Optical Fiber Harsh Environment Sensors

Various optical fiber harsh environment sensors were reported, including the miniaturized inline Fabry-Perot interferometer sensor by femtosecond laser micromachining, the long period fiber grating sensor and the inline core-cladding mode interferometer by CO2 laser irradiations

Simultaneous Measurement of Temperature and Pressure with Cascaded Extrinsic Fabry-Perot Interferometer and Intrinsic Fabry-Perot Interferometer Sensors

This paper presents an approach for simultaneous measurement of temperature and pressure using miniaturized fiber inline sensors. The approach utilizes the cascaded optical fiber inline intrinsic Fabry-Perot interferometer and extrinsic Fabry-Perot interferometer as temperature and pressure sensing elements, respectively. A CO2 laser was used to create a loss between them to balance their reflection power levels. The multiplexed signals were demodulated using a Fast Fourier transform-based wavelength tracking method. Experimental results showed that the sensing system could measure temperature and pressure unambiguously in a pressure range of 0 to 6.895 x 105 Pa and a temperature range from 20°C to 700°C

Fringe Visibility Enhanced Extrinsic Fabry-Perot Interferometer using a Graded Index Fiber Collimator

We report a fringe visibility-enhanced extrinsic Fabry-Perot interferometer (EFPI) by fusion splicing a quarter-pitch length of a graded-index fiber (GIF) to the lead-in single mode fiber (SMF). The performance of the GIF collimator is theoretically analyzed using a ray matrix model and experimentally verified through beam divergence angle measurements. The fringe visibility of the GIF-collimated EFPI is measured as a function of the cavity length and compared with that of a regular SMF-EFPI. At the cavity length of 500 μm, the fringe visibility of the GIF-EFPI is 0.8, while that of the SMF-EFPI is only 0.2. The visibility-enhanced GIF-EFPI may provide a better signal-to-noise ratio (SNR) for applications where a large dynamic range is desired

Macrophages as a Target for Treating Diabetic Foot Ulcers

In all stages of wound healing, macrophages play a pivotal role by coordinating the repair steps in a timely and accurate fashion. The successful completion of wound healing requires proper spatiotemporal presence and function of macrophages. Diabetes significantly alters the proliferation, polarization and functionality of macrophages, leading to a suboptimal but prolonged pro-inflammatory M1-like phenotype in wound macrophages and a failure of their late transition to a reparative M2-like phenotype. This defect in macrophage phenotype and the proper transition results in delayed or even failure of wound healing. Specifically in the diabetic foot ulcer (DFUs), this macrophage dysfunction results in chronic infection and potentially amputation. The abnormal macrophage phenotype in diabetes is not fully understood but is believed to mainly result from epigenetic changes in macrophages and altered interactions between macrophages and other cell types, such as fibroblasts, endothelial cells, neutrophils and T-cells. Recent research on DFUs has focused on developing strategies to improve diabetic wound repair through modulation of macrophage polarization. Treatment of DFUs will greatly benefit from a multi-modal therapy that includes controlling high blood glucose, topical support, prevention of secondary infection, resolution of sustained inflammation and application of cellular therapies targeting macrophages

A Systematic Literature Review of Researches on Urban Traffic Strategy Development

Abstract—With the advancement of computer science and the development of urban economy, the interest of human research on urban traffic strategy has been promoted. Number of vehicles in urban traffic network in a sharp increase, in order to solve the current status of China's traffic congestion, we hope to reduce urban vehicles greenhouse gas emissions and to reduce waiting time is a serious problem currently facing the city traffic. In order to solve this problem, it can be from two aspects. On the one hand, traffic signal control of traffic network, the other is to optimize the route of the vehicle. This paper respectively from tells the development of the traffic signal control strategy and vehicle routing process, and compares their advantages and disadvantages. The paper summarizes the urban traffic strategy and traffic optimization strategy in recent years, and systematically summarizes the present situation and existing problems of urban traffic optimization strategies at home and abroad, summarizes the development prospects of urban traffic optimization strategies, and provides the strategies for traffic optimization. In order to provide the strategy of scholars engaged in the transportation of new research perspectives and research data

The non-coding landscape of head and neck squamous cell carcinoma.

Head and neck squamous cell carcinoma (HNSCC) is an aggressive disease marked by frequent recurrence and metastasis and stagnant survival rates. To enhance molecular knowledge of HNSCC and define a non-coding RNA (ncRNA) landscape of the disease, we profiled the transcriptome-wide dysregulation of long non-coding RNA (lncRNA), microRNA (miRNA), and PIWI-interacting RNA (piRNA) using RNA-sequencing data from 422 HNSCC patients in The Cancer Genome Atlas (TCGA). 307 non-coding transcripts differentially expressed in HNSCC were significantly correlated with patient survival, and associated with mutations in TP53, CDKN2A, CASP8, PRDM9, and FBXW7 and copy number variations in chromosomes 3, 5, 7, and 18. We also observed widespread ncRNA correlation to concurrent TP53 and chromosome 3p loss, a compelling predictor of poor prognosis in HNSCCs. Three selected ncRNAs were additionally associated with tumor stage, HPV status, and other clinical characteristics, and modulation of their expression in vitro reveals differential regulation of genes involved in epithelial-mesenchymal transition and apoptotic response. This comprehensive characterization of the HNSCC non-coding transcriptome introduces new layers of understanding for the disease, and nominates a novel panel of transcripts with potential utility as prognostic markers or therapeutic targets

Inhalable particulate matter and mitochondrial DNA copy number in highly exposed individuals in Beijing, China: a repeated-measure study

Background: Mitochondria are both a sensitive target and a primary source of oxidative stress, a key pathway of air particulate matter (PM)-associated diseases. Mitochondrial DNA copy number (MtDNAcn) is a marker of mitochondrial damage and malfunctioning. We evaluated whether ambient PM exposure affects MtDNAcn in a highly-exposed population in Beijing, China. Methods: The Beijing Truck Driver Air Pollution Study was conducted shortly before the 2008 Beijing Olympic Games (June 15-July 27, 2008) and included 60 truck drivers and 60 office workers. Personal PM2.5 and elemental carbon (EC, a tracer of traffic particles) were measured during work hours using portable monitors. Post-work blood samples were obtained on two different days. Ambient PM10 was averaged from 27 monitoring stations in Beijing. Blood MtDNAcn was determined by real-time PCR and examined in association with particle levels using mixed-effect models. Results: In all participants combined, MtDNAcn was negatively associated with personal EC level measured during work hours (β=−0.059, 95% CI: -0.011; -0.0006, p=0.03); and 5-day (β=−0.017, 95% CI: -0.029;-0.005, p=0.01) and 8-day average ambient PM10 (β=−0.008, 95% CI: -0.043; -0.008, p=0.004) after adjusting for possible confounding factors, including study groups. MtDNAcn was also negatively associated among office workers with EC (β=−0.012, 95% CI: -0.022;-0.002, p=0.02) and 8-day average ambient PM10 (β=−0.030, 95% CI: -0.051;-0.008, p=0.007). Conclusions: We observed decreased blood MtDNAcn in association with increased exposure to EC during work hours and recent ambient PM10 exposure. Our results suggest that MtDNAcn may be influenced by particle exposures. Further studies are required to determine the roles of MtDNAcn in the etiology of particle-related diseases