Insulin contributes to atherosclerosis, but the potential mechanisms are kept unclear. In this study, insulin promoted proliferation of A7r5 cells. Microarray analysis indicated that insulin significantly changed 812 probe sets of genes, including 405 upregulated and 407 downregulated ones (fold change ≥ 1.5 or ≤ - 1.5; p  less then  0.05). Gene ontology analysis showed that the differentially expressed genes were involved in a number of processes, including the regulation of cell proliferation/migration/cycle, apoptotic process, oxidative stress, inflammatory response, mitogen-activated protein kinase (MAPK) activity, lipid metabolic process and extracellular matrix organization. Moreover, Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that the genes were involved in biosynthesis of amino acids, fatty acid metabolism, glycolysis/gluconeogenesis, metabolic pathways, regulation of autophagy, cell cycle and apoptosis, as well as the PI3K-Akt, MAPK, mTOR and NF-κB signaling pathways. Additionally, insulin enhanced phosphorylation of MAPK kinase 1/2 and Akt, suggesting activation of the MAPK and PI3K-Akt signaling pathways. Inhibition of ERK1/2 reduced insulin-induced proliferation. This study revealed the proliferative effects of insulin and displayed global gene expression profile of A7r5 cells stimulated by insulin, suggesting new insight into the molecular pathogenesis of insulin promoting atherosclerosis.Blackbuck (Antilope cervicapra) is a threatened species endemic to the Indian subcontinent. Many populations of blackbuck are found in southern India. Populations of blackbuck are negatively affected in many places for various reasons, such as habitat destruction and poaching. Their range decreased sharply during the 20th century. There is very limited information available on the population dynamics of blackbuck in southern India. For the phylogenetic and genetic diversity analyses of blackbuck populations among different distribution ranges in southern India, we sequenced mt DNA of cytochrome b (Cyt b) for 120, cytochrome c oxidase subunit-1 (COI) for 137 and the control region (CR) for 137 fecal pellets from eleven different locations in southern India. We analyzed the genetic structure of three mitochondrial markers, the CR, Cyt b and the COI region, separately and in a combined dataset. The haplotype diversity and nucleotide diversity of CR were 0.969 and 0.047, respectively, and were higher than those of Cyt b and COI. A Bayesian phylogeny and an MJ network based on the CR and combined dataset (105 sequences) signified several distinct haplotype clusters within blackbuck, whereas no clusters were identified with the Cyt b and COI phylogenetic analyses. The analysis of molecular variance of the combined data set revealed 52.46% genetic variation within the population. Mismatch distribution analysis revealed that blackbuck populations underwent complex changes with analysis of the combined dataset in each population and analysis of each marker separately in the overall population. The results provide evidence that blackbuck in different geographic locations has a distinct population structure due to habitat fragmentation after the formation of the Western and Eastern Ghats.Combination therapy has been considered as a potential method to overcome the BC chemoresistance. MicroRNAs (miRs) have been suggested as a therapeutic factor in the combination therapy of BC. This project aimed at examining the possible activity and molecular function of miR-424-5p and Taxol combination in the human BC cell line. MDA-MB-231 cells were treated with miR-424-5p mimics and Taxol, in a combined manner or separately. We used the MTT test for assessing the cell proliferation. In addition, flow-cytometry was used for evaluating apoptosis and cell-cycle. Expression levels of underlying molecular factors of miR-424-5p were assessed using western-blotting and qRT-PCR. The obtained results demonstrated that miR-424-5p repressed BC cell proliferation and sensitized these cells to Taxol treatment through the induction of apoptosis. Further investigations showed that miR-424-5p might increase BC chemosensitivity through the regulation of apoptosis-related factors including P53, Caspase-3, Bcl-2, and Bax as well as the proliferation-related gene c-Myc. Moreover, miR-424-5p restoration in combination with Taxol treatment decreased the colony formation by regulating Oct-4 and led to G2 arrest via modulating Cdk-2 expression. Western-blotting demonstrated that miR-424-5p may perform its anti-chemoresistance role by regulating the PD-L1 expression and controlling PTEN/PI3K/AKT/mTOR. Overall, the upregulation of miR-424-5p was indicated to upregulate the sensitivity of BC cells to treatment with Taxol. MiR-424-5p might regulate the chemosensitivity of the BC cell line by modulating PD-L1 and controlling the PTEN/mTOR axis. Therefore, the combination of miR-424-5p with Taxol would represent a novel procedure to treat against BC.Tumor necrosis factor alpha (TNF-α) is a pro-inflammatory cytokine involved in the regulation of the immune system and potentially the progression of cervical neoplastic lesions. In this study, we aimed to explore the possible relationship between polymorphisms of the TNF-α gene and susceptibility to cervical cancer. The relationship between a single nucleotide polymorphism (SNP) in the TNF-α gene (rs1800629) and the risk of cervical cancer was evaluated in a total of 445 subjects with (n = 153), or without (n = 292) cancer. Genotyping was performed using a Taq-Man based real time PCR method. Logistic regression analysis showed that individuals with AG/AA genotypes had an increased risk of cervical cancer compared to those with a GG genotype (OR 3.79, 95% CI 2.4-5.7,  less then  0.001). Our findings demonstrated that a genetic variant in the TNF-α gene (rs1800629) was associated with increased level and risk of developing cervical cancer, suggesting its potential use as a genetic risk factor for cervical neoplasia.Immune response plays a vital role in the pathogenesis of neuropathic pain. https://www.selleckchem.com/products/Chlorogenic-acid.html Immune response-targeted therapy becomes an effective strategy for treating neuropathic pain. Licochalcone A (Lic-A) possesses anti-inflammatory and neuroprotective effects. However, the potential of Lic-A to attenuate neuropathic pain has not been well explored. To investigate the protective effect and evaluate the underlying mechanism of Lic-A against neuropathic pain in a rat model. Chronic constriction injury (CCI) surgery was employed in rats to establish neuropathic pain model. Rats were intraperitoneally administrated with Lic-A (1.25, 2.50 and 5.00 mg/kg) twice daily. Mechanical withdrawal threshold and thermal withdrawal latency were used to evaluate neuropathic pain. After administration, the lumbar spinal cord enlargement of rats was collected for ELISA, Western blot and immunofluorescence analysis. Mechanical withdrawal threshold and thermal withdrawal latency results showed that Lic-A significantly attenuated CCI-evoked neuropathic pain in dose-dependent manner.