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Sarcopenia is characterized by progressive and generalized loss of skeletal muscle mass and strength, with a risk of adverse outcomes such as physical disability, poor quality of life, and death. Sarcopenic obesity is defined as having both sarcopenia and obesity, a condition reported to be associated with a higher risk for adverse outcomes including functional disability, frailty, poor quality of life, longer hospitalization, and higher mortality rates. The definition and diagnostic criteria for sarcopenia have been described by several working groups on the disease; however, there is no standardized definition and diagnostic criteria for sarcopenic obesity. In this review, we summarize nutrition, exercise, and pharmaceutical therapies for counteracting sarcopenic obesity in humans. Although there are some pharmaceutical therapies for both sarcopenia (i.e., testosterone, growth hormone, ghrelin, and vitamin D) and obesity (orlistat, lorcaserin, phentermine-topiramate, and vitamin D), therapies combining nutrition and exercise remain the first-line choice for preventing and treating sarcopenic obesity. Resistance training combined with supplements containing amino acids are considered most effective for treating sarcopenia. Low-calorie, high-protein diets combined with aerobic exercise and resistance training are recommended for preventing and treating obesity. Therefore, nutrition therapies (low-calorie, high-protein diets, protein and amino acid supplementation) and exercise therapies (resistance training and aerobic exercise) would be expected to be the most effective option for preventing and treating sarcopenic obesity. In cases of severe sarcopenic obesity or failure to achieve muscle gain and weight loss through nutrition and exercise therapies, it is necessary to add pharmaceutical therapies to treat the condition.

This work presents the design of a complex image processing IP developed completely in C. We present the latest advanced in ESL-synthesis and demonstrate its main advantages over conventional RT-level flows. In particular we focus on the ability of behavioral synthesis to shorten the design cycle, perform functional verification and explore quickly the design space obtaining multiple dominating implementations with unique area vs. speed characteristics from an initial untimed behavioral description. A feature extraction process is presented in detailed showing how automatic design space exploration can lead to Pareto optimal (non-dominant) designs ranging from 524,648 gates to 584,868 gates and latencies of 38 to 69 state counts for the smallest and fastest design respectively taking approximately 6.3 hours.

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Abstract. RELN (Reelin) is an extracellular glycoprotein that plays a critical role in neuronal migration. Here we show that the RELN gene is frequently silenced in gastric cancers (GCs) by aberrant promoter hypermethylation. Although RELN was strongly expressed in non-tumor gastric epithelia, its expression was weak, or absent, in GC cell lines and primary GC tumors. Absence of RELN expression significantly correlated with a more advanced stage of GC. Methylation of the RELN promoter was frequently found in GC cell lines and in primary GC tumors. These findings suggest that disruption of the RELN pathway may be involved in gastric carcinogenesis.