979 resultados para Toll roads.
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Transportation Department, Washington, D.C.
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"Publication no. FHWA-PL-93-008"--P. 4 of cover.
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"FHWA-PL-92-012."
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"October 2010"--Cover.
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Title from cover.
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Cover title.
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Includes an annoucement that the Illinois Dept. of Transportation, in cooperation with the Illinois State Toll Highway Authority, will be performing additional studies in support of the extension of I-355 through Will County, Illinois.
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Mode of access: Internet.
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Mode of access: Internet.
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Mode of access: Internet.
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Mode of access: Internet.
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We estimate the energy consumption of toll highway transport on a number of Spanish roads. Regression parameters are balanced according to coefficients from an empirical analysis based on survey data by vehicle type. The mean energy consumption and subsequent CO2 emissions on the toll highway sections are estimated as 1895 MJ/h/lane-km and 0.15 tCO2 eq./h/lane-km, values that increase to 2644 and 0.22 when energy and carbon emissions of transport infrastructure are considered based on the life cycle energy consumption for toll highway construction and use. If the energy intensity of infrastructure construction is allocated to the users according to traffic, it is much higher for motorcycles than for cars, and is significantly lower for articulated trucks than for vans.
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"Three of the papers ... have already appeared in the Atlantic monthly."
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[With his Popular exposition of the incorrectness of the tariffs of toll in use on the public improvements of the United States. Philadelphia, 1839]
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Cardiac arrhythmias are one of the main causes of death worldwide. Several studies have shown that inflammation plays a key role in different cardiac diseases and Toll-like receptors (TLRs) seem to be involved in cardiac complications. In the present study, we investigated whether the activation of TLR4 induces cardiac electrical remodeling and arrhythmias, and the signaling pathway involved in these effects. Membrane potential was recorded in Wistar rat ventricle. Ca(2+) transients, as well as the L-type Ca(2+) current (ICaL) and the transient outward K(+) current (Ito), were recorded in isolated myocytes after 24 h exposure to the TLR4 agonist, lipopolysaccharide (LPS, 1 μg/ml). TLR4 stimulation in vitro promoted a cardiac electrical remodeling that leads to action potential prolongation associated with arrhythmic events, such as delayed afterdepolarization and triggered activity. After 24 h LPS incubation, Ito amplitude, as well as Kv4.3 and KChIP2 mRNA levels were reduced. The Ito decrease by LPS was prevented by inhibition of interferon regulatory factor 3 (IRF3), but not by inhibition of interleukin-1 receptor-associated kinase 4 (IRAK4) or nuclear factor kappa B (NF-κB). Extrasystolic activity was present in 25% of the cells, but apart from that, Ca(2+) transients and ICaL were not affected by LPS; however, Na(+)/Ca(2+) exchanger (NCX) activity was apparently increased. We conclude that TLR4 activation decreased Ito, which increased AP duration via a MyD88-independent, IRF3-dependent pathway. The longer action potential, associated with enhanced Ca(2+) efflux via NCX, could explain the presence of arrhythmias in the LPS group.