WIMS-D4M user manual

The Winfrith Improved Multigroup Scheme (WIMS) code has been used extensively throughout the world for power and research reactor lattice physics analysis. There are many WIMS versions currently in use. The D4 version selected by the RERTR program was originally developed in 1980). It was chosen for the accurate lattice physics capability and an unrestricted distribution privilege. The code and its 69-group library tape 166259 generated in Winfrith were obtained from the Oak Ridge National Laboratory Radiation Shielding Information Center (RSIC) in 1992. Since that time the RERTR program has added three important features. The first was the capability to generate up to 20 broad-group bumup-dependent macroscopic or microscopic ISOTXS cross sections for each composition of the unit cell, a new ENDF/B-V based nuclear data library, and a new Supercell option. As a result of these modifications and other minor ones, the code is now named WIMS-D4M. A supplementary reference guide can be obtained from the RSIC that contains detailed explanations of all user options, library contents, along with several sample problems. Primary applications of WIMS for research reactor modeling do not require an extensive knowledge of all WIMS user options. This user guide is primarily addressed to the needs of the research reactor community although the code can be used for most thermal reactor lattices. The guide is written based on the experience of the RERTR staff with WIMS-D4M and will discuss only the most needed options for research reactor analyses

ROP: dumpster diving in RNA-sequencing to find the source of 1 trillion reads across diverse adult human tissues.

High-throughput RNA-sequencing (RNA-seq) technologies provide an unprecedented opportunity to explore the individual transcriptome. Unmapped reads are a large and often overlooked output of standard RNA-seq analyses. Here, we present Read Origin Protocol (ROP), a tool for discovering the source of all reads originating from complex RNA molecules. We apply ROP to samples across 2630 individuals from 54 diverse human tissues. Our approach can account for 99.9% of 1 trillion reads of various read length. Additionally, we use ROP to investigate the functional mechanisms underlying connections between the immune system, microbiome, and disease. ROP is freely available at https://github.com/smangul1/rop/wiki

History of clinical transplantation

How transplantation came to be a clinical discipline can be pieced together by perusing two volumes of reminiscences collected by Paul I. Terasaki in 1991-1992 from many of the persons who were directly involved. One volume was devoted to the discovery of the major histocompatibility complex (MHC), with particular reference to the human leukocyte antigens (HLAs) that are widely used today for tissue matching.1 The other focused on milestones in the development of clinical transplantation.2 All the contributions described in both volumes can be traced back in one way or other to the demonstration in the mid-1940s by Peter Brian Medawar that the rejection of allografts is an immunological phenomenon.3,4 © 2008 Springer New York

Centrilobular emphysema and coronary artery calcification: Mediation analysis in the SPIROMICS cohort

Background: Chronic obstructive pulmonary disease (COPD) is associated with a two-to-five fold increase in the risk of coronary artery disease independent of shared risk factors. This association is hypothesized to be mediated by systemic inflammation but this link has not been established. Methods: We included 300 participants enrolled in the SPIROMICS cohort, 75 each of lifetime non-smokers, smokers without airflow obstruction, mild-moderate COPD, and severe-very severe COPD. We quantified emphysema and airway disease on computed tomography, characterized visual emphysema subtypes (centrilobular and paraseptal) and airway disease, and used the Weston visual score to quantify coronary artery calcification (CAC). We used the Sobel test to determine whether markers of systemic inflammation mediated a link between spirometric and radiographic features of COPD and CAC. Results: FEV 1 /FVC but not quantitative emphysema or airway wall thickening was associated with CAC (p = 0.036), after adjustment for demographics, diabetes mellitus, hypertension, statin use, and CT scanner type. To explain this discordance, we examined visual subtypes of emphysema and airway disease, and found that centrilobular emphysema but not paraseptal emphysema or bronchial thickening was independently associated with CAC (p = 0.019). MMP3, VCAM1, CXCL5 and CXCL9 mediated 8, 8, 7 and 16% of the association between FEV 1 /FVC and CAC, respectively. Similar biomarkers partially mediated the association between centrilobular emphysema and CAC. Conclusions: The association between airflow obstruction and coronary calcification is driven primarily by the centrilobular subtype of emphysema, and is linked through bioactive molecules implicated in the pathogenesis of atherosclerosis. Trial Registration: ClinicalTrials.gov: Identifier: NCT01969344

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Decontamination as a precursor to decommissioning. Status report Task 2: process evaluation. [PWR; BWR]

As part of the US Nuclear Regulatory Commission's program to reduce occupational exposure and waste volumes, the Pacific Northwest Laboratory is studying decontamination as a precursor to decommissioning. Eleven processes or solvents were examined for their behavior in decontaminating BWR carbon steel samples. The solvents included NS-1, a proprietary solvent of Dow Chemical Corporation, designed for BWR use, and AP-Citrox, a well-known, two-step process designed for PWR stainless steel; it was used to provide a reference for later comparison to other systems and processes. The decontamination factors observed in the tests performed in a small laboratory scale recirculating loop ranged from about 1 (no effect) to 222 (about 99.6% of the initial activity removed. Coordinated corrosion measurements were made using twelve chemical solvents and eight metal alloys found in a range of reactor types