The Mechanical and Energy Release Performance of THV-Based Reactive Materials.

A polymer of tetrafluoroethylene, hexafluoropropylene, and vinylidene fluoride- (THV) based reactive materials (RMs) was designed to improve their density and energy release efficiency. The mechanical performances, fracture mechanisms, thermal behavior, energy release behavior, and reaction energy of four types of RMs (26.5% Al/73.5% PTFE, 5.29% Al/80% W/14.71% PTFE, 62% Hf/38% THV, 88% Hf/12% THV) were systematically researched by conducting compressive tests, scanning electron microscope (SEM), differential scanning calorimeter, thermogravimetric (DSC/TG) tests and ballistic experiments. The results show that the THV-based RMs have a unique strain softening effect, whereas the PTFE-based RMs have a remarkable strain strengthening effect, which is mainly caused by the different glass transition temperatures. Thermal analysis indicates that the THV-based RMs have more than one exothermic peak because of the complex component in THV. The energy release behavior of RMs is closely related to their mechanical properties, which could dominate the fragmentation behavior of materials. The introduction of tungsten (W) particles to PTFE RMs could not only enhance the density but also elevate the reaction threshold of RMs, whereas the reaction threshold of THV-based RMs is decreased when increasing Hf particles content. As such, under current conditions, the THV-based RMs (88% Hf/12% THV) with a high density of 7.83 g/cm3 are adapted to release a lot of energy in thin, confined spaces.

Failure Mechanism of the Fire Control Computer CPU Board inside the Tank under Transient Shock: Finite Element Simulations and Experimental Studies.

The electronic components inside a main battle tank (MBT) are the key components for the tank to exert its combat effectiveness. However, breakdown of the inner electronic components can easily occur inside the MBT due to the strong transient shock and large vibration during artillery fire. As a typical key electronic component inside an MBT, the fault mechanism and fault patterns of the CPU board of the fire control computer (FCC) are discussed through numerical simulation and experimental research. An explicit nonlinear dynamic analysis is performed to study the vibration features and fault mechanism under instantaneous shock load. By using finite element modal analysis, the first six nature frequencies of the CPU board are calculated. Meanwhile, curves of stress-frequency and strain-frequency of the CPU board under different harmonic loads are obtained, which are applied to further identify the peak response of the structure. Validation of the finite element model and simulation results are performed by comparing those obtained from the modal with experiments. Based on the dynamic simulation and experimental analysis, fault patterns of CPU board are discussed, and some optimization suggestions were proposed. The results shown in this work can provide a potential technical basis and reference for the optimization design of the electronic components that are commonly used in the modern weapon equipment and wartime support.

ACE2 Promotes the Synthesis of Pulmonary Surfactant to Improve AT II Cell Injury via SIRT1/eNOS Pathway.

OBJECTIVE: We aimed to explore the level of PS, cell viability, inflammatory factors, and apoptosis in neonatal respiratory distress syndrome (ARDS). Besides, we explored the potential relationship between ACE2, SIRT1/eNOS pathway, and hypoxia-induced AT II cell damage. METHODS: The hUC-MSC-derived AT II cells were verified by IF and ICC, whereas qRT-PCR was used for PS and AT II cell marker (CK-8 and KGF). The AT II cell damage model was established by hypoxia exposure. The enhanced expression of ACE2 was tested after transfection with pcDNA3.1-ACE2 by western blot. The effects of hypoxia and ACE2 on AT II cells were evaluated by MTT, western blot, ELISA, and flow cytometry. The involvement of the SIRT1/eNOS pathway in AT II cell's protective functions against NRDS was verified with the addition of SIRT1 inhibitor EX527. RESULTS: Based on the successful differentiation of AT II cells from hUC-MSCs and the buildup of AT II cell damage model, the overexpressed ACE2 impeded the hypoxia-induced cellular damage of AT II cells. It also counteracted the inhibitory effects of hypoxia on the secretion of PS. Overexpression of ACE2 rescued the cell viability and suppressed the secretion of inflammatory cytokines and the apoptosis of AT II cells triggered by hypoxia. And ACE2 activated the SIRT1/eNOS pathway to play its cell-protective and anti-inflammatory roles. CONCLUSION: Our findings provided information that ACE2 prevented AT II cells from inflammatory damage through activating the SIRT1/eNOS pathway, which suggested that ACE2 might become a novel protective agent applied in the protection and treatment of NRDS.

Resveratrol reduces drug resistance of SCLC cells by suppressing the inflammatory microenvironment and the STAT3/VEGF pathway.

DNA-damaging agents, such as doxorubicin (Adriamycin), are widely used for the treatment of small cell lung cancer (SCLC). However, drug resistance is one of the major challenges for treatment of SCLC. Herein, we investigated the mechanisms underlying drug resistance in SCLC cells and the effects of resveratrol (Res) on drug resistance. We report that Adriamycin treatment of H69AR (multidrug resistance phenotype) cells resulted in a lower rate of growth inhibition, up-regulation of MRP1 and P-glycoprotein (P-gp), and higher P-gp activity as compared with susceptible H69 cells treated with Adriamycin. Moreover, the signal transducer and activator of transcription 3/vascular endothelial growth factor (STAT3/VEGF) pathway was overactivated in H69AR cells, especially after interleukin-23 treatment. The inflammatory microenvironment promoted the drug resistance of H69AR cells by activating the STAT3/VEGF pathway. The addition of Res suppressed the expression levels of inflammatory mediators, inhibited the STAT3/VEGF pathway, impeded P-gp activity, and decreased the drug resistance of H69AR cells. H69AR cells exhibited Adriamycin resistance through activation of the STAT3/VEGF pathway, and Res ameliorated the inflammatory microenvironment to suppress the STAT3/VEGF pathway to reduce drug resistance. Our results suggest that Res may have therapeutic potential for SCLC treatment.

Exosomal long non-coding RNA LINC00662 promotes non-small cell lung cancer progression by miR-320d/E2F1 axis.

Non-small cell lung cancer (NSCLC) is the most common tumor affecting modern people and is associated with severe morbidity and high mortality. Exosomal long non-coding RNAs as crucial regulators are involved in cancer progression. However, the role of exosomal lncRNA LINC00662 in the development of NSCLC remains unclear. Here, we aimed to explore the impact of exosomal lncRNA LINC00662 on the NSCLC progression and the underlying mechanism. Significantly, we revealed that the expression of lncRNA LINC00662 was elevated in the plasma exosome of NSCLC patients. Exosomal LINC00662 promoted proliferation, invasion, and migration, and inhibited apoptosis and cell cycle arrest of NSCLC cells. Mechanically, LINC00662 was able to serve as a miR-320d sponge in NSCLC cells. MiR-320d could target E2F1 in NSCLC cells. Exosomal LINC00662 contributed to the progression of NSCLC by miR-320d/E2F1 axis in vitro. Remarkably, exosomal LINC00662 enhanced the tumor growth of NSCLC in vivo. Thus, we conclude that exosomal lncRNA LINC00662 promotes NSCLC progression by modulating miR-320d/E2F1 axis. Our finding provides new insights into the mechanism by which exosomal lncRNA LINC00662 contributes to the development of NSCLC. LncRNA LINC00662, miR-320d, and E2F1 may serve as potential targets for NSCLC therapy.