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The laser modification pretreatment method is an effective way to address the machining difficulties of silicon carbide (SiC), a typical hard-to-machine material. Therefore, the ablation behavior and modification mechanism of SiC under different laser energy were explored in this paper. A new multi-scale model of laser irradiation SiC that couples heat transfer and fluid motion is first established. Then, a series of experiments is carried out to evaluate the model's accuracy, and the interaction between laser and SiC is discussed in detail. The results show that the dominant modification mechanism changes from coulomb explosion to multiphoton absorption, incubation effect, and heat accumulation with the laser energy increase. This leads the surface topography of SiC to transition from nanoparticle formation to disorder to a melting state. In ablative state, micro/nano porous and humps are formed at the edge of ablation groove due to surface tension, generation and rupture of bubbles, respectively. Furthermore, the surface roughness is not proportional to the laser energy due to the plasma shielding effect, and the surface roughness can be reduced by enhancing the flow of the molten material. Amorphous Si–O–C, Si and spherical SiO2 exist in deposition area, leading to SiC elastic modulus decreases from 347 GPa to 103.82 GPa, and the shear strength decreases from 20.9 GPa to 17.25 GPa. The results of this study can provide references for parameters selection and theoretical support for improving the machinability of SiC.

Summary: Here, we provide a step-by-step protocol for generating human induced pluripotent stem cell (hiPSC)-based microglial mouse brain chimeras. In addition, we detail steps for intracerebral injection of pathological tau and magnetic cell isolation of human microglia from chimeric mouse brains for single-cell RNA sequencing. Human microglia developed in chimeric mouse brains recapitulate the pathophysiology of microglia in human brain tissue, offering unprecedented opportunities to study human microglial senescence in vivo.For complete details on the use and execution of this protocol, please refer to (Jin et al., 2022b). : Publisher’s note: Undertaking any experimental protocol requires adherence to local institutional guidelines for laboratory safety and ethics.

Summary: A conceptual framework for understanding abnormal endometrial decidualization, with considerable significance for the diagnosis and treatment of abnormal decidualization-related changes in non-receptive endometrium in implantation failure during early pregnancy is very important. Here, we found the expression levels of miR-29a in endometrial tissues were associated with the menstrual phases and pregnancy outcome. Inhibition of miR-29a led to decreased decidualization of endometrial stromal cells (ESCs) in vitro, whereas Tet methylcytosine dioxygenase 3 (TET3) and its potential demethylation target, the collagen type I alpha 1 chain (Col1A1), were restored. The binding capacity of TET3 to the Col1A1 promoter could be enhanced by the inhibition of miR-29a. Finally, deletion of TET3 rescued the inhibitory effect of the miR-29a antagomir on the proliferation of decidualized ESCs in vitro and embryo implantation in vivo. Thus, loss of miR-29a causes implantation failure because of the limitation of ESCs decidualization-related changes in non-receptive endometrium during early pregnancy.