scispace - formally typeset
Search or ask a question
Institution

Research Triangle Park

NonprofitDurham, North Carolina, United States
About: Research Triangle Park is a nonprofit organization based out in Durham, North Carolina, United States. It is known for research contribution in the topics: Population & Environmental exposure. The organization has 24961 authors who have published 35800 publications receiving 1684504 citations. The organization is also known as: RTP.


Papers
More filters
Journal ArticleDOI
TL;DR: In this article, the authors present a 10-a regional trend of NOx emissions in China from 1995 to 2004 using a bottom-up methodology and compare the emission trends with the NO2 column trends observed from GOME and SCIAMACHY, the two spaceborne instruments.
Abstract: [1] A rapid increase of NO2 columns over China has been observed by satellite instruments in recent years. We present a 10-a regional trend of NOx emissions in China from 1995 to 2004 using a bottom-up methodology and compare the emission trends with the NO2 column trends observed from GOME and SCIAMACHY, the two spaceborne instruments. We use a dynamic methodology to reflect the dramatic change in China's NOx emissions caused by energy growth and technology renewal. We use a scenario analysis approach to identify the possible sources of uncertainties in the current bottom-up inventory, in comparison with the satellite observation data. Our best estimates for China's NOx emissions are 10.9 Tg in 1995 and 18.6 Tg in 2004, increasing by 70% during the period considered. NOx emissions and satellite-based NO2 columns show broad agreement in temporal evolution and spatial distribution. Both the emission inventory data and the satellite observations indicate a continuous and accelerating growth rate between 1996 and 2004 over east central China. However, the growth rate from the emission inventory is lower than that from the satellite observations. From 1996 to 2004, NOx emissions over the region increased by 61% according to the inventory, while a 95% increase in the NO2 columns measured by satellite was observed during the same period. We found good agreement during summertime but a large discrepancy during wintertime. The consistency between the summertime trends suggests that the bias cannot be due to systematic error of activity data or emission factors. The reasons for the discrepancy cannot yet be fully identified, but possible explanations include an underestimation in seasonal emission variations, variability of meteorology, NOx injection height, and the increasing trend of sulfate aerosols.

465 citations

Journal ArticleDOI
TL;DR: Results indicate that calcium-calmodulin plays a central role in the calcium-dependent regulation of tyrosine phosphorylation by G protein-coupled receptors in some systems, and indicate that in HEK-293 cells, the Gβγ subunit-mediated α2A-AR- and the Gαq/11-mediated βARK1ct-mediated Erk1/2 activation pathways converge at the level of phospholipase C.

465 citations

Journal ArticleDOI
TL;DR: Cyp4a10 and Cyp4a14 represented the group of genes induced by PB only in CAR-null mice, indicating that CAR may be a transcription blocker that prevents these genes from being induced or repressed by PB.
Abstract: Phenobarbital (PB) induces various gene encoding drug/steroid-metabolizing enzymes such as cytochromes P450 (P450s) and transferases. Although the nuclear orphan constitutive active receptor (CAR) has been identified as a key transcription factor that regulates the induction of CYP2B, the full scope of CAR-regulated genes still remains a major question. To this end, reverse transcriptase-polymerase chain reaction and cDNA microarray techniques were employed to examine gene expression in wild-type and CAR-null mice. The results show that a total of 138 genes were detected to be either induced or repressed in response to PB treatment, of which about half were under CAR regulation. Including CYP2B10, CYP3A11, and NADPH-CYP reductase, CAR regulated a group of the PB-induced drug/steroid-metabolizing enzymes. Enzymes such as amino levulinate synthase 1 and squalene epoxidase displayed CAR-independent induction by PB. Cyp4a10 and Cyp4a14 represented the group of genes induced by PB only in CAR-null mice, indicating that CAR may be a transcription blocker that prevents these genes from being induced by PB. Additionally, the group of genes encoding enzymes and proteins involved in basic biological processes such as energy metabolism underwent the CAR-dependent repression by PB. Thus, CAR seems to have diverse roles, both as a positive and negative regulator, in the regulation of hepatic genes in response to PB beyond drug/steroid metabolism.

