JAK/STAT pathway regulation of GABAA receptor expression after differing severities of experimental TBI.

Synaptic inhibition in the adult brain is primarily mediated by the γ-aminobutyric acid (GABA) type A receptor (GABA(A)R). The distribution, properties, and dynamics of these receptors are largely determined by their subunit composition. Alteration of subunit composition after a traumatic brain injury (TBI) may result in abnormal increased synaptic firing and possibly contribute to injury-related pathology.

Glucuronic acid and the ethanol metabolite ethyl-glucuronide cause toll-like receptor 4 activation and enhanced pain.

We have previously observed that the non-opioid morphine metabolite, morphine-3-glucuronide, enhances pain via a toll-like receptor 4 (TLR4) dependent mechanism. The present studies were undertaken to determine whether TLR4-dependent pain enhancement generalizes to other classes of glucuronide metabolites. In silico modeling predicted that glucuronic acid alone and ethyl glucuronide, a minor but long-lasting ethanol metabolite, would dock to the same MD-2 portion of the TLR4 receptor complex previously characterized as the docking site for morphine-3-glucuronide.

Athletic participation in severe hemophilia: bleeding and joint outcomes in children on prophylaxis.

Objectives: We sought to determine joint outcomes relative to impact level of athletic participation among school-aged children who had hemophilia and were taking prophylactic factor replacement, as well as to investigate prognostic factors for joint outcomes.

Methods: School-aged boys with severe hemophilia A or B at a single center were included in the study. Clinical data on baseline joint status, BMI, hemophilia treatment, bleeding episodes, joint assessments, athletic participation, and injuries were retrospectively reviewed.