795, P < .001; 0.757, P = .001; 0.717, P = .005, respectively). All 3 markers were correlated with the presence of carcinoid syndrome (AUROC = 0.702, P = .006; 0.701, P = .006; 0.697, P = .007, respectively), carcinoid heart disease (AUROC = 0.896; 0.887; 0.923, P < .001, respectively, P < .001), and liver metastatic involvement greater than 30% (AUROC = 0.827; 0.807; 0.849, P < .001, respectively, P < .001), independent from other traditional prognostic factors. Biomarker levels were similar between patients with optimal or suboptimal diet observance. Ou5HIAA and p5HIAA could be used as more convenient alternatives to 24u5HIAA in patients with metastatic midgut NETs. Prospective long-term studies with repeated dosages are needed.Ou5HIAA and p5HIAA could be used as more convenient alternatives to 24u5HIAA in patients with metastatic midgut NETs. 2',3'-cGAMP clinical trial Prospective long-term studies with repeated dosages are needed.This is Part I of a three-part series on community empowerment as a route to greater health equity. We argue that community 'empowerment' approaches in the health field are increasingly restricted to an inward gaze on community psycho-social capacities and proximal neighbourhood conditions, neglecting the outward gaze on political and social transformation for greater equity embedded in foundational statements on health promotion. We suggest there are three imperatives if these approaches are to contribute to increased equity. First, to understand pathways from empowerment to health equity and drivers of the depoliticisation of contemporary empowerment practices. Second, to return to the original concept of empowerment processes that support communities of place/interest to develop capabilities needed to exercise collective control over decisions and actions in the pursuit of social justice. Third, to understand, and engage with, power dynamics in community settings. Based on our longitudinal evaluation of a major English community empowerment initiative and research on neighbourhood resilience, we propose two complementary frameworks to support these shifts. The Emancipatory Power Framework presents collective control capabilities as forms of positive power. The Limiting Power Framework elaborates negative forms of power that restrict the development and exercise of a community's capabilities for collective control. Parts II and III of this series present empirical findings on the operationalization of these frameworks. Part II focuses on qualitative markers of shifts in emancipatory power in BL communities and Part III explores how power dynamics unfolded in these neighbourhoods. Information on the extent of patient medication adherence and the use of interventions to advance adherence are scarce in clinical practice. This study aimed to assess medication adherence and risk factors for non-adherence among the caregivers of children with tuberculosis (TB). This prospective study was conducted among the caregivers of 443 child TB patients registered during the study. Caregivers of children were queried using a structured questionnaire consisting of sociodemographic and socio-economic factors and the role of healthcare workers during the treatment course. Risk factors for non-adherence were estimated using a logistic regression model. In multivariate analysis, the independent variables that had a statistically significant positive association with non-adherence were male sex (adjusted odds ratio [AOR] 5.870 [95% confidence interval CI 1.99 to 17.29]), age ≥45y (AOR 5.627 [95% CI 1.88 to 16.82]), caregivers with no formal education (AOR 3.905 [95% CI 1.29 to 11.79]), financial barriers (AOR 30.297 [95% CI 6.13 to 149.54]), insufficient counselling by healthcare workers (AOR 5.319 [95% CI 1.62 to 17.42]), insufficient counselling by health professionals (AOR 4.117 [95% CI 1.05 to 16.05]) and unfriendly attitude and poor support from healthcare professionals (AOR 11.150 [95% CI 1.91 to 65.10]). Treatment adherence in the present study was 86% using the Morisky Green Levine Medication Adherence Scale and 90.7% using the visual analogue scale tool. Predictors of non-adherence need to be a focus and caregivers should be given complete knowledge about the importance of adherence to TB treatment.Treatment adherence in the present study was 86% using the Morisky Green Levine Medication Adherence Scale and 90.7% using the visual analogue scale tool. Predictors of non-adherence need to be a focus and caregivers should be given complete knowledge about the importance of adherence to TB treatment. Skeletal muscle is the primary site for insulin-stimulated glucose disposal, and muscle insulin resistance is central to abnormal glucose metabolism in obesity. Whether muscle insulin signaling to the level of Akt/AS160 is intact in insulin-resistant obese humans is controversial. We defined a linear range of insulin-stimulated systemic and leg glucose uptake in 14 obese and 14 nonobese volunteers using a 2-step insulin clamp (Protocol 1) and then examined the obesity-related defects in muscle insulin action in 16 nonobese and 25 obese male and female volunteers matched for fitness using a 1-step, hyperinsulinemic, euglycemic clamp coupled with muscle biopsies (Protocol 2). Insulin-stimulated glucose disposal (Si) was reduced by > 60% (P < 0.0001) in the obese group in Protocol 2; however, the phosphorylation of Akt and its downstream effector AS160 were not different between nonobese and obese groups. The increase in phosphorylation of Akt2 in response to insulin was positively correlated with Si for both the nonobese (r = 0.53, P = 0.03) and the obese (r = 0.55, P = 0.01) groups. Total muscle GLUT4 protein was 17% less (P < 0.05) in obese subjects. We suggest that reduced muscle glucose uptake in obesity is not due to defects in the insulin signaling pathway at the level of Akt/AS160, which suggests there remain significant gaps in our knowledge of muscle insulin resistance in obesity. Our data imply that models of acute lipotoxicity do not replicate the pathophysiology of obesity.We suggest that reduced muscle glucose uptake in obesity is not due to defects in the insulin signaling pathway at the level of Akt/AS160, which suggests there remain significant gaps in our knowledge of muscle insulin resistance in obesity. Our data imply that models of acute lipotoxicity do not replicate the pathophysiology of obesity.