Evidence map›Paper›PMID 32671850›Full record

ArticleAnnals of the New York Academy of Sciences2020

Magnetic resonance imaging analysis of long-term neuropathology after exposure to the nerve agent soman: correlation with histopathology and neurological dysfunction.

Sandesh D Reddy, Xin Wu, Ramkumar Kuruba, Vidya Sridhar, Doodipala Samba Reddy

Open access · greenAbstract read
In one paragraph

Article in Annals of the New York Academy of Sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Sandesh D ReddyDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas.
Xin WuDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas.
Ramkumar KurubaDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas.
Vidya SridharTexas A&M Institute for Preclinical Studies, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Texas.
Doodipala Samba ReddyDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas.ORCID 0000-0003-2735-9550
Texas A&M Health Science Center · USTexas A&M University · US

Funding

Neurosteroid Treatment for OP IntoxicationU01NS083460 · NINDS · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI REDDY, DOODIPALA SAMBA · 2013 to 2017
$3.4M
Epigenetic Attenuation of Long-Term Effects of Nerve AgentsR21NS099009 · NINDS · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI REDDY, DOODIPALA SAMBA · 2017 to 2018
$408k
NINDS NIH HHS R21 NS099009NINDS NIH HHS U01 NS083460
6 · The paper itself

Abstract

Nerve agents (NAs) produce acute and long-term brain injury and dysfunction, as evident from the Japan and Syria incidents. Magnetic resonance imaging (MRI) is a versatile technique to examine such chronic anatomical, functional, and neuronal damage in the brain. The objective of this study was to investigate long-term structural and neuronal lesion abnormalities in rats exposed to acute soman intoxication. T2-weighted MRI images of 10 control and 17 soman-exposed rats were acquired using a Siemens MRI system at 90 days after soman exposure. Quantification of brain tissue volumes and T2 signal intensity was conducted using the Inveon Research Workplace software and the extent of damage was correlated with histopathology and cognitive function. Soman-exposed rats showed drastic hippocampal atrophy with neuronal loss and reduced hippocampal volume (HV), indicating severe damage, but had similar T2 relaxation times to the control group, suggesting limited scarring and fluid density changes despite the volume decrease. Conversely, soman-exposed rats displayed significant increases in lateral ventricle volumes and T2 times, signifying strong cerebrospinal fluid expansion in compensation for tissue atrophy. The total brain volume, thalamic volume, and thalamic T2 time were similar in both groups, however, suggesting that some brain regions remained more intact long-term after soman intoxication. The MRI neuronal lesions were positively correlated with the histological markers of neurodegeneration and neuroinflammation 90 days after soman exposure. The predominant MRI hippocampal atrophy (25%) was highly consistent with massive reduction (35%) of neuronal nuclear antigen-positive (NeuN

Indexed as

HippocampusInterneuronsMagnetic Resonance ImagingMemory DisordersNeurodegenerative DiseasesNeuroimagingAnimalsMaleNerve AgentsRatsRats, Sprague-DawleySomanTime FactorsNerve AgentsSomanepilepsyhippocampusmemoryMRInerve agentneuroimagingorganophosphatesoman

Identifiers

PMID32671850
PMCPMC7708405
OpenAlexW3042666257

What OpenQuestion holds

Textmetadata
LicenceTDM
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.