Allergic conjunctivitis is a common problem that significantly impairs patients’ quality of life. Whether air pollution serves as a risk factor for the development of allergic conjunctivitis remains elusive. In this paper, we assess the relationship between air pollutants and weather conditions with outpatient visits for allergic conjunctivitis. By using a time-series analysis based on the largest dataset ever assembled to date, we found that the number of outpatient visits for allergic conjunctivitis was significantly correlated with the levels of NO2, O3, and temperature, while its association with humidity was statistically marginal. No associations between PM10, PM2.5, SO2, or wind velocity and outpatient visits were seen. Subgroup analyses showed that sex seemed to modify the effects of humidity on outpatient visits for allergic conjunctivitis, but not for NO2, O3, or temperature. People younger than 40 were found to be susceptible to changes of all four parameters, while those older than 40 were only consistently affected by NO2 levels. Our findings revealed that higher levels of ambient NO2, O3, and temperature increase the chances of outpatient visits for allergic conjunctivitis. Ambient air pollution and weather changes may contribute to the worsening of allergic conjunctivitis.

Background The short-term effects of particulate matter (PM) exposure on childhood asthma exacerbation and disease control rate is not thoroughly assessed in Chinese population yet. The previous toxic effects of PM exposure are either based on long-term survey or experimental data from cell lines or mouse models, which also needs to be validated by real-world evidences. Methods We evaluated the short-term effects of PM exposure on asthma exacerbation in a Chinese population of 3106 pediatric outpatientsand disease control rate (DCR) in a population of 3344 children using case-crossover design. All the subjects enrolled are non-hospitalized outpatients. All data for this study were collected from the electronic health record (EHR) in the period between January 1, 2016 and June 30, 2018 in Xiamen, China. Results We found that exposure to PM 2.5 and PM 10 within the past two weeks was significantly associated with elevated risk of exacerbation (OR = 1.049, p < 0.001 for PM 2.5 and OR = 1.027, p < 0.001 for PM 10 ). In addition, exposure to PM 10 was associated with decreased DCR (OR = 0.976 for PM 10 , p < 0.001). Conclusions Our results suggest that exposure to both PM 10 and PM 2.5 has significant short-term effects on childhood asthma exacerbation and DCR, which serves as useful epidemiological parameters for clinical management of asthma risk in the sensitive population. Electronic supplementary material The online version of this article (10.1186/s12887-019-1530-7) contains supplementary material, which is available to authorized users.

The somatic landscape of the cancer genome results from different mutational processes represented by distinct "mutational signatures". Although several mutagenic mechanisms are known to cause specific mutational signatures in cell lines, the variation of somatic mutational activities in patients, which is mostly attributed to somatic selection, is still poorly explained. Here we introduce a quantitative trait, mutational propensity (MP), and describe an integrated method to infer genetic determinants of variations in the mutational processes in 3,566 cancers with specific underlying mechanisms. As a result, we report 2,314 candidate determinants with both significant germline and somatic effects on somatic selection of mutational processes, of which 485 act via cancer gene expression and 1,427 act through the tumor immune microenvironment.These data demonstrate that the genetic determinants of MPs provide complementary information to known cancer driver genes, clonal evolution, and clinical biomarkers.

We evaluated the effects of air pollutants, age, allergic history, family allergic history, treatment, treatment steps, and compliance on uncontrolled childhood asthma in Xiamen, China. The clinical data of children with asthma in the pediatric outpatient department of the First Affiliated Hospital of Xiamen University from January 2016 to June 2018 were analyzed retrospectively. According to the assessment of the patients' outcome including well-controlled, partly-controlled and uncontrolled, 7,211 cases of 3,268 patients were selected. Rank sum test and ordered multi-class logistic regression analysis were used. In the rank sum test, age, allergic history, family allergic history, season, treatment, treatment steps and compliance were found associated with uncontrolled rate (all P < 0.001). Logistic regression analysis showed that PM10, NO2, and SO2 raised uncontrolled-asthma rate (aOR 1.311, aOR 1.281, aOR 1.252, respectively). Older children had lower uncontrolled rate (OR = 0.849, 95% CI: 0.758–0.950), children with higher treatment steps had higher uncontrolled rate (OR = 1.227, 95%CI: 1.040–1.448), and children with better treatment compliance have lower uncontrolled rate (OR = 0.374 95% CI: 0.331–0.424). The order of the uncontrolled rate of asthma from high to low was winter, spring, autumn, and summer. PM10, NO2, SO2, age, season, treatment steps, and treatment compliance have significance for predicting the control rate of childhood asthma in Xiamen, China.

Background: Particulate Matter (PM) is known to cause inflammatory responses in human. Although prior studies verified the immunogenicity of PM in cell lines and animal models, the effectors of PM exposure in the respiratory system and the regulators of the immunogenicity of PM is not fully elucidated. Methods: To identify the potential effector of PM exposure in human respiratory system and to better understand the biology of the immunogenicity of PM, We performed gene-expression profiling of peripheral blood mononuclear cells from 171 heathy subjects in northern China to identify co-expressed gene modules associated with PM exposure. We inferred transcription factors regulating the co-expression and validated the association to Tcell differentiation in both primary T-cells and mice treated with PM. Results: We report two transcription factors, IRF4 and STAT3, as regulators of the gene expression in response to PM exposure in human. We confirmed that the activation of IRF4 and STAT3 by PM is strongly associated with imbalanced differentiation of T-cells in the respiratory tracts in a time-sensitive manner in mouse. We also verified the consequential inflammatory responses of the PM exposure. Moreover, we show that the protein levels of phosphorylated IRF4 and STAT3 increase with PM exposure. Conclusions: Our study suggests the regulatory activities of IRF4 and STAT3 are associated with the Th17-mediated inflammatory responses to PM exposure in the respiratory tracts, which informs the biological background of the immunogenicity of particulate matters.

<p>The clinical information of 60 LUAD patients which received chemotherapy and target therapies.</p>

No abstract

Background Allelic imbalance (AI) in tumors is caused by chromosomal and sub-chromosomal gains and losses. Results We evaluated AI at 109,086 germline exonic SNP loci in four cancer types, and identified a set of SNPs that demonstrate strong tumor allele specificity in AI events. Further analyses demonstrated that these alleles show consistently different frequencies in the cancer population compared to the healthy population and are significantly enriched for predicted protein-damaging variants. Moreover, genes harboring SNPs that demonstrate allele specificity are enriched for cancer-related biological processes and are more likely to be essential in cancer cells. Conclusions In summary, our study provides a unique and complementary method to identify genes and variants that are relevant to carcinogenesis.