This study was designed to evaluate the effects of pregnancy on the solubility of halogenated volatile anaesthetics in rat blood and tissues. Tissue samples from 10 pregnant and 10 non-pregnant adult female Sprague Dawley rats, including the heart, liver, kidney and brain, were obtained and made into respective homogenates. Blood/gas and tissue/gas partition coefficients for halothane, sevoflurane and isoflurane were determined by the method of two-stage headspace equilibration by gas chromatography with each of the homogenates. Values were analysed by t-test or one-way analysis of variance. The solubility within blood and brain for halothane in the pregnant group (2.90 ± 0.44, 5.55 ± 0.73) was significantly lower than that of the non-pregnant group (3.42±0.23, 6.33±0.64; P <0.05). However, there were no significant differences between the two groups for liver, kidney or heart solubility. For sevoflurane and isoflurane, there were no significant differences in solubility between the two groups. In conclusion, pregnancy decreased the solubility of halothane within the blood and brain, whereas the solubility of halothane in other tissues including the liver, kidney and heart showed no significant alteration. Pregnancy did not affect the solubility of sevoflurane or isoflurane within blood or the other tissues studied.
Background Macrophages have been demonstrated to promote the rupture of the atherosclerotic lesion, a primary cause of ischemic events, by modulating the formation of plaque necrosis. We aimed to search the key factors of genetic macrophages in concerns of carotid ruptured plaques.Methods The database of the gene expressed GSE41571 is retrieved from the Gene Expression Omnibus (GEO) to differentially obtain the measured expression genes (DEGs) by tendering the tool usage of GEO2R. The enriched pathways of ontology at DEGs performances with DAVID interacted the constructions of protein to protein networking by the analysis of STRING and Cytoscape software. And also the identified PPI networks in the significance of hub genes module plugged into respective Cytohubba and MCODE Cytoscape.Result A total of 1481 DEGs in macrophages from ruptured and stable carotid atherosclerotic plaques are noticed, by including 568 up-regulation genes and 913 down-regulation genes. The analyzed GO shows a DEGs are mainly involved in protein ubiquitination, endocytosis, mRNA processing, and mitotic cell cycle. KEGG pathway enrichment analysis revealed that some major protein catabolism pathways, including the ubiquitin-proteasome, autophagy, and endocytosis systems, play key roles in the progressive carotid plaque clotting. The genes of the hub in the PPI network included POLR2E , PPP2R1A , HSP90AA1 , and CBL . The modules were mainly associated with ubiquitin-mediated proteolysis, endocytosis, spliceosome, proteasome.Conclusion Our findings offer novel molecular insights into the mechanisms by which macrophages drive formation and vulnerability of plaques. The candidate DEGs and potential biological pathways might be used as diagnostic targets, and facilitate the development of novel macrophage-targeting therapies for unstable atherosclerosis.
This study investigated the effects of and cofilin-2 (CFL2) in regulating epithelial-mesenchymal transition (EMT) in ovarian cancer. The level of miR-200c was lower in invasive SKOV3 cells than that in non-invasive OVCAR3 cells, whereas CFL2 showed the opposite trend. Bioinformatics analysis and dual-luciferase reporter gene assays indicated that CFL2 was a direct target of miR-200c. Furthermore, SKOV3 and OVCAR3 cells were transfected with miR-200c mimic or inhibitor, pCDH-CFL2 (CFL2 overexpression), or CFL2 shRNA (CFL2 silencing). MiR-200c inhibition and CFL2 overexpression resulted in elevated levels of both CFL2 and vimentin while reducing E-cadherin expression. They also increased ovarian cancer cell invasion and migration in vitro and in vivo and increased the tumor volumes. Conversely, miR-200c mimic and CFL2 shRNA exerted the opposite effects as those aforementioned. In addition, the effects of pCDH-CFL2 and CFL2 shRNA were reversed by the miR-200c mimic and inhibitor, respectively. This finding suggested that miR-200c could be a potential tumor suppressor by targeting CFL2 in the EMT process.
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