Evolution of anthropogenic air pollutant emissions in Guangdong Province, China, from 2006 to 2015

Guangdong Province (GD), one of the most prosperous and populous regions in China, still experiences haze events and growing ozone pollution in spite of the substantial air-quality improvement in recent years. Integrated control of fine particulate matter (PM2.5) and ozone in GD calls for a systematic review of historical emissions. In this study, emission trends, spatial variations, source-contribution variations, and reduction potentials of sulfur dioxide (SO2), nitrogen oxides (NO), PM2.5, inhalable particles (PM10), carbon monoxide (CO), ammonia (NH3), and volatile organic compounds (VOCs) in GD from 2006 to 2015 were first examined using a dynamic methodology, taking into account economic development, technology penetration, and emission controls. The relative change rates of anthropogenic emissions in GD during 2006-2015 are -48% for SO2, -0.5% for NO, -16% for PM2.5, -22% for PM10, 13% for CO, 3% for NH3, and 13% for VOCs. The declines of SO2, NO, PM2.5, and PM10 emissions in the whole province mainly resulted from the stringent emission control in the Pearl River delta (PRD) region, where most previous control measures were focused, especially on power plants (SO2 and NO), industrial combustion (SO2, PM2.5, PM10), on-road mobile sources (NO), and dust sources (PM2.5 and PM10). Emissions from other areas (non-PRD, NPRD), nevertheless, remain relatively stable due to the lax control measures and rapidly growing energy consumption. In addition, emission leaks of SO2 and NO from industries are observed from PRD to NPRD in 2010 and 2011. As a result, emissions in NPRD are increasingly important in GD, particularly those from industrial combustion. The contribution of NPRD to the total SO2 emissions in GD, for example, increased from 27% in 2006 to 48% in 2015. On-road mobile sources and solvent use are the two key sources that should receive more effective control measures in GD. Current control-driven emission reductions from on-road mobile sources are neutralized by the substantial growth of the vehicle population, while VOC emissions in GD steadily increase due to the growth of solvent use and the absence of effective control measures. Besides, future work could focus on power plants and industrial combustion in GD and industrial process sources in NPRD, which still have large emission reduction potentials. The historical emission inventory developed in this study not only helps to understand the emission evolution in GD, but also provides robust data to quantify the impact of emission and meteorology variations on air quality and unveil the primary cause of significant air-quality change in GD in the recent decade

CD133-Positive Cells Might Be Responsible for Efficient Proliferation of Human Meningioma Cells

Owing to lack of appropriate model systems, investigations of meningioma biology have come to a stop. In this study, we developed a comprehensive digestion method and defined a culture system. Using this method and system, primary meningioma cells in conditioned suspension medium and a hypoxic environment could be amplified in spheres and were passaged for more than ten generations. Meningioma sphere cells were positive for meningioma cell markers and negative for markers of neural cell types. Importantly, we found the cells expressed the stem cell marker, CD133, but not nestin. All of the tumor sphere cell populations showed a slower degree of cell proliferation than that of human glioma cells and fetal neural stem cells (NSCs). Further studies showed that the proliferative rate was positively correlated with CD133 expression. The higher the CD133 expression, the faster the cell proliferation. With the increase in cell generations, the cell proliferation rate gradually slowed down, and CD133 expression also decreased. Single CD133+ cells rather than CD133− cells could form spheres. Thus, the results above indicated that those cells expressing CD133 in spheres might be stem-like cells, which may be responsible for efficient amplification of human meningioma cells. Decreased expression of CD133 may lead to the failure of long-term passaging

Identification of recurrent USP48 and BRAF mutations in Cushing’s disease

Abstract Cushing’s disease results from corticotroph adenomas of the pituitary that hypersecrete adrenocorticotropin (ACTH), leading to excess glucocorticoid and hypercortisolism. Mutations of the deubiquitinase gene USP8 occur in 35–62% of corticotroph adenomas. However, the major driver mutations in USP8 wild-type tumors remain elusive. Here, we report recurrent mutations in the deubiquitinase gene USP48 (predominantly encoding p.M415I or p.M415V; 21/91 subjects) and BRAF (encoding p.V600E; 15/91 subjects) in corticotroph adenomas with wild-type USP8. Similar to USP8 mutants, both USP48 and BRAF mutants enhance the promoter activity and transcription of the gene encoding proopiomelanocortin (POMC), which is the precursor of ACTH, providing a potential mechanism for ACTH overproduction in corticotroph adenomas. Moreover, primary corticotroph tumor cells harboring BRAF V600E are sensitive to the BRAF inhibitor vemurafenib. Our study thus contributes to the understanding of the molecular mechanism of the pathogenesis of corticotroph adenoma and informs therapeutic targets for this disease

Whole-genome and whole-exome sequencing of bladder cancer identifies frequent alterations in genes involved in sister chromatid cohesion and segregation

Bladder cancer is one of the most common cancers worldwide, with transitional cell carcinoma (TCC) being the predominant form. Here we report a genomic analysis of TCC by both whole-genome and whole-exome sequencing of 99 individuals with TCC. Beyond confirming recurrent mutations in genes previously identified as being mutated in TCC, we identified additional altered genes and pathways that were implicated in TCC. Notably, we discovered frequent alterations in STAG2 and ESPL1, two genes involved in the sister chromatid cohesion and segregation (SCCS) process. Furthermore, we also detected a recurrent fusion involving FGFR3 and TACC3, another component of SCCS, by transcriptome sequencing of 42 DNA-sequenced tumors. Overall, 32 of the 99 tumors (32%) harbored genetic alterations in the SCCS process. Our analysis provides evidence that genetic alterations affecting the SCCS process may be involved in bladder tumorigenesis and identifies a new therapeutic possibility for bladder cancer