Experimental and Numerical Study on Dynamic Response of Foam-Nickel Sandwich Panels under Near-Field Blast Loading.

The explosion products, such as shock waves, fragments and heat energy formed by explosion, act on the plate structure, which may cause structural damage, material failure and even phase transformation of material. In this paper, the damage mechanism and protective effect of near-field blast load on sandwich structure based on foam-nickel core material were studied. Firstly, the near-field explosion test was conducted to investigate the blast response of the foam-nickel sandwich structure subjected to blast shock from 8701 explosive at near-field position. The deformation characteristics and stress history of the sandwich structure on the acting location of blast load were carefully investigated via experimental methods. A finite element model of near-field explosion was established for effective numerical modelling of the dynamic behaviour of the sandwich structure using the explicit dynamics software ANSYS/LS-DYNA for more comprehensive investigations of the blast shock response of the sandwich structure. The finite element model is reasonable and validated by mesh independence verification and comparing the simulated response behaviour to that from the experimental results for the sandwich structure subjected to near-field blast load. On this basis, the damage mechanism and protection effect of the near-field explosion impact on foam-nickel cores with different density and porosity are simulated more systematically. The investigated results from the experiments and a series of numerical simulations show the large deformation effect due to the extensive energy absorption, which suggests that the sandwich structure based on foam-nickel core material may be expected to become a new choice of protective structure under near-field blast load.

Immune checkpoint molecule TIGIT manipulates T cell dysfunction in septic patients.

Sepsis is a dysregulated host response to infection. T cell dysfunction results in the failure to eradicate pathogens and the increased susceptibility to nosocomial infections and mortality during sepsis. Although PD-1 has shown to be a promising target to interfere with T cells dysfunction, the role of other coinhibitory receptors in sepsis remains largely elusive. Here we demonstrated that the immune checkpoint molecule TIGIT on lymphocytes and the critical role of TIGIT in regulating T cell responses in sepsis. Fifty septic patients and seventeen healthy donors were prospectively enrolled. The expression patterns of TIGIT and other molecules on lymphocytes were quantitated by flow cytometry. Ex vivo functional assays were also conducted. Results show that TIGIT expression on T cells was significantly upregulated in sepsis and septic shock patients relative to healthy donors. Elevated frequencies of TIGIT+ T cells correlated with aggravated inflammatory response and organ injuries. Of note, TIGIT expression on CD8+ T cells showed a competitive capability to predict ICU mortality in sepsis. TIGIT+ T cells expressed higher levels of PD-1, lower levels of CD226, and released fewer cytokines. Strikingly, ex vivo blockade of TIGIT using anti-TIGIT antibody restored the frequencies of cytokine-producing T cells from septic patients. These data illustrate that TIGIT on T cells is being used not only as a clinical predictor of poor prognosis but also as a potential target of novel immunotherapeutic intervention during sepsis.