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Trichloroethanol (TCOH), as a metabolite of trichloroethylene, has sensitization in the pathogenesis of trichloroethylene-induced hypersensitivity dermatitis (TIHD) which the human leukocyte antigen (HLA)-B∗13:01 gene is strongly associated with it. However, it is still obscure how TCOH participates in the pathogenesis of TIHD. Here, we demonstrate that TLR2 and TLR4 signaling through MyD88 and TRAF6-dependent pathway could activate NF-κB by promoting degradation of the inhibitor IκB-α to stimulate the process of NF-κB nuclear translocation. Besides, the crucial molecules of antigen processing and presentation, including TAP1, LMP2, LMP7, and HLA-B* 13:01, were all enhanced and the abundance of HLA-B* 13:01 on the surface of CIR-B* 13:01 cells was also up-regulated with the TCOH concentration increasing. Notably, we used 50 μM pyrrolidinedithiocarbamate (ammonium) to effectively inhibit the activation of NF-κB, which could effectively reverse the stimulation of antigen processing and presentation in TCOH-treated CIR-B* 13:01 cells. Taken together, we speculated that TCOH could promote the abundance of HLA complex on the antigen-presenting cells via TLR2 and TLR4/NF-κB to induce the severe reactivation of T lymphocytes, leading to the extreme immune response.

Recently, Trichloroethylene (TCE) induced TCE hypersensitivity syndrome (THS) has attracted the attention of many researchers in the field of environmental and occupational health. Studies have revealed that Human leukocyte antigen (HLA) polymorphisms were the important genetic determinants of the diseases, but the potential molecular mechanism remains unclear.This study aimed to investigate the association between THS and HLA at the molecular level.We chose the human B-lymphoblastoid cell line Hmy2.C1R transfected with cDNA of HLA-B*13:01 and HLA-B*13:02 to analyze the characteristics of HLA-B-binding peptides and investigate the effect of TCE on the binding affinity of peptides to the HLA-B molecules. Further, the mathematical model was used to identify the possible interaction between TCE and HLA-B*13:01 or HLA-B*13:02 molecule.54 HLA-B*13:01-binding peptides and 85 HLA-B*13:02-binding peptides were identified. Comparing the protein sequences of HLA-B*13:01 and HLA-B*13:02, amino acids were different at positions 94, 95 and 97. The results of the binding affinity of self-peptides to HLA molecules in the presence of TCE showed that TCE significantly decreased the binding affinity of peptides to HLA-B*13:01 only, but did not affect that of HLA-B*13:02. Molecular docking model showed that there was a unique high-affinity binding mode between TCE and HLA-B*13:01 (but not HLA-B*13:02), and the binding site located in the region of F pocket, suggesting that the unique structure of the F pocket of HLA-B*13:01 might provide the possibility of binding TCE. The pathogenesis of interaction between HLA-B*13:01 and TCE might belong to the model of the alteration of the HLA-presented self-peptide repertoire.This study explored the molecular mechanism of the association between THS and HLA-B*13:01, and had important implications for understanding the role of gene-environment interaction in the development of complex environment-related diseases.

Coke oven emissions are a complex mixture of particulate matter and gases, some with carcinogenicity, released during coke production. Lung cancer caused by coke oven emissions has been listed as a statutory occupational cancer in China and many countries.In this study, coke oven emissions-induced lung cancer was mainly found in the manufacturing industries. Coke oven workers exposed to higher levels of polycyclic aromatic hydrocarbons in different workplaces had a high risk of occupational lung cancer.It is necessary to take efforts to greatly reduce emissions from coke production and effectively monitor the health of workers.

