Evidence map›Paper›PMID 31119176›Full record

ArticleBioMed research international2019

Serum Amyloid A Protein as a Potential Biomarker for Severity and Acute Outcome in Traumatic Brain Injury.

Evan Wicker, Leah Benton, Kershina George, William Furlow, Sonia Villapol

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  18. The interaction between brain and liver regulates lipid metabolism in the TBI pathology.Biochimica et biophysica acta. Molecular basis of disease · 2021
    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

5 authors at 2 institutions in 1 country.

Evan WickerDepartment of Pharmacology & Physiology, Georgetown University, Washington, D.C., USA.ORCID 0000-0003-4242-7849
Leah BentonM.S. Biochemistry and Molecular Biology Program, Georgetown University, Washington, D.C., USA.
Kershina GeorgeM.S. Biochemistry and Molecular Biology Program, Georgetown University, Washington, D.C., USA.
William FurlowM.S. Biochemistry and Molecular Biology Program, Georgetown University, Washington, D.C., USA.
Sonia VillapolCenter for Neuroregeneration and Department of Neurosurgery, Houston Methodist Research Institute, Houston, TX, USA.ORCID 0000-0002-6174-4113
Georgetown University · USHouston Methodist · US

Funding

The role of peripheral serum amyloid A on brain inflammation after TBIR03NS095038 · NINDS · GEORGETOWN UNIVERSITY · PI VILLAPOL, SONIA · 2016 to 2017
$156k
NINDS NIH HHS R03 NS095038
6 · The paper itself

Abstract

Traumatic brain injury (TBI) causes a wide variety of neuroinflammatory events. These neuroinflammatory events depend, to a greater extent, on the severity of the damage. Our previous studies have shown that the liver produces serum amyloid A (SAA) at high levels in the initial hours after controlled cortical impact (CCI) injury in mice. Clinical studies have reported detectable SAA in the plasma of brain injury patients, but it is not clear if SAA levels depend on TBI severity. To evaluate this question, we performed a mild to severe CCI injury in wild-type mice. We collected blood samples and brains at 1, 3, and 7 days after injury for protein detection by western blotting, enzyme-linked immunosorbent assay, or immunohistochemical analysis. Our results showed that severe CCI injury compared to mild CCI injury or sham mice caused an increased neuronal death, larger lesion volume, increased microglia/macrophage density, and augmented neutrophil infiltration. Furthermore, we found that the serum levels of SAA protein ascended in the blood in correlation with high neuroinflammatory and neurodegenerative responses. Altogether, these results suggest that serum SAA may be a novel neuroinflammation-based, and severity-dependent, biomarker for acute TBI.

Indexed as

AnimalsBiomarkersBrainBrain Injuries, TraumaticDisease Models, AnimalHumansMiceSerum Amyloid A ProteinTrauma Severity IndicesBiomarkersSerum Amyloid A Protein

Identifiers

PMID31119176
PMCPMC6500682
OpenAlexW2935739875

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.