Dynamics of a structured slug population model in the absence of seasonal variation

We develop a novel, nonlinear structured population model for the slug Deroceras reticulatum, a highly significant agricultural pest of great economic impact, in both organic and non-organic settings. In the absence of seasonal variations, we numerically explore the effect of life history traits that are dependent on an individual's size and measures of population biomass. We conduct a systematic exploration of parameter space and highlight the main mechanisms and implications of model design. A major conclusion of this work is that strong size dependent predation significantly adjusts the competitive balance, leading to non-monotonic steady state solutions and slowly decaying transients consisting of distinct generational cycles. Furthermore, we demonstrate how a simple ratio of adult to juvenile biomass can act as a useful diagnostic to distinguish between predated and non-predated environments, and may be useful in agricultural settings

On the computational power of probabilistic and quantum branching program

In this paper, we show that one-qubit polynomial time computations are as powerful as NC1 circuits. More generally, we define syntactic models for quantum and stochastic branching programs of bounded width and prove upper and lower bounds on their power. We show that any NC1 language can be accepted exactly by a width-2 quantum branching program of polynomial length, in contrast to the classical case where width 5 is necessary unless NC 1 = ACC. This separates width-2 quantum programs from width-2 doubly stochastic programs as we show the latter cannot compute the middle bit of multiplication. Finally, we show that bounded-width quantum and stochastic programs can be simulated by classical programs of larger but bounded width, and thus are in NC1. For read-once quantum branching programs (QBPs), we give a symmetric Boolean function which is computable by a read-once QBP with O (log n) width, but not by a deterministic read-once BP with o (n) width, or by a classical randomized read-once BP with o (n) width which is "stable" in the sense that its transitions depend on the value of the queried variable but do not vary from step to step. Finally, we present a general lower bound on the width of read-once QBPs, showing that our O (log n) upper bound for this symmetric function is almost tight. © 2005 Elsevier Inc. All rights reserved

Identification of genes expressed by immune cells of the colon that are regulated by colorectal cancer-associated variants.

A locus on human chromosome 11q23 tagged by marker rs3802842 was associated with colorectal cancer (CRC) in a genome-wide association study; this finding has been replicated in case-control studies worldwide. In order to identify biologic factors at this locus that are related to the etiopathology of CRC, we used microarray-based target selection methods, coupled to next-generation sequencing, to study 103 kb at the 11q23 locus. We genotyped 369 putative variants from 1,030 patients with CRC (cases) and 1,061 individuals without CRC (controls) from the Ontario Familial Colorectal Cancer Registry. Two previously uncharacterized genes, COLCA1 and COLCA2, were found to be co-regulated genes that are transcribed from opposite strands. Expression levels of COLCA1 and COLCA2 transcripts correlate with rs3802842 genotypes. In colon tissues, COLCA1 co-localizes with crystalloid granules of eosinophils and granular organelles of mast cells, neutrophils, macrophages, dendritic cells and differentiated myeloid-derived cell lines. COLCA2 is present in the cytoplasm of normal epithelial, immune and other cell lineages, as well as tumor cells. Tissue microarray analysis demonstrates the association of rs3802842 with lymphocyte density in the lamina propria (p = 0.014) and levels of COLCA1 in the lamina propria (p = 0.00016) and COLCA2 (tumor cells, p = 0.0041 and lamina propria, p = 6 × 10(-5)). In conclusion, genetic, expression and immunohistochemical data implicate COLCA1 and COLCA2 in the pathogenesis of colon cancer. Histologic analyses indicate the involvement of immune pathways

Identification and evaluation of epidemic prediction and forecasting reporting guidelines : a systematic review and a call for action

NGR reports funding by NIGMS grant R35GM119582. BMA is supported by Bill and Melinda Gates Foundation through the Global Good Fund. SP and IMB were funded by the Armed Forces Health Surveillance Branch (GEIS: P0116_19_WR_03.11).Introduction: High quality epidemic forecasting and prediction are critical to support response to local, regional and global infectious disease threats. Other fields of biomedical research use consensus reporting guidelines to ensure standardization and quality of research practice among researchers, and to provide a framework for end-users to interpret the validity of study results. The purpose of this study was to determine whether guidelines exist specifically for epidemic forecast and prediction publications. Methods: We undertook a formal systematic review to identify and evaluate any published infectious disease epidemic forecasting and prediction reporting guidelines. This review leveraged a team of 18 investigators from US Government and academic sectors. Results: A literature database search through May 26, 2019, identified 1467 publications (MEDLINE n = 584, EMBASE n = 883), and a grey-literature review identified a further 407 publications, yielding a total 1777 unique publications. A paired-reviewer system screened in 25 potentially eligible publications, of which two were ultimately deemed eligible. A qualitative review of these two published reporting guidelines indicated that neither were specific for epidemic forecasting and prediction, although they described reporting items which may be relevant to epidemic forecasting and prediction studies. Conclusions: This systematic review confirms that no specific guidelines have been published to standardize the reporting of epidemic forecasting and prediction studies. These findings underscore the need to develop such reporting guidelines in order to improve the transparency, quality and implementation of epidemic forecasting and prediction research in operational public health.Publisher PDFPeer reviewe

