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Summary The recent increase in demand for performance-driven and outcome-based transportation planning makes accurate and reliable performance measures essential. Vehicle miles traveled (VMT), the total miles traveled by all vehicles on roadways, has been utilized widely as a proxy for traffic impact assessment, vehicle emissions, gasoline consumption, and crashes. Accordingly, a number of studies estimate VMT using diverse data sources. This study estimates VMT in the urban area of Bucheon, South Korea, by predicting the annual average daily traffic for unmeasured locations using spatial interpolation techniques (i.e., regression kriging and linear regression). The predictive performance of this method is compared with that of the existing Highway Performance Monitoring System (HPMS) method. The results show that regression kriging could provide more accurate VMT estimates than the HPMS method and linear regression, especially with a small sample size. Copyright © 2016 John Wiley & Sons, Ltd.

Background and Purpose cAMP as a second messenger stimulates expression of microphthalmia-associated transcription factor (MITF) or the tyrosinase gene in UVB-induced skin pigmentation. Diphenylmethylene hydrazinecarbothioamide (QNT 3-80) inhibits α-melanocyte-stimulating hormone (α-MSH)-induced melanin production in B16 murine melanoma cells but its molecular basis remains to be defined. Here, we investigated the mechanism underlying the amelioration of skin hyperpigmentation by QNT 3-80. Experimental Approach We used melanocyte cultures with raised levels of cAMP and UVB-irradiated dorsal skin of guinea pigs for pigmentation assays. Immunoprecipitation, kemptide phosphorylation, fluorescence analysis and docking simulation were applied to elucidate a molecular mechanism of QNT 3-80. Key Results QNT 3-80 inhibited melanin production in melanocyte cultures with elevated levels of cAMP, including those from human foreskin. This compound also ameliorated hyperpigmentation in vivo in UVB-irradiated dorsal skin of guinea pigs. As a mechanism, QNT 3-80 directly antagonized cAMP binding to the regulatory subunit of PKA, nullified the dissociation and activation of inactive PKA holoenzyme in melanocytes and fitted into the cAMP-binding site on the crystal structure of human PKA under the most energetically favourable simulation. QNT 3-80 consequently inhibited cAMP- or UVB-induced phosphorylation (activation) of cAMP-responsive element-binding protein in vitro and in vivo, thus down-regulating expression of genes for MITF or tyrosinase in the melanogenic process. Conclusions and Implications Our data suggested that QNT 3-80 could contribute significantly to the treatment of skin disorders with hyperpigmented patches with the cAMP-binding site of PKA as its molecular target.

We implemented a novel i-PR (in-cell Black Stripe Patterned Retarder) pixel structure by using a simple driving scheme. This approach improves the 2D aperture ratio but has the unique problem of inducing TFT (Thin Film Transistor) thermal instability. This is caused by a bias temperature stress in TCON TFT during 3D mode. Therefore, we developed an advanced drain dual-gate TFT application to improve the high-temperature reliability. This novel TFT structure could have its own VLT (VGS of Luminance Threshold) margin during the reset process, although the VLT shift is as much as that for a normal TCON TFT.