Abstract. Extremely severe and persistent haze occurred in January 2013 over eastern and northern China. The record-breaking high concentrations of fine particulate matter (PM 2.5 ) of more than 700 µg m −3 on hourly average and the persistence of the episodes have raised widespread, considerable public concerns. During that period, 7 of the top 10 polluted cities in China were within the Hebei Province. The three cities in southern Hebei (Shijiazhuang, Xingtai, and Handan) have been listed as the top three polluted cities according to the statistics for the first half of the year 2013. In this study, the Mesoscale Modeling System Generation 5 (MM5) and the Models-3/Community Multiscale Air Quality (CMAQ) modeling system are applied to simulate the 2013 severe winter regional hazes in East Asia and northern China at horizontal grid resolutions of 36 and 12 km, respectively, using the Multi-resolution Emission Inventory for China (MEIC). The source contributions of major source regions and sectors to PM 2.5 concentrations in the three most polluted cities in southern Hebei are quantified by aiming at the understanding of the sources of the severe haze pollution in this region, and the results are compared with December 2007, the haziest month in the period 2001-2010. Model evaluation against meteorological and air quality observations indicates an overall acceptable performance and the model tends to underpredict PM 2.5 and coarse particulate matter (PM 10 ) concentrations during the extremely polluted episodes. The MEIC inventory is proven to be a good estimation in terms of total emissions of cities but uncertainties exist in the spatial allocations of emissions into fine grid resolutions within cities. The source apportionment shows that emissions from northern Hebei and the Beijing-Tianjin city cluster are two major regional contributors to the pollution in January 2013 in Shijiazhuang, compared with those from Shanxi and northern Hebei for December 2007. For Xingtai and Handan, the emissions from northern Hebei and Henan are important. The industrial and domestic sources are the most significant local contributors, and the domestic and agricultural emissions from Shandong and Henan are non-negligible regional sources, especially for Xingtai and Handan. Even in the top two haziest months (i.e., January 2013 and December 2007), a large fraction of PM 2.5 in the three cities may originate from quite different regional sources. These results indicate the importance of establishing a regional joint framework of policymaking and action system to effectively mitigate air pollution in this area, not only over the Beijing-Tianjin-Hebei area, but also surrounding provinces such as Henan, Shandong, and Shanxi.

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BackgroundRecently, the concept of sepsis was redefined by an international task force. This international task force of experts recommended using the quick Sequential Organ Failure Assessment (qSOFA) criteria instead of the systemic inflammatory response syndrome (SIRS) criteria to classify patients at high risk for death. However, the added value of these new criteria in the emergency department (ED) remains unclear. Thus, we performed this meta-analysis to determine the diagnostic accuracy of the qSOFA criteria in predicting mortality in ED patients with infections and compared the performance with that of the SIRS criteria.MethodsPubMed, EMBASE and Google Scholar (up to April 2018) were searched for related articles. A 2 × 2 contingency table was constructed according to mortality and qSOFA score (< 2 and ≥ 2) or SIRS score (< 2 and ≥ 2) in ED patients with infections. Two investigators independently assessed study eligibility and extracted data. We used a bivariate meta-analysis model to determine the prognostic value of qSOFA and SIRS in predicting mortality. We used the I2 index to test heterogeneity. The bivariate random-effects regression model was used to pool the individual sensitivity, specificity, diagnostic odds ratio (DOR), positive likelihood ratio (PLR), and negative likelihood ratio (NLR). The summary receiver operating characteristic curve (SROC) was constructed to assess the overall diagnostic accuracy.ResultsEight studies with a total of 52,849 patients were included. A qSOFA score ≥ 2 was associated with a higher risk of mortality in ED patients with infections, with a pooled risk ratio (RR) of 4.55 (95% CI, 3.38–6.14) using a random-effects model (I2 = 91.1%). A SIRS score ≥ 2 was a prognostic marker of mortality in ED patients with infections, with a pooled RR of 2.75 (95% CI, 1.96–3.86) using a random-effects model (I2 = 89%). When comparing the performance of qSOFA and SIRS in predicting mortality, a qSOFA score ≥ 2 was more specific; however a SIRS score ≥ 2 was more sensitive. The initial qSOFA values were of limited prognostic value in ED patients with infections.ConclusionsA qSOFA score ≥ 2 and SIRS score ≥ 2 are strongly associated with mortality in ED patients with infections. However, it is also clear that qSOFA and SIRS have limitations as risk stratification tools for ED patients with infections.Electronic supplementary materialThe online version of this article (10.1186/s13049-018-0527-9) contains supplementary material, which is available to authorized users.

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To elucidate the genetic effect involved in the premalignant progression of chronic inflammation to cancer, we performed microRNA and mRNA profiling in oral lichen planus (OLP), oral squamous cell carcinoma (OSCC), and normal tissue from the same patients. We demonstrate the involvement of a suppressive microRNA, miR-375, in the regulation of this premalignant progression via KLF5, a transcription factor that modulates the expression of genes contributing to proliferation and apoptosis. We found that miR-375 abundance decreased in tissues with progression from the normal state to OLP and subsequently to OSCC. Restoration of miR-375 by transduction of a synthetic mimic into OSCC cells repressed cellular proliferation and promoted apoptosis, with concomitant down-regulation of KLF5, and vice versa. The direct binding of miR-375 to the 3′-untranslated region of KLF5 was further confirmed. Additionally, Survivin (BIRC5), a target of KLF5, was also regulated by miR-375, explaining the susceptibility of miR-375-mimic transfected cells to apoptosis. Further analysis of clinical specimens suggested that expression of KLF5 and BIRC5 is up-regulated during the progression from inflammation to cancer. Our findings provide novel insights into the involvement of microRNAs in progression of inflammation to carcinoma and suggest a potential early-stage biomarker or therapy target for oral carcinoma.