Fast and accurate tilt-shift-immune phase-shifting algorithm based on self-adaptive selection of interferogram subblocks and principal component analysis.

To eliminate the effect of tilt-shift error on the accuracy of phase-shifting interferometry (PSI), a fast and accurate tilt-shift-immune phase-shifting algorithm based on the self-adaptive selection of interferogram subblocks and principal component analysis (SSPCA) is proposed. First, each interferogram is divided into several subblocks, and principal component analysis and the least-squares method (LSM) are applied to obtain the phase-shift value of each subblock. Next, according to the correlation coefficients between each phase-shift curve, valid and invalid subblocks can be distinguished. Finally, all phase-shift values of the valid subblocks are used to fit the tilt phase-shift plane, and phase results can be obtained using the LSM. Simulations indicate that the accuracy of SSPCA can reach 0.03 rad both for small (1 rad) and large (${2}\pi $2π rad) tilt amplitudes, and it takes only one-tenth or less of the processing time of iterative algorithms. Experiments proved that SSPCA can be applied even without a precision phase shifter and thus provides a low-cost approach for PSI with both high precision and speed.

Metformin promotes proliferation and suppresses apoptosis in Ox-LDL stimulated macrophages by regulating the miR-34a/Bcl2 axis.

Background: Metformin, an antidiabetic drug, has been reported to be involved in atherosclerosis (AS). In this study, the effects of metformin on oxidized low-density lipoprotein (Ox-LDL)-induced macrophage apoptosis were investigated, and the mechanisms involved in this process were examined. Methods: qRT-qPCR analysis was performed to detect the expression of miR-34a in macrophage cells. Cell proliferation was determined by MTT assays and colony formation assays. Cell apoptosis was assessed by the detection of apoptotic rate and caspase 3 activity. Western blot analysis was performed to evaluate the expression of Bcl2 protein. Results: Metformin treatment promoted proliferation and suppressed apoptosis in macrophages following the treatment of oxidized low-density lipoprotein (Ox-LDL). Metformin could inhibit miR-34a in macrophages. miR-34a overexpression could reverse the effect of metformin on proliferation and apoptosis in Ox-LDL-treated macrophages. Moreover, metformin could increase the expression of the miR-34a target gene Bcl2. Furthermore, metformin treatment exerted the pro-proliferation and anti-apoptosis effect through regulating Bcl2 expression in Ox-LDL-stimulated macrophages. Conclusion: Metformin facilitated proliferation and inhibited apoptosis of macrophages treated with Ox-LDL through the miR-34a/Bcl2 axis, indicating the potential value of metformin in AS therapy.