Merrillalexandersen8053

OBJECTIVE The aim of this study was to describe practices for weaning from mechanical ventilation (MV), in terms of the use of protocols, methods, and criteria, in pediatric ICUs (PICUs), neonatal ICUs (NICUs), and mixed neonatal/pediatric ICUs (NPICUs) in Brazil. METHODS This was a cross-sectional survey carried out by sending an electronic questionnaire to a total of 298 NICUs, PICUs, and NPICUs throughout Brazil. RESULTS Completed questionnaires were assessed for 146 hospitals, NICUs accounting for 49.3% of the questionnaires received, whereas PICUs and NPICUs accounted for 35.6% and 15.1%, respectively. Weaning protocols were applied in 57.5% of the units. In the NICUs and NPICUs that used weaning protocols, the method of MV weaning most commonly employed (in 60.5% and 50.0%, respectively) was standardized gradual withdrawal from ventilatory support, whereas that employed in most (53.0%) of the PICUs was spontaneous breathing trial (SBT). During the SBTs, the most common ventilation mode, in all ICUs, was pressure-support ventilation (10.03 ± 3.15 cmH2O) with positive end-expiratory pressure. The mean SBT duration was 35.76 ± 29.03 min in the NICUs, compared with 76.42 ± 41.09 min in the PICUs. The SBT parameters, weaning ventilation modes, and time frame considered for extubation failure were not found to be dependent on the age profile of the ICU population. The findings of the clinical evaluation and arterial blood gas analysis are frequently used as criteria to assess readiness for extubation, regardless of the age group served by the ICU. CONCLUSIONS In Brazil, the clinical practices for weaning from MV and extubation appear to vary depending on the age group served by the ICU. It seems that weaning protocols and SBTs are used mainly in PICUs, whereas gradual withdrawal from ventilatory support is more widely used in NICUs and NPICUs.in English, Portuguese OBJETIVO Este estudo visou avaliar a adequação da prescrição de profilaxia de tromboembolismo venoso (TEV) após a implementação do protocolo. MÉTODOS Trata-se de um estudo antes e depois realizado em um hospital de cuidados terciários no Rio Grande do Sul, Brasil. Pacientes clínicos e cirúrgicos internados, com 18 anos ou mais, foram avaliados para o risco de TEV e, posteriormente, para adequação da tromboprofilaxia, de acordo com o risco. As avaliações ocorreram antes e depois de uma estratégia de implementação de protocolo, que consistiu em uma plataforma on-line para acessar o protocolo, uma postagem pública do diagrama do protocolo, alertas clínicos na sala de convívio médico, alertas de e-mail e alertas pop-up no sistema informatizado de prescrição médica. O Desfecho principal foi a adequação da prescrição de profilaxia do TEV de acordo com o protocolo. RESULTADOS Foram avaliados 429 pacientes para adequação da tromboprofilaxia (213 antes e 216 depois). A prevalência de adequação aumentou de 54% para 63% (pré e pós-intervenção, respectivamente) e após o ajuste por tipo de paciente e fase do estudo, a razão de prevalência atingiu (RP) = 1,20, intervalo de confiança de 95% (IC) 1,02-1,42. CONCLUSÕES os resultados mostraram que a adequação geral da prescrição de tromboprofilaxia foi discretamente melhorada. Apesar desses resultados, este estudo fornece evidências, até o momento, de uma série de estratégias para implementar o protocolo em instituições privadas em países de renda média com uma equipe médica aberta, pois há poucas pesquisas investigando esse tipo de intervenção simples e pragmática.Given the global burden of tuberculosis, shortened treatment regimens with existing or repurposed drugs are needed to contribute to tuberculosis control. The long duration of treatment of drug-susceptible tuberculosis (DS-TB) is associated with nonadherence and loss to follow up, and the treatment success rate of multidrug-resistant tuberculosis (MDR-TB) is low (approximately 50%) with longer regimens. In this review article, we report recent advances and ongoing clinical trials aimed at shortening regimens for DS-TB and MDR-TB. We discuss the role of high-dose rifampin, as well as that of clofazimine and linezolid in regimens for DS-TB. There are at least 5 ongoing clinical trials and 17 observational studies and clinical trials evaluating shorter regimens for DS-TB and MDR-TB, respectively. We also report the results of observational studies and clinical trials evaluating a standardized nine-month moxifloxacin-based regimen for MDR-TB. Further studies, especially randomized clinical trials, are needed to evaluate regimens including newer drugs, drugs proven to be or highly likely to be efficacious, and all-oral drugs in an effort to eliminate the need for injectable drugs.PURPOSE Patients with diabetes are vulnerable to myocardial I/R (ischaemia/reperfusion) injury, but are not responsive to IPO (ischaemic post-conditioning). Dactinomycin We hypothesized that decreased cardiac Adiponectin (APN) is responsible for the loss of diabetic heart sensitivity to IPO cardioprotecton. METHODS Diabetic rats were subjected to I/R injury (30 min of LAD occlusion followed by 120 min of reperfusion). Myocardial infarct area was determined by TTC staining. Cardiac function was monitored by a microcatheter. ANP, 15-F2t-isoprostane, nitrotyrosine and MDA were measured by assay kits. Levels of p-Akt, total-Akt and GAPDH were determined by Western Blot. RESULTS Diabetic rats subjected to myocardial IR exhibited severe myocardial infarction and oxidative stress injury, lower APN in the plasma and cardiac p-Akt expression ( P less then 0.05). IPO significantly attenuated myocardial injury and up-regulated plasma APN content and cardiac p-Akt expression in non-diabetic rats but not in diabetic rats. Linear correlation analysis showed that the expression of adiponectin was positively correlated with p-Akt and negatively correlated with myocardial infarction area ( P less then 0.01). CONCLUSION Protective effect of IPO was tightly correlated with the expression of adiponectin, exacerbation of I/R injury and ineffectiveness of IPO was partially due to the decline of adiponectin and inactivation of Akt in diabetes mellitus.