Alkane-Strengthened Viscoelasticity in Micellar Solutions of Surface-Active Ionic Liquids and Their Potential Application in Enhanced Oil Recovery

Wormlike micelles (WLMs) are highly sensitive to alkanes, resulting in structural destruction and loss of viscosity. Therefore, the study of WLMs against alkanes holds great significant importance. Surface-active ionic liquids have shown increasing promise for different situations for customizing molecular structures with the specialty of flexible functional assembly. In this paper, we found that WLMs constructed from the long-chain fatty acid surface-active ionic liquid (N,N-dimethylbenzylamine-oleic acid, abbreviated as BD-OA) exhibit strengthened viscoelasticity with the introduction of alkanes, expanding the resistance range to alkane damage. Here, the rheological behavior, microstructure, and dissipative particle dynamics (DPD) simulations of BD-OA WLMs were investigated at macro-, micro-, and mesoscopic scales, before (and after) the introduction of alkane. Our findings confirm the structural transformation of the micellar system from WLMs to lamellar micelles with higher viscoelasticity after alkane induction. The rearrangement of the micelle configuration may be attributed to the infiltration of alkane molecules into the fence layer formed by the BD-OA WLMs, leading to an increase in the boundary accumulation parameter and ultimately resulting in the formation of lower curvature lamellar micelles. More importantly, the against alkanes BD-OA WLMs have exhibited excellent in enhanced oil recovery, which has a promise for substituting common oil-displacing agents in tertiary oil recovery processes

The Association between <i>RAD23B</i> Ala249Val Polymorphism and Cancer Susceptibility: Evidence from a Meta-Analysis

<div><p>Background</p><p>A number of studies have investigated associations of genetic variation in <i>RAD23B</i> Ala249Val (rs1805329 C>T) with cancer susceptibility; however, the findings are inconsistent. We performed a meta-analysis to acquire a more precise estimation of the relationship.</p><p>Method</p><p>We searched literatures from PubMed, Embase and Web of Science. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the association between Ala249Val polymorphism and cancer risk.</p><p>Results</p><p>A total of 23 studies consisting of 10837 cases and 13971 controls were included in this meta-analysis. Overall, no significant associations were found between <i>RAD23B</i> Ala249Val polymorphism and cancer risk (Val/Val vs. Ala/Ala: OR = 0.97, 95% CI = 0.75–1.25; Ala/Val vs. Ala/Ala: OR = 1.08, 95% CI = 0.96–1.22; recessive model: OR = 0.93, 95% CI = 0.76–1.14 and dominant model: OR = 1.07, 95% CI = 0.94–1.20). We did not find any significant associations in the further stratification analyses by cancer type, ethnicity and source of control.</p><p>Conclusions</p><p>Despite some limitations, this meta-analysis indicates that it is unlikely that the <i>RAD23B</i> 249Val/Val polymorphism may contribute to the individual susceptibility to cancer risk. However, further advanced designed studies with larger sample size and different ethnicities should be conducted to confirm our results.</p></div

Meta-analysis of the association between <i>RAD23B</i> Ala249Val polymorphism and cancer risk.

<p>PB, Population based; HB, Hospital based.</p>a<p><i>P</i> value of the Q-test for heterogeneity test.</p

Flow chart for the process of selecting the 23 included studies for this meta-analysis.

<p>Flow chart for the process of selecting the 23 included studies for this meta-analysis.</p

Stratification analysis for associations between <i>PLCE1</i> variant genotypes and GA risk.

<p>GA, gastric adenocarcinoma; SNP, single-nucleotide polymorphism; CI, confidence interval; OR, odds ratio.</p>a<p>Obtained in logistic regression models with adjustment for age, sex, smoking status and drinking status.</p><p>The results were in bold, if the 95% CI excluded 1 or <i>P</i><0.05.</p

Forest plot showing associations between <i>PLCE1</i> rs2274223 and gastric cancer risk.

<p>A) The ORs and 95% CIs were obtained using AG vs. AA. B) The ORs and 95% CIs were obtained using GG vs. AA. The axis corresponds to the OR. The diamonds and the horizontal bars represent the overall ORs with 95% CIs given by their width.</p

Distributions of selected variables in GA cases and cancer-free controls.

<p>GA, gastric adenocarcinoma.</p>a<p>Two-sided <i>χ²</i> test for distributions between cases and controls.</p>b<p>Data are mean ± SD and P value from Student's <i>t</i> test.</p

Logistic regression analysis of associations between the genotypes of <i>PLCE1</i> and GA risk.

<p>GA, gastric adenocarcinoma; SNP, single-nucleotide polymorphism; CI, confidence interval; OR, odds ratio.</p>a<p>Chi square test for genotype distributions between cases and controls.</p>b<p>Adjusted for age, sex, smoking status and drinking status in logistic regress models.</p>c<p>for additive genetic models.</p>d<p>for dominant genetic models.</p>f<p>at allelic levels.</p><p>The results were in bold, if the 95% CI excluded 1 or <i>P</i><0.05.</p

Coronary-Heart-Disease-Associated Genetic Variant at the COL4A1/COL4A2 Locus Affects COL4A1/COL4A2 Expression, Vascular Cell Survival, Atherosclerotic Plaque Stability and Risk of Myocardial Infarction

Genome-wide association studies have revealed an association between coronary heart disease (CHD) and genetic variation on chromosome 13q34, with the lead single nucleotide polymorphism rs4773144 residing in the COL4A2 gene in this genomic region. We investigated the functional effects of this genetic variant. Analyses of primary cultures of vascular smooth muscle cells (SMCs) and endothelial cells (ECs) from different individuals showed a difference between rs4773144 genotypes in COL4A2 and COL4A1 expression levels, being lowest in the G/G genotype, intermediate in A/G and highest in A/A. Chromatin immunoprecipitation followed by allelic imbalance assays of primary cultures of SMCs and ECs that were of the A/G genotype revealed that the G allele had lower transcriptional activity than the A allele. Electrophoretic mobility shift assays and luciferase reporter gene assays showed that a short DNA sequence encompassing the rs4773144 site interacted with a nuclear protein, with lower efficiency for the G allele, and that the G allele sequence had lower activity in driving reporter gene expression. Analyses of cultured SMCs from different individuals demonstrated that cells of the G/G genotype had higher apoptosis rates. Immunohistochemical and histological examinations of ex vivo atherosclerotic coronary arteries from different individuals disclosed that atherosclerotic plaques with the G/G genotype had lower collagen IV abundance and thinner fibrous cap, a hallmark of unstable, rupture-prone plaques. A study of a cohort of patients with angiographically documented coronary artery disease showed that patients of the G/G genotype had higher rates of myocardial infarction, a phenotype often caused by plaque rupture. These results indicate that the CHD-related genetic variant at the COL4A2 locus affects COL4A2/COL4A1 expression, SMC survival, and atherosclerotic plaque stability, providing a mechanistic explanation for the association between the genetic variant and CHD risk

Association between SNP rs4773144 and MI incidence/prevalence in CHD patients.

<p>Association between SNP rs4773144 and MI incidence/prevalence in CHD patients.</p