Sexually Predatory Behavior in an Adolescent Female.

This report describes a rare case of an adolescent female with a history of unspecified depressive disorder, disinhibited social engagement disorder, and significant history of sexual trauma at an early age, who initially presented with suicidal ideation. During the initial evaluation, the patient was found to have engaged in sexually predatory behavior toward younger boys, including solicitation and inappropriate sexual behavior. This report discusses relevant literature on the prevalence, risk factors, and treatment for this behavior among female adolescent sexual predators, as sex offenders are primarily thought to be men. General recommendations for health care professionals caring for female sexual offenders are addressed as well as the importance of early treatment and appropriate training for professionals. The patient has been deidentified.

Ceramide mediates vascular dysfunction in diet-induced obesity by PP2A-mediated dephosphorylation of the eNOS-Akt complex.

Vascular dysfunction that accompanies obesity and insulin resistance may be mediated by lipid metabolites. We sought to determine if vascular ceramide leads to arterial dysfunction and to elucidate the underlying mechanisms. Pharmacological inhibition of de novo ceramide synthesis, using the Ser palmitoyl transferase inhibitor myriocin, and heterozygous deletion of dihydroceramide desaturase prevented vascular dysfunction and hypertension in mice after high-fat feeding. These findings were recapitulated in isolated arteries in vitro, confirming that ceramide impairs endothelium-dependent vasorelaxation in a tissue-autonomous manner. Studies in endothelial cells reveal that de novo ceramide biosynthesis induced protein phosphatase 2A (PP2A) association directly with the endothelial nitric oxide synthase (eNOS)/Akt/Hsp90 complex that was concurrent with decreased basal and agonist-stimulated eNOS phosphorylation. PP2A attenuates eNOS phosphorylation by preventing phosphorylation of the pool of Akt that colocalizes with eNOS and by dephosphorylating eNOS. Ceramide decreased the association between PP2A and the predominantly cytosolic inhibitor 2 of PP2A. We conclude that ceramide mediates obesity-related vascular dysfunction by a mechanism that involves PP2A-mediated disruption of the eNOS/Akt/Hsp90 signaling complex. These results provide important insight into a pathway that represents a novel target for reversing obesity-related vascular dysfunction.