Numerical simulations of transport phenomena is one of the valid methods in investigation of crystal silicon growth by CVD for various types of reactors. The present review provides the key summary on the development of fluid dynamic simulations on polysilicon of CVD and hopefully aid in future improvement of this technology. In the solution of CVD reactor models for polysilicon production, the influence of the deposition process on temperature, the transport phenomena and the surface reactions have to be taken into account when discussing the silicon growth rate.
Objective To fine-map the NF-κB activating protein-like ( NKAPL ) locus identified in a prior genome-wide study as a possible rheumatoid arthritis (RA) risk locus and thereby delineate additional variants with stronger and/or independent disease association. Methods Genotypes for 101 SNPs across the NKAPL locus on chromosome 6p22.1 were obtained on 1368 Canadian RA cases and 1471 controls. Single marker associations were examined using logistic regression and the most strongly associated NKAPL locus SNPs then typed in another Canadian and a US-based RA case/control cohort. Results Fine-mapping analyses identified six NKAPL locus variants in a single haplotype block showing association with p≤5.6×10 −8 in the combined Canadian cohort. Among these SNPs, rs35656932 in the zinc finger 193 gene and rs13208096 in the NKAPL gene remained significant after conditional logistic regression, contributed independently to risk for disease, and were replicated in the US cohort (P comb =4.24×10 −10 and 2.44×10 −9 , respectively). These associations remained significant after conditioning on SNPs tagging the HLA-shared epitope (SE) DRB1*0401 allele and were significantly stronger in the HLA-SE negative versus positive subgroup, with a significant negative interaction apparent between HLA-DRB1 SE and NKAPL risk alleles. Conclusions By illuminating additional NKAPL variants with highly significant effects on risk that are distinct from, but interactive with those arising from the HLA-DRB1 locus, our data conclusively identify NKAPL as an RA susceptibility locus.
Abstract Objective To examine the association of previously identified autoimmune disease susceptibility loci with granulomatosis with polyangiitis (Wegener's) (GPA), and to determine whether the genetic susceptibility profiles of other autoimmune diseases are associated with those of GPA. Methods Genetic data from 2 cohorts were meta‐analyzed. Genotypes for 168 previously identified single‐nucleotide polymorphisms (SNPs) associated with susceptibility to different autoimmune diseases were ascertained in a total of 880 patients with GPA and 1,969 control subjects of European descent. Single‐marker associations were identified using additive logistic regression models. Associations of multiple SNPs with GPA were assessed using genetic risk scores based on susceptibility loci for Crohn's disease, type 1 diabetes, systemic lupus erythematosus, rheumatoid arthritis (RA), celiac disease, and ulcerative colitis. Adjustment for population substructure was performed in all analyses, using ancestry‐informative markers and principal components analysis. Results Genetic polymorphisms in CTLA4 were significantly associated with GPA in the single‐marker meta‐analysis (odds ratio [OR] 0.79, 95% confidence interval [95% CI] 0.70–0.89, P = 9.8 × 10 −5 ). The genetic risk score for RA susceptibility markers was significantly associated with GPA (OR 1.05 per 1‐unit increase in genetic risk score, 95% CI 1.02–1.08, P = 5.1 × 10 −5 ). Conclusion RA and GPA may arise from a similar genetic predisposition. Aside from CTLA4 , other loci previously found to be associated with common autoimmune diseases were not statistically significantly associated with GPA in this study.
Background: Previous studies have demonstrated that lncRNAs play functional roles in regulating cancer cells proliferation, invasion and apoptosis. Recent studies confirmed that lncRNA 00312 has important biological functions in lung and colorectal cancer. However, the role of lncRNA 00312 in renal cell carcinoma (RCC) remains unclear. Our aim was to explore the function of lncRNA 00312 in RCC and its potential molecular mechanism.Methods: RCC cell lines A498, ACHN, were used as in vitro models in this study. RT-PCR was performed to determine lncRNA 00312, miR-34a-5p, ASS1 mRNA expression. Proliferation, and invasion were examined by CCK-8 and transwell assay to confirm the function role of lncRNA 00312. Western blot analysis was used to examine the expression of apoptotic proteins Bax and Bcl-2.Findings: We confirmed that lncRNA 00312 is mainly expressed in cytoplasm of RCC cells and is down-regulated in RCC tissues. Overexpression of lncRNA 00312 suppressed cell proliferation and invasion, while promoted apoptosis. Our results verified that miR-34a-5p could directly bind to lncRNA 00312, and revealed the role of miR-103 in RCC. Furthermore, we confirmed that lncRNA 00312 plays its role through ASS1, a functional gene in many tumors, which was closely related with miR-34a-5p.Interpretation: The functional role of lncRNA 00312 on proliferation, invasion and apoptosis could be partially reversed by miR-34a-5p overexpression or ASS1 silencing. Our study demonstrated that lncRNA 00312/miR-34a-5p/ASS1 axis may play a functional role in the progression of RCC, which provides new insights for RCC clinical treatment.Funding Statement: This work was supported by the sub-topics of National Basic Research Program of China (973 Program; 2015CB755402-043) and Science and Technology Department of Sichuan Province (2015SZ0117; 2019YJ0701).Declaration of Interests: The authors declared no conflict of interest.Ethics Approval Statement: This study was approved by the Human Ethics Committees Review Board at the Mianyang Central Hospital (S201400048, S2018085).
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