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The aim of the study was to evaluate the risk and threshold doses of lens opacity among residents exposed to low-dose radiation. Residents aged ≥45 years were recruited from a high natural background radiation (HNBR) area in Yangjiang City and a control area selected from nearby Enping City. Lens opacities (LOPs) were classified according to the Lens Opacities Classification System (LOCS) III system. Face-to-face interviews were conducted to collect information on lifestyles, migration and medical history. Life-time cumulative doses were estimated using gender, age, occupancy factors and environmental radiation doses received indoors and outdoors. Logistic regression analyses were conducted to estimate the dose response and determine thresholds. In the HNBR area, among 479 study participants, 101 (21.1%), 245(51.1%) and 23 cases (4.8%), respectively, of cortical, nuclear and posterior subcapsular (PSC) LOPs were found. In the control area, those types of LOPs were identified among 58 cases (12.6%), 206 cases (51.2%) and 6 cases (1.3%) of 462 examinees, respectively. Cumulative eye lens dose was estimated to be 189.5 ± 36.5 mGy in the HNBR area. Logistic analyses gave odds ratios at 100 mGy of 1.26 [95% confidence interval (CI) 1.00–1.60], 0.81 (95% CI 0.64–1.01) and 1.73 (95% CI 1.05–2.85) for cortical, nuclear and PSC LOPs, respectively. For cortical LOPs, a logistic analysis with a threshold dose gave a threshold estimate of 140 mGy (90% CI 110–160 mGy). The results indicated that population exposed to life-time, low-dose-rate environmental radiation was at an elevated risk of cortical and PSC LOPs. A statistically significant threshold dose was obtained for cortical LOPs and no threshold dose for PSC LOPs.

High mobility group box 1 (HMGB1) has been known to involve in the pathogenesis of many inflammatory diseases. The aim of this study was to establish animal model of acute rhinosinusitis (ARS), and determine whether ethyl pyruvate (EP) attenuate inflammatory response of sinonasal mucosa by inhibiting HMGB1 in ARS animals. Thirty-six Sprague Dawley (SD) rat were used as follows: six normal controls without intervention (group 1); thirty rats were used for establishment of ARS rats model by nasal insertion of Merocel sponge, and model rats without any treatments (group 2), treated with nasal drops of sterile saline (group 3), 10 μl EP (group 4), and 20 μl EP (group 5), twice a day for 5 days, respectively. Bacterial culture was done regularly and the main bacterial strains were identified using matrix-assisted laser desorption/ionization time of flight mass spectrometry. HMGB1 expression in sinonasal mucosa was detected by immunohistochemistry and RT-PCR. Serum levels of HMGB1, IL-6, and TNF-α were determined by ELISA. Data from 29 of 36 rats that had completed research were analyzed. Bacterial colony formation unit (CFU) of nasal secretion was significantly higher in each group of ARS rats compared with controls (p < 0.001). ARS rats treated with EP had only slightly decreased CFU, but significantly attenuated inflammatory response of sinonasal mucosa and decreased HMGB1 expression compared to those treated with saline alone (p < 0.001). Serum levels of HMGB1, IL-6 and TNF-α were significantly higher in ARS rats compared to controls, and decreased by EP treatments (p < 0.001). Nasal sponge packing led to acute inflammatory response of nasal sinus in rats, and increased the expression of HMGB1, IL-6, and TNF-α. Nasal drops with EP could attenuate the inflammation of sinonasal mucosa through inhibiting the expression of HMGB1, IL-6 and TNF-α in ARS rats.

