Evidence map›Paper›PMID 30037420›Full record

ArticleThe American journal of pathology2018

Matrix-Assisted Laser Desorption Ionization Mapping of Lysophosphatidic Acid Changes after Traumatic Brain Injury and the Relationship to Cellular Pathology.

Whitney S McDonald, Elizabeth E Jones, Jonathan M Wojciak, Richard R Drake, Roger A Sabbadini, Neil G Harris

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Making a difference.European journal of translational myology · 2024
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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

6 authors at 3 institutions in 1 country.

Whitney S McDonaldUCLA Brain Injury Research Center, Department of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California.
Elizabeth E JonesMedical University of South Carolina Proteomics Center, Charleston, South Carolina.
Jonathan M WojciakLpath, Inc., San Diego, California.
Richard R DrakeMedical University of South Carolina Proteomics Center, Charleston, South Carolina.
Roger A SabbadiniLpath, Inc., San Diego, California.
Neil G HarrisUCLA Brain Injury Research Center, Department of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California. Electronic address: ngharris@ucla.edu.
Lpath (United States) · USMedical University of South Carolina · USUniversity of California, Los Angeles · US

Funding

A mechanism for stunted map plasticity after TBIR01NS091222 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HARRIS, NEIL · 2015 to 2019
$1.7M
Novel Anti-LPA Antibody for the Treatment of Traumatic Brain InjuryR44NS087641 · NINDS · LPATH THERAPEUTICS, INC. · PI HARRIS, NEIL, SABBADINI, ROGER A · 2014 to 2014
$224k
NINDS NIH HHS R01 NS091222NINDS NIH HHS R44 NS087641
6 · The paper itself

Abstract

Lysophosphatidic acid (LPA) levels increase in the cerebrospinal fluid and blood within 24 hours after traumatic brain injury (TBI), indicating it may be a biomarker for subsequent cellular pathology. However, no data exist that document this association after TBI. We, therefore, acquired matrix-assisted laser desorption ionization imaging mass spectrometry data of LPA, major LPA metabolites, and hemoglobin from adult rat brains at 1 and 3 hours after controlled cortical impact injury. Data were semiquantitatively assessed by signal intensity analysis normalized to naïve rat brains acquired concurrently. Gray and white matter pathology was assessed on adjacent sections using immunohistochemistry for cell death, axonal injury, and intracellular LPA, to determine the spatiotemporal patterning of LPA corresponding to pathology. The results revealed significant increases in LPA and LPA precursors at 1 hour after injury and robust enhancement in LPA diffusively throughout the brain at 3 hours after injury. Voxel-wise analysis of LPA by matrix-assisted laser desorption ionization and β-amyloid precursor protein by immunohistochemistry in adjacent sections showed significant association, raising the possibility that LPA is linked to secondary axonal injury. Total LPA and metabolites were also present in remotely injured areas, including cerebellum and brain stem, and in particular thalamus, where intracellular LPA is associated with cell death. LPA may be a useful biomarker of cellular pathology after TBI.

Indexed as

AnimalsBiomarkersBrain Injuries, TraumaticLysophospholipidsMaleRatsRats, Sprague-DawleySpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationBiomarkerslysophosphatidic acidLysophospholipids

Identifiers

PMID30037420
PMCPMC6099387
OpenAlexW2883068130

What OpenQuestion holds

Textmetadata
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.