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Long-range distributed vibration sensing based on internal-modulation OFDR
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作者 Yaoli Yue Jing Zeng +3 位作者 Zhenyang Ding Teng Zhang Haohan Guo Tiegen Liu 《Nanotechnology and Precision Engineering》 CSCD 2024年第4期8-15,共8页
Presented here is long-range distributed vibration sensing based on internal-modulation optical frequency domain reflectometry(OFDR).In the proposed system with internal modulation,a silicon-based photonic-chip laser i... Presented here is long-range distributed vibration sensing based on internal-modulation optical frequency domain reflectometry(OFDR).In the proposed system with internal modulation,a silicon-based photonic-chip laser is used as the laser source,and by controlling the output voltage curve of an arbitrary waveform generator to induce temperature change in the external cavity of the laser,a 10-GHz optical frequency tuning range is achieved.The complexity of the proposed internal-modulation system is lower than that of the traditional external-modulation OFDR system that combines a narrow-linewidth laser with a single-sideband modulator to achieve wavelength tuning.Cross-correlation analysis is used as a sensing mechanism to evaluate the similarity between Rayleigh scatter signals and to achieve vibration event localization.Experimental comparison is made of the vibration sensing performance of the external-and internal-modulation systems,and for a vibration event generated at a distance of 100.95 km,they locate it with a sensing spatial resolution of 43.0 m and 16.8 m,respectively.The results indicates that the proposed distributed vibration sensing based on internal modulation has better sensing performance and lower complexity compared to the traditional external-modulation system.In addition,the proposed system is single-ended and involves no optical amplification,which makes it very suitable for ultra-long-range sensing. 展开更多
关键词 Distributed optical fiber sensing Distributed vibration sensing Optical frequency domain reflectometry internal modulation
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Switched-mode AGC circuits with internally created reset module for burst-mode unbalanced data optical receiver
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作者 Wang Rong Wang Zhigong +2 位作者 Wang Weibai Xu Jian Guan Zhiqiang 《High Technology Letters》 EI CAS 2011年第3期317-324,共8页
This paper presents an innovative switched-mode auto gain control (AGC) circuit with internally created reset module for DC-10Mb/s burst-mode unbalanced (BMU) optical data transmission. Conventional AGC circuit is... This paper presents an innovative switched-mode auto gain control (AGC) circuit with internally created reset module for DC-10Mb/s burst-mode unbalanced (BMU) optical data transmission. Conventional AGC circuit is inappropriate for BMU data transmission because it is based on average level detection and requires considerable time to settle on a predefined gain. Therefore, we adopt a fast switched-mode AGC based on peak level detection. After the gain is adjusted, the peak level detectors need to re-detect the peak level of the input signal. Thus, we develop an internally created reset module. This AGC with reset module exhibits a fast operation and achieves an adjusted stable gain within one-bit, avoiding any bit loss up to 10Mb/s data rate. During power-up, the peak level detectors possibly hold an uncertain level resulting in the bit-errors. We propose a power-up reset circuit to solve this problem. Designed in a 0.5μm CMOS technology, the circuit achieves an optical sensitivity of better than -30dBm and a wide dynamic range of over 30dB with a power dissipation of only 30 mW from a 5V supply. 展开更多
关键词 burst-mode unbalanced (BMU) data optical receiver auto gain control (AGC) internally created reset module bit loss
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CREG inhibits VSMCs proliferation by modulating the internalization of IGFII
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作者 YAN Cheng-hui,HAN Ya-ling,TAO Jie,DENG Jie,LUAN Bo,WU Guang-zhe,ZHANG Xiao-lin (Department of Cardiology,Cardiovascular Institute of PLA, Shenyang Northern Hospital,Shenyang 310016,China) 《岭南心血管病杂志》 2011年第S1期194-195,共2页
Background To study the molecular mechanisms of CREG(the cellular repressor of E1A-stimulated gene) on proliferation of VSMCs in vitro.Methods The pRc/CMV-CREG plasmid or the pSM2-siCREG plasmid was transferred into h... Background To study the molecular mechanisms of CREG(the cellular repressor of E1A-stimulated gene) on proliferation of VSMCs in vitro.Methods The pRc/CMV-CREG plasmid or the pSM2-siCREG plasmid was transferred into human vascular smooth muscle cells(hVSMCs) to produce the cell clone that over-expression or down-expression of CREG respectively.BrdU assay and FACS cell cycle analysis were used to detect the proliferation of cells.Western blotting and immunocytochemistry show the expression and localization of IGF2R in hVSMCs.RT-PCR and ELISA assay determined the expression and secretion of IGFII factor. Alex488-labeled rhIGFII was used to investigate the endocysis of cells.And the blockade of IGFII internalization by treatment both the neutralized antibody of anti-IGF2R and rsIGF2R detected the effect of IGFII on VSMCs growth. Furthermore,Western blotting and signal pathway inhibitor were used to analysis the activation of PI3K/AKT and ERK on VSMCs proliferation.Results Western blotting identified that the expression of CREG in hVSMCs-CREG cells increased compared to control cell,and the decreased obviously in hVSMCs-siCREG cells.Meanwhile,the overexpression of CREG in cells was detected to inhibit the proliferation of VSMCs and to enhance the distribution of IGF2R in cellular membrane.Furthermore,overexpression of CREG also accelerated the endocysis of IGFII in hVSMCs-CREG,and attenuate the secretion of IGFII into cell medium by ELISA analysis and Alex488 labeled IGFII analysis.Blockade experiments both neutralized antibody of IGF2R and rhIGF2R fragment determined that enhancement of IGFII secretion promoted the VSMCs proliferation,and PI3K/AKT and ERK signal pathway mediated the effect of IGFII on VSMCs.Conclusions Altogether, these data indicate that CREG inhibits the proliferation of hVSMCs through interfering into the internalization pathway of IGF2R-IGFII. 展开更多
关键词 CREG inhibits VSMCs proliferation by modulating the internalization of IGFII
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