Anisotropic elastic constants calculation of stainless steel cladded layers of pressure vessel steel plate

Cladding stainless steel layer on the inner surface of ferrite pressure vessel is a common method to improve the corrosion resistance and save the economic cost. However, the movement of heat source and temperature gradient in the process of cladded welding will lead to the anisotropy of cladded layer material. When measuring the residual stress of pressure vessel steel plate with stainless steel cladded layers (SSCL) by contour method, it is necessary to know the elastic mechanical properties of stainless steel cladded layers accurately. The assumption of transversely isotropy (TI) was employed, and the relationship between the material compliance matrix and the elastic modulus of transversely isotropic material was utilized. Based on the elastic modulus of each cladded layer and the whole steel plate from the longitudinal direction (0°) until the transverse direction (90°) measured by the experiment, the independent constants S11, S13, S33 and S44 in the compliance matrix of each cladded layer and the whole steel plate were obtained by regression analysis method. Furthermore, by using the relationship between the independent constants of the stiffness matrix of the transversely isotropic material and the single crystal material, the independent constant S12 in the compliance matrix of each stainless steel cladded layer and the whole steel plate were obtained. And then the independent constants of the stiffness matrix of each cladded layer and the whole steel plate were acquired. Hence, a method for calculating the anisotropic elastic constants of the stainless steel cladded layer and the whole steel plate was proposed. The results will provide material data support for measuring residual stress of pressure vessel steel plate with stainless steel cladded layers by contour method

PAX9 polymorphism and susceptibility to sporadic non-syndromic severe anodontia: a case-control study in southwest China

Our research aimed to look into the clinical traits and genetic mutations in sporadic non-syndromic anodontia and to gain insight into the role of mutations of PAX9, MSX1, AXIN2 and EDA in anodontia phenotypes, especially for the PAX9. Material and Methods The female proband and her family members from the ethnic Han families underwent complete oral examinations and received a retrospective review. Venous blood samples were obtained to screen variants in the PAX9, MSX1, AXIN2, and EDA genes. A case-control study was performed on 50 subjects with sporadic tooth agenesis (cases) and 100 healthy controls, which genotyped a PAX9 gene polymorphism (rs4904210). Results Intra-oral and panoramic radiographs revealed that the female proband had anodontia denoted by the complete absence of teeth in both the primary and secondary dentitions, while all her family members maintained normal dentitions. Detected in the female proband were variants of the PAX9 and AXIN2 including A240P (rs4904210) of the PAX9, c.148C>;T (rs2240308), c.1365A>;G (rs9915936) and c.1386C>;T (rs1133683) of the AXIN2. The same variants were present in her unaffected younger brother. The PAX9 variations were in a different state in her parents. Mutations in the MSX1 and EDA genes were not identified. No significant diferences were found in the allele and genotype frequencies of the PAX9 polymorphism between the controls and the subjects with sporadic tooth agenesis. Conclusions These results suggest that the association of A240P with sporadic tooth agenesis still remains obscure, especially for different populations. The genotype/phenotype correlation in congenital anodontia should be verified

Neuropilin-1 Identifies a New Subpopulation of TGF-β-Induced Foxp3 Regulatory T Cells With Potent Suppressive Function and Enhanced Stability During Inflammation

CD4Foxp3 regulatory T cells (Tregs) play a crucial role in preventing autoimmunity and inflammation. There are naturally-derived in the thymus (tTreg), generated extrathymically in the periphery (pTreg), and induced culture (iTreg) with different characteristics of suppressiveness, stability, and plasticity. There is an abundance of published data on neuropilin-1 (Nrp-1) as a tTreg marker, but little data exist on iTreg. The fidelity of Nrp-1 as a tTreg marker and its role in iTreg remains to be explored. This study found that Nrp-1 was expressed by a subset of Foxp3CD4T cells in the central and peripheral lymphoid organs in intact mice, as well as in iTreg. Nrp-1iTreg and Nrp-1iTreg were adoptively transferred into a T cell-mediated colitis model to determine their ability to suppress inflammation. Differences in gene expression between Nrp-1 and Nrp-1iTreg were analyzed by RNA sequencing. We demonstrated that the Nrp-1 subset of the iTreg exhibited enhanced suppressive function and stability compared to the Nrp-1 counterpart both and , partly depending on IL-10. We found that Nrp-1 is not an exclusive marker of tTreg, however, it is a biomarker identifying a new subset of iTreg with enhanced suppressive function, implicating a potential for Nrp-1iTreg cell therapy for autoimmune and inflammatory diseases

PAX9 polymorphism and susceptibility to sporadic non-syndromic severe anodontia: a case-control study in southwest China

Our research aimed to look into the clinical traits and genetic mutations in sporadic non-syndromic anodontia and to gain insight into the role of mutations of PAX9, MSX1, AXIN2 and EDA in anodontia phenotypes, especially for the PAX9. Material and Methods The female proband and her family members from the ethnic Han families underwent complete oral examinations and received a retrospective review. Venous blood samples were obtained to screen variants in the PAX9, MSX1, AXIN2, and EDA genes. A case-control study was performed on 50 subjects with sporadic tooth agenesis (cases) and 100 healthy controls, which genotyped a PAX9 gene polymorphism (rs4904210). Results Intra-oral and panoramic radiographs revealed that the female proband had anodontia denoted by the complete absence of teeth in both the primary and secondary dentitions, while all her family members maintained normal dentitions. Detected in the female proband were variants of the PAX9 and AXIN2 including A240P (rs4904210) of the PAX9, c.148C>T (rs2240308), c.1365A>G (rs9915936) and c.1386C>T (rs1133683) of the AXIN2. The same variants were present in her unaffected younger brother. The PAX9 variations were in a different state in her parents. Mutations in the MSX1 and EDA genes were not identified. No significant diferences were found in the allele and genotype frequencies of the PAX9 polymorphism between the controls and the subjects with sporadic tooth agenesis. Conclusions These results suggest that the association of A240P with sporadic tooth agenesis still remains obscure, especially for different populations. The genotype/phenotype correlation in congenital anodontia should be verified