Creep aging behavior of retrogression and re-aged 7150 aluminum alloy

Creep aging behavior of retrogression and re-aged(RRAed)7150 aluminum alloy(AA7150)was systematically investigated using the creep aging experiments,mechanical properties tests,electrical conductivity tests and transmission electron microscope(TEM)observations.Creep aging results show that the steady-state creep mechanism of RRAed alloys is mainly dislocation climb(stress exponent≈5.8),which is insensitive to the grain interior and boundary precipitates.However,the total creep deformation increases over the re-aging time.In addition,the yield strength and tensile strength of the four RRAed samples are essentially the same after creep aging at 140℃ for 16 h,but the elongation decreases slightly with the re-aging time.What’s more,the retrogression and re-aging treatment are beneficial to increase the hardness and electrical conductivity of the creep-aged 7150 aluminum alloy.It can be concluded that the retrogression and re-aging treatment before creep aging forming process can improve the microstructure within grain and at grain boundary,forming efficiency and comprehensive performance of mechanical properties and electrical conductivity of 7150 aluminum alloy.

The Philadelphia chromosome in leukemogenesis

The truncated chromosome 22 that results from the reciprocal translocation t(9;22)(q34;q11) is known as the Phila?delphia chromosome(Ph) and is a hallmark of chronic myeloid leukemia(CML).In leukemia cells,Ph not only impairs the physiological signaling pathways but also disrupts genomic stability.This aberrant fusion gene encodes the breakpoint cluster region?proto?oncogene tyrosine?protein kinase(BCR?ABL1) oncogenic protein with persistently enhanced tyrosine kinase activity.The kinase activity is responsible for maintaining proliferation,inhibiting differentia?tion,and conferring resistance to cell death.During the progression of CML from the chronic phase to the accelerated phase and then to the blast phase,the expression patterns of different BCR?ABL1 transcripts vary.Each BCR?ABL1 transcript is present in a distinct leukemia phenotype,which predicts both response to therapy and clinical outcome.Besides CML,the Ph is found in acute lymphoblastic leukemia,acute myeloid leukemia,and mixed?phenotype acute leukemia.Here,we provide an overview of the clinical presentation and cellular biology of different phenotypes of Ph?positive leukemia and highlight key findings regarding leukemogenesis.

Interleukin- 13 interferes with activation-induced t-ce apoptosis by repressing p53 expression

The etiology and the underlying mechanism of CD4＋ T-cell polarization are unclear. This study sought to investigate the mechanism by which interleukin （IL）-13 prevents the activation-induced apoptosis of CD4＋ T cells. Here we report that CD4＋ T cells expressed IL-13 receptor a2 in the intestine of sensitized mice. IL-13 suppressed both the activation-induced apoptosis of CD4＋ T cells and the expression of p53 and FasL. Exposure to recombinant IL-13 inhibited activation-induced cell death （AICD） along with the expression of p53, caspase 3, and tumor necrosis factor-a in CD4＋ T cells. Administration of an anti-lL-13 antibody enhanced the effect of specific immunotherapy on allergic inflammation in the mouse intestine, enforced the expression of p53 in intestinal CD4＋ T cells, and enhanced the frequency of CD4＋ T-cell apoptosis upon challenge with specific antigens. In summary, blocking IL-13 enhances the therapeutic effect of antigen-specific immunotheraov by regulating aDoptosis and thereby enforcing AICD in CD4＋ T cells.