RESUMEN
Silica aerogels, which are constructed with silica nanoparticles and numerous nanoscale pores, have many outstanding attributes, but they are usually brittle and hydrophilic. For the construction of a robust aerogel, the novel polyhedral oligomeric silsesquioxane (POSS) was introduced to prepare a series of aerogels possessing particles covered with elastic cushion to improve the mechanical property. The multialkoxy POSS, which possessed stiff Si-O-Si nanocages and flexible alkyl chains, was synthesized via thiol-ene click chemistry. After a facile and efficient approach, a partially ordered structure of SiO2 nanoparticles and organic elastic cushion would form spontaneously within the aerogels. With the POSS as the only precursor, several outstanding attributes were achieved in a single aerogel such as high specific surface area (SSA), high compression strength, high compression modulus, and noticeable compression flexibility. Meanwhile, the aerogel was superhydrophobic of which the contact angle (CA) was higher than 153°. Moreover, the potential application of oil-water separation is also presented.
RESUMEN
Purpose: Inflammatory indexes, including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII) and lymphocyte-to-monocyte ratio (LMR), have been confirmed as prognostic factors in multiple manigances. However, the prognostic value of these parameters in bevacizumab-treated non-small-cell lung cancer (NSCLC) is still not clear. Methods: We retrospectively studied 119 patients with advanced NSCLC who received bevacizumab treatment. The associations of pretreatment NLR, PLR, SII and LMR with progression-free survival (PFS) and overall survival (OS) were analyzed. Results & Conclusion: The median PFS and OS of patients with high baseline NLR, PLR and SII and low LMR were significantly decreased than those of patients with low baseline NLR, PLR and SII and high LMR. Multivariable analysis indicated that high baseline SII was independently related with inferior prognosis, and baseline LMR was an independent predictor for OS.
RESUMEN
Accumulating evidence suggests that celecoxib and artemisinin could mediate ovarian cancer development and metastasis. The present study investigated the effects of celecoxib and artemisinin on the epithelial-mesenchymal transition (EMT) characteristics of the human ovarian epithelial adenocarcinoma cell line, SKOV3. SKOV3 cells were incubated with celecoxib (10 µM) for different periods of time to establish an EMT cell model. Subsequently, artemisinin (20, 40 and 80 µM) was used to establish a cell model of the reverse process, mesenchymal-epithelial transition (MET). Cell proliferation, metastasis, invasiveness and the expression of vimentin and E-cadherin were measured using Cell Counting Kit-8, wound healing assay, western blotting, flow cytometry and immunofluorescence. The EMT cell model exhibited enhanced proliferative capacity, increased migration, increased vimentin expression and decreased E-cadherin expression. By contrast, artemisinin decreased proliferative capacity, decreased migration, decreased vimentin expression and increased E-cadherin expression of EMT model cells, indicating that MET was induced. These results demonstrated that artemisinin may reverse celecoxib-induced epithelial-mesenchymal transition in SKOV3 cells.
RESUMEN
Accumulating evidence suggests that acetyl-CoA acetryltransferase 1 (ACAT-1) may mediate tumor development and metastasis. However, the specific function served by ACAT-1 in lung cancer is not well understood. Therefore, the present study initially verified that ACAT-1 was overexpressed in Lewis lung carcinoma (LLC) tissues compared with non-LLC mice and that this overexpression promoted the proliferation, invasion and metastasis of these LLC samples. Western blotting, immunofluorescence microscopy and flow cytometry allowed the present study to determine that the ACAT-1 inhibitor avasimibe significantly reduced the expression of ACAT-1 in LLC compared with LLC cells that are not treated with avasimibe (P<0.05). A combination of Cell Counting Kit-8 and wound healing assays demonstrated that downregulating ACAT-1 expression sufficiently inhibited the proliferation of LLC cells. Avasimibe promoted LLC cell apoptosis as assessed by a Annexin V/propidium iodide double staining assay. Furthermore, avasimibe inhibited tumor growth in vivo and improved immune responses, with tissue biopsies from LLC model mice exhibiting higher levels of ACAT-1 compared with in healthy controls. Altogether, the results of the present study reveal that avasimibe may inhibit the progression of LLC by downregulating the expression of ACAT-1, which may thus be a potential novel therapeutic target for lung cancer treatment.