Amplification of rotation velocity using weak measurements in Sagnac's interferometer

We study the amplification of rotation velocity with the Sagnac interferometer based on the concept of weak-value amplification. By using a different scheme to perform the Sagnac interferometer with the probe in momentum space, we have demonstrated the new weak measure protocol to detect the small rotation velocity by amplifying the phase shift of the Sagnac effect. At the given the maximum incident intensity of the initial spectrum, the detection limit of the intensity of the spectrometer and the accuracy of angular velocity measurement, we can theoretical give the appropriate potselection and the minimum of optical path area before experiment. In addition, we put forward a new optical design to increase the optical path area and decrease the size of the interferometer to overcome the limit of instrument size. Finally, our modified Sagnac's interferometer based on weak measurement is innovative and efficient probing the small rotation velocity signal.Comment: arXiv admin note: text overlap with arXiv:1203.0827 by other author

Trichlorophenyl-benzoxime induces apoptosis in human colon carcinoma cells via activation of mitochondria dependent pathway

Purpose: To determine the apoptotic effect of trichlorophenyl-benzoxime (TCPB) on colorectal cancer (CRC) cells, and to elucidate the mechanism of action. Methods: Colon carcinoma cell lines (DLD-1 and HT-29) were used in this study. The cells were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10 % fetal bovine serum (FBS) and 1 % penicillin/streptomycin at 37 ˚C in an atmosphere of 5 % CO2 and 95 % air. When the cells attained 60 - 70 % confluency, they were treated with serum-free medium and graded concentrations of TCPB (1.0 – 6.0 μM) for 24 h. Cell viability and apoptosis were assessed using 3-(4, 5-dimethylthiazol-2-yl) 2, 5-diphenyltetrazolium bromide (MTT) and flow cytometric assays, respectively. Western blotting and 2', 7' dichlorofluorescein diacetate (DCFH DA) assays were used for the determination of expression levels of apoptotic proteins, and levels of reactive oxygen species (ROS), respectively. Results: Treatment of DLD-1 and HT-29 cells with TCPB led to significant and dose-dependent reductions in their viability, as well as significant and dose-dependent increases in the number of apoptotic cells (p < 0.05). Treatment of HT-29 cells with TCPB led to significant increases in the population of cells in the G0/G1 phase, but significant reduction of cell proportion in S and G2/M phases (p < 0.05). It also significantly and dose-dependently upregulated the expressions of caspase-3 and bax, down-regulation of the expression of bcl-2 (p < 0.05). TCPB treatment upregulated the expressions of p53, cytochrome c (cyt c), procaspase-3, and procaspase-9, but down-regulated the expression of pAkt dose-dependently (p < 0.05). The expression of Akt in HT-29 cells was not significantly affected by TCPB (p > 0.05). However, TCPB significantly enhanced the cleavage of PARP1, and significantly and dose-dependently increased the levels of ROS in HT-29 cells (p < 0.05). Conclusion: These results suggest that TCPB exerts apoptotic effect on CRC cells via activation of mitochondria-dependent pathway, and thus can be suitably developed for the management of colon cancer