SUMMARY:The regulatory mechanism of miRNA induction in response to Mycobacterium tuberculosis (MTB) infection has not been clearly established. Autophagy has recently been identified as an effective way to control intracellular survival of MTB. In the present study, we demonstrate a novel role of miR-30A in the negative regulation of the autophagy-mediated anti-MTB response. We found that overexpression of miR-30A suppresses the elimination of intracellular MTB through the inhibition of autophagy. Furthermore, there was a negative correlation between concentrations of miR-30A and beclin-1 in MTB positive patients and miR-30A expression decreased after anti-TB treatment. Our results indicate that miR-30A plays a key role in immune response against MTB and, therefore, may serve as a potential target for future treatments of tuberculosis infection.

Stack gas emissions were characterized for a steam-generating boiler commonly used in China. The boiler was tested when fired with a newly formulated boiler briquette coal (BB-coal) and when fired with conventional raw coal (R-coal). The stack gas emissions were analyzed to determine emission rates and emission factors and to develop chemical source profiles. A dilution source sampling system was used to collect PM on both Teflon membrane filters and quartz fiber filters. The Teflon filters were analyzed gravimetrically for PM 10 and PM 2.5 mass concentrations and by X-ray fluorescence (XRF) for trace elements. The quartz fiber filters were analyzed for organic carbon (OC) and elemental carbon (EC) using a thermal/optical IMPLICATIONS Source emission data are highly desirable for numerous small and middle-size boilers commonly used in China. This paper presents a database of emission rates and emission factors of PM 10 , PM 2.5 , SO 2 , and CO, as well as elemental source profiles for a typical boiler fired with R-coal and with the newly formulated BB-coal. The database can be used in various applications, such as ambient air quality prediction, source apportionment, and emission inventory development. Important implications of control strategies may be drawn from comparison of the emissions from the two types of coal tested in the study. reflectance technique. Sulfur dioxide was measured using the standard wet chemistry method. Carbon monoxide was measured using an Orsat combustion analyzer.The emission rates of the R-coal combustion (in kg/hr), determined using the measured stack gas concentrations and the stack gas emission rates, were 0.74 for PM 10 , 0.38 for PM 2.5 , 20.7 for SO 2 , and 6.8 for CO, while those of the BB-coal combustion were 0.95 for PM 10 , 0.30 for PM 2.5 , 7.5 for SO 2 , and 5.3 for CO. The fuel-mass-based emission factors (in g/kg) of the R-coal, determined using the emission rates and the fuel burn rates, were 1.68 for PM 10 , 0.87 for PM 2.5 , 46.7 for SO 2 , and 15 for CO, while those of the BB-coal were 2.51 for PM 10 , 0.79 for PM 2.5 , 19.9 for SO 2 , and 14 for CO. The task-based emission factors (in g/ton steam generated) of the R-coal, determined using the fuel-mass-based emission factors and the coal/ steam conversion factors, were 0.23 for PM 10 , 0.12 for PM 2.5 , 6.4 for SO 2 , and 2.0 for CO, while those of the BB-coal were 0.30 for PM 10 , 0.094 for PM 2.5 , 2.4 for SO 2 , and 1.7 for CO. PM 10 and PM 2.5 elemental compositions are also presented for both types of coal tested in the study.

Simple, inexpensive, preformed vanadiumSchiff base complexes were facilely prepared and used in enantioselective sulfoxidation. Both the amount of aqueous H 2 O 2 and reaction time greatly influenced the ee values and yields of chiral sulfoxides. High enantioselectivities (up to 99% ee) and reasonable yields ( > 40%) for various chiral sulfoxides were achieved by combining enantioselective sulfoxidation and appropriate concomitant kinetic resolution.

To assess the effect of the NFKB1 -94ins/del polymorphism on cancer, we conducted a meta-analysis based on 25 studies including 8,750 cases and 9,170 controls. Overall, the -94ins/del polymorphism was associated with cancer risk in the pooled analysis and in Asian population, whereas no association was observed in Caucasian population. Stratified analysis by subtypes of cancer showed that the -94ins/del polymorphism was associated with oral squamous cell carcinoma and ovarian cancer risk, but had no association with colorectal cancer, bladder cancer, and renal cell cancer. Our meta-analysis suggests the NFKB1 -94ins/del polymorphism affects cancer susceptibility, and the association is ethnic-specific.

Helicobacter pylori (H. pylori) infection is the major cause of chronic active gastritis and peptic ulcer disease. Upregulation of IL-17A is associated with H. pylori infection in the gastric mucosa; however, the factors involved in the regulation of interleukin (IL)-17A-induced inflammatory responses in H. pylori-associated gastritis remain unknown. MicroRNAs (miRNAs) serve as key post-transcriptional regulators of gene expression and are associated with the H. pylori infection. The present study aimed to analyze the effects of IL-17A on the expression of miR-146a upon infection with H. pylori, as well as to identify the possible impact of miR-146a dysregulation on the inflammatory response in vivo and in vitro. Reverse transcription-quantitative polymerase chain reaction analysis was used to determine the expression levels of miR-146a in gastric epithelial cells upon IL-17A stimulation. The effects of miR-146a mimics on IL-17A-induced inflammatory responses in SGC-7901 cells were evaluated. The effects of miR-146a mimics on the expression levels of IL-1 receptor-associated kinase 1 (IRAK1) and tumor necrosis factor receptor-associated factor 6 (TRAF6) upon IL-17A treatment were analyzed, and the IL-17A-stimulated inflammation following the silencing of IRAK1 and TRAF6 was observed. In addition, the correlation between miR-146a and IL-17A in human gastric mucosa with H. pylori was examined. The results indicated that IL-17A-induced miR-146a may regulate the inflammatory response during the infection of H. pylori in a nuclear factor-κB-dependent manner. Furthermore, the expression of miR-146a and IL-17A are positively correlated in human gastric mucosa infected with H. pylori. These data suggested that miR-146a may serve as a biomarker or therapeutic target in gastritis therapy.