Four key effectiveness moderators of lifestyle interventions for GDM prevention.

Matrix-assisted laser desorption/ionization (MALDI) mass spectrometry is an important technique to characterize the average molecular weights, oligomer repeat units, and end groups of polymer materials. Although MALDI methods have been developed for a broad variety of different synthetic polymers, MALDI continues to struggle with polymer samples having broad polydispersity (PD). We have combined MALDI and gel permeation chromatography (GPC) analyses for broad PD polymer samples with the use of a liquid chromatography (LC) interface. The LC interface uses heated sheath gas and a capillary nozzle to remove most of the mobile phase and deposit the GPC eluants on the precoated matrix on a moving MALDI plate. Our experiments demonstrate that the combination of GPC-LC interface-MALDI can aid in the characterization of broad PD samples, the verification of the presence of low-intensity, high-mass oligomers, and the detection of minor series in polymer samples.

MicroRNAs (miRNAs) are vital in the regulation of tumor progression and invasion. Dysregulation of miRNAs has been linked to the development of various types of human cancers, including non-small-cell lung cancer (NSCLC). However, the effect of miRNA-34a (miR-34a), a key regulator of tumor suppression, on the tumorigenesis of NSCLC has not been fully elaborated. Herein, we reveal that miR-34a is significantly downregulated in NSCLC tissues and cell lines, suggesting that miR-34a might function as a tumor suppressor in lung cancer. We also confirmed that epidermal growth factor receptor (EGFR) is a direct target of miR-34a, and our data reveal that siRNA knockdown of EGFR can inhibit cell proliferation, promote apoptosis and arrest cell-cycle progression. In addition, EGFR can reverse the suppressive function of miR-34a overexpression on proliferation and cell apoptosis. Furthermore, in vivo experiments demonstrated that miR-34a suppress tumor growth, both in the A549 xenograft model, as well as in the metastatic tumors in nude mice. Taken together, our findings suggest that miR-34a inhibits NSCLC tumor growth and metastasis through targeting EGFR.

The quantities of lipid sorbed to continuous-wear PureVision lenses are significantly different from those previously reported by other authors in a similarly conducted experiment. This difference suggests that any hypothesis of silicone hydrogel lenses based on these previous lipid data should be reconsidered.

Aim To evaluate the expression of Foxp3‐positive lymphocytes around newly formed tissue after regenerative endodontic treatment (RET) in vivo and investigate the effects of stem cells from the apical papilla (SCAP) on the conversion of CD4+CD25− T cells to CD4+CD25+Foxp3+ regulatory T cells (Tregs) in vitro. Methodology Three 6‐month‐old beagles with nine doubled‐rooted premolars in each dog were randomly assigned to the RET group and the control group. RET was performed after apical periodontitis had been induced in the experimental immature teeth. Three months later, the expression of Foxp3 was detected in the histological sections by immunofluorescent staining. Human SCAP and CD4+CD25− T cells from mice spleens (1 : 1 and 1 : 5) were co‐cultured in cell–cell contact or in Transwells, respectively, for 24 and 72 h in vitro. The percentage of Tregs was evaluated by flow cytometry. The results were analysed using the Fisher's exact test and analysis of variance. P < 0.05 was regarded as statistically significant. Results Inflammatory cells were present with tissue regeneration in the RET group, and Foxp3‐positive T cells were enriched around the newly formed tissues. SCAP promoted Treg conversion after 72 h in vitro. Cell–cell contact played an important role after the 24 h co‐culture, whilst soluble factors were also involved after 72 h (P < 0.05). Conclusions SCAP promoted the conversion of pro‐inflammatory T cells to Tregs in vitro. Tregs were enriched around the regenerating tissues in the root canals after RET, which may create a suitable immune microenvironment for the differentiation of SCAP. This study provides an underlying mechanism for tissue regeneration during RET.

This study investigated the antitumour and chemosensitizing effects of celecoxib in the treatment of advanced colorectal cancer. A total of 90 patients were randomly divided into two groups: group CF was treated with a combination of celecoxib and the folinic acid-fluorouracil-oxaliplatin (FOLFOX4) regimen; and group F was treated with the FOLFOX4 regimen alone. Immunohisto chemical analysis of tumour tissues for cyclooxygenase-2 (COX-2) protein was performed. With regard to short-term efficacy, the response and disease control rates were significantly greater in group CF than group F. A log-rank test showed that the 3-year survival rate was significantly greater in group CF than group F. It was concluded that the addition of celecoxib to the FOLFOX4 regimen increased the short-term efficacy and the 3-year survival rate, and improved the quality of life of patients with advanced colorectal cancer. The antitumour and chemo sensitizing effects of celecoxib appeared to be independent of COX-2.

This study investigated the effect of ginsenoside Rg1 on the functions of ex vivo cultivated endothelial progenitor cells (EPCs) and whether ginsenoside Rg1 prevented EPC senescence. EPCs isolated from peripheral blood from healthy volunteers were incubated with different concentrations of ginsenoside Rg1 and the effects were observed at different time points. Cell proliferation and in vitro vasculogenesis were assayed and flow cytometry was used to determine the effects of ginsenoside Rg1 on the cell cycle. Senescence and telomerase activity in EPCs were also assayed. It was found that ginsenoside Rg1 promoted EPC proliferation and vasculogenesis in dose-and time-dependent manners. Cell-cycle analysis showed that ginsenoside Rg1 increased the proliferative phase and decreased the resting phase of EPCs. β-Galactosidase and telomerase activities increased. These results support the view that ginsenoside Rg1 induces EPC proliferation and angiogenesis, and inhibits EPC senescence.

BackgroundContinuous and excessive application of deltamethrin (DM) has resulted in the rapid development of insecticide resistance in Culex pipiens pallens. The quantitative trait loci (QTL) responsible for resistance to DM had previously been detected in Cx. pipiens pallens. But locating the QTLs on the chromosomes remained difficult. An available approach is to first characterize DNA molecular markers linked with the phenotype, and then identify candidate genes.MethodsIn this study, the amplified fragment length polymorphism (AFLP) marker L3A8.177 associated with the QTL, was characterized. We searched for potential candidate genes in the flank region of L3A8.177 in the genome sequence of the closely related Cx. pipiens quinquefasciatus and conducted mRNA expression analysis of the candidate gene via quantitative real-time PCR. Then the relationship between DM resistance and the candidate gene was identified using RNAi and American CDC Bottle Bioassay in vivo. We also cloned the ORF sequences of the candidate gene from both susceptible and resistant mosquitoes.ResultsThe genes CYP6CP1 and protease m1 zinc metalloprotease were in the flank region of L3A8.177 and had significantly different expression levels between susceptible and resistant strains. Protease m1 zinc metalloprotease was significantly up-regulated in the susceptible strains compared with the resistant and remained over-expressed in the susceptible field-collected strains. For deduced amino acid sequences of protease m1 zinc metalloprotease, there was no difference between susceptible and resistant mosquitoes. Knockdown of protease m1 zinc metalloprotease not only decreased the sensitivity of mosquitoes to DM in the susceptible strain but also increased the expression of CYP6CP1, suggesting the role of protease m1 zinc metalloprotease in resistance may be involved in the regulation of the P450 gene expression.ConclusionOur study represents an example of candidate genes derived from the AFLP marker associated with the QTL and provides the first evidence that protease m1 zinc metalloprotease may play a role in the regulation of DM resistance in Cx. pipiens pallens.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-016-1450-4) contains supplementary material, which is available to authorized users.