Evidence map›Paper›PMID 30846842›Full record

ArticleCellular & molecular immunology2019

Dissemination of brain inflammation in traumatic brain injury.

Kaibin Shi, Jianning Zhang, Jing-Fei Dong, Fu-Dong Shi

Abstract read
In one paragraph

Article in Cellular & molecular immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

88 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
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  6. Article
  7. Rubicon modulates neuroimmune responses following traumatic brain injury.bioRxiv : the preprint server for biology · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Compromised blood-brain barrier in traumatic brain injury model ofIranian journal of basic medical sciences · 2026
    Article
  12. Review
  13. Article
  14. Reticuline modulates astrocyte and microglial responses to enhance prognosis after traumatic brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  15. Article
  16. Hybridoma-inspired strategy crafts tailored multifunctional exosomes for precision therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Article
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  19. Article
  20. Article

28 more citing papers are in PubMed but not listed here.

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

4 authors.

Kaibin ShiDepartments of Neurology and Neurosurgery, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Jianning ZhangDepartments of Neurology and Neurosurgery, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Jing-Fei DongBloodWorks Northwest Research Institute, Division of Hematology, Department of Medicine, School of Medicine, University of Washington, Seattle, WA, 98195, USA.
Fu-Dong ShiDepartments of Neurology and Neurosurgery, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China. fshi66@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) is recognized as a global health problem due to its increasing occurrence, challenging treatment, and persistent impacts on brain pathophysiology. Neural cell death in patients with TBI swiftly causes inflammation in the injured brain areas, which is recognized as focal brain inflammation. Focal brain inflammation causes secondary brain injury by exacerbating brain edema and neuronal death, while also exerting divergent beneficial effects, such as sealing the damaged limitans and removing cellular debris. Recent evidence from patients with TBI and studies on animal models suggest that brain inflammation after TBI is not only restricted to the focal lesion but also disseminates to remote areas of the brain. The dissemination of inflammation has been detected within days after the primary injury and persists chronically. This state of inflammation may be related to remote complications of TBI in patients, such as hyperthermia and hypopituitarism, and may lead to progressive neurodegeneration, such as chronic traumatic encephalopathy. Future studies should focus on understanding the mechanisms that govern the initiation and propagation of brain inflammation after TBI and its impacts on post-trauma brain pathology.

Indexed as

AnimalsBrainBrain Injuries, TraumaticEncephalitisFree RadicalsHumansNeuronsNeurotoxinsFree RadicalsNeurotoxinsdisseminated brain inflammationmicrogliapost-injury neurodegenerationtraumatic brain injury

Identifiers

PMID30846842
PMCPMC6804599

What OpenQuestion holds

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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.