ObjectivesTrichloroethylene (TCE) -induced hypersensitivity syndrome (TIHS) is a potentially life-threatening disease. Several genetic susceptibility biomarkers have been found to be associated with TIHS, and this systematic prospective study has been conducted to evaluate the utility of these genetic susceptibility biomarkers in preventing the disease.MethodsThe newly hired TCE-exposed workers were recruited from March 2009 to October 2010. HLA-B*13:01 genotyping and 3-month follow-up procedure were conducted. All workers were monitored for adverse reaction by telephone interview every week. The workers with early symptoms of TIHS were asked to go to the hospital immediately for further examination, diagnosis and treatment. The medical expense record data of patients with TIHS were collected for cost-effectiveness analysis in 2018.ResultsAmong 1651 workers, 158 (9.57%) were found to carry the HLA-B*13:01 allele and 16 (0.97%) were diagnosed with TIHS. HLA-B*13:01 allele was significantly associated with an increased TIHS risk (relative risk=28.4, 95% CI 9.2 to 86.8). As a risk predictor of TIHS, HLA-B*13:01 testing had a sensitivity of 75%, a specificity of 91.1% and an area under curve of 0.83 (95% CI 0.705 to 0.955), the positive and negative predictive values were 7.6% and 99.7%, respectively. The incidence of TIHS was significantly decreased in HLA-B*13:01 non-carriers (0.27%) compared with all workers (0.97%, p=0.014). Cost-effectiveness analysis showed that HLA-B*13:01 screening could produce an economic saving of $4604 per TIHS avoided.ConclusionsProspective HLA-B*13:01 screening may significantly reduce the incidence of TIHS and could be a cost effective option for preventing the disease in TCE-exposed workers.

An autoencoder-residual (AE-Res) network is designated to assist the linearization of the wideband photonic scanning channelized receiver. It is capable of adaptively suppressing spurious distortions over multiple octaves of signal bandwidth, obviating the need for calculating the multifactorial nonlinear transfer functions. Proof-of-concept experiments indicate that the improvement of the third-order spur-free dynamic range (SFDR2/3) is 17.44 dB. Moreover, the results for real wireless communication signals demonstrate that the improvement of the spurious suppression ratio (SSR) is 39.69 dB and the reduction of the noise floor is ∼10 dB.

In this paper, a broadband microwave photonic channelized receiver based on optical frequency comb (OFC) injection locking technology is illustrated. The simulation results show that, with more than 80 comb lines generated from OFC, this receiver enables channelized scanning and reception of broadband signal up to 40 GHz with instantaneous bandwidth of 1 GHz. Meanwhile, the channels selected using optical injection locking (OIL) technology, perform high gain and low phase noise with suppression ratio between the selected comb line and other comb lines is 28.7 dB. Due to OIL technology, the wideband tunability of this receiver would not depend on the optical filter or demultiplexer, and the band limitation and operation resolution introduced by optical components are broken through. The OIL technology also lead to the architecture of receiver more compact and feasible in practical.

Many important molecules show strong characteristic vibrational transitions in the mid-infrared (MIR) part of the electromagnetic spectrum. This leads to applications in spectroscopy, chemical and bio-molecular sensing, security and industry, especially over the mid- and long- wave infrared atmospheric transmission windows of 3-5 μm and 8-13 μm. In this paper, we review some of our more recent experimental and simulation work aimed at developing new light sources based on chalcogenide glass optical fibres that can help us utilize this spectral region for biomedical applications. This includes the development of supercontinuum and bright luminescent sources and our progress towards fibre-based lasers. We place these developments in the context of MIR imaging and spectroscopy in order to show how they bring the promise a new era in healthcare and clinical diagnostics.

Exposure to diesel engine exhaust (DEE) was associated with various adverse health effects including lung cancer. Particle size distribution and profiles of organic compounds in both particle and gas phases of DEE that could provide valuable insights into related health effects were measured in a diesel engine testing workshop. Concentrations of urinary 6 mono-hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) in 137 DEE-exposed workers and 127 non-DEE-exposed workers were determined. Benchmark dose method was applied to estimate lower limit of benchmark dose (BMDL) of urinary OH-PAHs most specific to DEE exposure for previously reported cancer biomarkers. We found that 84.3% of diesel exhaust particles were ultrafine particles. Indeno[123-cd]pyrene and phenanthrene were the most abundant carcinogenic and noncarcinogenic PAHs in the particle phase of DEE, respectively. Principal component analysis demonstrated that urinary hydroxyphenanthrene (OHPhe) had highest loading value on principal component (PC) representative of DEE exposure and lowest loading value on PC representative of smoking status. BMDLs of urinary OHPhe from best-fitting models for cancer biomarkers including micronucleus and 1,N6-ethenodeoxyadenosine were 1.08 μg/g creatinine and 2.82 μg/g creatinine, respectively. These results provided basis for understanding DEE exposure induced health effects and potential threshold for regulating DEE levels in an occupational setting.

