Evidence map›Paper›PMID 27513538›Full record

ArticleCritical care medicine2016

Computational Analysis Supports an Early, Type 17 Cell-Associated Divergence of Blunt Trauma Survival and Mortality.

Andrew Abboud, Rami A Namas, Mostafa Ramadan, Qi Mi, Khalid Almahmoud, Othman Abdul-Malak, Nabil Azhar, Akram Zaaqoq, Rajaie Namas, Derek A Barclay and 7 more

Open access · greenAbstract read
In one paragraph

Article in Critical care medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 2 institutions in 1 country.

Andrew Abboud1Department of Surgery, University of Pittsburgh, Pittsburgh, PA. 2Department of Sports Medicine and Nutrition, University of Pittsburgh, Pittsburgh, PA. 3Department of Computational & Systems Biology, University of Pittsburgh, Pittsburgh, PA. 4Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA. 5Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI. 6Center for Inflammation and Regenerative Modeling, McGowan Institute for Regenerative Medicine, Pittsburgh, PA.
Rami A Namas
Mostafa Ramadan
Qi Mi
Khalid Almahmoud
Othman Abdul-Malak
Nabil Azhar
Akram Zaaqoq
Rajaie Namas
Derek A Barclay
Jinling Yin
Jason Sperry
Andrew Peitzman
Ruben Zamora
Richard L Simmons
Timothy R Billiar
Yoram Vodovotz
University of Pittsburgh · USUniversity of Michigan–Ann Arbor · US

Funding

Regulation of Intestinal Mucosal Injury & Repair After Trauma/Hemorrhagic ShockP50GM053789 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BILLIAR, TIMOTHY R · 1997 to 2013
$18.0M
TRAINING IN TRAUMA AND SEPSIS RESEARCHT32GM008516 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TIMOTHY R BILLIAR · 1994 to 2026
$9.4M
NIGMS NIH HHS P50 GM053789NIGMS NIH HHS T32 GM008516
6 · The paper itself

Abstract

objectiveBlunt trauma patients may present with similar demographics and injury severity yet differ with regard to survival. We hypothesized that this divergence was due to different trajectories of systemic inflammation and utilized computational analyses to define these differences.

designRetrospective clinical study and experimental study in mice.

settingLevel 1 trauma center and experimental laboratory. PATIENTS: From a cohort of 493 victims of blunt trauma, we conducted a pairwise, retrospective, case-control study of patients who survived over 24 hours but ultimately died (nonsurvivors; n = 19) and patients who, after ICU admission, went on to be discharged(survivors; n = 19).

interventionsNone in patients. Neutralizing anti-interleukin-17A antibody in mice. MEASUREMENTS AND MAIN

resultsData on systemic inflammatory mediators assessed within the first 24 hours and over 7 days were analyzed with computational modeling to infer dynamic networks of inflammation. Network density among inflammatory mediators in nonsurvivors increased in parallel with organ dysfunction scores over 7 days, suggesting the presence of early, self-sustaining, pathologic inflammation involving high-mobility group protein B1, interleukin-23, and the Th17 pathway. Survivors demonstrated a pattern commensurate with a self-resolving, predominantly lymphoid response, including higher levels of the reparative cytokine interleukin-22. Mice subjected to trauma/hemorrhage exhibited reduced organ damage when treated with anti-interleukin-17A.

conclusionsVariable type 17 immune responses are hallmarks of organ damage, survival, and mortality after blunt trauma and suggest a lymphoid cell-based switch from self-resolving to self-sustaining inflammation.

Indexed as

Models, BiologicalAnimalsAntibodiesCase-Control StudiesFemaleHMGB1 ProteinHumansInflammationInterleukin-17Interleukin-22Interleukin-23InterleukinsMaleMiddle AgedOrgan Dysfunction ScoresRetrospective StudiesAntibodiesHMGB1 ProteinInterleukin-17Interleukin-22Interleukin-23Interleukins

Identifiers

PMID27513538
PMCPMC5201164
OpenAlexW2513924918

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.