Astrocyte Gi-GPCR signaling corrects compulsive-like grooming and anxiety-related behaviors in Sapap3 knockout mice.

Astrocytes are morphologically complex cells that serve essential roles. They are widely implicated in central nervous system (CNS) disorders, with changes in astrocyte morphology and gene expression accompanying disease. In the Sapap3 knockout (KO) mouse model of compulsive and anxiety-related behaviors related to obsessive-compulsive disorder (OCD), striatal astrocytes display reduced morphology and altered actin cytoskeleton and Gi-G-protein-coupled receptor (Gi-GPCR) signaling proteins. Here, we show that normalizing striatal astrocyte morphology, actin cytoskeleton, and essential homeostatic support functions by targeting the astrocyte Gi-GPCR pathway using chemogenetics corrected phenotypes in Sapap3 KO mice, including anxiety-related and compulsive behaviors. Our data portend an astrocytic pharmacological strategy for rescuing phenotypes in brain disorders that include compromised astrocyte morphology and tissue support.

A recurrent retrohepatic abscess secondary to a dropped appendicolith.

Appendicoliths can drop into the peritoneal cavity during the course of an appendicectomy, or more commonly as a result of perforated appendicitis. We report the case of a patient with a history of recurrent retrohepatic abscesses over 7-year period due to a retained appendicolith and review the literature on perihepatic abscesses caused by retained appendicoliths. The abscess had been drained percutaneously 4 times without retrieval of the appendicolith and eventually the patient needed a laparotomy, drainage of the abscess, and extraction of the appendicolith. Treatment of abscesses secondary to dropped appendicoliths may be percutaneous, laparoscopic, or via conventional open surgery, but it is important to retrieve the appendicolith if recurrent abscess formation is to be avoided.