Sickle cell disease has been very well characterized as a single amino acid molecular
disorder of hemoglobin leading to its pathological polymerization, with resulting red cell …

Since the discovery of sickle cell disease (SCD) in 1910, enormous strides have been made
in the elucidation of the pathogenesis of its protean complications, which has inspired recent …

Sickle cell disease (SCD) is caused by a mutation in both beta globin genes, resulting in
chronic hemolysis and multiorgan disease that ultimately leads to premature death …

A single amino acid substitution in hemoglobin comprises the molecular basis for sickle cell
anemia, but evolution of the corresponding clinical disease is extraordinarily complicated …

Many mechanisms contribute to the complex pathophysiology of sickle cell disease (SCD),
with dysfunction of the vascular endothelium as a unifying theme. Specifically, hemolysis …

Sickle cell disease (SCD) is characterized by the presence of sickle hemoglobin, which has
the unique property of polymerizing when deoxygenated. The pathophysiology of acute and …

Much of the morbidity and mortality of sickle cell anemia is accounted for by a chronic
vasculopathy syndrome. There is currently no identified therapy, interventional or …

Homozygous sickle cell disease (SCD) is an autosomal recessive genetic disease that
results from the substitution of valine for glutamic acid at position 6 of the β-globin gene …

The first coherent pathophysiological scheme for sickle cell disease (SCD) emerged in the
sixties-seventies based on an extremely detailed description of the molecular mechanism by …

Sickle cell disease (SCD) is an autosomal recessive disorder in the gene encoding the β-
chain of hemoglobin. Deoxygenation causes the mutant hemoglobin S to polymerize …