RESUMEN

A new dynamical core, known as the Finite-Volume Cubed-Sphere (FV3) and developed at both NASA and NOAA, is used in NOAA's Global Forecast System (GFS) and in limited-area models for regional weather and air quality applications. NOAA has also upgraded the operational FV3GFS to version 16 (GFSv16), which includes a number of significant developmental advances to the model configuration, data assimilation, and underlying model physics, particularly for atmospheric composition to weather feedback. Concurrent with the GFSv16 upgrade, we couple the GFSv16 with the Community Multiscale Air Quality (CMAQ) model to form an advanced version of the National Air Quality Forecasting Capability (NAQFC) that will continue to protect human and ecosystem health in the US. Here we describe the development of the FV3GFSv16 coupling with a "state-of-the-science" CMAQ model version 5.3.1. The GFS-CMAQ coupling is made possible by the seminal version of the NOAA-EPA Atmosphere-Chemistry Coupler (NACC), which became a major piece of the next operational NAQFC system (i.e., NACC-CMAQ) on 20 July 2021. NACC-CMAQ has a number of scientific advancements that include satellite-based data acquisition technology to improve land cover and soil characteristics and inline wildfire smoke and dust predictions that are vital to predictions of fine particulate matter (PM2.5) concentrations during hazardous events affecting society, ecosystems, and human health. The GFS-driven NACC-CMAQ model has significantly different meteorological and chemical predictions compared to the previous operational NAQFC, where evaluation of NACC-CMAQ shows generally improved near-surface ozone and PM2.5 predictions and diurnal patterns, both of which are extended to a 72 h (3 d) forecast with this system.

RESUMEN

Elevated tropospheric ozone is harmful to human health and plants. It is formed through the photochemical reactions involving volatile organic compounds (VOCs) and nitrogen oxides (NO(x)). The elevated ozone episodes occur mainly in summer months in the United States, while the high-ozone episodes frequently occur during the fall in Taiwan. The unique landscape of Taiwan produces tremendous amounts of biogenic VOCs in the mountain regions that are adjacent to concentrated urban areas. The urban areas, in turn, generate prodigious amounts of anthropogenic emissions. Biogenic VOC emissions have direct influence on tropospheric ozone formation. To explore the air quality problems in Taiwan, this study attempts to develop a biogenic VOC emission model suitable for air quality applications in Taiwan. The emission model is based on the Biogenic Emissions Inventory System Version 2 and coupled with a detailed Taiwan land use database. The 1999 total Taiwan biogenic VOC emissions were estimated at 214,000 metric tons. The emissions of isoprene, monoterpenes, and other VOCs were about 37.2%, 30.4%, and 32.4% of total biogenic VOC emissions, respectively. The annual total biogenic VOC emission per unit area was more than two times the value of that in any European country, implying that detailed emissions estimates in any size of region will benefit the global biogenic emission inventories.

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RESUMEN

Flavonoids are widely distributed in plants, but their biological functions are still unclear. In the present study, in vitro and in vivo experiments were performed to demonstrate the inhibitory activities of rutin, wogonin, and quercetin on lipopolysaccharide-induced nitric oxide (NO) and prostaglandin E(2) production in RAW 264.7 macrophages, primary peritoneal macrophages, and Balb/c mice, respectively. In vitro results showed that wogonin and quercetin dose-dependently suppressed lipopolysaccharide-induced NO production in RAW 264.7 macrophages and primary peritoneal macrophages without a notable cytotoxic effect on either cell types associated with a decrease in inducible nitric oxide synthase (iNOS) protein expression in both cells. Rutin, at 80 microM only, had a slight but obvious inhibitory effect on lipopolysaccharide-induced NO production in primary peritoneal macrophages. Both wogonin and quercetin attenuated lipopolysaccharide-induced prostaglandin E(2) production in vitro. Intravenous injection of lipopolysaccharide (10 mg/kg, i.v.) resulted in a time-dependent induction of NO production in serum, and pretreatment with the L-arginine analog N-nitro-L-arginine methyl ester (L-NAME) blocked this induction. Intravenous pretreatment of Balb/c mice with rutin, wogonin or quercetin for 1 h followed by lipopolysaccharide treatment significantly inhibited lipopolysaccharide-induced NO production, but no inhibition of prostaglandin E(2) production was found. A decrease in iNOS protein, but not cyclooxygenase-2 protein, was detected in liver and lung specimens of lipopolysaccharide-treated Balb/c mice in the presence of rutin, wogonin or quercetin. In conclusion, data obtained both in vitro and in vivo suggest that wogonin and quercetin exert inhibitory activity on lipopolysaccharide-induced NO production through suppression of iNOS expression.

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