Weight Loss Improves Cardio-Metabolic and Inflammatory State in Subjects with Metabolic Syndrome

Metabolic syndrome (MetS) is a condition characterized by a constellation of reversible major risk factors for cardiovascular disease (CVD) and type 2 diabetes (T2DM). While it has been widely demonstrated that weight reduction by 5\u201310% decreases CVD and T2DM risk factors, including atherogenic dyslipidemia, on the other hand, its effects on comprehensive serum cytokine profile and endotoxemia are less investigated. Furthermore, the impact of weight loss on these parameters was studied especially in subjects with morbid obesity, often after bariatric surgery; while the studies on the effects of a physiological weight reduction with a balanced hypocaloric diet in overweight and moderately obese subjects showed contradictory results

Prevalence of refractive errors in children in India: a systematic review

Uncorrected refractive error is an avoidable cause of visual impairment which affects children in India. The objective of this review is to estimate the prevalence of refractive errors in children ≤ 15 years of age. The Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines were followed in this review. A detailed literature search was performed to include all population and school‐based studies published from India between January 1990 and January 2017, using the Cochrane Library, Medline and Embase. The quality of the included studies was assessed based on a critical appraisal tool developed for systematic reviews of prevalence studies. Four population‐based studies and eight school‐based studies were included. The overall prevalence of refractive error per 100 children was 8.0 (CI: 7.4–8.1) and in schools it was 10.8 (CI: 10.5–11.2). The population‐based prevalence of myopia, hyperopia (≥ +2.00 D) and astigmatism was 5.3 per cent, 4.0 per cent and 5.4 per cent, respectively. Combined refractive error and myopia alone were higher in urban areas compared to rural areas (odds ratio [OR]: 2.27 [CI: 2.09–2.45]) and (OR: 2.12 [CI: 1.79–2.50]), respectively. The prevalence of combined refractive errors and myopia alone in schools was higher among girls than boys (OR: 1.2 [CI: 1.1–1.3] and OR: 1.1 [CI: 1.1–1.2]), respectively. However, hyperopia was more prevalent among boys than girls in schools (OR: 2.1 [CI: 1.8–2.4]). Refractive error in children in India is a major public health problem and requires concerted efforts from various stakeholders including the health care workforce, education professionals and parents, to manage this issue

MIRO-1 Determines Mitochondrial Shape Transition upon GPCR Activation and Ca^(2+) Stress

Mitochondria shape cytosolic calcium ([Ca^(2+)]_c) transients and utilize the mitochondrial Ca_2^+ ([Ca^(2+)]_m) in exchange for bioenergetics output. Conversely, dysregulated [Ca^(2+)]_c causes [Ca^(2+)]_m overload and induces permeability transition pore and cell death. Ablation of MCU-mediated Ca^(2+) uptake exhibited elevated [Ca^(2+)]_c and failed to prevent stress-induced cell death. The mechanisms for these effects remain elusive. Here, we report that mitochondria undergo a cytosolic Ca^(2+)-induced shape change that is distinct from mitochondrial fission and swelling. [Ca^(2+)]_c elevation, but not MCU-mediated Ca^(2+) uptake, appears to be essential for the process we term mitochondrial shape transition (MiST). MiST is mediated by the mitochondrial protein Miro1 through its EF-hand domain 1 in multiple cell types. Moreover, Ca^(2+)-dependent disruption of Miro1/KIF5B/tubulin complex is determined by Miro1 EF1 domain. Functionally, Miro1-dependent MiST is essential for autophagy/mitophagy that is attenuated in Miro1 EF1 mutants. Thus, Miro1 is a cytosolic Ca^(2+) sensor that decodes metazoan Ca^(2+) signals as MiST

MIRO-1 Determines Mitochondrial Shape Transition upon GPCR Activation and Ca^(2+) Stress

Mitochondria shape cytosolic calcium ([Ca^(2+)]_c) transients and utilize the mitochondrial Ca_2^+ ([Ca^(2+)]_m) in exchange for bioenergetics output. Conversely, dysregulated [Ca^(2+)]_c causes [Ca^(2+)]_m overload and induces permeability transition pore and cell death. Ablation of MCU-mediated Ca^(2+) uptake exhibited elevated [Ca^(2+)]_c and failed to prevent stress-induced cell death. The mechanisms for these effects remain elusive. Here, we report that mitochondria undergo a cytosolic Ca^(2+)-induced shape change that is distinct from mitochondrial fission and swelling. [Ca^(2+)]_c elevation, but not MCU-mediated Ca^(2+) uptake, appears to be essential for the process we term mitochondrial shape transition (MiST). MiST is mediated by the mitochondrial protein Miro1 through its EF-hand domain 1 in multiple cell types. Moreover, Ca^(2+)-dependent disruption of Miro1/KIF5B/tubulin complex is determined by Miro1 EF1 domain. Functionally, Miro1-dependent MiST is essential for autophagy/mitophagy that is attenuated in Miro1 EF1 mutants. Thus, Miro1 is a cytosolic Ca^(2+) sensor that decodes metazoan Ca^(2+) signals as MiST