Background Arsenic (As) with various chemical forms, including inorganic arsenic and organic arsenic, is the most prevalent water and environmental toxin. This metalloid occurs worldwide and many of its forms, especially arsenite [As(III)], cause various diseases including cancer. Organification of arsenite is an effective way for organisms to cope with arsenic toxicity. Microbial communities are vital contributors to the global arsenic biocycle and represent a promising way to reduce arsenite toxicity. Methods Brevundimonas sp. M20 with arsenite and roxarsone resistance was isolated from aquaculture sewage. The arsHRNBC cluster and the metRFHH operon of M20 were identified by sequencing. The gene encoding ArsR/methyltransferase fusion protein, arsR M , was amplified and expressed in Escherichia coli BL21 (DE3), and this strain showed resistance to arsenic in the present of 0.25–6 mM As(III), aresenate, or pentavalent roxarsone. The methylation activity and regulatory action of ArsR M were analyzed using Discovery Studio 2.0, and its functions were confirmed by methyltransferase activity analysis and electrophoretic mobility shift assays. Results The minimum inhibitory concentration of the roxarsone resistant strain Brevundimonas sp. M20 to arsenite was 4.5 mM. A 3,011-bp arsenite resistance ars cluster arsHRNBC and a 5649-bp methionine biosynthesis met operon were found on the 3.315-Mb chromosome. Functional prediction analyses suggested that ArsR M is a difunctional protein with transcriptional regulation and methyltransferase activities. Expression of ArsR M in E. coli increased its arsenite resistance to 1.5 mM. The arsenite methylation activity of ArsR M and its ability to bind to its own gene promoter were confirmed. The As(III)-binding site (ABS) and S -adenosylmethionine-binding motif are responsible for the difunctional characteristic of ArsR M . Conclusions We conclude that ArsR M promotes arsenite methylation and is able to bind to its own promoter region to regulate transcription. This difunctional characteristic directly connects methionine and arsenic metabolism. Our findings contribute important new knowledge about microbial arsenic resistance and detoxification. Future work should further explore how ArsR M regulates the met operon and the ars cluster.

The inhibitory receptor T-cell immunoglobulin and mucin domain-3 (Tim-3) has emerged as a critical regulator of the T-cell dysfunction that develops in chronic viral infections and cancers. However, little is known regarding the signalling pathways that drive Tim-3 expression. Here, we demonstrate that interleukin (IL)-27 induces nuclear factor, interleukin 3 regulated (NFIL3), which promotes permissive chromatin remodelling of the Tim-3 locus and induces Tim-3 expression together with the immunosuppressive cytokine IL-10. We further show that the IL-27/NFIL3 signalling axis is crucial for the induction of Tim-3 in vivo . IL-27-conditioned T helper 1 cells exhibit reduced effector function and are poor mediators of intestinal inflammation. This inhibitory effect is NFIL3 dependent. In contrast, tumour-infiltrating lymphocytes from IL-27R −/− mice exhibit reduced NFIL3, less Tim-3 expression and failure to develop dysfunctional phenotype, resulting in better tumour growth control. Thus, our data identify an IL-27/NFIL3 signalling axis as a key regulator of effector T-cell responses via induction of Tim-3, IL-10 and T-cell dysfunction. Tim-3 is an inhibitory molecule that suppresses T-cell responses. Here the authors show that the cytokine IL-27, acting through the transcription factor NFIL3, induces Tim-3 in vivo , and that IL-27-conditioned Th1 cells have poor effector function.

Presently, in the context of the novel coronavirus pneumonia epidemic, several antibiotics are overused in hospitals, causing heavy pressure on the hospital’s wastewater treatment process. Therefore, developing stable, safe, and efficient hospital wastewater treatment equipment is crucial. Herein, a bench-scale electrooxidation equipment for hospital wastewater was used to evaluate the removal effect of the main antibiotic levofloxacin (LVX) in hospital wastewater using response surface methodology (RSM). During the degradation process, the influence of the following five factors on total organic carbon (TOC) removal was discussed and the best reaction condition was obtained: current density, initial pH, flow rate, chloride ion concentration, and reaction time of 39.6 A/m2, 6.5, 50 mL/min, 4‰, and 120 min, respectively. The TOC removal could reach 41% after a reaction time of 120 min, which was consistent with the result predicted by the response surface (40.48%). Moreover, the morphology and properties of the electrode were analyzed. The degradation pathway of LVX was analyzed using high-performance liquid chromatography–mass spectrometry (LC–MS). Subsequently, the bench-scale electrooxidation equipment was changed into onboard-scale electrooxidation equipment, and the onboard-scale equipment was promoted to several hospitals in Dalian.

