Evidence map›Paper›PMID 20698760›Full record

ArticleJournal of neurotrauma2010

Neuroproteomics: a biochemical means to discriminate the extent and modality of brain injury.

Andrew K Ottens, Liliana Bustamante, Erin C Golden, Changping Yao, Ronald L Hayes, Kevin K W Wang, Frank C Tortella, Jitendra R Dave

Open access · greenAbstract read
In one paragraph

Article in Journal of neurotrauma, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  7. iTRAQ-Based Quantitative Proteomics Reveals the New Evidence Base for Traumatic Brain Injury Treated with Targeted Temperature Management.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018
    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

8 authors at 2 institutions in 1 country.

Andrew K OttensDepartment of Anatomy, Medical College of Virginia at Virginia Commonwealth University, Richmond, Virginia 23298-0709, USA. akottens@vcu.edu
Liliana Bustamante
Erin C Golden
Changping Yao
Ronald L Hayes
Kevin K W Wang
Frank C Tortella
Jitendra R Dave
University of Florida · USBanyan Biomarkers (United States) · US

Funding

Dynamics of the Traumatic Brain Injury Degradome.K25NS055012 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI OTTENS, ANDREW K · 2006 to 2009
$670k
NINDS NIH HHS NS055012
6 · The paper itself

Abstract

Diagnosis and treatment of stroke and traumatic brain injury remain significant health care challenges to society. Patient care stands to benefit from an improved understanding of the interactive biochemistry underlying neurotrauma pathobiology. In this study, we assessed the power of neuroproteomics to contrast biochemical responses following ischemic and traumatic brain injuries in the rat. A middle cerebral artery occlusion (MCAO) model was employed in groups of 30-min and 2-h focal neocortical ischemia with reperfusion. Neuroproteomes were assessed via tandem cation-anion exchange chromatography-gel electrophoresis, followed by reversed-phase liquid chromatography-tandem mass spectrometry. MCAO results were compared with those from a previous study of focal contusional brain injury employing the same methodology to characterize homologous neocortical tissues at 2 days post-injury. The 30-min MCAO neuroproteome depicted abridged energy production involving pentose phosphate, modulated synaptic function and plasticity, and increased chaperone activity and cell survival factors. The 2-h MCAO data indicated near complete loss of ATP production, synaptic dysfunction with degraded cytoarchitecture, more conservative chaperone activity, and additional cell survival factors than those seen in the 30-min MCAO model. The TBI group exhibited disrupted metabolism, but with retained malate shuttle functionality. Synaptic dysfunction and cytoarchitectural degradation resembled the 2-h MCAO group; however, chaperone and cell survival factors were more depressed following TBI. These results underscore the utility of neuroproteomics for characterizing interactive biochemistry for profiling and contrasting the molecular aspects underlying the pathobiological differences between types of brain injuries.

Indexed as

Analysis of VarianceAnimalsBlotting, WesternBrain InjuriesBrain IschemiaChromatography, Ion ExchangeChromatography, LiquidDisease Models, AnimalMaleProteomicsRatsRats, Sprague-DawleyReperfusion InjuryTandem Mass Spectrometry

Identifiers

PMID20698760
PMCPMC2953930
OpenAlexW2137885865

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.