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The oxidation of six Cu-xNi alloys (x = 0.2, 0.6, 1, 2, 3, 4 at.%) was studied at 800 °C under 1 atm O2. All of the binary Cu-Ni alloys underwent an internal oxidation of Ni in the presence of an external scale of Cu2O and CuO, in agreement with the theoretical expectations for a finite range of Ni contents. However, the behavior of internal oxidation deviates significantly from the classical behavior of internal oxidation described by Wagner, in particular for the absence of a well-defined front of internal oxidation.

Osteogenic differentiation of human bone marrow-derived mesenchymal stem cells (hBMSCs) is vital for bone formation, and its dysfunction is linked to osteoporosis (OP). In this work, we explored the function of long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) in regulating osteogenic differentiation of hBMSCs. In the present study, the expression of SNHG14 in hBMSCs obtained from OP patients was measured by quantitative real-time polymerase chain reaction (qRT-PCR). SNHG14 was over-expressed or knocked down in hBMSCs, and the expression levels of OP-related genes (ALP, OCN, and OPN) in hBMSCs were detected by qRT-PCR and Western blot. StarBase database and miRanda database were used to predict the binding sites between SNHG14 and miR-185-5p, and between miR-185-5p and 3'UTR of WNT1 inducible signaling pathway protein 2 (WISP2), respectively. Luciferase reporter gene assay was used to validate the binding relationship between SNHG14 and miR-185-5p, and miR-185-5p and 3'UTR of WISP2, respectively. Here, we report that SNHG14 was significantly down-regulated in hBMSCs obtained from patients with OP. Overexpression of SNHG14 promoted osteogenic differentiation, while knockdown of SNHG14 worked oppositely. Mechanistically, miR-185-5p was demonstrated to be a target of SNHG14, and could reverse the function of SNHG14. Additionally, WISP2 was identified as a target gene of miR-185-5p in hBMSCs and could be indirectly regulated by SNHG14. Taken together, down-regulation of SNHG14 in hBMSCs accelerated the progression of OP via regulating miR-185-5p/WISP2 axis., (Copyright 2020 Biolife Sas. www.biolifesas.org.)

Objective: To investigate the association of HLA class II alleles/haplotypes, type I C2 deficiency gene, and tumor necrosis factor a gene promoter allele (TNF2) with systemic lupus erythematosus (SLE) in the Chinese population in Taiwan., Methods: The HLA-DRB1 and DQB1 alleles were studied in 105 SLE patients and 115 controls by the polymerase chain reaction (PCR)/sequence-specific oligonucleotide probe method, the subtyping of DRB1*15/16 and DRB5 by PCR with sequence-specific primers, type I C2 deficiency gene by PCR, and TNF2 by PCR-Nco I restriction fragment length polymorphism., Results: The frequencies of the HLA class II alleles DRB1*02, DRB1*1502, DRB5*0102, DQB1*0501, and DQB1*0602 and DR2-associated haplotypes DRB1* 1501,DRB5*0101,DQB1*0602 and DRB1*1502,DRB5* 0102,DQB1*0501 were higher among SLE patients than among controls; however, only DQB1*0501 was statistically significantly associated with SLE. No specific allele/haplotype was significantly associated with lupus nephritis. No subject had type I C2 deficiency. SLE patients had a marginally higher percentage of TNF2, which was in linkage disequilibrium with DR3. Since DR3 was not associated with SLE in this Taiwanese Chinese population, TNF2 might play a role in the immunopathogenesis of SLE., Conclusion: Although no HLA-DRB1 allele was found to be significantly associated with SLE, the associations with DQB1*0501 and TNF2 suggest that DQB1 and tumor necrosis factor a may be important genetic factors in SLE susceptibility in the Chinese population in Taiwan.

Spleen cytotoxic T cells killing influenza virus-infected target cells are cross-reactive for the different type A influenza viruses, in contrast to the circulating antibodies, which show fine specificity for each A virus subtype variant. This finding has raised the question of whether a single T cell can recognize cells infected with all type A viruses. T-killer cell lines with specificity for alloantigens and the male Y antigen can be selected by means of growth factors present in the supernatant of T cells stimulated with concanavalin A (refs 3-7). We report here that we have been able to establish clones of mouse T cells killing target cells infected with influenza virus. Our cell line maintains the same specificity as the heterogeneous spleen cell population from infected mice, in as far as the T-killer cells are specific for A influenza virus, but do not discriminate between the different type A viruses. The cell line maintains H-2 restriction and does not kill cells infected with B influenza virus. The cells grow in the presence of T-cell growth factor and do not require antigen for growth although they maintain their receptors for type A virus. They can also be stimulated by irradiated T-helper cells from mice primed by type A influenza infection in the presence of type A virus-infected cells.