Numerical simulation of laser ultrasonic detection of the surface microdefects on laser powder bed fusion additive manufactured 316L stainless steel

A numerical model is presented in this article to investigate the interactions between laser generated ultrasonic and the microdefects(0.01 to 0.1 mm),which are on the surface of the laser powder bed fusion additive manufactured 316L stainless steel.Firstly,the influence of the transient sound field and detection positions on Rayleigh wave signals are investigated.The interactions between the varied microdefects and the laser ultrasonic are studied.It is shown that arrival time of reflected Rayleigh(RR)waves wave is only related to the location of defects.The depth can be checked from the feature point Q,the displacement amplitude and time delay of converted transverse(RS)wave,while the width information can be evaluated from the RS wave time delay.With the aid of fitting curves,it is found to be linearly related.This simulation study provides a theoretical basis for quantitative detection of surface microdefects of additive manufactured 316L stainless steel components.

Dlg1 Knockout Inhibits Microglial Activation and Alleviates Lipopolysaccharide-Induced Depression-Like Behavior in Mice

Microglia-mediated neuroinflammation is widely perceived as a contributor to numerous neurological diseases and mental disorders including depression.Discs large homolog 1(Dlg1),an adaptor protein,regulates cell polarization and the function of K?channels,which are reported to regulate the activation of microglia.However,little is known about the role of Dlg1 in microglia and the maintenance of central nervous system homeostasis.In this study,we found that Dlg1 knockdown suppressed lipopolysaccharide(LPS)-induced inflammation by downregulating the activation of nuclear factor-jB signaling and the mitogen-activated protein kinase pathway in microglia.Moreover,using an inducible Dlg1 microglia-specific knockout(Dlg1flox/flox;CX3CR1CreER)mouse line,we found that microglial Dlg1 knockout reduced the activation of microglia and alleviated the LPS-induced depressionlike behavior.In summary,our results demonstrated that Dlg1 plays a critical role in microglial activation and thus provides a potential therapeutic target for the clinical treatment of depression.