Evidence map›Paper›PMID 33149233›Full record

ArticleScientific reports2020

Singular manifolds of proteomic drivers to model the evolution of inflammatory bowel disease status.

Ian Morilla, Thibaut Léger, Assiya Marah, Isabelle Pic, Hatem Zaag, Eric Ogier-Denis

Abstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

6 authors.

Ian MorillaUniversité Sorbonne Paris Nord, LAGA, CNRS, UMR 7539, Laboratoire d'excellence Inflamex, F-93430, Villetaneuse, France. morilla@math.univ-paris13.fr.
Thibaut LégerUMR 7592 CNRS, Institut Jacques Monod, Université Paris Diderot, Paris, France.
Assiya MarahInception IBD Inc., Montreal, Canada.
Isabelle PicInception IBD Inc., Montreal, Canada.
Hatem ZaagUniversité Sorbonne Paris Nord, LAGA, CNRS, UMR 7539, Laboratoire d'excellence Inflamex, F-93430, Villetaneuse, France.
Eric Ogier-DenisINSERM, Research Centre of Inflammation, Laboratoire d'excellence Inflamex, BP 416, Paris, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The conditions used to describe the presence of an immune disease are often represented by interaction graphs. These informative, but intricate structures are susceptible to perturbations at different levels. The mode in which that perturbation occurs is still of utmost importance in areas such as cell reprogramming and therapeutics models. In this sense, module identification can be useful to well characterise the global graph architecture. To help us with this identification, we perform topological overlap-related measures. Thanks to these measures, the location of highly disease-specific module regulators is possible. Such regulators can perturb other nodes, potentially causing the entire system to change behaviour or collapse. We provide a geometric framework explaining such situations in the context of inflammatory bowel diseases (IBD). IBD are severe chronic disorders of the gastrointestinal tract whose incidence is dramatically increasing worldwide. Our approach models different IBD status as Riemannian manifolds defined by the graph Laplacian of two high throughput proteome screenings. It also identifies module regulators as singularities within the manifolds (the so-called singular manifolds). Furthermore, it reinterprets the characteristic nonlinear dynamics of IBD as compensatory responses to perturbations on those singularities. Then, particular reconfigurations of the immune system could make the disease status move towards an innocuous target state.

Indexed as

Disease SusceptibilityProteomeProteomicsAlgorithmsBiomarkersColitis, UlcerativeComputational BiologyCrohn DiseaseDisease ProgressionHumansInflammation MediatorsInflammatory Bowel DiseasesModels, BiologicalReproducibility of ResultsBiomarkersInflammation MediatorsProteome

Identifiers

PMID33149233
PMCPMC7643119

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.