These flavonoids improve GLUT-4 expression and translocation to plasma membrane by activation of insulin-sensitive PI3K/Akt signaling and insulin-independent AMPK, SIRT-1 and MOR activation pathways for regulation of glucose homeostasis, and improve fat oxidation and reduce lipid synthesis by regulation of related genes for lipid homeostasis in the body of obese diabetic animals. In this chapter, we have highlighted all these beneficial anti-obesity and antidiabetic potentials of some dietary plant flavonoids along with their molecular actions, bioavailability and pharmacokinetics. In addition, the present understanding and management of obesity and diabetes are also focused. Morbidity of inflammatory gastrointestinal (GI) diseases continues to grow resulting in worsen quality of life and increased burden on public medical systems. Complex and heterogenous illnesses, inflammatory bowel diseases (IBDs) encompass several inflammation -associated pathologies including Crohn's disease and ulcerative colitis. IBD is often initiated by a complex interplay between host genetic and environmental factors, lifestyle and diet, and intestinal bacterial components. IBD inflammatory signature was linked to the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) signaling pathway that is currently targeted by IBD therapies. Sphingolipid signaling was identified as one of the key mediators and regulators of pro-inflammatory conditions, and, specifically, TNF-α related signaling. All GI tissues and circulating immune/blood cells contain activated sphingolipid-metabolizing enzymes, including sphingosine kinases (SphK1 and SphK2) that generate sphingosine-1-phosphate (S1P), a bioactive lipid and ligand for five G-protein coupled membrane S1P receptors (S1PRs). Numerous normal and pathogenic inflammatory responses are mediated by SphK/S1P/S1PRs signaling axis including lymphocyte trafficking and activation of cytokine signaling machinery. SphK1/S1P/S1PRs axis has recently been defined as a target for the treatment of GI diseases including IBD/colitis. Several SphK1 inhibitors and S1PRs antagonists have been developed as novel anti-inflammatory agents. In this review, we discuss the mechanisms of SphK/S1P signaling in inflammation-linked GI disorders. The potential role of SphK/S1PRs inhibitors in the prevention and treatment of IBD/colitis is critically evaluated. AutoInflammatory Diseases (AIDs) are a group of innate immune system disorders characterized by sterile inflammation without evidence of pathogenic autoantibodies or auto-reactive T lymphocytes.  https://www.selleckchem.com/products/ipi-549.html  An expanding spectrum of genes and molecular pathways are associated with AIDs. Inflammasomopathies are secondary to dysregulation of multi-protein complexes, called inflammasomes, leading to an excessive maturation and secretion of IL1β and IL18. Patients present with persistent or recurrent systemic inflammation, abdominal and chest pain, skin rashes and are sensible to IL1 inhibitors. Unfolded proteins response causes a small number of AIDs that we propose to call immuno-proteinopathies, characterized by recurrent fevers and deep tissues inflammation. Other inflammatory conditions can occur in case of abnormalities of actin polymerization and the term of immuno-actinopathies is proposed. Generalized pustular psoriasis is a marker of autoinflammation mainly affecting the keratinocytes. Specific treatment targeting the p40 subunit of IL12 and IL23 or IL-17 are usually effective. Granulomatous inflammation characterizes AIDs related to NOD2 signaling defects. Defects in the ubiquitin-proteasome system cause a group of relopathies and some interferonopathies related to defect of the proteasome function (CANDLE syndrome). Gain of function of proteins regulating the production of type I interferons lead to severe inflammatory conditions, called interferonopathies. The JAK/STAT inhibitors are usually effective in these latter conditions. In conclusions, the identification of the main intracellular pathways involved in rare monogenic AIDs allows not only the proper classification of different conditions, but also highlight a pivotal role of possible novel therapeutic targets for the future. BACKGROUND Cardiopulmonary exercise testing (CPET) identifies high-risk patients before major surgery. In addition to using oxygen uptake and ventilatory efficiency to assess functional capacity, CPET can be used to identify underlying myocardial dysfunction through the assessment of the oxygen uptake to heart rate response (oxygen pulse response). We examined the relationship of oxygen pulse response, in combination with other CPET variables and known cardiac risk factors, with mortality after colorectal cancer surgery. METHODS This work focused on a retrospective cohort study of patients who had CPET and underwent colorectal cancer surgery. The primary outcome was a composite of in-hospital and 30-day mortality. Ventilatory inefficiency (Ve/Vco2>34) and exercise-induced myocardial dysfunction (abnormal oxygen pulse response) were investigated for an association with mortality using bivariable analysis and multivariable Cox regression. RESULTS A total of 1214 patients who underwent colorectal cancer surgery were included, and the primary outcome occurred in 26 patients (2.1%). Multivariable Cox regression showed abnormal oxygen pulse response was independently associated with the primary outcome (odds ratio [OR]=2.75; 95% confidence interval [CI], 1.17-6.47). Bivariable analysis showed that Ve/Vco2 >34 was associated with the primary outcome (OR=3.43; 95% CI, 1.47-8.01). Combining Ve/Vco2 >34 and abnormal oxygen pulse response conferred an increased risk for the primary outcome (OR=4.47; 95% CI, 1.62-12.34), compared with Ve/Vco2 >34 and normal oxygen pulse response. CONCLUSION Ventilatory inefficiency and an abnormal oxygen pulse response were independently associated with short- (30-day) and long-term (2-yr) mortality. Oxygen pulse response may provide additional information when considering perioperative risk stratification. Intelligent control systems are being developed for the control of plants with complex dynamics. However, the simplicity of the PID (proportional-integrative-derivative) controller makes it still widely used in industrial applications and robotics. This paper proposes an intelligent control system based on a deep reinforcement learning approach for self-adaptive multiple PID controllers for mobile robots. The proposed hybrid control strategy uses an actor-critic structure and it only receives low-level dynamic information as input and simultaneously estimates the multiple parameters or gains of the PID controllers. The proposed approach was tested in several simulated environments and in a real time robotic platform showing the feasibility of the approach for the low-level control of mobile robots. From the simulation and experimental results, our proposed approach demonstrated that it can be of aid by providing with behavior that can compensate or even adapt to changes in the uncertain environments providing a model free unsupervised solution.