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Non-communicable diseases (NCDs) are a major health concern in India and were estimated to account for 63% of all deaths in 2016, and if left unaddressed, they could cost India approximately US$3.55 trillion in economic losses by 2030. The National Programme for Prevention and Control of Cancer, Diabetes, Cardiovascular Diseases & Stroke (NPCDCS) has identified community engagement to enable behaviour change as a top intervention to manage various NCDs. Community engagement initiatives in India are plagued with multiple issues such as a lack of long-term focus, non-clarity on budgets, ineffective programme planning and the absence of visionary leadership and governance. This article attempts to understand the role of community engagement in providing access to NCD awareness and to support action on prevention, screening, diagnosis, treatment and compliance, so that the community is empowered to proactively behave in a way to prevent and manage NCDs effectively and hence reduce the incidence of NCDs. The article is based on research study using a mixed-method approach in a five-step manner, which included secondary and primary research. After scanning 200 initiatives across the spectrum of community engagement globally, 20 were shortlisted and detailed case studies of the initiatives were analysed and presented. In addition, primary research was pursued to propose recommendations for community engagement across the areas of visioning and planning, leadership and governance, and community involvement. Some guiding principles were recommended to create an environment of shared leadership and collaboration for community engagement, consequently creating greater positive influence on NCD management within the community. [ABSTRACT FROM AUTHOR]

Obesity comorbidities such as diabetes and cardiovascular disease are pressing public health concerns. Overconsumption of calories leads to weight gain; however, neural mechanisms underlying excessive food consumption are poorly understood. Here, we demonstrate that dopamine receptor D1 (Drd1) expressed in the agouti-related peptide/neuropeptide Y (AgRP/NPY) neurons of the arcuate hypothalamus is required for appropriate responses to a high-fat diet (HFD). Stimulation of Drd1 and AgRP/NPY co-expressing arcuate neurons is sufficient to induce voracious feeding. Delivery of a HFD after food deprivation acutely induces dopamine (DA) release in the ARC, whereas animals that lack Drd1 expression in ARCAgRP/NPY neurons (Drd1AgRP-KO) exhibit attenuated foraging and refeeding of HFD. These results define a role for the DA input to the ARC that encodes acute responses to food and position Drd1 signaling in the ARCAgRP/NPY neurons as an integrator of the hedonic and homeostatic neuronal feeding circuits. [Display omitted] • Dopamine is released in the ARC in response to food • ARCDrd1 neurons regulate feeding and energy homeostasis • Stimulation of ARCDrd1/AgRP/NPY neurons is sufficient to induce feeding • Drd1 signaling in the ARCAgRP/NPYneurons promotes HFD consumption Zhang et al. show that DA release in the ARC is modulated by metabolic states and encodes the energy density of the available food. The Drd1-expressing neurons in the ARC including a subpopulation of ARCAgRP/NPYneurons induce feeding. Genetic ablation of Drd1 in ARCAgRP/NPYneurons attenuates HFD-induced hyperphagia. [ABSTRACT FROM AUTHOR]

In the Categorical Clustering problem, we are given a set of vectors (matrix) A = { a 1 , ... , a n } over Σ m , where Σ is a finite alphabet, and integers k and B. The task is to partition A into k clusters such that the median objective of the clustering in the Hamming norm is at most B. Fomin, Golovach, and Panolan [ICALP 2018] proved that the problem is fixed-parameter tractable for the binary case Σ = { 0 , 1 }. We extend this algorithmic result to a popular capacitated clustering model, where in addition the sizes of the clusters are lower and upper bounded by integer parameters p and q , respectively. Our main theorem is that the problem is solvable in time 2 O (B log ⁡ B) | Σ | B ⋅ (m n) O (1). [ABSTRACT FROM AUTHOR]

The widespread availability of energy-dense, rewarding foods is correlated with the increased incidence of obesity across the globe. Overeating during mealtimes and unscheduled snacking disrupts timed metabolic processes, which further contribute to weight gain. The neuronal mechanism by which the consumption of energy-dense food restructures the timing of feeding is poorly understood. Here, we demonstrate that dopaminergic signaling within the suprachiasmatic nucleus (SCN), the central circadian pacemaker, disrupts the timing of feeding, resulting in overconsumption of food. D1 dopamine receptor (Drd1)-null mice are resistant to diet-induced obesity, metabolic disease, and circadian disruption associated with energy-dense diets. Conversely, genetic rescue of Drd1 expression within the SCN restores diet-induced overconsumption, weight gain, and obesogenic symptoms. Access to rewarding food increases SCN dopamine turnover, and elevated Drd1-signaling decreases SCN neuronal activity, which we posit disinhibits downstream orexigenic responses. These findings define a connection between the reward and circadian pathways in the regulation of pathological calorie consumption. • Diet-induced obesity (DIO) requires dopamine (DA)-Drd1 signaling • DA-Drd1 signaling in the central circadian clock (SCN) instigates DIO • SCN DA-Drd1 signaling disinhibits hedonic food consumption in between meals • Diet drives dysbiosis and peripheral circadian desynchrony independent of Drd1 Palatable diets rich in fat and sugar incentivize overeating, which leads to obesity. Grippo and Tang et al. discover a unique role for dopamine signaling in the central circadian clock that promotes overconsumption outside of mealtimes. [ABSTRACT FROM AUTHOR]