Nigrostriatal degeneration determines dynamics of glial inflammatory and phagocytic activity.

Glial cells are key players in the initiation of innate immunity in neurodegeneration. Upon damage, they switch their basal activation state and acquire new functions in a context and time-dependent manner. Since modulation of neuroinflammation is becoming an interesting approach for the treatment of neurodegenerative diseases, it is crucial to understand the specific contribution of these cells to the inflammatory reaction and to select experimental models that recapitulate what occurs in the human disease.

Apolipoprotein E Polymorphisms in Andean Population of Jujuy, Argentina.

The pleiotropic nature of the apolipoprotein E () gene is associated with complex diseases in different populations. We analyzed polymorphisms in 76 individuals from Jujuy - Argentina using NGS technology. The observed genotypes align with the expected Hardy-Weinberg equilibrium.

Heparin-induced thrombocytopenia: a rare presentation with skin necrosis.

Heparin-induced thrombocytopenia is the most clinically relevant non-hemorrhagic complication of heparin and is characterized by the presence of anti-platelet factor 4 (PF4)/heparinimmunoglobulin G (IgG) antibodies. The circulating PF4/heparinIgG immune complex binds to platelets their FcyIIa receptors, activating them and promoting their aggregation, with consequent platelet consumption, thrombocytopenia, and thrombotic phenomena. Despite thrombocytopenia, this condition is not typically associated with bleeding complications.