Evidence map›Paper›PMID 32131477›Full record

ArticleBrain sciences2020

Modeling the Genetic Basis of Individual Differences in Susceptibility to Gulf War Illness.

Byron C Jones, Diane B Miller, Lu Lu, Wenyuan Zhao, David G Ashbrook, Fuyi Xu, Megan K Mulligan, Robert W Williams, Daming Zhuang, Carolina Torres-Rojas and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Observational
  6. Article
  7. Article
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  9. Exploring the Role of Chemokine Receptor 6 (Frontiers in neuroscience · 2020
    Article
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

11 authors at 2 institutions in 1 country.

Byron C JonesDepartment of Genetics, Genomics and Informatics, Department of Pharmacology, University of Tennessee Health Science Center, 71 South Manassas Street, Memphis, TN 38163, USA.
Diane B MillerMolecular Neurotoxicology Laboratory, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.
Lu LuDepartment of Genetics, Genomics and Informatics, Department of Pharmacology, University of Tennessee Health Science Center, 71 South Manassas Street, Memphis, TN 38163, USA.
Wenyuan ZhaoDepartment of Genetics, Genomics and Informatics, Department of Pharmacology, University of Tennessee Health Science Center, 71 South Manassas Street, Memphis, TN 38163, USA.
David G AshbrookDepartment of Genetics, Genomics and Informatics, Department of Pharmacology, University of Tennessee Health Science Center, 71 South Manassas Street, Memphis, TN 38163, USA.
Fuyi XuDepartment of Genetics, Genomics and Informatics, Department of Pharmacology, University of Tennessee Health Science Center, 71 South Manassas Street, Memphis, TN 38163, USA.
Megan K MulliganDepartment of Genetics, Genomics and Informatics, Department of Pharmacology, University of Tennessee Health Science Center, 71 South Manassas Street, Memphis, TN 38163, USA.
Robert W WilliamsDepartment of Genetics, Genomics and Informatics, Department of Pharmacology, University of Tennessee Health Science Center, 71 South Manassas Street, Memphis, TN 38163, USA.
Daming ZhuangDepartment of Genetics, Genomics and Informatics, Department of Pharmacology, University of Tennessee Health Science Center, 71 South Manassas Street, Memphis, TN 38163, USA.
Carolina Torres-RojasDepartment of Genetics, Genomics and Informatics, Department of Pharmacology, University of Tennessee Health Science Center, 71 South Manassas Street, Memphis, TN 38163, USA.
James P O'CallaghanMolecular Neurotoxicology Laboratory, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.
University of Tennessee Health Science Center · USCenters for Disease Control and Prevention · US

Funding

U.S. Department of Defense CDMRP grant W81XWH-17-1-0472
6 · The paper itself

Abstract

Between 25% and 30% of the nearly one million military personnel who participated in the 1991 Persian Gulf War became ill with chronic symptoms ranging from gastrointestinal to nervous system dysfunction. This disorder is now referred to as Gulf War Illness (GWI) and the underlying pathophysiology has been linked to exposure-based neuroinflammation caused by organophosphorous (OP) compounds coupled with high circulating glucocorticoids. In a mouse model of GWI we developed, corticosterone was shown to act synergistically with an OP (diisopropylflurophosphate) to dramatically increase proinflammatory cytokine gene expression in the brain. Because not all Gulf War participants became sick, the question arises as to whether differential genetic constitution might underlie individual differences in susceptibility. To address this question of genetic liability, we tested the impact of OP and glucocorticoid exposure in a genetic reference population of 30 inbred mouse strains. We also studied both sexes. The results showed wide differences among strains and overall that females were less sensitive to the combined treatment than males. Furthermore, we identified one OP-glucocorticoid locus and nominated a candidate gene-

Indexed as

BXD micecandidate genecorticosteroneDFPneuroinflammationrecombinant inbred strains

Identifiers

PMID32131477
PMCPMC7139661
OpenAlexW3008729059

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.