Routine organic air emissions at the Radioactive Waste Management Complex Waste Storage Facilities fiscal year 1995 report

This report presents the data and results of the routine organic air emissions monitoring performed in the Radioactive Waste Management Complex Waste Storage Facility, WMF-628, from January 4, 1995 to September 3, 1995. The task objectives were to systematically identify and measure volatile organic compound (VOC) concentrations within WMF-628 that could be emitted into the environment. These routine measurements implemented a dual method approach using Open-Path Fourier Transform Infrared Spectroscopy (OP-FTIR) monitoring and the Environmental Protection Agency (EPA) analytical method TO-14, Summa{reg_sign} Canister sampling. The data collected from the routine monitoring of WNF-628 will assist in estimating the total VOC emissions from WMF-628

Monitoring plan for routine organic air emissions at the Radioactive Waste Management Complex Waste Storage Facilities

This monitoring plan provides the information necessary to perform routine organic air emissions monitoring at the Waste Storage Facilities located at the Transuranic Storage Area of the Radioactive Waste Management Complex at the Idaho National Engineering Laboratory. The Waste Storage Facilities include both the Type I and II Waste Storage Modules. The plan implements a dual method approach where two dissimilar analytical methodologies, Open-Path Fourier Transform Infrared Spectroscopy (OP-FTIR) and ancillary SUMMA{reg_sign} canister sampling, following the US Environmental Protection Agency (EPA) analytical method TO-14, will be used to provide qualitative and quantitative volatile organic concentration data. The Open-Path Fourier Transform Infrared Spectroscopy will provide in situ, real time monitoring of volatile organic compound concentrations in the ambient air of the Waste Storage Facilities. To supplement the OP-FTIR data, air samples will be collected using SUMMA{reg_sign}, passivated, stainless steel canisters, following the EPA Method TO-14. These samples will be analyzed for volatile organic compounds with gas chromatograph/mass spectrometry analysis. The sampling strategy, procedures, and schedules are included in this monitoring plan. The development of this monitoring plan is driven by regulatory compliance to the Resource Conservation and Recovery Act, State of Idaho Toxic Air Pollutant increments, Occupational Safety and Health Administration. The various state and federal regulations address the characterization of the volatile organic compounds and the resultant ambient air emissions that may originate from facilities involved in industrial production and/or waste management activities

A trans-acting locus regulates an anti-viral expression network and type 1 diabetes risk

Combined analyses of gene networks and DNA sequence variation can provide new insights into the aetiology of common diseases that may not be apparent from genome-wide association studies alone. Recent advances in rat genomics are facilitating systems-genetics approaches. Here we report the use of integrated genome-wide approaches across seven rat tissues to identify gene networks and the loci underlying their regulation. We defined an interferon regulatory factor 7 (IRF7)-driven inflammatory network (IDIN) enriched for viral response genes, which represents a molecular biomarker for macrophages and which was regulated in multiple tissues by a locus on rat chromosome 15q25. We show that Epstein-Barr virus induced gene 2 (Ebi2, also known as Gpr183), which lies at this locus and controls B lymphocyte migration, is expressed in macrophages and regulates the IDIN. The human orthologous locus on chromosome 13q32 controlled the human equivalent of the IDIN, which was conserved in monocytes. IDIN genes were more likely to associate with susceptibility to type 1 diabetes (T1D)-a macrophage-associated autoimmune disease-than randomly selected immune response genes (P = 8.85 x 10(-6)). The human locus controlling the IDIN was associated with the risk of T1D at single nucleotide polymorphism rs9585056 (P = 7.0 x 10(-10); odds ratio, 1.15), which was one of five single nucleotide polymorphisms in this region associated with EBI2 (GPR183) expression. These data implicate IRF7 network genes and their regulatory locus in the pathogenesis of T1D

Prismatic edge dislocations in graphite

Dislocations are a central concept in materials science, which dictate the plastic deformation and damage evolution in materials. Layered materials such as graphite admit two general types of interlayer dislocations: basal and prismatic dislocations, of which prismatic dislocations have been relatively less studied. Using density functional theory (DFT) calculations, we have examined different prismatic core structures in graphite and evaluated their structure, energetics and mobility. We find close energetic interplay between bonded and “free-standing” core structures in both zigzag and armchair directions, with a reconstructed stable zigzag core identified. We explore grain boundaries and prismatic dislocation pile-up, identifying metastable structures which may be important in energy storage. The role of interlayer stacking in core structure, dislocation glide and climb is also considered in-depth. Our calculations suggest that the prismatic dislocation core is stable up to high temperatures of approximately 1500 K in bulk graphite. Above this temperature, the breaking of bonds in the dislocation core can facilitate climb, grain-boundary motion, and the annealing of damage through prismatic dislocation glide. © 2021 Elsevier LtdANR-20-CE08-0026, TUBITAK-2219; Engineering and Physical Sciences Research Council, EPSRC: EP/P020232/1, EP/R005745/1This work was supported by the United Kingdom EPSRC grant EP/R005745/1 , Mechanisms of Retention and Transport of Fission Products in Virgin and Irradiated Nuclear Graphite. Kenny Jolley and Pavlos Mouratidis also gratefully acknowledge funds from EDF energy generation 2016–2021 . The authors gratefully acknowledge the use of Athena at HPC Midlands+, which was funded by the EPSRC grant EP/P020232/1 as part of the HPC Midlands + consortium. CE and AI acknowledge ANR-16-CE24-0008-01 “EdgeFiller” and ANR-20-CE08-0026 “OPIFCat” for funding. DE acknowledges support from the TUBITAK-2219 post-doctoral research abroad fund.This work was supported by the United Kingdom EPSRC grant EP/R005745/1, Mechanisms of Retention and Transport of Fission Products in Virgin and Irradiated Nuclear Graphite. Kenny Jolley and Pavlos Mouratidis also gratefully acknowledge funds from EDF energy generation 2016?2021. The authors gratefully acknowledge the use of Athena at HPC Midlands+, which was funded by the EPSRC grant EP/P020232/1 as part of the HPC Midlands + consortium. CE and AI acknowledge ANR-16-CE24-0008-01 ?EdgeFiller? and ANR-20-CE08-0026 ?OPIFCat? for funding. DE acknowledges support from the TUBITAK-2219 post-doctoral research abroad fund

Thrombocytopenia with Absent Radii (TAR) syndrome is cause by compound inheritance of low-frequency regulatory SNPs and a rare null mutation in exon-junction complex subunit RBM8A

Genetics of disease, diagnosis and treatmen