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Obesity is a complex medical condition that affects multiple organs in the body. However, the underlying mechanisms of obesity, as well as its treatment, are largely unexplored. The focus of this research was to use bioinformatics to discover possible treatment targets for obesity. To begin, the GSE133099 database was used to identify 364 differentially expressed genes (DEGs). Then, DEGs were subjected to tissue-specific analyses and enrichment analyses, followed by the creation of a protein-protein interaction (PPI) network and generation of a drug-gene interaction database to screen key genes and potential future drugs targeting obesity. Findings have illustrated that the tissue-specific expression of neurologic markers varied significantly (34.7%, 52/150). Among these genes, Lep, ApoE, Fyn, and FN1 were the key genes observed in the adipocyte samples from obese patients relative to the controls. Furthermore, nine potential therapeutic drugs (dasatinib, ocriplasmin, risperidone, gemfibrozil, ritonavir, fluvastatin, pravastatin, warfarin, atorvastatin) that target the key genes were also screened and selected. To conclude the key genes discovered (Lep, ApoE, Fyn, and FN1), as well as 9 candidate drugs, could be used as therapeutic targets in treating obesity.Mirtazapine is an antidepressant drug that has been proven to possess a cognitive enhancer efficiency. In this study, we evaluated the potential protective effects of mirtazapine on BV2 microglia in response to isoflurane exposure. Our results show that mirtazapine attenuated isoflurane-induced expression of microglia-specific protein Iba1 in BV2 microglia. find more Mirtazapine prevented isoflurane-induced production of the pro-inflammatory factors interleukin (IL)-1β and IL-18 by inhibiting the activation of the nod-like receptor family protein 3 (NLRP3) inflammasome in BV2 microglia. The increased reactive oxygen species (ROS) production and elevated expression level of NADPH oxidase 4 (NOX4) in isoflurane-induced BV2 microglia were mitigated by mirtazapine. Isoflurane exposure reduced triggering receptor expressed on myeloid cells 2 (TREM2) expression in BV2 microglia, which was restored by mirtazapine. Moreover, silencing of TREM2 abolished the inhibitory effects of mirtazapine on ionized calcium-binding adapter molecule 1 (Iba1) expression and inflammation in BV2 microglia. From these results, we could infer that mirtazapine exerted a protective effect on BV2 microglia against isoflurane exposure-caused microglia activation, neuroinflammation, and oxidative stress via inducing TREM2 activation. Hence, mirtazapine might be a potential intervention strategy to prevent isoflurane exposure-caused cognitive dysfunction in clinical practice.Multiple studies have confirmed that adipokines are compactly relevant to insulin resistance and participate in the pathogenesis of gestational diabetes mellitus (GDM). This paper aimed to study the effects of C1q/tumor necrosis factor related protein (CTRP)6 on the phenotypes of trophoblast cells, covering cell proliferation, invasion and migration, and initially explore the mechanism. High glucose was used to induce trophoblast cells to establish an in vitro model. The expression levels of CTRP6 were firstly determined, and then the effects of CTRP6 knockdown on cell viability, apoptosis, migration and invasion were assessed using CCK8, TUNEL, wound healing, Transwell assays. Moreover, the role of peroxisome proliferator-activated receptor gamma (PPARγ), probable target of CTRP6, was evaluated through co-transfection with PPARγ overexpression vector. The results of the present study revealed that CTRP6 and PPARγ were both upregulated in high glucose-induced cells. And CTRP6 knockdown could significantly elevate the abilities of cell viability, migration and invasion, and avoid cell apoptosis. In addition, PPARγ overexpression was found to restrain the protective effects of CTRP6 knockdown on the above aspects, indicating CTRP6 played a role in trophoblast cells via inhibiting PPARγ expression. In conclusion, CTRP6 regulated the viability, migration and invasion of high glucose-induced gestational trophoblast cells through PPARγ signaling.The intestinal epithelial tight junctions (TJs) provide barrier against paracellular permeation of lumenal antigens. Defects in TJ barrier such as increased levels of pore-forming TJ protein CLDN2 (claudin-2) is associated with inflammatory bowel disease. We have previously reported that starvation-induced macroautophagy/autophagy enhances the TJ barrier by degrading pore-forming CLDN2. In this study, we examined the molecular mechanism underlying autophagy-induced CLDN2 degradation. CLDN2 degradation was persistent in multiple modes of autophagy induction. Immunolocalization, membrane fractionation, and pharmacological inhibition studies showed increased clathrin-mediated CLDN2 endocytosis upon starvation. Inhibition of clathrin-mediated endocytosis negated autophagy-induced CLDN2 degradation and enhancement of the TJ barrier. The co-immunoprecipitation studies showed increased association of CLDN2 with clathrin and adaptor protein AP2 (AP2A1 and AP2M1 subunits) as well as LC3 and lysosomes upon starvation, unit alpha 1; AP2M1 adaptor related protein complex 2 subunit mu 1; ATG7 autophagy related 7; CAL calcitriol; Cas9 CRISPR-associated protein 9; Con control; CPZ chlorpromazine; DSS dextran sodium sulfate; EBSS Earle's balanced salt solution; IBD inflammatory bowel disease; TER trans-epithelial resistance; KD knockdown; KO knockout; MAP1LC3/LC3 microtubule associated protein 1 light chain 3; MβCD Methyl-β-cyclodextrin; MET metformin; MG132 carbobenzoxy-Leu-Leu-leucinal; MTOR mechanistic target of rapamycin kinase; NT non target; RAPA rapamycin; RES