43 research outputs found
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Atmospheric relative concentrations in building wakes
This report documents the ARCON96 computer code developed for the U.S. Nuclear Regulatory Commission Office of Nuclear Reactor Regulation for potential use in control room habitability assessments. It includes a user`s guide to the code, a description of the technical basis for the code, and a programmer`s guide to the code. The ARCON96 code uses hourly meteorological data and recently developed methods for estimating dispersion in the vicinity of buildings to calculate relative concentrations at control room air intakes that would be exceeded no more than five percent of the time. The concentrations are calculated for averaging periods ranging from one hour to 30 days in duration. ARCON96 is a revised version of ARCON95, which was developed for the NRC Office of Nuclear Regulatory Research. Changes in the code permit users to simulate releases from area sources as well as point sources. The method of averaging concentrations for periods longer than 2 hours has also been changed. The change in averaging procedures increases relative concentrations for these averaging periods. In general, the increase in concentrations is less than a factor of two. The increase is greatest for relatively short averaging periods, for example 0 to 8 hours and diminishes as the duration of the averaging period increases
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Detailed Time-Histories of Concentrations Resulting from Puff and Short-Period Releases of an Inert Radioactive Gas: A Volume of Atmospheric Diffusion Data.
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Radiological Assessment System for Consequence Analysis (RASCAL) Version 3.0
The Radiological Assessment System for Consequence AnaLysis, Version 3.0 (RASCAL 3.0) is the U.S. Nuclear Regulatory Commission�s (NRC) main computational tool for use during radiological emergencies. RASCAL estimates doses from radiological accidents for comparison with Protective Action Guides and acute health effects thresholds. It includes six computational tools: ST-Dose, FM-Dose, Decay, BackCalc, UF6Plume, and MetProc. ST-Dose computes time-dependent nuclide release rates, atmospheric transport, radiological decay, and doses. FM-Dose computes doses from environmental concentrations of nuclides. Decay computes radiological decay and daughter in-growth. BackCalc estimates a distribution of possible release rates from field measurements. UF6Plume computes uranium exposures and HF concentrations from a UF6 release. MetProc prepares meteorological data for use by ST-Dose and UF6Plume
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Genetic analysis reveals a hierarchy of interactions between polycystin-encoding genes and genes controlling cilia function during left-right determination
During mammalian development, left-right (L-R) asymmetry is established by a cilia-driven leftward fluid flow within a midline embryonic cavity called the node. This ‘nodal flow’ is detected by peripherally-located crown cells that each assemble a primary cilium which contain the putative Ca2+ channel PKD2. The interaction of flow and crown cell cilia promotes left side-specific expression of Nodal in the lateral plate mesoderm (LPM). Whilst the PKD2-interacting protein PKD1L1 has also been implicated in L-R patterning, the underlying mechanism by which flow is detected and the genetic relationship between Polycystin function and asymmetric gene expression remains unknown. Here, we characterize a Pkd1l1 mutant line in which Nodal is activated bilaterally, suggesting that PKD1L1 is not required for LPM Nodal pathway activation per se, but rather to restrict Nodal to the left side downstream of nodal flow. Epistasis analysis shows that Pkd1l1 acts as an upstream genetic repressor of Pkd2. This study therefore provides a genetic pathway for the early stages of L-R determination. Moreover, using a system in which cultured cells are supplied artificial flow, we demonstrate that PKD1L1 is sufficient to mediate a Ca2+ signaling response after flow stimulation. Finally, we show that an extracellular PKD domain within PKD1L1 is crucial for PKD1L1 function; as such, destabilizing the domain causes L-R defects in the mouse. Our demonstration that PKD1L1 protein can mediate a response to flow coheres with a mechanosensation model of flow sensation in which the force of fluid flow drives asymmetric gene expression in the embryo
Both tumour cells and infiltrating T-cells in equine sarcoids express FOXP3 associated with an immune-supressed cytokine microenvironment
The Role of Passenger Leukocytes in Rejection and “Tolerance” after Solid Organ Transplantation: A Potential Explanation of a Paradox
Effects of Anacetrapib in Patients with Atherosclerotic Vascular Disease
BACKGROUND:
Patients with atherosclerotic vascular disease remain at high risk for cardiovascular events despite effective statin-based treatment of low-density lipoprotein (LDL) cholesterol levels. The inhibition of cholesteryl ester transfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipoprotein (HDL) cholesterol levels. However, trials of other CETP inhibitors have shown neutral or adverse effects on cardiovascular outcomes.
METHODS:
We conducted a randomized, double-blind, placebo-controlled trial involving 30,449 adults with atherosclerotic vascular disease who were receiving intensive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92 mg per deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol per liter). The patients were assigned to receive either 100 mg of anacetrapib once daily (15,225 patients) or matching placebo (15,224 patients). The primary outcome was the first major coronary event, a composite of coronary death, myocardial infarction, or coronary revascularization.
RESULTS:
During the median follow-up period of 4.1 years, the primary outcome occurred in significantly fewer patients in the anacetrapib group than in the placebo group (1640 of 15,225 patients [10.8%] vs. 1803 of 15,224 patients [11.8%]; rate ratio, 0.91; 95% confidence interval, 0.85 to 0.97; P=0.004). The relative difference in risk was similar across multiple prespecified subgroups. At the trial midpoint, the mean level of HDL cholesterol was higher by 43 mg per deciliter (1.12 mmol per liter) in the anacetrapib group than in the placebo group (a relative difference of 104%), and the mean level of non-HDL cholesterol was lower by 17 mg per deciliter (0.44 mmol per liter), a relative difference of -18%. There were no significant between-group differences in the risk of death, cancer, or other serious adverse events.
CONCLUSIONS:
Among patients with atherosclerotic vascular disease who were receiving intensive statin therapy, the use of anacetrapib resulted in a lower incidence of major coronary events than the use of placebo. (Funded by Merck and others; Current Controlled Trials number, ISRCTN48678192 ; ClinicalTrials.gov number, NCT01252953 ; and EudraCT number, 2010-023467-18 .)
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Evaluation of potential releases from single-shell tanks
Potential toxic chemical concentrations in the air near vents of single-shell tanks have been evaluated using three scenarios. The first scenario duplicates the conditions existing the morning of January 28, 1992, when several workers reported exposure to toxic or irritating gases near the BX and BY tank farms in the 200-East Area at Hanford. The results of this scenario indicate that it is unlikely that a tank in either tank farm could have been the source of the gases associated with the incident. In the other two scenarios, maximum potential concentrations under worst-cast and bounding conditions were examined. The results of theses scenario show that air concentrations of all toxic gases reported to be in the tanks fall below their time-weighted average, threshold limiting values within 5 m of tank vents under worst-case conditions involving a restricted air flow to the tanks. When unrestricted air flow to the tanks and worst-case conditions are assumed, the maximum gas concentrations fall below time-weighted average, threshold limiting values within 15 m of vents