This study assesses the effects of long-term exposure to ambient air pollutants on inflammatory response and lung function. We selected 390 male coke oven workers with exposure to polycyclic aromatic hydrocarbons (PAHs) and fine particulate matter (PM2.5) and 115 control workers. The average duration in the exposed group was 9.10 years. The total amount of PAHs was more enriched in PM2.5 which collected from the coke oven workshops compared with the control areas. Correspondingly, the internal PAHs exposure indicated by urinary 1-hydroxypyrene (1-OHP) in the exposure group increased 25.7-fold compared to that of the control group. Moreover, the increasing level of urinary 1-OHP was associated with the decrease of forced expiratory volume in 1 s to forced vital capacity ratio (FEV1/FVC). In non-current smokers of exposure group, inverse correlation of 1-OHP with FEV1/FVC was also found. Particularly, an exposure duration-dependent decline in FEV1/FVC and mean forced expiratory flow between 25% and 75% of f...

Background: Exposure to fine particulate matter (PM2.5) pollution is associated with increased morbidity and mortality from respiratory diseases. However, few population-based studies have been conducted to assess the alterations in circulating pulmonary proteins due to long-term PM2.5 exposure. Methods: We designed a two-stage study. In the first stage (training set), we assessed the associations between PM2.5 exposure and levels of pulmonary damage markers (CC16, SP-A and SP-D) and lung function in a coke oven emission (COE) cohort with 558 coke plant workers and 210 controls. In the second stage (validation set), significant initial findings were validated by an independent diesel engine exhaust (DEE) cohort with 50 DEE exposed workers and 50 controls. Results: Serum CC16 levels decreased in a dose response manner in association with both external and internal PM2.5 exposures in the two cohorts. In the training set, serum CC16 levels decreased with increasing duration of occupational PM2.5 exposure history. An interquartile range (IQR) (122.0μg/m3) increase in PM2.5 was associated with a 5.76% decrease in serum CC16 levels, whereas an IQR (1.06μmol/mol creatinine) increase in urinary 1-hydroxypyrene (1-OHP) concentration was associated with a 5.36% decrease in serum CC16 levels in the COE cohort. In the validation set, the concentration of serum CC16 in the PM2.5 exposed group was 22.42% lower than that of the controls and an IQR (1.24μmol/mol creatinine) increase in urinary 1-OHP concentration was associated with a 12.24% decrease in serum CC16 levels in the DEE cohort. Conclusions: Serum CC16 levels may be a sensitive marker for pulmonary damage in populations with high PM2.5 exposure. Keywords: Fine particulate matter, Pulmonary injury, Club cell protein, Surfactant protein A, Surfactant protein D, 1-Hydroxypyren

Diesel exhaust (DE) as the major source of vehicle-emitted particle matter in ambient air impairs lung function. The objectives were to assess the contribution of local (eg, the fraction of exhaled nitric oxide [FeNO] and serum Club cell secretory protein [CC16]) and systemic (eg, serum C-reaction protein [CRP] and interleukin-6 [IL-6]) inflammation to DE-induced lung function impairment using a unique cohort of diesel engine testers (DETs, n = 137) and non-DETs (n = 127), made up of current and noncurrent smokers. Urinary metabolites, FeNO, serum markers, and spirometry were assessed. A 19% reduction in CC16 and a 94% increase in CRP were identified in DETs compared with non-DETs (all p values

The efficacy of traditional tablets, drop pills and soft capsules of bergenin is far lower than expected. Therefore, bergenin was modified in this paper to connect with amino polylactic acid, a kind of biodegradable material, for chemical immobilization. The bergenin-amino PLA thus obtained was controllable with small molecular weight and excellent thermal stability. Its release in vitro could be extended with the increase in molecular weight. According to tests of biological compatibility and anti-tumor in vitro, bergenin-amino PLA at a proportion of 1 to 100 was characterized by better biological compatibility and lower cytotoxicity than control group at a concentration of 0.4 μ g/m L. The chemical immobilization of bergenin not only provides patients with an excellent way of drug administration but lays a good foundation for sustained drug release.

