The Value of the Biomarkers Neuron-Specific Enolase and S100 Calcium-Binding Protein for Prediction of Mortality in Children Resuscitated After Cardiac Arrest.

The aim of the present study was to assess the ability of the biomarkers neuron-specific enolase (NSE) and S100 calcium-binding protein b (S100b) to predict 30 day mortality in children resuscitated from cardiac arrest (CA). It was a prospective observational study at a single tertiary heart centre. Consecutive children were admitted after resuscitated in-hospital and out-of-hospital CA. Levels of NSE and S100b were analyzed from 12 to 24 hours, from 24 to 48 hours, and from 48 to 72 hours after admission. The primary endpoint was 30-day mortality. Differences in biomarker levels between survivors and non-survivors were analyzed with the Mann-Whitney U test. Receiver operating characteristics (ROC) curves were applied to assess the predictive ability of the biomarkers and the areas under the ROC curves (AUC) were presented. A total of 32 resuscitated CA patients were included, and 12 (38%) patients died within 30 days after resuscitation. We observed significantly higher levels of NSE and S100b in non-survivors compared to survivors at all timepoints from 12 to 72 hours after CA. NSE achieved AUCs from 0.91-0.98 for prediction of 30 day mortality, whereas S100b achieved AUCs from 0.93-0.94. An NSE cut-off of 61 µg/L sampled between 12-24 hours from admission achieved a sensitivity of 80% and a specificity of 100% for prediction of 30 day mortality. In children resuscitated from CA, the biomarkers NSE and S100b appear to be solid predictors of mortality after 30 days.

Effects of different doses of exercise and diet-induced weight loss on beta-cell function in type 2 diabetes (DOSE-EX): a randomized clinical trial.

Diet-induced weight loss is associated with improved beta-cell function in people with type 2 diabetes (T2D) with remaining secretory capacity. It is unknown if adding exercise to diet-induced weight loss improves beta-cell function and if exercise volume is important for improving beta-cell function in this context. Here, we carried out a four-armed randomized trial with a total of 82 persons (35% females, mean age (s.d.) of 58.2 years (9.8)) with newly diagnosed T2D (<7 years). Participants were randomly allocated to standard care (n = 20), calorie restriction (25% energy reduction; n = 21), calorie restriction and exercise three times per week (n = 20), or calorie restriction and exercise six times per week (n = 21) for 16 weeks. The primary outcome was beta-cell function as indicated by the late-phase disposition index (insulin secretion multiplied by insulin sensitivity) at steady-state hyperglycemia during a hyperglycemic clamp. Secondary outcomes included glucose-stimulated insulin secretion and sensitivity as well as the disposition, insulin sensitivity, and secretion indices derived from a liquid mixed meal tolerance test. We show that the late-phase disposition index during the clamp increases more in all three intervention groups than in standard care (diet control group, 58%; 95% confidence interval (CI), 16 to 116; moderate exercise dose group, 105%; 95% CI, 49 to 182; high exercise dose group, 137%; 95% CI, 73 to 225) and follows a linear dose-response relationship (P > 0.001 for trend). We report three serious adverse events (two in the control group and one in the diet control group), as well as adverse events in two participants in the diet control group, and five participants each in the moderate and high exercise dose groups. Overall, adding an exercise intervention to diet-induced weight loss improves glucose-stimulated beta-cell function in people with newly diagnosed T2D in an exercise dose-dependent manner (NCT03769883).