465 citations

Journal ArticleDOI
TL;DR: Exposure of humans to as low a level as 0.08 ppm for 6.6 h is sufficient to initiate an inflammatory reaction in the lung, and exposure to 0.10 ppm ozone resulted in significant increases in PMNs, PGE2, LDH, IL-6, alpha 1-antitrypsin, and decreased phagocytosis via the complement receptor.
Abstract: An acute (2 h) exposure of humans to 0.4 ppm ozone initiates biochemical changes in the lung that result in the production of components mediating inflammation and acute lung damage as well as components having the potential to lead to long-term effects such as fibrosis. However, many people are exposed to lower levels of ozone than this, but for periods of several hours. Therefore, it is important to determine if a prolonged exposure to low levels of ozone is also capable of causing cellular and biochemical changes in the lung. Nonsmoking males were randomly exposed to filtered air and either 0.10 ppm ozone or 0.08 ppm ozone for 6.6 h with moderate exercise (40 liters/min). Bronchoalveolar lavage (BAL) was performed 18 h after each exposure, and cells and fluid were analyzed. The BAL fluid of volunteers exposed to 0.10 ppm ozone had significant increases in neutrophils (PMNs), protein, prostaglandin E2 (PGE2), fibronectin, interleukin-6 (IL-6), and lactate dehydrogenase (LDH) compared with BAL fluid from the same volunteers exposed to filtered air. In addition, there was a decrease in the ability of alveolar macrophages to phagocytize yeast via the complement receptor. Exposure to 0.08 ppm ozone resulted in significant increases in PMNs, PGE2, LDH, IL-6, alpha 1-antitrypsin, and decreased phagocytosis via the complement receptor. However, BAL fluid protein and fibronectin were no longer significantly elevated. We conclude that exposure of humans to as low a level as 0.08 ppm for 6.6 h is sufficient to initiate an inflammatory reaction in the lung.

465 citations

Journal ArticleDOI
TL;DR: The proposed technique enables the implementation of high-efficiency high-power-density fully regulated fully regulated CEET systems suitable for applications with a wide input and load range.
Abstract: A high-performance contactless electrical energy transmission (CEET) technique which employs the inductive energy transmission principle is described. The proposed technique enables the implementation of high-efficiency high-power-density fully regulated CEET systems suitable for applications with a wide input and load range. A high efficiency of the system is achieved by recovering the energy stored in the leakage inductances of the transformer by incorporating them in the operation of the circuit, and by employing high-frequency-inverter and controlled-rectifier topologies that allow a controlled bidirectional power flow through the transformer. In addition, a feedforward variable-switching-frequency control of the inverter is used to maintain approximately constant power transfer through the transformer with the input voltage changes, whereas the output-side rectifier employs a local pulsewidth-modulation control to achieve a tight regulation of the output in the presence of load variations. Specifically, the described CEET system is suitable for use in universal-input battery chargers.

464 citations


Authors

Showing all 25006 results

NameH-indexPapersCitations
Douglas G. Altman2531001680344
Lewis C. Cantley196748169037
Ronald Klein1941305149140
Daniel J. Jacob16265676530
Christopher P. Cannon1511118108906
James B. Meigs147574115899
Lawrence Corey14677378105
Jeremy K. Nicholson14177380275
Paul M. Matthews14061788802
Herbert Y. Meltzer137114881371
Charles J. Yeo13667276424
Benjamin F. Cravatt13166661932
Timothy R. Billiar13183866133
Peter Brown12990868853
King K. Holmes12460656192
Network Information
Related Institutions (5)
University of North Carolina at Chapel Hill
185.3K papers, 9.9M citations

90% related

University of Minnesota
257.9K papers, 11.9M citations

89% related

University of Washington
305.5K papers, 17.7M citations

89% related

University of Pittsburgh
201K papers, 9.6M citations

89% related

National Institutes of Health
297.8K papers, 21.3M citations

88% related

Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202317
202277
2021988
20201,001
20191,035
20181,051