Trichloroethylene (TCE) -induced hypersensitivity syndrome (TIHS) is a potentially life-threatening disease. Several genetic susceptibility biomarkers have been found to be associated with TIHS, and this systematic prospective study has been conducted to evaluate the utility of these genetic susceptibility biomarkers in preventing the disease.The newly hired TCE-exposed workers were recruited from March 2009 to October 2010.Among 1651 workers, 158 (9.57%) were found to carry theProspective

We demonstrate a maximum gain of 4.6 dB at a signal wavelength of 5.28 μm in a 4.1 μm resonantly pumped Pr3+-doped selenide-based chalcogenide glass fibre amplifier of length 109 mm, as well as a new signal excited-stated absorption (ESA) at signal wavelengths around 5.5 μm. This work to the best of our knowledge is the first experimental demonstration of gain at mid-infrared (MIR) wavelengths in a Pr3+-doped chalcogenide fibre amplifier. The signal ESA of the fibre is attributed to the transition 3H6 → (3F4, 3F3) after the pump ESA (3H5 → 3H6) at a pump wavelength of 4.1 μm, which absorbs the MIR signal at wavelengths of 5.37, 5.51 and 5.57 μm, and so spoils the amplifier’s performance at these wavelengths. Thus, this signal ESA should be suppressed in a resonantly pumped Pr3+-doped selenide-based chalcogenide fibre amplifier.

In this contribution it is shown that broadband emission stretching from 2000 nm up to 6000 nm can be achieved when using selenide-chalcogenide glass. It is also shown experimentally that by appropriate selection of pumping wavelengths the shape of the output spectrum can be varied to suit a particular application.

We demonstrate a maximum gain of 4.6 dB at a signal wavelength of 5.28 μm in a 4.1 μm resonantly pumped Pr3+-doped selenide-based chalcogenide glass fibre amplifier of length 109 mm, as well as a new signal excited-stated absorption (ESA) at signal wavelengths around 5.5 μm. This work to the best of our knowledge is the first experimental demonstration of gain at mid-infrared (MIR) wavelengths in a Pr3+-doped chalcogenide fibre amplifier. The signal ESA of the fibre is attributed to the transition 3H6 → (3F4, 3F3) after the pump ESA (3H5 → 3H6) at a pump wavelength of 4.1 μm, which absorbs the MIR signal at wavelengths of 5.37, 5.51 and 5.57 μm, and so spoils the amplifier’s performance at these wavelengths. Thus, this signal ESA should be suppressed in a resonantly pumped Pr3+-doped selenide-based chalcogenide fibre amplifier.

We report a multiwavelength mid-infrared laser based on intracavity difference frequency generation in an MgO-doped periodically poled LiNbO3 optical parametric oscillator, which was pumped by a dual-wavelength fiber MOPA consisting of two parts: dual-wavelength seed and power amplifier. The maximum output power of the linearly polarized pump laser was 65.3 W, and the wavelengths were 1060 and 1080 nm. Three idler emissions with different wavelengths of 3127, 3303 and 3346 nm were obtained under the maximum pump power, and the total idler output reached 7.38 W, indicating a 15% pump-to-idler slope efficiency. The signal laser generated in the experiment had two wavelengths, which were 1594 and 1604 nm under the maximum pump power. Three nonlinear progresses occurred in the experiment, two of them being optical parametric oscillation and the one left being difference frequency generation.

The experimental study of frequency down-conversion processof a dual-wavelength fiber laser by using an MgO:PPLN nonlinear crystal was presented. The dual-wavelength fiber laser was a home-made linearly polarized fiber laser with a maximal output power of 74.1 W at 1060 nm and 1080 nm. A total idler output power of 6.36 W with dual idler-waves at 3125 nm and 3323 nm was obtained. The corresponding pump-to-idler slope efficiency was 11.4%. In the experiment, only one signal wavelength of 1603 nm was observed, which indicated that only one optical parametric oscillation occurred while the other pump laser was contributed to the intra-cavity difference frequency generation (DFG) process. This work provides an effective approach to generate dual-wavelength mid-infrared (MIR) lasers for its features of convenience and controllability.

