Update on aspirin exacerbated respiratory disease with chronic rhinosinusitis.

Purpose Of Review: This review provides the current understanding on the mechanism, diagnosis, and treatment of aspirin exacerbated respiratory disease (AERD) with chronic rhinosinusitis (CRS).

Recent Findings: Updates focus on the current understanding of type 2 inflammation as a disease driver, alterations in gene expression in nasal polyps, and use of biologics in treating aspirin exacerbated respiratory disease. Recent findings include altered expression of GATA binding protein 3 (GATA3), interleukin (IL)-4, IL-5, and IL-17 in nasal polyps supports the current understanding that type 2 inflammation predominantly drives the pathophysiology of AERD with CRS.

Decreased dopamine receptor 1 activity and impaired motor-skill transfer in Dyt1 ΔGAG heterozygous knock-in mice.

DYT1 dystonia is a movement disorder caused by a trinucleotide deletion (ΔGAG) in DYT1 (TOR1A), corresponding to a glutamic acid loss in the C-terminal region of torsinA. Functional alterations in the basal ganglia circuits have been reported in both DYT1 dystonia patients and rodent models. Dyt1 ΔGAG heterozygous knock-in (KI) mice exhibit motor deficits and decreased striatal dopamine receptor 2 (D2R) binding activity, suggesting a malfunction of the indirect pathway.