The Elastic Constants Measurement of Metal Alloy by Using Ultrasonic Nondestructive Method at Different Temperature

The ultrasonic nondestructive method is introduced into the elastic constants measurement of metal material. The extraction principle of Poisson’s ratio, elastic modulus, and shear modulus is deduced from the ultrasonic propagating equations with two kinds of vibration model of the elastic medium named ultrasonic longitudinal wave and transverse wave, respectively. The ultrasonic propagating velocity is measured by using the digital correlation technique between the ultrasonic original signal and the echo signal from the bottom surface, and then the elastic constants of the metal material are calculated. The feasibility of the correlation algorithm is verified by a simulation procedure. Finally, in order to obtain the stability of the elastic properties of different metal materials in a variable engineering application environment, the elastic constants of two kinds of metal materials in different temperature environment are measured by the proposed ultrasonic method

Interleukin-33 promoting Th1 lymphocyte differentiation dependents on IL-12

No abstract available.The pro-Th2 cytokine IL-33 is now emerging as an important Th1 cytokine-IFN-γ inducer in murine CD4+ T cells that is essential for protective cell-mediated immunity against viral infection in mice. However, whether IL-33 can promote human Th1 cell differentiation and how IL-33 polarizes Th1 cells is less understood. We assessed the ability of IL-33 to induce Th1 cell differentiation and IFN-γ production in vitro and in vivo. We report here that IL-33 alone had no ability in Th1 cell polarization. However it potentiated IL-12-mediated Th1 cell differentiation and IFN-γ production in TCR-stimulated murine and human CD4+ T cells in vitro and in vivo. IL-33 promoted Th1 cell development via MyD88 and synergized with IL-12 to enhance St2 and IL-12R expression in CD4+ T cells. These data therefore provide a novel mechanism for Th1 cell differentiation and optimal induction of a Type 1 response. Thus, IL-33 is capable of inducing IL-12-dependent Th1 cell differentiation in human and mouse CD4+ T cells

β-lactam hypersensitivity involves expansion of circulating and skin-resident Th22 cells

Background: β-lactam hypersensitivity has been classified according to the phenotype and function of drug-specific T-cells; however, new T-cell subsets have not been considered. Objective: The objective of this study was use piperacillin as a model of β-lactam hypersensitivity to study the nature of the drug-specific T-cell response induced in the blood and skin of hypersensitive patients and healthy volunteers. Methods: Drug-specific T-cells were cloned from blood and inflamed skin and cellular phenotype and function was explored. Naïve T cells from healthy volunteers were primed to piperacillin, cloned and subjected to the similar analyses. Results: PBMC and T-cell clones (n=570, 84% CD4+) from blood of piperacillin hypersensitive patients proliferated and secreted Th1/2 cytokines alongside IL-22 following drug stimulation. IL-17A secretion was not detected. Drug-specific clones from inflamed skin (n=96, 83% CD4+) secreted a similar profile of cytokines, but displayed greater cytolytic activity, secreting perforin, granzyme B and Fas L when activated. Blood- and skin-derived clones expressed high levels of skin-homing chemokine receptors and migrated in the presence of the ligands CCL17 and CCL27. Piperacillin-primed naïve T-cells from healthy volunteers also secreted IFN-γ, IL-13, IL-22 and cytolytic molecules. Aryl hydrocarbon (ArH) receptor blockade prevented differentiation of the naïve T-cells into antigen-specific Il-22 secreting cells. Conclusion: Together our results reveal that circulating and skin resident antigen-specific IL-22 secreting T-cells are detectable in patients with β-lactam hypersensitivity. Furthermore, differentiation of naïve T-cells into antigen-specific Th22 cells is dependent on ArH receptor signalling

Anti-Toll-like receptor 2 and 4 antibodies suppress inflammatory response in mice

Toll-like receptors (TLRs) 2 and 4 recognize different endogenous and exogenous agonists and play a distinct role in infection and inflammation. However, their ultimate effect in a given infectious and inflammatory disease is less understood. We produced polyclonal anti-murine TLR2 and TLR4 antibodies and investigated their effect on cutaneous leishmaniasis and inflammatory arthritis. Administration of these antibodies to susceptible BALB/c mice, infected in the footpad with Leishmania major, reduced footpad swelling but not the parasite load compared with mice treated with control IgG. The antibodies synergistically reduced leishmanial-specific T-cell proliferation, T helper type 1 and type 2 cytokine production, specific IgG1 and IgG2a antibody synthesis, and T-cell receptor and co-stimulatory molecule expression on dendritic cells in infected mice. We then tested the effect of these antibodies on collagen-induced arthritis (CIA) in DBA/1 mice, a classic model of chronic inflammation. Both antibodies markedly suppressed the development of clinical parameters with concomitant reduction of pro-inflammatory cytokine production. These data therefore suggest that anti-TLR2 and 4 antibodies may have a synergistic therapeutic effect on inflammatory disease in vivo