Immunohistochemical, ultrastructural and functional analysis of axonal regeneration through peripheral nerve grafts containing Schwann cells expressing BDNF, CNTF or NT3

Objective  To establish reference values for activated coagulation time (ACT) in normal cats and dogs, by visual assessment of clot formation using the MAX-ACTTM tube. Subjects  We recruited 43 cats and 50 dogs for the study; 11 cats and 4 dogs were excluded from the statistical analysis because of abnormalities on clinical examination or laboratory testing including anaemia, prolonged prothrombin time (PT) or activated partial thromboplastin time (APTT), or insufficient plasma volume for comprehensive laboratory coagulation testing. Procedure  Blood samples were collected via direct venipuncture for MAX-ACT, packed cell volume/total solids, manual platelet estimation and PT/APTT measurement. Blood (0.5 mL) was mixed gently in the MAX-ACT tube at 37°C for 30 s, then assessed for clot formation every 5 to 10 s by tipping the tube gently on its side and monitoring for magnet movement. The endpoint was defined as the magnet lodging in the clot. The technique was tested with 10 dogs by collecting two blood samples from the same needle insertion and running a MAX-ACT on each simultaneously. Results  In normal cats the mean MAX-ACT was 66 s (range 55–85 s). In normal dogs the mean was 71 s (range 55–80 s). There was no statistical difference between the first and second samples collected from the same needle insertion. Conclusions and Clinical Relevance  In both cats and dogs, a MAX-ACT result >85 s should be considered abnormal and further coagulation testing should be performed. Additionally, failure to discard the first few drops of the sample does not appear to significantly affect results

Identification and Evaluation of Epidemic Prediction and Forecasting Reporting Guidelines: A Systematic Review and a Call for Action

INTRODUCTION: High quality epidemic forecasting and prediction are critical to support response to local, regional and global infectious disease threats. Other fields of biomedical research use consensus reporting guidelines to ensure standardization and quality of research practice among researchers, and to provide a framework for end-users to interpret the validity of study results. The purpose of this study was to determine whether guidelines exist specifically for epidemic forecast and prediction publications. METHODS: We undertook a formal systematic review to identify and evaluate any published infectious disease epidemic forecasting and prediction reporting guidelines. This review leveraged a team of 18 investigators from US Government and academic sectors. RESULTS: A literature database search through May 26, 2019, identified 1467 publications (MEDLINE n = 584, EMBASE n = 883), and a grey-literature review identified a further 407 publications, yielding a total 1777 unique publications. A paired-reviewer system screened in 25 potentially eligible publications, of which two were ultimately deemed eligible. A qualitative review of these two published reporting guidelines indicated that neither were specific for epidemic forecasting and prediction, although they described reporting items which may be relevant to epidemic forecasting and prediction studies. CONCLUSIONS: This systematic review confirms that no specific guidelines have been published to standardize the reporting of epidemic forecasting and prediction studies. These findings underscore the need to develop such reporting guidelines in order to improve the transparency, quality and implementation of epidemic forecasting and prediction research in operational public health

Mule Regulates the Intestinal Stem Cell Niche via the Wnt Pathway and Targets EphB3 for Proteasomal and Lysosomal Degradation

The E3 ubiquitin ligase Mule is often overexpressed in human colorectal cancers, but its role in gut tumorigenesis is unknown. Here, we show in vivo that Mule controls murine intestinal stem and progenitor cell proliferation by modulating Wnt signaling via c-Myc. Mule also regulates protein levels of the receptor tyrosine kinase EphB3 by targeting it for proteasomal and lysosomal degradation. In the intestine, EphB/ephrinB interactions position cells along the crypt-villus axis and compartmentalize incipient colorectal tumors. Our study thus unveils an important new avenue by which Mule acts as an intestinal tumor suppressor by regulation of the intestinal stem cell niche