The International Agency for Research on Cancer has classified carbon black (CB) as a possible (Group 2B) human carcinogen. Given that most CB manufacturing processes result in the emission of various types of chemicals, it is uncertain if the adverse health effects that have been observed in CB-exposed workers are related to CB specifically or are due to other exposures. To address this issue, we conducted a cross-sectional molecular epidemiology study in China of 106 male factory workers who were occupationally exposed to pure CB and 112 unexposed male workers frequency-matched by age and smoking status from the same geographic region. Repeated personal exposure measurements were taken in workers before biological sample collection. Peripheral blood from all workers was used for the complete blood cell count and lymphocyte subsets analysis. Compared to unexposed workers, eosinophil counts in workers exposed to CB were increased by 30.8% (P = 0.07) after adjusting for potential confounders. When stratified by smoking status, statistically significant differences in eosinophils between CB exposed and unexposed workers were only present among never smokers (P = 0.040). Smoking is associated with alterations in various cell counts; however, no significant interaction between CB exposure and smoking status for any cell counts was observed. Given that inflammation, characterized in part by elevated eosinophils in peripheral blood, may be associated with increased cancer risk, our findings provide new biologic insights into the potential relationship between CB exposure and lung carcinogenesis. Environ. Mol. Mutagen., 2016. © 2016 Wiley Periodicals, Inc.

Diesel engine exhaust (DEE) was found to induce lipid peroxidation (LPO) in animal exposure studies. LPO is a class of oxidative stress and can be reflected by detecting the levels of its production, such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), and etheno-DNA adducts including 1,N(6)-etheno-2'-deoxyadenosine (ɛdA) and 3,N(4)-etheno-2'-deoxycytidine (ɛdC). However, the impact of DEE exposure on LPO has not been explored in humans. In this study, we evaluated urinary MDA, 4-HNE, ɛdA, and ɛdC levels as biomarkers of LPO among 108 workers with exclusive exposure to DEE and 109 non-DEE-exposed workers. Results showed that increased levels of urinary MDA and ɛdA were observed in subjects occupationally exposed to DEE before and after age, body mass index (BMI), smoking status, and alcohol use were adjusted (all p 0.001). There was a statistically significant relationship between the internal exposure dose (urinary ΣOH-PAHs) and MDA, 4-HNE, and ɛdA (all p 0.001). Furthermore, significant increased relations between urinary etheno-DNA adduct and MDA, 4-HNE were observed (all p 0.05). The findings of this study suggested that the level of LPO products (MDA and ɛdA) was increased in DEE-exposed workers, and urinary MDA and ɛdA might be feasible biomarkers for DEE exposure. LPO induced DNA damage might be involved and further motivated the genomic instability could be one of the pathogeneses of cancer induced by DEE-exposure. However, additional investigations should be performed to understand these observations.

To estimate the benchmark dose( BMD) of the reproduction /developmental toxicity screening test in rats and compare with the non-observed adverse effect level( NOAEL).A total of 120 SD rats were divided into 4 groups and feed with nitrile compound at 0, 12. 5, 50, 200 mg/kg BW for females and 0, 10, 40, 150 mg/kg BW for males, respectively. Rats were orally dosed with the substance for a period of 54 days. The toxic signs, body weight, food consumption, organ weight, organ weight coefficient and pathological lesion of genital organs of parent rats, and the number of live and dead births, litter weight and abnormalities were observed. The results was analyzed and estimated by benchmark dose method by software of BMDS 2. 6. The lower confidence limit on the benchmark dose( BMDL) can be obtained to calculate the reference dose.After 1, 2, 5 and 6 week administration, the daily food consumption of female rats in high-dose group(( 16. 39 ± 0. 75), ( 16. 57 ± 0. 24), ( 43. 65 ± 1. 94) and( 31. 18 ± 6. 93) g), decreased significantly, compared with control group(( 20. 79 ± 0. 11), ( 18. 30 ± 0. 87), ( 46. 20 ± 1. 90) and( 43. 57 ± 10. 67) g)( P0. 01). The body weight of 20 days pregnant rats in high-dose group(( 353. 67 ±29. 73) g), significantly decreased, compared with control group(( 389. 83 ± 29. 46) g)( P0. 01). The litter weight of live pups at day 0(( 64. 97 ± 37. 75) g) and day 4( 108. 66 ± 62. 67) g) in high-dose group decreased obviously, compared with control group(( 94. 39 ± 23. 00) g, ( 156. 37 ± 29. 06) g)( P0. 05). The implantation loss rates increased in medium and high-dose groups( 19. 6% and 47. 0%) with significant difference, compared with control group( 5. 7%)( P0. 01). The key toxic effect was implantation loss and NOAEL of the chemical was 12. 5 mg/kg BW. The BMDL was 17. 8mg/kg BW, from the nested data of implantation loss.In the reproduction /developmental toxicity screening test, the reference dose obtained from BMD method is17. 8 mg/kg BW.

