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Similar in principle to recent implementations of a lidar system at 355 nm [Opt. Lett. 25, 1231 (2000), Appl. Opt. 44, 6023 (2005)], an incoherent-detection Mie Doppler wind lidar at 1064 nm was developed and deployed in 2005 [Opt. Rev. 12, 409 (2005)] for wind measurements in the low troposphere, taking advantage of aerosol scattering for signal enhancement. We present a number of improvements made to the original 1064 nm system to increase its robustness for long-period operation. These include a multimode fiber for receiving the reference signal, a mode scrambler to allow uniform illumination over the Fabry-Perot interferometer, and a fast scannable Fabry-Perot interferometer for calibration and for the determination of outgoing laser frequency during the wind observation. With these improvements in stability, the standard deviation of peak transmission and FWHM of the Fabry-Perot interferometer was determined to be 0.49% and 0.36%, respectively. The lidar wind measurements were validated within a dynamic range of +/-40 m/s. Comparison experiments with both wind profiler radar and Vaisala wiresonde show good agreement with expected observation error. An example of 24 h continuous observations of wind field and aerosol backscatter coefficients in the boundary layer with 1 min and 30 m temporal and spatial resolution and 3 m/s tolerated wind velocity error is presented and fully demonstrates the stability and robustness of this lidar.

The purpose of this study was to characterize the expression of procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD2), a membrane-bound homodimeric enzyme that specifically hydroxylates lysine in the telopeptide of procollagens, and assess the clinical significance of PLOD2 in colorectal cancer (CRC). Our results show that PLOD2 is highly expressed in CRC tumor tissues and cell lines, both at the mRNA and protein levels. Next, we found that PLOD2 was positively correlated with tumor grade (P = 0.001), T stage (P = 0.001), N stage (P < 0.001), and an advanced TNM stage (P < 0.001). Knockdown of PLOD2 attenuated CRC cell proliferation, migration, and invasiveness, in vitro. Our analysis of the mechanism behind the effects of PLOD2 suggests that PLOD2 affected glycolysis by regulating the expression of hexokinase 2 (HK2). HK2 reverses the inhibitory effects of PLOD2 knockdown in CRC. Furthermore, the data suggest that PLOD2 regulates the expression of HK2 via the STAT3 signaling pathway. Survival analysis revealed that high expression levels of PLOD2 (HR = 3.800, P < 0.001) and HK2 expression (HR = 10.222, P < 0.001) correlated with the overall survival rate. After analyzing their expression and correlation, PLOD2 positively correlated with HK2 (r = 0.590, P < 0.001). Our findings have revealed that PLOD2 is a novel regulatory factor in glucose metabolism, exerted via controlling HK2 expression in CRC cells, suggesting PLOD2 as a promising therapeutic target for CRC treatment.

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