A Three-Dimensional Equivalent Stiffness Model of Composite Laminates with Wrinkle Defects.

The stiffness of composite laminates is easily affected by wrinkle defects. In this paper, a new effective analytical model was proposed to predict the three-dimensional equivalent elastic properties of multidirectional composite laminates with wrinkle defects. Firstly, a geometric model was established according to the microscopic characteristics of wrinkle defects. Then, based on the classical laminate theory and homogenization method, the constitutive equation and flexibility matrix of the wrinkle region were established. Finally, the equivalent stiffness parameters of unidirectional and multidirectional laminates were derived, and the effects of different wrinkle parameters and ply-stacking sequences on the stiffness of unidirectional and multidirectional laminates were studied by using the analytical model. The results show that the mechanical properties of the lamina and laminates are affected by the out-of-plane angle and in-plane angle of the wrinkle defects. The accuracy of the analytical model has been verified by the numerical model and other theoretical models, and it has the characteristics of few parameters and a high efficiency. The analytical model can be used to predict the stiffness of composite structures with wrinkle defects simply, effectively, and quantitatively. It can also be used as a tool to provide the mechanical response information of laminates with wrinkle defects.

MiR-513a-3p promotes radiation-induced apoptosis of human lung cells by inhibiting glutathione S-transferase P1.

Radiotherapy is a common treatment for lung cancer. However, radiation pneumonitis caused by radiotherapy can affect the quality of life and prognosis of lung cancer patients. miR-513a-3p has been found to sensitize human lung adenocarcinoma cells to chemotherapy by targeting glutathione S-transferase P1 (GSTP1). Here, we found that x-ray induced the apoptosis of BEAS-2B and miR-513a-3p expression in a dose- and time-dependent manner, and miR-513a-3p-mimic significantly increased x-ray induced apoptosis, while miR-513a-3p-inhibitor significantly decreased x-ray induced apoptosis. Dual luciferase gene reporter system showed that miR-513a-3p targeted to inhibit the expression of GSTP1 in BEAS-2B cells. Moreover, knockdown of GSTP1 significantly increased, while overexpression of GSTP1 decreased the apoptosis of BEAS-2B induced by x-ray. Importantly, overexpression of GSTP1 significantly reduced miR-513a-3p-mimic elevated x-ray -induced apoptosis in BEAS-2B cells. In conclusion, x-ray caused increased expression of miR-513a-3p, and miR-513a-3p promoted x-ray-induced apoptosis of human lung cells by inhibiting GSTP1.

MiR-363-3p attenuates neonatal hypoxic-ischemia encephalopathy by targeting DUSP5.

Neonatal hypoxic-ischemia encephalopathy (HIE) refers to hypoxic-ischemic brain damage caused by perinatal asphyxia. Increasing evidence has revealed the crucial roles of microRNAs (miRNAs) in neonatal HIE. In the current research, we aimed to explore the biological role of miR-363-3p in neonatal HIE. For this purpose, we established in vitro models of PC-12 and SH-SY5Y cells subjected to oxygen-glucose deprivation and reperfusion (OGD/R) and an in vivo rat model subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) treatment. First, using H&E staining, TTC staining, and western blot analysis, we observed that DUSP5 knockdown suppressed HIE in vivo. Then, by performing flow cytometric analysis, western blotting, RT-qPCR, and MTT assays, we observed that DUSP5 silencing suppressed OGD/R-induced cell injury in vitro. Subsequently, we explored the potential regulatory mechanism of DUSP5 in OGD/R-treated cells with luciferase reporter assays and RT-qPCR analysis. The results demonstrated that DUSP5 was targeted by miR-363-3p. Next, functional assays, including flow cytometric analysis, MTT assays, western blotting and RT-qPCR, were conducted to explore the biological functions of miR-363-3p in SH-SY5Y and PC-12 cells. Our data showed that miR-363-3p overexpression suppressed OGD/R-induced cell injury. Finally, the results from rescue experiments showed that enhanced DUSP5 expression counteracted the effect of miR-363-3p overexpression. In conclusion, our data suggested that miR-363-3p attenuates neonatal HIE by targeting DUSP5.

Narciclasine attenuates LPS-induced acute lung injury in neonatal rats through suppressing inflammation and oxidative stress.

Acute lung injury (ALI) is a life-threatening disorder related to serious pulmonary inflammation. Narciclasine exhibits strong anti-inflammation activity and attenuates the reactive oxygen species (ROS) production. The present study aims to investigate the underlying mechanism related to the effect of narciclasine on the pathogenesis of neonatal acute lung injury (ALI). Narciclasine attenuated LPS-induced pathological injury and pulmonary edema. In addition, narciclasine suppressed the secretion of inflammatory cytokines, including necrosis factor-α (TNF-α), Interleukin (IL-6), IL-1ß, monocyte chemotactic protein-1 (MCP-1) in serum, and inhibited the expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in lung tissues of neonatal ALI rats. Furthermore, narciclasine alleviated oxidative stress and apoptosis in lung tissues. Importantly, narciclasine exerted an inhibition effect on NF-κB nuclear translocation and activation of Toll-like Receptor 4 (TLR4)/Nuclear factor (NF)-κB/Cyclooxygenase 2 (Cox2) signaling pathway. Taken together, narciclasine protected against lung injury via inhibition effect on excessive inflammation, oxidative stress and apoptosis, hence, narciclasine may be considered as an effective and novel agent for clinical therapeutic strategy of ALI Treatment.