This study assesses the effects of long-term exposure to ambient air pollutants on inflammatory response and lung function. We selected 390 male coke oven workers with exposure to polycyclic aromatic hydrocarbons (PAHs) and fine particulate matter (PM

Etheno-DNA adducts are biomarkers for assessing oxidative stress. In this study, the aim was to detect the level of etheno-DNA adducts and explore the relationship between the etheno-DNA adducts and genotoxicity biomarkers of the diesel engine exhaust (DEE)-exposed workers. We recruited 86 diesel engine testing workers with long-term exposure to DEE and 99 non-DEE-exposed workers. The urinary mono-hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) and etheno-DNA adducts (edA and edC) were detected by HPLC-MS/MS and UPLC-MS/MS, respectively. Genotoxicity biomarkers were also evaluated by comet assay and cytokinesis-block micronucleus assay. The results showed that urinary edA was significantly higher in the DEE-exposed workers (p

In this Letter, we report, for the first time to our knowledge, on a continuous-wave, singly resonant optical parametric oscillator using an MgO: PPLN crystal pumped by an all-fiberized master-oscillator power amplifier structured amplified random fiber laser. An idler output power of 2.46 W at 3752 nm is achieved with excellent beam quality, and the corresponding pump-to-idler conversion efficiency is 9.6% at room temperature. The idler output power exhibits a peak-to-peak power stability better than 12.7%, and the corresponding standard deviation is better than 3.6% RMS in about 20 min at the maximum output power. Meanwhile, other characteristics of the generated signal and idler laser are studied in detail and not only offered an effective guide in the research of optical parametric processes in the case of a continuous spectrum, but also broadened the range of random fiber laser applications.

The efficacy of bergenin prepared with osmotic-pump-controlled release is much lower than expected. In this study, biodegradable polylactic acid is used to modify bergenin and immobilize it with chemical methods. Bergenin-PLA obtained by this method has low molecular weight and good thermal stability, as well as prolonged in vitro release time along with increased molecular weight. Biocompatibility tests and in vitro antitumor tests showed that bergenin-PLA at a ratio of 1:30 has good biological properties and low cytotoxicity at t three concentrations, and its antitumor activity was significantly increased compared to bergenin. The chemical immobilization of bergenin not only provides a good mode of administration for patients but also provides a good foundation for the sustained release of drugs over time.

Total alkaloids of Alstonia scholaris leaves (ASAs) are extracted from the lamp leaves, which have positive anti-inflammatory activity and remarkable effects in treating bronchitis. Due to its short half-life, we used a degradable mPEG-PLA to physically encapsulate the total alkali of the lamp stage, and prepared a sustained-release microsphere by double-emulsion method. The ASAs-loaded mPEG10000-PLA microspheres were screened for better performance by testing the morphology, average particle size, embedding rate and drug loading of different molecular weight mPEG-PLA microspheres, which can stably and continuously release for 15 days at 37 &deg, C. The results of cytotoxicity and blood compatibility indicated that the drug-loaded microspheres have beneficial biocompatibility. Animal experiments showed that the drug-loaded microspheres had a beneficial anti-inflammatory effect. These results all indicated that mPEG-PLA is a controlled release carrier material suitable for ASAs.

In this contribution, a comprehensive experimental study of photoluminescence from Pr3+/Dy3+ co-doped selenide-chalcogenide multimode fiber samples is discussed. The selenide-chalcogenide multimode fiber samples co-doped with 500 ppm of Pr3+ ions and 500 ppm of Dy3+ ions are prepared using conventional melt-quenching. The main objective of the study is the analysis of the pumping wavelength selection on the shape of the output spectrum. For this purpose, the Pr3+/Dy3+ co-doped selenide-chalcogenide multimode fiber samples are illuminated at one end using pump lasers operating at the wavelengths of 1.32 µm, 1.511 µm and 1.7 µm. The results obtained show that the Pr3+/Dy3+ ion co-doped selenide-chalcogenide multimode fiber emits photoluminescence spanning from 2 µm to 6 µm. Also it is demonstrated that, by varying the output power and wavelength of the pump sources, the spectral shape of the emitted luminescence can be modified to either reduce or enhance the contribution of radiation within a particular wavelength band. The presented results confirm that Pr3+/Dy3+ co-doped selenide-chalcogenide multimode fiber is a good candidate for the realization of broadband spontaneous emission fiber sources with shaped output spectrum for the mid-infrared wavelength region.