resveratrol; SMER small-molecule enhancer 28; SQSTM1 sequestosome 1; ST starvation; ULK1 unc-51 like autophagy activating kinase 1; WT wild type.We aimed to evaluate if protein source (PS) alterations during IVM affect embryo sex/development and gene expression profile in cumulus cells (CCs). Bovine oocytes were matured and cultured in the presence of FBS or BSA. Then, the PS effect during IVM on gene expression (GPC4, VCAN, GHR, PTGS2, and ALCAM) was determined. CC biopsy was removed before and after IVM treatments. After fertilization and cultured, CCs were grouped according to their fate into CCs from immature COCs, CCs from COCs that did or did not result in embryos (according to PS). Results showed that when the culture was performed in FBS presence, blastocyst rate was higher (p  0.05) were observed between immature and mature CCs groups in gene expression, regardless of their fate. Only the GHR gene was related to embryo production but just with FBS on IVM. In conclusion, PS can affect embryo development when using the serum on IVM and IVC, influences CCs gene expression, and has to be considered when studying oocyte quality markers.Candida albicans is a commensal yeast fungus of the human oral, gastrointestinal, and genital mucosal surfaces, and skin. Antibiotic-induced dysbiosis, iatrogenic immunosuppression, and/or medical interventions that impair the integrity of the mucocutaneous barrier and/or perturb protective host defense mechanisms enable C. albicans to become an opportunistic pathogen and cause debilitating mucocutaneous disease and/or life-threatening systemic infections. In this review, we synthesize our current knowledge of the tissue-specific determinants of C. albicans pathogenicity and host immune defense mechanisms.Deficient bone regeneration causes bone defects or nonunion in a substantial proportion of trauma patients that urges for novel therapies. To develop a reliable therapy, we investigated the effect of negative pressure wound therapy (NPWT) on bone regeneration in vivo in a rat calvarial defect model. Negative pressure (NP) treatment in vitro was mimicked to test its effect on osteoblast differentiation in rat mesenchymal stem cells (MSCs) and MC3T3-E1 cells. Transcriptomic analyses, pharmaceutical interventions, and shRNA knockdowns were conducted to explore the underlying mechanism and their clinical relevance was investigated in samples from patients with nonunion. The potential application of a combined therapy of MSCs in hydrogels with negative pressure was tested in the rat critical-size calvarial defect model. We found that NPWT promoted bone regeneration in vivo and NP treatment induced osteoblast differentiation in vitro. NP induced osteogenesis via activating macroautophagy/autophagy by AMPK-ULK1 sign 2; SBI, SBI-0206965; SPP1/OPN, secreted phosphoprotein 1; THY1/CD90, Thy-1 cell surface antigen; SQSTM1, sequestosome 1; TGFB3, transforming growth factor beta 3; ULK1/Atg1, unc-51 like autophagy activating kinase 1.To investigate the effects of ginsenosides on the memory impairment in Sprague-Dawley rats (SD rats) after anesthesia through the administration of propofol SPF, SD rats were randomly divided into four groups control group (Group I), propofol-treated group (Group II), low dose of ginsenosides-treated group (Group III) and high dose of ginsenosides-treated group (Group IV). These rats were subjected to fear memory test in shuttle box, Y-maze test and Morris water maze test. Immediately after the test, the expression levels of nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) were further detected by ELISA method. Ginsenosides could ameliorate the impairment on the functions of fear memory, working memory and spatial memory in rats caused by anesthesia via the injection of Propofol. Furthermore, the expression levels of NGF and BDNF on rat hippocampus were significant increased by the treatment of ginsenosides at both two doses compared with the control group (both P less then 0.05). Ginsenosides hold potential to be developed as a novel therapeutic agent for those patients suffering from postoperative cognitive dysfunction caused by anesthesia via the treatment of propofol.The phosphoprotein phosphatase catalytic subunit (PPPCs) family has been shown to play an important role in the development and progression of various malignancies, but its expression patterns and biological functions in breast cancer (BC) remain unclear. Therefore, we aimed to investigate the clinical significance and biological functions of the PPPCs family to understand its possible significance in the diagnosis, prognosis and treatment of breast cancer. We comprehensively investigated the expression levels, diagnostic accuracy, prognostic outcomes, biological functions and effects on immune cell infiltration of the PPPCs family in breast cancer using online databases. Except for PPP1CB, PPP1CC, PPP5C and PPEF1, the mRNA expression levels of the PPPCs family in breast cancer tissues were significantly different from those in paracancerous tissues. The differentially expressed genes (DEGs) were associated with the clinicopathological parameters and prognosis of breast cancer. The DEGs were mainly associated with the WNT signaling pathway, antigen presentation and DNA repair. In addition, the DEGs significantly affected the infiltration of immune cells in breast cancer tissues. Among the PPPCs family, PPP1CA and PPP4C played a prominent role in the progression of breast cancer, and inhibition of PPP1CA and PPP4C expression by siRNA can significantly inhibit breast cancer cells proliferation and migration. In conclusion, the PPPCs family, especially PPP1CA and PPP4C, could be used as new biomarkers to improve diagnostic accuracy, predict prognosis and novel targets for the treatment of breast cancer.