15 research outputs found

    Air\u2013Sea/Land Interaction in the Coastal Zone

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    Atmospheric turbulence measurements made at the U.S. Army Corps of Engineers Field Research Facility (FRF) located on the Atlantic coast near the town of Duck, North Carolina during the CASPER-East Program (October\u2013November 2015) are used to study air\u2013sea/land coupling in the FRF coastal zone. Turbulence and mean meteorological data were collected at multiple levels (up to four) on three towers deployed at different landward distances from the shoreline, with a fourth tower located at the end of a 560-m-long FRF pier. The data enable comparison of turbulent fluxes and other statistics, as well as investigations of surface-layer scaling for different footprints, including relatively smooth sea-surface conditions and aerodynamically rough dry inland areas. Both stable and unstable stratifications were observed. The drag coefficient and diurnal variation of the sensible heat flux are found to be indicators for disparate surface footprints. The drag coefficient over the land footprint is significantly greater, by as much as an order of magnitude, compared with that over the smooth sea-surface footprint. For onshore flow, the internal boundary layer in the coastal zone was either stable or (mostly) unstable, and varied dramatically at the land-surface discontinuity. The offshore flow of generally warm air over the cooler sea surface produced a stable internal boundary layer over the ocean surface downstream from the coast. While the coastal inhomogeneities violate the assumptions underlying Monin\u2013Obukhov similarity theory (MOST), any deviations from MOST are less profound for the scaled standard deviations and the dissipation rate over both water and land, as well as for stable and unstable conditions. Observations, however, show a poor correspondence with MOST for the flux-profile relationships. Suitably-averaged, non-dimensional profiles of wind speed and temperature vary significantly among the different flux towers and observation levels, with high data scatter. Overall, the statistical dependence of the vertical gradients of scaled wind speed and temperature on the Monin\u2013Obukhov stability parameter in the coastal area is weak, if not non-existent

    Primary pulmonary hypertension: the pressure rises for a gene

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    Primary pulmonary hypertension (PPH) represents the end stage of a disruption of pulmonary vascular integrity, of unknown cause. Although PPH is associated with several systemic disorders, there have hitherto been few clues as to the aetiological factors responsible for the pathogenesis of this condition. As an example of the application of modern molecular genetics and positional cloning, this leader desribes the range of studies currently under way, which aim to find the gene that underlies PPH, and summarises the implications of the identification of such a gene. Key Words: pulmonary hypertension • genetics • chromosome 2q3

    Association of CYP2C9*2 With Bosentan-Induced Liver Injury

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    Bosentan (Tracleer) is an endothelin receptor antagonist prescribed for the treatment of pulmonary arterial hypertension (PAH). Its use is limited by drug-induced liver injury (DILI). To identify genetic markers of DILI, association analyses were performed on 56 Caucasian PAH patients receiving bosentan. Twelve functional polymorphisms in five genes (ABCB11, ABCC2, CYP2C9, SLCO1B1, and SLCO1B3) implicated in bosentan pharmacokinetics were tested for associations with alanine aminotransferase (ALT), aspartate aminotransferase (AST), and DILI. After adjusting for body mass index, CYP2C9*2 was the only polymorphism associated with ALT, AST, and DILI (β = 2.16, P = 0.024; β = 1.92, P = 0.016; odds ratio 95% CI = 2.29-∞, P = 0.003, respectively). Bosentan metabolism by CYP2C9*2 in vitro was significantly reduced compared with CYP2C9*1 and was comparable to that by CYP2C9*3. These results suggest that CYP2C9*2 is a potential genetic marker for prediction of bosentan-induced liver injury and warrants investigation for the optimization of bosentan treatment
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