Reconfiguring redundancy management

A redundancy management system is described wherein input signals from a sensor are provided redundantly in parallel so that a primary control signal may be selected. Median value signals for groups of three sensors are detected in median value selectors of selection filter. The detected median value signals are then also compared in a subtractor/comparator to determine whether any of them exceed the others by an amount greater than the signal level for a failed sensor. If so, the exceeding detected medium value signal is sent to a control computer as the primary control signal. If not, the lowest level detected medium value signal is sent as the primary control signal

Unlike particle correlations and the strange quark matter distillation process

We present a new technique for observing the strange quark matter distillation process based on unlike particle correlations. A simulation is presented based on the scenario of a two-phase thermodynamical evolution model.Comment: 15 pages, 2 figures, 1 tabl

Imaging Sources with Fast and Slow Emission Components

We investigate two-proton correlation functions for reactions in which fast dynamical and slow evaporative proton emission are both present. In such cases, the width of the correlation peak provides the most reliable information about the source size of the fast dynamical component. The maximum of the correlation function is sensitive to the relative yields from the slow and fast emission components. Numerically inverting the correlation function allows one to accurately disentangle fast dynamical from slow evaporative emission and extract details of the shape of the two-proton source.Comment: 13 pages, 4 figure

Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis

© The Author(s). Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.Primary sclerosing cholangitis (PSC) is an immune-mediated disease of the bile ducts that co-occurs with inflammatory bowel disease (IBD) in almost 90% of cases. Colorectal cancer is a major complication of patients with PSC and IBD, and these patients are at a much greater risk compared to patients with IBD without concomitant PSC. Combining flow cytometry, bulk and single-cell transcriptomics, and T and B cell receptor repertoire analysis of right colon tissue from 65 patients with PSC, 108 patients with IBD and 48 healthy individuals we identified a unique adaptive inflammatory transcriptional signature associated with greater risk and shorter time to dysplasia in patients with PSC. This inflammatory signature is characterized by antigen-driven interleukin-17A (IL-17A)+ forkhead box P3 (FOXP3)+ CD4 T cells that express a pathogenic IL-17 signature, as well as an expansion of IgG-secreting plasma cells. These results suggest that the mechanisms that drive the emergence of dysplasia in PSC and IBD are distinct and provide molecular insights that could guide prevention of colorectal cancer in individuals with PSC.This work was supported by the Leona M. and Harry B. Helmsley Charitable trust (SHARE), the Digestive Diseases Research Core Center C-IID P30 DK42086 at the University of Chicago, the PSC Partners Seeking a Cure Canada and the Sczholtz Family Foundation. K.R.M. is supported by grant no. NS124187. S.C.S. is supported by an American Gastroenterological Association Research Scholar Award, Veterans Affairs Career Development Award (no. ICX002027A01) and the San Diego Digestive Diseases Research Center (no. P30 DK120515). C.Q. is supported by the BBSRC Core Strategic Programme Grant (BB/CSP1720/1, BBS/E/T/000PR9818 and BBS/E/T/000PR9817). I.H.J. is supported by a Rosalind Franklin Fellowship from the University of Groningen and a Netherlands Organization for Scientific Research VIDI grant no. 016.171.047. D.G.S. is supported by grant no. F30DK121470.info:eu-repo/semantics/publishedVersio