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However, the QoL related to low socio-economic factors gave mixed results and physical activity, education and type of footwear can influence the outcomes. [https://www.selleckchem.com/products/ad80.html selleck products] There is a general gender-dependent higher prevalence of DFS in men, although it depends on the geographical area. DFS often co-occurs with other diabetes-induced complications (retinopathy, nephropathy and cardiovascular disorders) and comorbid obesity generally worsens it. CONCLUSIONS Accessibility to health services aimed at reducing inequalities and constant health education and promotion and care regarding psychological and socio-economic issues should be continuously undertaken for individuals with DFS in order to improve their QoL. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Adhesion G Protein-Coupled Receptor 116 (GPR116) is an orphan receptor known for the function and variety of extracellular signalling, cell- cell adhesion, angiogenesis and cell migration. Many studies have shown that different GPCRs are over expressed in several cancers. GPR116 could be a pharmacologically important drug target for triple negative breast cancer (TNBC), because previous studies have found that the knockdown of GPR116 results in suppression of cell migration and invasion. However no drugs targeting GPR116 were identified until now. OBJECTIVE In this study, GPR116 is considered as a selective target for triple negative breast cancer treatment. METHODS Computational molecular characterisation of GPR116 was carried out to identify crucial amino acids. In this regard Food and Drug Administration (FDA) approved breast cancer drugs were selected as ligands and performed molecular docking study with insilico protein structure of GPR116 receptor. Molecular dynamics simulations have been useal amino acid . To investigate further in vitro/in vivo assay to confirm the active site in breast cancer functional receptor and crucial amino acid to confirm active drug molecular interaction. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Tyramine derivatives 3-16 were prepared and tested first time for their α-glucosidase (Sources Saccharomyces cerevisiae) inhibitory activity by using an in vitro mechanism-based biochemical assay. All the compounds were found to be new, except compounds 3, 10 and 11, 12 and 16. OBJECTIVE In continuation of our research to synthesize and identify potent inhibitors of an α-glucosidase enzyme, we intended to synthesize new inhibitors of α-glucosidase enzyme with enhanced efficacy in order to provide the basis for the better treatment of the type-II diabetic. METHODS Tyramine (1) was allowed to react with variety of aryl chlorides (2) to yield the corresponding amides. Synthesized compounds were then purified through normal phase column chromatography. Compounds 3-16 were then assessed for their α-glucosidase inhibitory activity in an in vitro biochemical assay. The cytotoxicity of compounds 3-16 was determined by using 3T3 mouse fibroblast cell lines. RESULTS Compounds 3-5, 8, 13, and 15-16 were found to be more active (IC50 = 103.1±0.46, 37.3±4.51, 56.7±4.2, 23.9±2.31, 43.6±2.88, 55.8±1.73, and 38.2±0.86 µM, respectively) than the acarbose, the standard inhibitor of an α-glucosidase enzyme, (IC50= 840.0±1.73 µM). To determine the dissociation constants and mode of inhibition, the kinetic studies were also performed for compounds 4 and 8 (the most potent inhibitors). It was observed that compounds 4 and 8 possess non-competitive properties as the inhibitors of α-glucosidase. All the compounds were found to be non-cytotoxic, except 5 and 12 (IC50= 14.7± 0.24 and 6.6± 0.38 µM, respectively). CONCLUSION The current study gives the facile synthesis and identification of potent inhibitors of α-glucosidase. The new inhibitors reported here may be investigated further for the designing and development of novel anti-diabetic agents. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.PURPOSE The current study was conducted in order to investigate the role of Forkhead box O1 and p21-mediated macrophage polarization in postoperative cognitive dysfunction induced by sevoflurane. METHODS There involved a total of 30 healthy mice that were randomly divided into two groups control group (without any treatment) and anaesthesia group (treated with sevoflurane inhalation). The effects of sevoflurane on cognitive function (memory) in mice were studied by trace fear conditioned reflex, and the effects of systemic inflammation and behavior after operation were measured by enzyme-linked immunosorbent assay (Elisa), the concentrations of CD163 and tumor necrosis factor -α (TNF- α) were measured. The expression of macrophage phenotype was observed by immunofluorescence staining, the expression levels of M1 and M2 markers mRNA were detected by real-time fluorescence quantitative PCR (RT-PCR), and the expression levels of FoxO1 and p21 were analyzed by immunoblotting (Western blot). RESULTS Compared with those in the control group (P less then 0.05). Compared with the control group, the expression of FoxO1 and p21 protein in the anesthesia group was significantly lower than that in the control group with significant statistical difference (P less then 0.01). CONCLUSION This study offers theoretical basis and insight for further understanding the prevention and treatment of cognitive dysfunction induced by anesthetic drugs. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.OBJECTIVES Alzheimer's disease (AD), also known as senile dementia, is a common neurodegenerative disease characterized by progressive cognitive impairment and personality changes. Numerous evidences have suggested that microRNAs(miRNAs) are involved in the pathogenesis and development of AD. However, the exact role of miR-335-5p in the progressionof AD is still not clearly clarified. METHODS The protein and mRNA levels were measured by western blotand RNA extraction and quantitative real-time PCR (qRT-PCR), respectively. The relationship between miR-335-5p and c-jun-N-terminal kinase 3 (JNK3) was confirmed by dual luciferase reporter assay. SH-SY5Y cells were transfected with APP mutant gene to establish the in vitro AD cell model. Flow cytometry and western blot were performed to evaluate cell apoptosis. The APP/PS1 transgenic mice was used as an in vivo AD model.Morris water maze test was performed to assess the effect of miR-335-5p on the cognitive deficits in APP/PS1 transgenic mice. RESULTS The JNK3 mRNA expression and protein levels of JNK3 and β-Amyloid (Aβ) were significantly up-regulated,and the mRNA expression of miR-335-5p was down-regulated in the brain tissues of AD patients.