Evidence map›Paper›PMID 26725466›Full record

ArticleJournal of applied toxicology : JAT2016

Systems toxicology of chemically induced liver and kidney injuries: histopathology-associated gene co-expression modules.

Jerez A Te, Mohamed Diwan M AbdulHameed, Anders Wallqvist

Open access · hybridAbstract read
In one paragraph

Article in Journal of applied toxicology : JAT, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 24 citations in OpenAlex.

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  10. A Novel Open Access Web Portal for Integrating Mechanistic and Toxicogenomic Study Results.Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Article
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  12. Assessing Chemical-Induced Liver InjuryFrontiers in genetics · 2019
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Jerez A TeDepartment of Defense Biotechnology High Performance Computing Software Applications Institute, Telemedicine and Advanced Technology Research Center, U.S. Army Medical Research and Materiel Command, Fort Detrick, MD, 21702, USA.
Mohamed Diwan M AbdulHameedDepartment of Defense Biotechnology High Performance Computing Software Applications Institute, Telemedicine and Advanced Technology Research Center, U.S. Army Medical Research and Materiel Command, Fort Detrick, MD, 21702, USA.
Anders WallqvistDepartment of Defense Biotechnology High Performance Computing Software Applications Institute, Telemedicine and Advanced Technology Research Center, U.S. Army Medical Research and Materiel Command, Fort Detrick, MD, 21702, USA.
United States Army Medical Research and Development Command · USTelemedicine & Advanced Technology Research Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Organ injuries caused by environmental chemical exposures or use of pharmaceutical drugs pose a serious health risk that may be difficult to assess because of a lack of non-invasive diagnostic tests. Mapping chemical injuries to organ-specific histopathology outcomes via biomarkers will provide a foundation for designing precise and robust diagnostic tests. We identified co-expressed genes (modules) specific to injury endpoints using the Open Toxicogenomics Project-Genomics Assisted Toxicity Evaluation System (TG-GATEs) - a toxicogenomics database containing organ-specific gene expression data matched to dose- and time-dependent chemical exposures and adverse histopathology assessments in Sprague-Dawley rats. We proposed a protocol for selecting gene modules associated with chemical-induced injuries that classify 11 liver and eight kidney histopathology endpoints based on dose-dependent activation of the identified modules. We showed that the activation of the modules for a particular chemical exposure condition, i.e., chemical-time-dose combination, correlated with the severity of histopathological damage in a dose-dependent manner. Furthermore, the modules could distinguish different types of injuries caused by chemical exposures as well as determine whether the injury module activation was specific to the tissue of origin (liver and kidney). The generated modules provide a link between toxic chemical exposures, different molecular initiating events among underlying molecular pathways and resultant organ damage. Published 2016. This article is a U.S. Government work and is in the public domain in the USA. Journal of Applied Toxicology published by John Wiley & Sons, Ltd.

Indexed as

Gene Regulatory NetworksAnimalsBiomarkersDatabases, FactualDose-Response Relationship, DrugEndpoint DeterminationGene Expression ProfilingGene Expression RegulationGenomicsKidneyLiverMaleModels, BiologicalPrincipal Component AnalysisRatsRats, Sprague-DawleyBiomarkersXenobioticsadverse outcome pathwaysco-expression moduleshepatotoxicityhistopathologynephrotoxicitysystems toxicologytoxicogenomics

Identifiers

PMID26725466
PMCPMC5064727
OpenAlexW2225006655

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.