l-Arginine supplementation improves rats' antioxidant system and exercise performance.

Reactive species have great importance in sports performance, once they can directly regulate energy production, muscular contraction, inflammation, and fatigue. Therefore, the redox control is essential for athletes' performance. Studies demonstrated that l-arginine has an important role in the synthesis of urea, cell growth and production of nitric oxide, moreover, there are indications that it is also able to induce benefits to muscle antioxidant system through the upregulation of some antioxidant enzymes, and by inhibiting some pathways of reactive species production. Therefore, the aim of this study was to evaluate the effects of l-arginine supplementation on performance and oxidative stress of male rats (trained or not), submitted to a single session of high intensity exercise. Forty male Wistar rats were divided into four groups, control (C), control+l-arginine (C + A), trained (T), and trained+l-arginine (T + A). The aerobic training was conducted for 8 weeks. Data of maximum speed and time from tests were used as indicators of performance. Variables related to oxidative stress and antioxidant system were also evaluated. Aerobic training was capable to induce enhancements on animals' exercise performance and on their redox state. Additionally, supplementation improved rats' physical performance on both groups, control and trained. Different improvements between groups on the antioxidant capacity were observed. Nevertheless, considering the ergogenic effect of l-arginine and the lack of all positive adaptations promoted by the exercise training, untrained animals may be more exposed to oxidative damages after the practice of intense exercises.

Carbapenem-resistant Enterobacteriaceae on a cardiac surgery intensive care unit: successful measures for infection control.

BACKGROUND: Carbapenem-resistant Enterobacteriaceae (CRE) cause surgical site infections (SSIs) in intensive care units (ICUs). This study aimed to evaluate the impact of intervention and control measures to reduce CRE colonization and infection rates among patients in the ICU of a cardiac surgery hospital following a CRE outbreak. METHODS: An observational study of the pre- and postintervention status of a cohort of colonized or infected patients in the postoperative adult cardiac surgery ICU was performed between April 2013 and December 2014. As well as the usual measures of screening and cohort nursing, the control measures were enhanced during the intervention period by providing alcohol gel at the bedside, daily bathing with no-rinse 2% chlorhexidine-impregnated wash cloths, and disinfection of surfaces around the patient three times per day. RESULTS: The rates of CRE colonization (P<0.001), primary central-line-associated bloodstream infections (P<0.002) and SSIs (P< 0.003) decreased significantly during the postintervention period. CONCLUSION: The implemented measures were effective in controlling colonization and infection with CRE in the cardiac surgery ICU.

Agrin-induced phosphorylation of the acetylcholine receptor regulates cytoskeletal anchoring and clustering.

At the developing neuromuscular junction, a motoneuron-derived factor called agrin signals through the muscle-specific kinase receptor to induce postsynaptic aggregation of the acetylcholine receptor (AChR). The agrin signaling pathway involves tyrosine phosphorylation of the AChR beta subunit, and we have tested its role in receptor localization by expressing tagged, tyrosine-minus forms of the beta subunit in mouse Sol8 myotubes. We find that agrin-induced phosphorylation of the beta subunit occurs only on cell surface AChR, and that AChR-containing tyrosine-minus beta subunit is targeted normally to the plasma membrane. Surface AChR that is tyrosine phosphorylated is less detergent extractable than nonphosphorylated AChR, indicating that it is preferentially linked to the cytoskeleton. Consistent with this, we find that agrin treatment reduces the detergent extractability of AChR that contains tagged wild-type beta subunit but not tyrosine-minus beta subunit. In addition, agrin-induced clustering of AChR containing tyrosine-minus beta subunit is reduced in comparison to wild-type receptor. Thus, we find that agrin-induced phosphorylation of AChR beta subunit regulates cytoskeletal anchoring and contributes to the clustering of the AChR, and this is likely to play an important role in the postsynaptic localization of the receptor at the developing synapse.