Protective Orders for Male Perpetrators of Intimate Partner Violence: Differences Between Violators and Non-Violators.

The goal of this study was to determine the profile of the aggressors of intimate partner violence (IPV), who tend to violate protective orders (POs). A cohort of 200 men convicted of IPV (120 violators and 80 non-violators of the POs) was studied. Male perpetrators were more likely to belong to the PO violator group when they had a prior criminal history, they inflicted more severe physical violence, they were drug users, and they had a low education level. Using the risk factors identified here when dealing with males who perpetrate IPV and taking appropriate measures may help to prevent revictimization.

Two Cases of Consecutive Toxic Anterior Segment Syndrome after Uneventful Trabeculectomy Surgeries in a Tertiary Center.

Toxic anterior segment syndrome (TASS) is a severe, acute, sterile intraocular inflammation that occurs the same day or in the early stages after intraocular surgery. It has been most commonly reported after phacoemulsification. We report 2 cases that developed TASS after sequential uneventful trabeculectomy surgeries, in which a quaternary ammonium compound was used for the disinfection of surgical instruments. Good outcomes were achieved, possibly related to the fast treatment initiation.

Angiotensin II causes hypertension and cardiac hypertrophy through its receptors in the kidney.

Essential hypertension is a common disease, yet its pathogenesis is not well understood. Altered control of sodium excretion in the kidney may be a key causative feature, but this has been difficult to test experimentally, and recent studies have challenged this hypothesis. Based on the critical role of the renin-angiotensin system (RAS) and the type I (AT1) angiotensin receptor in essential hypertension, we developed an experimental model to separate AT1 receptor pools in the kidney from those in all other tissues. Although actions of the RAS in a variety of target organs have the potential to promote high blood pressure and end-organ damage, we show here that angiotensin II causes hypertension primarily through effects on AT1 receptors in the kidney. We find that renal AT1 receptors are absolutely required for the development of angiotensin II-dependent hypertension and cardiac hypertrophy. When AT1 receptors are eliminated from the kidney, the residual repertoire of systemic, extrarenal AT1 receptors is not sufficient to induce hypertension or cardiac hypertrophy. Our findings demonstrate the critical role of the kidney in the pathogenesis of hypertension and its cardiovascular complications. Further, they suggest that the major mechanism of action of RAS inhibitors in hypertension is attenuation of angiotensin II effects in the kidney.