Improved technique for measuring the size distribution of black carbon particles in liquid water

<p>We developed an improved technique for measuring the size distribution of black carbon (BC) particles suspended in liquid water to facilitate quantitative studies of the wet deposition of BC. The measurement system, which consists of a nebulizer and a single-particle soot photometer, incorporates two improvements into the system that we developed earlier. First, we extended the upper limit of the detectable BC size from 0.9 μm to about 4.0 μm by modifying the photo-detector for measuring the laser-induced incandescence signal. Second, we introduced a pneumatic nebulizer (Marin-5) with a high extraction efficiency (∼50.0%) that was independent of particle diameter up to 2.0 μm. For BC mass concentrations less than 70 μg L⁻¹, we experimentally showed that the diameters of BC particles did not appreciably change during the Marin-5 extraction process, consistent with theoretical calculations. Finally, we demonstrated by laboratory experiments that the size distributions of ambient BC particles changed little during their growth into cloud droplets under supersaturation of water vapor. Using our improved system, we measured the size distributions of BC particles simultaneously in air and rainwater in Tokyo during summer 2014. We observed that the size distributions of BC particles in rainwater shifted to larger sizes compared with those observed in ambient air, indicating that larger BC particles in air were removed more efficiently by precipitation.</p> <p>Copyright © 2016 American Association for Aerosol Research</p

Proportions for hospital admission in the development and validation cohorts.

<p>Proportions for hospital admission in the development and validation cohorts.</p

Patients’ demographics and laboratory data on ED arrival according to J-ERATO score in the validation cohort.

<p>Patients’ demographics and laboratory data on ED arrival according to J-ERATO score in the validation cohort.</p

Heat-related illness patients’ demographics, prehospital findings, and event characteristics between development and validation cohorts.

<p>Heat-related illness patients’ demographics, prehospital findings, and event characteristics between development and validation cohorts.</p

Logistic regression analysis for prediction of hospital admission in patients with heat-related illness.

<p>Logistic regression analysis for prediction of hospital admission in patients with heat-related illness.</p

Calibration curve comparing the distribution of patients in relation to observed and estimated probability using logistic regression.

<p>Calibration curve comparing the distribution of patients in relation to observed and estimated probability using logistic regression.</p

Patient selection.

<p>Patient selection.</p

Associations of the J-ERATO score with the outcomes in patients with heat-related illness.

<p>Associations of the J-ERATO score with the outcomes in patients with heat-related illness.</p

LATS2 Positively Regulates Polycomb Repressive Complex 2

<div><p>LATS2, a pivotal Ser/Thr kinase of the Hippo pathway, plays important roles in many biological processes. LATS2 also function in Hippo-independent pathway, including mitosis, DNA damage response and epithelial to mesenchymal transition. However, the physiological relevance and molecular basis of these LATS2 functions remain obscure. To understand novel functions of LATS2, we constructed a <i>LATS2</i> knockout HeLa-S3 cell line using TAL-effector nuclease (TALEN). Integrated omics profiling of this cell line revealed that <i>LATS2</i> knockout caused genome-wide downregulation of Polycomb repressive complex 2 (PRC2) and H3K27me3. Cell-cycle analysis revealed that downregulation of PRC2 was not due to cell cycle aberrations caused by <i>LATS2</i> knockout. Not LATS1, a homolog of LATS2, but LATS2 bound PRC2 on chromatin and phosphorylated it. LATS2 positively regulates histone methyltransferase activity of PRC2 and their expression at both the mRNA and protein levels. Our findings reveal a novel signal upstream of PRC2, and provide insight into the crucial role of LATS2 in coordinating the epigenome through regulation of PRC2.</p></div

Long-Term Pancreatic Beta Cell Exposure to High Levels of Glucose but Not Palmitate Induces DNA Methylation within the Insulin Gene Promoter and Represses Transcriptional Activity

<div><p>Recent studies have implicated epigenetics in the pathophysiology of diabetes. Furthermore, DNA methylation, which irreversibly deactivates gene transcription, of the insulin promoter, particularly the cAMP response element, is increased in diabetes patients. However, the underlying mechanism remains unclear. We aimed to investigate insulin promoter DNA methylation in an over-nutrition state. INS-1 cells, the rat pancreatic beta cell line, were cultured under normal-culture-glucose (11.2 mmol/l) or experimental-high-glucose (22.4 mmol/l) conditions for 14 days, with or without 0.4 mmol/l palmitate. DNA methylation of the rat insulin 1 gene (<i>Ins1</i>) promoter was investigated using bisulfite sequencing and pyrosequencing analysis. Experimental-high-glucose conditions significantly suppressed insulin mRNA and increased DNA methylation at all five CpG sites within the <i>Ins1</i> promoter, including the cAMP response element, in a time-dependent and glucose concentration-dependent manner. DNA methylation under experimental-high-glucose conditions was unique to the <i>Ins1</i> promoter; however, palmitate did not affect DNA methylation. Artificial methylation of <i>Ins1</i> promoter significantly suppressed promoter-driven luciferase activity, and a DNA methylation inhibitor significantly improved insulin mRNA suppression by experimental-high-glucose conditions. Experimental-high-glucose conditions significantly increased DNA methyltransferase activity and decreased ten-eleven-translocation methylcytosine dioxygenase activity. Oxidative stress and endoplasmic reticulum stress did not affect DNA methylation of the <i>Ins1</i> promoter. High glucose but not palmitate increased ectopic triacylglycerol accumulation parallel to DNA methylation. Metformin upregulated insulin gene expression and suppressed DNA methylation and ectopic triacylglycerol accumulation. Finally, DNA methylation of the <i>Ins1</i> promoter increased in isolated islets from Zucker diabetic fatty rats. This study helps to clarify the effect of an over-nutrition state on DNA methylation of the <i>Ins1</i> promoter in pancreatic beta cells. It provides new insights into the irreversible pathophysiology of diabetes.</p></div