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Jarvis, N.

Publications and source records attributed to Jarvis, N..

2 recordsLinked to original sources

Relational Graph Convolutional Networks for Glioblastoma Biomarker Discovery via ceRNA and Copy Number Variation Analysis

Glioblastoma (GBM) is a highly aggressive brain tumor with a five-year survival rate of 6.9%, attributable in substantial part to the shortage of reliable biomarkers. Competing endogenous RNA (ceRNA) and copy number variation (CNV) analyses each carry biomarker-identification potential, but existing work treats them separately and does not integrate multiple regulatory mechanisms. We therefore applied relational graph convolutional networks (RGCNs) to ceRNA and CNV knowledge graphs under a late-fusion ensemble architecture. Across 10-fold cross-validation the RGCN discriminated best among the graph architectures tested (AUCROC 0.874 {+/-} 0.070), significantly exceeding graph convolutional, graph attention and relational attention networks. Combining the ceRNA and CNV branches at the decision level gave the best overall performance (AUCROC 0.883 {+/-} 0.072; PR-AUC 0.208 {+/-} 0.152) and improved on the ceRNA-only model in precision--recall terms, although that improvement does not survive correction for multiple comparisons and we therefore report it as suggestive. Screening the late-fusion ranking against the existing glioma literature left five candidates that are absent from the curated glioblastoma biomarker set and the subject of at most one prior glioma report, among them hsa-miR-203b and hsa-miR-5683, each differentially expressed by more than fivefold on a log_2 scale. All five are computational predictions. Relational graph learning over a ceRNA network, combined with genomic dosage at the decision level, is thus a workable framework for biomarker prioritization, and the five loci give targeted experimental work a place to start.

bioinformatics↗

A new tractable method for generating Human Alveolar Macrophage Like cells in vitro to study lung inflammatory processes and diseases

Alveolar macrophages (AMs) are unique lung resident cells that contact airborne pathogens and environmental particulates. The contribution of human AMs (HAM) to pulmonary diseases remains poorly understood due to difficulty in accessing them from human donors and their rapid phenotypic change during in vitro culture. Thus, there remains an unmet need for cost-effective methods for generating and/or differentiating primary cells into a HAM phenotype, particularly important for translational and clinical studies. We developed cell culture conditions that mimic the lung alveolar environment in humans using lung lipids, i.e., Infasurf (calfactant, natural bovine surfactant) and lung-associated cytokines (GM-CSF, TGF-{beta}, and IL-10) that facilitate the conversion of blood-obtained monocytes to an AM-Like (AML) phenotype and function in tissue culture. Similar to HAM, AML cells are particularly susceptible to both Mycobacterium tuberculosis and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections. This study reveals the importance of alveolar space components in the development and maintenance of HAM phenotype and function, and provides a readily accessible model to study HAM in infectious and inflammatory disease processes, as well as therapies and vaccines. IMPORTANCEMillions die annually from respiratory disorders. Lower respiratory track gas-exchanging alveoli maintain a precarious balance between fighting invaders and minimizing tissue damage. Key players herein are resident AMs. However, there are no easily accessible in vitro models of HAMs, presenting a huge scientific challenge. Here we present a novel model for generating AML cells based on differentiating blood monocytes in a defined lung component cocktail. This model is non-invasive, significantly less costly than performing a bronchoalveolar lavage, yields more AML cells than HAMs per donor and retains their phenotype in culture. We have applied this model to early studies of M. tuberculosis and SARS-CoV-2. This model will significantly advance respiratory biology research.

immunology↗