Recently, the concept of random fiber lasers has attracted a great deal of attention for its feature to generate incoherent light without a traditional laser resonator, which is free of mode competition and insure the stationary narrow-band continuous modeless spectrum. In this Letter, we reported the first, to the best of our knowledge, optical parametric oscillator (OPO) pumped by an amplified 1070 nm random fiber laser (RFL), in order to generate stationary mid-infrared (mid-IR) laser. The experiment realized a watt-level laser output in the mid-IR range and operated relatively stable. The use of the RFL seed source allowed us to take advantage of its respective stable time-domain characteristics. The beam profile, spectrum and time-domain properties of the signal light were measured to analyze the process of frequency down-conversion process under this new pumping condition. The results suggested that the near-infrared (near-IR) signal light ‘inherited’ good beam performances from the pump light. Those would be benefit for further develop about optical parametric process based on different pumping circumstances.

Bmi-1, the first functionally identified polycomb gene family member, plays critical roles in cell cycle regulation, cell immortalization, and cell senescence. Bmi-1 is involved in the development and progression of carcinomas and is a potent target for cancer therapy. One important pathway regulated by Bmi-1 is that involving two cyclin-dependent kinase inhibitors, p16(Ink4a) and p19(Arf), as Bmi-1 represses the INK4a locus on which they are encoded. A close correlation between the up-regulation of Bmi-1 and down-regulation of p16 has been demonstrated in various tumors; however, how Bmi-1 regulates p16 expression is not clear. In this study, we revealed that Bmi-1 regulates the expression of p16 by binding directly to the Bmi-1-responding element (BRE) within the p16 promoter. The BRE resided at bp -821 to -732 upstream of the p16 ATG codon. BRE alone was sufficient to allow Bmi-1-mediated regulation of the CMV promoter. Bmi-1 typically functions by forming a complex with Ring2; however, regulation of p16 was independent of Ring2. Chromatin immunoprecipitation sequencing of Bmi-1-precipitated chromatin DNA revealed that 1536 genes were targeted by Bmi-1, including genes involved in tissue-specific differentiation, cell cycle, and apoptosis. By analyzing the binding sequences of these genes, we found two highly conserved Bmi-1-binding motifs, which were required for Bmi-1-mediated p16 promoter regulation. Taken together, our results revealed the molecular mechanism of Bmi-1-mediated regulation of the p16 gene, thus providing further insights into the functions of Bmi-1 as well as a sensitive high-throughput platform with which to screen Bmi-1-targeted small molecules for cancer therapy.

The International Agency for Research on Cancer has classified carbon black (CB) as a possible (Group 2B) human carcinogen. Given that most CB manufacturing processes result in the emission of various types of chemicals, it is uncertain if the adverse health effects that have been observed in CB-exposed workers are related to CB specifically or are due to other exposures. To address this issue, we conducted a cross-sectional molecular epidemiology study in China of 106 male factory workers who were occupationally exposed to pure CB and 112 unexposed male workers frequency-matched by age and smoking status from the same geographic region. Repeated personal exposure measurements were taken in workers before biological sample collection. Peripheral blood from all workers was used for the complete blood cell count and lymphocyte subsets analysis. Compared to unexposed workers, eosinophil counts in workers exposed to CB were increased by 30.8% (P = 0.07) after adjusting for potential confounders. When stratified by smoking status, statistically significant differences in eosinophils between CB exposed and unexposed workers were only present among never smokers (P = 0.040). Smoking is associated with alterations in various cell counts; however, no significant interaction between CB exposure and smoking status for any cell counts was observed. Given that inflammation, characterized in part by elevated eosinophils in peripheral blood, may be associated with increased cancer risk, our findings provide new biologic insights into the potential relationship between CB exposure and lung carcinogenesis. Environ. Mol. Mutagen. 57:589-604, 2016. © 2016 Wiley Periodicals, Inc.