Evidence map›Paper›PMID 32635699›Full record

ArticleClinical and experimental emergency medicine2020

Effect of complement C1-esterase inhibitor on brain edema and inflammation after mild traumatic brain injury in an animal model.

Eric Weiss, Teena Dhir, Abigail Collett, Michal Reola, Mark Kaplan, Corrado Minimo, Laurel Omert, Pak Leung

Open access · diamondAbstract read
In one paragraph

Article in Clinical and experimental emergency medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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  3. Article
  4. Review
  5. Article
  6. Tackling Neuroinflammation After Traumatic Brain Injury: Complement Inhibition as a Therapy for Secondary Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  7. Article
  8. Review
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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 3 institutions in 1 country.

Eric WeissDepartment of Surgery, Einstein Healthcare Network, Philadelphia, PA, USA.
Teena DhirDepartment of Surgery, Einstein Healthcare Network, Philadelphia, PA, USA.
Abigail CollettPhiladelphia College of Osteopathic Medicine, Philadelphia, PA, USA.
Michal ReolaDepartment of Surgery, Einstein Healthcare Network, Philadelphia, PA, USA.
Mark KaplanDepartment of Surgery, Einstein Healthcare Network, Philadelphia, PA, USA.
Corrado MinimoDepartment of Surgery, Einstein Healthcare Network, Philadelphia, PA, USA.
Laurel OmertDepartment of Surgery, Einstein Healthcare Network, Philadelphia, PA, USA.
Pak LeungDepartment of Surgery, Einstein Healthcare Network, Philadelphia, PA, USA.
Einstein Healthcare Network · USPhiladelphia College of Osteopathic Medicine · USThomas Jefferson University · US

Funding

Albert Einstein Society 8579
6 · The paper itself

Abstract

objectiveTraumatic brain injury (TBI) is characterized by damage to the blood-brain barrier, inflammation, and edema formation. In this pilot study, we aimed to investigate the effects of a complement inhibitor, C1-esterase inhibitor (C1 INH), on brain edema and inflammation in a rat model of mild TBI.

methodsThirty-six male Sprague Dawley rats were randomly assigned to control, TBI, or TBI plus C1 INH groups. TBI and TBI plus C1 INH rats received an injection of saline or 25 IU/kg C1 INH, respectively, with TBI using a weight drop model. Control rats received saline only. Rats were subsequently euthanized and their brain tissue harvested for analysis. The primary outcome was the extent of edema as assessed by the brain's water content. Secondary outcomes included enzyme-linked immunosorbent assays to determine levels of pro-inflammatory mediators.

resultsTumor necrosis factor-α levels were significantly greater in TBI rats than control rats, indicating that inflammation was generated by the weight drop impact. Brain water content following TBI was significantly different between TBI rats treated with C1-INH (78.7%±0.12), untreated TBI rats (79.3%±0.12), and control rats (78.6%±0.15, P=0.001). There was a significant decrease in C3a and interleukin 2 levels among C1 INH-treated rats compared with untreated TBI rats, but no change in levels of tumor necrosis factor-α and S100β.

conclusionC1-INH inhibited the complement pathway, suggesting that C1-INH may have a therapeutic benefit in TBI. Further studies are needed to investigate the effect of C1-INH on clinical outcomes.

Indexed as

Brain injuries, traumaticComplement system proteinsCytokinesEdemaInflammation

Identifiers

PMID32635699
PMCPMC7348678
OpenAlexW3040279377

What OpenQuestion holds

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LicenceCC BY-NC
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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.