Arsenic (As) with various chemical forms, including inorganic arsenic and organic arsenic, is the most prevalent water and environmental toxin. This metalloid occurs worldwide and many of its forms, especially arsenite [As(III)], cause various diseases including cancer. Organification of arsenite is an effective way for organisms to cope with arsenic toxicity. Microbial communities are vital contributors to the global arsenic biocycle and represent a promising way to reduce arsenite toxicity. Brevundimonas sp. M20 with arsenite and roxarsone resistance was isolated from aquaculture sewage. The arsHRNBC cluster and the metRFHH operon of M20 were identified by sequencing. The gene encoding ArsR/methyltransferase fusion protein, arsR.sup.M, was amplified and expressed in Escherichia coli BL21 (DE3), and this strain showed resistance to arsenic in the present of 0.25-6 mM As(III), aresenate, or pentavalent roxarsone. The methylation activity and regulatory action of ArsR.sup.M were analyzed using Discovery Studio 2.0, and its functions were confirmed by methyltransferase activity analysis and electrophoretic mobility shift assays. The minimum inhibitory concentration of the roxarsone resistant strain Brevundimonas sp. M20 to arsenite was 4.5 mM. A 3,011-bp arsenite resistance ars cluster arsHRNBC and a 5649-bp methionine biosynthesis met operon were found on the 3.315-Mb chromosome. Functional prediction analyses suggested that ArsR.sup.M is a difunctional protein with transcriptional regulation and methyltransferase activities. Expression of ArsR.sup.M in E. coli increased its arsenite resistance to 1.5 mM. The arsenite methylation activity of ArsR.sup.M and its ability to bind to its own gene promoter were confirmed. The As(III)-binding site (ABS) and S-adenosylmethionine-binding motif are responsible for the difunctional characteristic of ArsR.sup.M. We conclude that ArsR.sup.M promotes arsenite methylation and is able to bind to its own promoter region to regulate transcription. This difunctional characteristic directly connects methionine and arsenic metabolism. Our findings contribute important new knowledge about microbial arsenic resistance and detoxification. Future work should further explore how ArsR.sup.M regulates the met operon and the ars cluster.

Mycobacterium smegmatis strain MC2 155 is an attractive model organism for the study of M. tuberculosis and other mycobacterial pathogens, as it can grow well using cholesterol as a carbon resource. However, its global transcriptomic response remains largely unrevealed. In this study, M. smegmatis MC2 155 cultivated in androstenedione, cholesterol and glycerol supplemented media were collected separately for a RNA-Sequencing study. The results showed that 6004, 6681 and 6348 genes were expressed in androstenedione, cholesterol and glycerol supplemented media, and 5891 genes were expressed in all three conditions, with 237 specially expressed in cholesterol added medium. A total of 1852 and 454 genes were significantly up-regulated by cholesterol compared with the other two supplements. Only occasional changes were observed in basic carbon and nitrogen metabolism, while almost all of the genes involved in cholesterol catabolism and mammalian cell entry (MCE) were up-regulated by cholesterol, but not by androstenedione. Eleven and 16 gene clusters were induced by cholesterol when compared with glycerol or androstenedione, respectively. This study provides a comprehensive analysis of the cholesterol responsive transcriptome of M. smegmatis. Our results indicated that cholesterol induced many more genes and increased the expression of the majority of genes involved in cholesterol degradation and MCE in M. smegmatis, while androstenedione did not have the same effect.

