmolarity. However,

Galactose epimerase deficiency is an inborn error of metabolism due to uridine diphosphate-galactose-4'-epimerase (GALE) deficiency. We report the clinical presentation, genetic and biochemical studies in two siblings with generalized GALE deficiency.Patient 1: The first child was born with a