Urban particulate matter (UPM) exerts negative effects on various human organs. Transient receptor potential vanilloid 1 (TRPV1) is a polymodal sensory transducer that can be activated by multiple noxious stimuli. This study aimed to explore the effects of the UPM 1648a on the expression of TRPV1, and its regulatory mechanisms in HaCaT cells. UPM enhanced TRPV 1 promoter-luciferase reporter activity. UPM also increased expression of the TRPV 1 gene as evidenced by increased mRNA and protein levels of TRPV 1. In addition, elucidation of the underlying mechanism behind the UPM-mediated effects on TRPV 1 expression revealed that UPM can upregulate expression of the TRPV1 gene by activating activator protein-1 (AP-1) and nuclear factor kappa B (NF-κB). The UPM treatment also altered Ca2+ influx and cell proliferation, as well as production of interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β). In addition, these UPM-induced effects were attenuated by SB203580 and ammonium pyrrolidinedithiocarbamate (PDTC). However, SP600125 and PD98059 did not alter the UPM-induced effects. Taken together, these findings indicate that UPM upregulates expression of the TRPV 1 gene, which is mediated by the p38 mitogen-activated protein kinase (MAPK) and NF-κB signaling pathways and suggest that UPM is a potential irritant that can induce skin processes such as aging and inflammatory responses.

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Using data on per capita income among 13 regions in Korea over the period 1985-2002, regional convergence is evaluated. This study uses panel cointegration tests and a random coefficient model that allows both regional differences and similarities to estimate the Solow growth model. The model also corrects for heteroscedasticity and serial correlation. Evidence is found in favour of regional convergence in Korea, with a rate of convergence of around 8% a year. The results also indicate that the investment rate in physical capital has a significantly positive effect and the population growth has a significantly negative effect on the growth rate of per capita income, holding its initial level constant.

BACKGROUND: Some studies have provided the possibility that adipose tissue may mediate air pollution-induced lung dysfunction. Studies using quantified fat mass data are needed to understand the biological mechanisms between adipocyte and air pollution in lung function. We aimed to investigate whether abdominal adiposity measured by computed tomography (CT) modifies the effects of air pollution on lung function in Korean men. METHODS: A total of 1876 men who visited one of two health checkup centers were recruited for this study. Adiposity traits such as visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) and total adipose tissue (TAT) areas were measured by CT. We used the annual mean concentrations of ambient air pollutants including nitrogen dioxide (NO 2 ) and particulate matter with an aerodynamic diameter ⩽ 10 μm (PM 10 ). RESULTS: Interquartile range (IQR) increase in annual mean concentration of NO 2 was significantly associated with a 2.5% lower forced expiratory volume in 1 s (FEV 1 ) and 2.9% lower forced vital capacity (FVC) (both P o0.05). The decrease in lung function was more strongly associated with adiposity traits than with body mass index. In a stratified analysis of adiposity, compared with subjects with low-VAT area (VAT ⩽ 200 cm 2 ), those with high-VAT area (VAT4200 cm 2 ) showed a rapid decrease in FEV 1 with each IQR increase in PM 10 (β = -0.0812; 95% confidence interval (CI) = -0.1590, -0.0035) and NO 2 (β = -0.0979; 95% CI = -0.1611, -0.0346). In the high-VAT group, each IQR increase in NO 2 content was significantly associated with a 10.6% decrease (β = -0.1056; 95% CI = -0.1770, -0.0343) in FVC. SAT and TAT areas showed similar patterns. CONCLUSIONS: We report the first finding that abdominal adiposity intensifies the inverse relationship between air pollution and lung function.

SIMT architectures improve performance and efficiency by exploiting control and memory-access structure across data-parallel threads. Value structure occurs when multiple threads operate on values that can be compactly encoded, e.g., by using a simple function of the thread index. We characterize the availability of control, memory-access, and value structure in typical kernels and observe ample amounts of value structure that is largely ignored by current SIMT architectures. We propose three microarchitectural mechanisms to exploit value structure based on compact affine execution of arithmetic, branch, and memory instructions. We explore these mechanisms within the context of traditional SIMT microarchitectures (GP-SIMT), found in general-purpose graphics processing units, as well as fine-grain SIMT microarchitectures (FG-SIMT), a SIMT variant appropriate for compute-focused data-parallel accelerators. Cycle-level modeling of a modern GP-SIMT system and a VLSI implementation of an eight-lane FG-SIMT execution engine are used to evaluate a range of application kernels. When compared to a baseline without compact affine execution, our approach can improve GP-SIMT cycle-level performance by 4-17% and can improve FG-SIMT absolute performance by 20-65% and energy efficiency up to 30% for a majority of the kernels.