Metamorphosis is a critical stage in the adaptive development of amphibians from aquatic to terrestrial animals. Metamorphosis of the Chinese giant salamander is mainly manifested by the loss of external gills with consequent changes in the respiratory pattern. The loss of the external gill is regulated by the pathway of apoptosis in which caspase genes are the key factors. This study cloned and expressed the caspase 3/7/8/9 genes of the Chinese giant salamander. The main results were as follows: the complete open reading frames (ORFs) were 885 bp, 960 bp, 1461 bp and 1279 bp, respectively; caspase 3/7/8/9 genes all contained the CASc domain, and most of the motifs were located in CASc domain; and caspase 8 possessed two DED structural domains and caspase 9 possessed a CARD structural domain. Furthermore, results from the tissue distribution analysis indicated that caspase 3/7/8/9 genes were all significantly expressed in the external gill, and at 9 and 10 months of age (MOA), which is the peak time for the loss, the EXPRESSION level of caspase 3/7/8/9 genes was obviously high, which was consistent with the histological result. Moreover, the loss of external gills of the Chinese giant salamander may result from activation of both the apoptosis-related death receptor pathway and the mitochondrial pathway. Finally, it was discovered that thyroid hormone (TH) treatment could both advance the time point at which the external gills of the Chinese giant salamander began to degenerate and shorten this process. Interestingly, at the peak of its metamorphosis (9 MOA), the Chinese giant salamander further accelerated the metamorphosis rate of TH treatment, which suggested a promotive effect on the loss of external gills via the superimposition of the exogenous TH and caspase genes. The study of caspase genes in this experiment was conducive to understanding the mechanism of external gill loss in the Chinese giant salamander, as well as improving our understanding of the metamorphosis development of some Caudata species.

Metamorphosis is a critical stage in the adaptive development of amphibians from aquatic to terrestrial animals. Metamorphosis of the Chinese giant salamander is mainly manifested by the loss of external gills with consequent changes in the respiratory pattern. The loss of the external gill is regulated by the pathway of apoptosis in which caspase genes are the key factors. This study cloned and expressed the caspase 3/7/8/9 genes of the Chinese giant salamander. The main results were as follows: the complete open reading frames (ORFs) were 885 bp, 960 bp, 1461 bp and 1279 bp, respectively; caspase 3/7/8/9 genes all contained the CASc domain, and most of the motifs were located in CASc domain; and caspase 8 possessed two DED structural domains and caspase 9 possessed a CARD structural domain. Furthermore, results from the tissue distribution analysis indicated that caspase 3/7/8/9 genes were all significantly expressed in the external gill, and at 9 and 10 months of age (MOA), which is the peak time for the loss, the EXPRESSION level of caspase 3/7/8/9 genes was obviously high, which was consistent with the histological result. Moreover, the loss of external gills of the Chinese giant salamander may result from activation of both the apoptosis-related death receptor pathway and the mitochondrial pathway. Finally, it was discovered that thyroid hormone (TH) treatment could both advance the time point at which the external gills of the Chinese giant salamander began to degenerate and shorten this process. Interestingly, at the peak of its metamorphosis (9 MOA), the Chinese giant salamander further accelerated the metamorphosis rate of TH treatment, which suggested a promotive effect on the loss of external gills via the superimposition of the exogenous TH and caspase genes. The study of caspase genes in this experiment was conducive to understanding the mechanism of external gill loss in the Chinese giant salamander, as well as improving our understanding of the metamorphosis development of some Caudata species.

Mycobacterium smegmatis strain MC super(2) 155 is an attractive model organism for the study of M. tuberculosis and other mycobacterial pathogens, as it can grow well using cholesterol as a carbon resource. However, its global transcriptomic response remains largely unrevealed. In this study, M. smegmatis MC super(2) 155 cultivated in androstenedione, cholesterol and glycerol supplemented media were collected separately for a RNA-Sequencing study. The results showed that 6004, 6681 and 6348 genes were expressed in androstenedione, cholesterol and glycerol supplemented media, and 5891 genes were expressed in all three conditions, with 237 specially expressed in cholesterol added medium. A total of 1852 and 454 genes were significantly up-regulated by cholesterol compared with the other two supplements. Only occasional changes were observed in basic carbon and nitrogen metabolism, while almost all of the genes involved in cholesterol catabolism and mammalian cell entry (MCE) were up-regulated by cholesterol, but not by androstenedione. Eleven and 16 gene clusters were induced by cholesterol when compared with glycerol or androstenedione, respectively. This study provides a comprehensive analysis of the cholesterol responsive transcriptome of M. smegmatis. Our results indicated that cholesterol induced many more genes and increased the expression of the majority of genes involved in cholesterol degradation and MCE in M.smegmatis, while androstenedione did not have the same effect.