Patients exposed to a surgical safety checklist experience better postoperative outcomes, but this could simply reflect wider quality of care in hospitals where checklist use is routine.

There is no conclusive evidence in this review to support or refute inspiratory muscle training for asthma. The evidence was limited by the small number of trials with few participants together with the risk of bias. More well conducted randomised controlled trials are needed. Future trials should investigate the following outcomes: lung function, exacerbation rate, asthma symptoms, hospital admissions, use of medications and days off work or school. Inspiratory muscle training should also be assessed in people with more severe asthma and conducted in children with asthma.

Background Hypertrophic cardiomyopathy (HCM) is a common genetic disorder caused mainly by mutations in sarcomeric proteins and is characterized by maladaptive myocardial hypertrophy, diastolic heart failure, increased myofilament Ca2+ sensitivity and high susceptibility to sudden death. We tested the following hypothesis: correction of the increased myofilament sensitivity can delay or prevent the development of the HCM phenotype. Methods and Results We used an HCM mouse model with an E180G mutation in α-tropomyosin (Tm180) that demonstrates increased myofilament Ca2+ sensitivity, severe hypertrophy and diastolic dysfunction. To test our hypothesis, we reduced myofilament Ca2+ sensitivity in Tm180 mice by generating a double transgenic (DTG) mouse line. We crossed Tm180 mice with mice expressing a pseudo-phosphorylated cardiac troponin I (cTnI) (S23D and S24D; TnI-PP). TnI-PP mice demonstrated a reduced myofilament Ca2+ sensitivity compared to wild-type mice. The development of pathological hypertrophy did not occur in mice expressing both Tm180 and TnI-PP. Left ventricle performance was improved in DTG compared to their Tm180 littermates, which express wild-type cTnI. Hearts of DTG mice demonstrated no changes in expression of phospholamban (PLN) and Serca2a, increased levels of PLN and TnT phosphorylation, and reduced phosphorylation of TnI compared to Tm180 mice. Moreover, expression of TnI-PP in Tm180 hearts inhibited modifications in the activity of ERK1/2 and GATA-4 in Tm180 hearts. Conclusions Our data strongly indicate that reduction of myofilament sensitivity to Ca2+ and associated correction of abnormal relaxation can delay or prevent development of HCM and should be considered as a therapeutic target for HCM.

BackgroundRecently, some studies have evaluated the role of adiposity measures in the prediction of hypertension risk, but the results are conflicting. Thus, the aim of this study was to compare which of the four indicators of adiposity (waist circumference–WC, body mass index–BMI, body adiposity index–BAI, and visceral adiposity index–VAI) were better associated with hypertension in a Brazilian population.Methods and findingsFor this study, were selected 1627 individuals (both genders, and aged over 18 years) resident in the municipality of Baependi, a city located in the Southeast of Brazil. WC, BMI, BAI and VAI were determined according to a standard protocol. Hypertension was defined as mean systolic blood pressure ≥ 140 mmHg and/or diastolic blood pressure ≥ 90 mmHg, and/or antihypertensive drug use. The indicators of adiposity WC, BMI, BAI, and VAI were higher in hypertensive when compared to non-hypertensive individuals. In addition, WC and BMI were most strongly associated with hypertension in men and women, respectively. The area under the curve (AUC) of WC was significantly higher than VAI in men. In women, both AUC of BMI and WC showed higher discriminatory power to predict hypertension than BAI and VAI.ConclusionsThe indicators of adiposity WC and BMI were better associated with hypertension than BAI and VAI, in both genders, and it could be a useful tools for the screening of hypertensive patients.