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Endothelial cell activation and dysfunction are the foundation of atherosclerosis, including coronary artery disease (CAD). Endothelial cell activation is mediated by the level of gene transcription. Early growth response 3 (Egr3) is a critical determinant of vascular endothelial growth factor (VEGF) signalling in activated endothelial cells. If endothelial cells are excessively activated, it may lead to vasculopathic diseases, such as pathologic angiogenesis, inflammation, and atherosclerosis. The aim of the present study was to assess the association between the Egr3 gene polymorphisms and CAD.
Two independent case-control studies that involved the Han group (409 CAD patients and 351 control subjects) and the Uygur group (299 CAD patients and 303 control subjects) analysed the relationship between Egr3 SNPs (rs1996147 and rs1008949) and CAD. Genotyping was undertaken using the TaqMan SNP genotyping assay.
The entire Uygur group and the males in the Uygur group showed a higher frequency of the A allele (rs1996147) in CAD patients than in the control subjects (P = 0.003 and P = 0.005, respectively). Additionally, the distribution of the recessive model of rs1996147 (AA vs GG + AG) for the total sample and the males was significantly different between CAD patients and control participants (P = 0.002 and P = 0.003, respectively), and the difference remained statistically significant following multivariate adjustment (Total: OR = 1.705; 95% CI: 1.166-2.494, P = 0.006; males: OR = 1.908, 95% CI: 1.189-3.062, P = 0.007). However, for Uygur females, we did not observe a difference in the allele frequency or genotypic distribution of rs1996147 between CAD patients and control participants. Similarly, the distribution of the rs1996147 allele frequency or genotypes showed no significant difference between patients with CAD and control participants in the Han group. The distribution of rs1008949 genotypes, dominant model, recessive model, and allele frequency did not show a significant difference between patients with CAD and the control subjects in the Han and Uygur groups.
rs1996147 may be a novel polymorphism of the Egr3 gene associated with CAD in males of the Chinese Uygur population.
Egr3, Coronary artery disease, Polymorphism
Association of Egr3 genetic polymorphisms and coronary artery disease in the Uygur and Han of China
Xia Li,#1 Yi-Tong Ma,corresponding author1 Xiang Xie,#1 Yi-Ning Yang,1 Xiang Ma,1 Ying-Ying Zheng,1 Shuo Pan,1 Fen Liu,2 and Bang-Dang Chen2
To describe and compare outcomes from in-patient rehabilitation (IPR) in working-aged adults across different groups of long-term neurological conditions, as defined by the UK National Service Framework.
Analysis of a large Australian prospectively collected dataset for completed IPR episodes (n = 28,596) from 2003-2012.
De-identified data for adults (16-65 years) with specified neurological impairment codes were extracted, cleaned and divided into ‘Sudden-onset’ conditions: (Stroke (n = 12527), brain injury (n = 7565), spinal cord injury (SCI) (n = 3753), Guillain-Barre syndrome (GBS) (n = 805)) and ‘Progressive/stable’ conditions (Progressive (n = 3750) and Cerebral palsy (n = 196)). Key outcomes included Functional Independence Measure (FIM) scores, length of stay (LOS), and discharge destination.
Mean LOS ranged from 21-57 days with significant group differences in gender, source of admission and discharge destination. All six groups showed significant change (p<0.001) between admission and discharge that was likely to be clinically important across a range of items. Significant between-group differences were observed for FIM Motor and Cognitive change scores (Kruskal-Wallis p<0.001), and item-by-item analysis confirmed distinct patterns for each of the six groups. SCI and GBS patients were generally at the ceiling of the cognitive subscale. The ‘Progressive/stable’ conditions made smaller improvements in FIM score than the ‘Sudden-onset conditions’, but also had shorter LOS. Conclusion All groups made gains in independence during admission, although pattern of change varied between conditions, and ceiling effects were observed in the FIM-cognitive subscale. Relative cost-efficiency between groups can only be indirectly inferred. Limitations of the current dataset are discussed, together with opportunities for expansion and further development.
Comparison of Rehabilitation Outcomes for Long Term Neurological Conditions: A Cohort Analysis of the Australian Rehabilitation Outcomes Centre Dataset for Adults of Working Age
Lynne Turner-Stokes, 1 ,* Roxana Vanderstay, 1 Tara Stevermuer, 2 Frances Simmonds, 2 Fary Khan, 3 and Kathy Eagar 2
Atrial septal defect (ASD) is the third most frequent type of congenital heart anomaly, featuring shunting of blood between the two atria. Gene-environment interaction remains to be an acknowledged cause for ASD occurrence. A recent European genome-wide association study (GWAS) of congenital heart disease (CHD) identified 3 susceptibility SNPs at chromosome 4p16 associated with ASD: rs870142, rs16835979 and rs6824295. A Chinese-GWAS of CHD conducted in the corresponding period did not reveal the 3 susceptibility SNPs, but reported 2 different risk SNPs: rs2474937 and rs1531070. Therefore, we aimed to investigate the associations between the 3 European GWAS-identified susceptibility SNPs and ASD risk in the Han population in southwest China. Additionally, to increase the robustness of our current analysis, we conducted a meta-analysis combining published studies and our current case-control study. We performed association, linkage disequilibrium, and haplotype analysis among the 3 SNPs in 190 ASD cases and 225 age-, sex-, and ethnicity-matched healthy controls. Genotype and allele frequencies among the 3 SNPs showed statistically significant differences between the cases and controls. Our study found that individuals carrying the allele T of rs870142, the allele A of rs16835979, and the allele T of rs6824295 had a respective 50.1% (odds ratio (OR) = 1.501, 95% confidence interval (CI) = 1.122-2.009, PFDR-BH = 0.018), 48.5% (OR = 1.485, 95%CI = 1.109-1.987, PFDR-BH = 0.012), and 38.6% (OR = 1.386, 95%CI = 1.042-1.844, PFDR-BH = 0.025) increased risk to develop ASD than wild-type allele carriers in our study cohort. In the haplotype analysis, we identified a disease-risk haplotype (TAT) (OR = 1.540, 95%CI = 1.030-2.380, PFDR-BH = 0.016). Our meta-analysis also showed that the investigated SNP was associated with ASD risk (combined OR (95%CI) = 1.35 (1.24-1.46), P < 0.00001). Our study provides compelling evidence to motivate better understanding of the etiology of ASD.
Association between the European GWAS-Identified Susceptibility Locus at Chromosome 4p16 and the Risk of Atrial Septal Defect: A Case-Control Study in Southwest China and a Meta-Analysis
Li Zhao,# 1 Bei Li,# 1 Ke Dian, 2 Binwu Ying, 1 Xiaojun Lu, 1 Xuejiao Hu, 1 Qi An, 2 Chunxia Chen, 1 Chunyan Huang, 1 Bin Tan, 1 and Li Qin 1 ,