Evidence map›Paper›PMID 12162731›Full record

ReviewJournal of anatomy2002

Blood-brain barrier breakdown in septic encephalopathy and brain tumours.

D C Davies

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Journal of anatomy, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03133208 (Serum Biomarkers in Sepsis Associated Encephalopathy), which is not on this map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed
8.0field-weighted citation impact, top 3% 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.

NCT03133208 active not recruitingnot on this mapstarted 2017, after this paper: background citation

Serum Biomarkers in Sepsis Associated Encephalopathy (SAE)

TypeobservationalSponsorUniversity of FloridaRan2017 to 2026Enrolled90ConditionsSepsis, Altered Mental Status, Sepsis-Associated Delirium, Sepsis Associated EncephalopathyArmsBlood draws
3 · Its place in the literature

Who cites it

141 citing papers in PubMed, 308 citations in OpenAlex.

  1. Trial
  2. Article
  3. Lung endothelial cytopathic tau is sufficient to impair long-term potentiation during infection.American journal of respiratory cell and molecular biology · 2026
    Article
  4. Article
  5. Endothelial αvβ3 integrin induction during hypoxia protects blood-brain barrier integrity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Treatment advances in high-grade gliomas.Frontiers in oncology · 2024
    Review
  19. Aquaporins in sepsis- an update.Frontiers in immunology · 2024
    Review
  20. Article

81 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

1 author at 1 institution in 1 country.

D C DaviesDepartment of Anatomy and Developmental Biology, St George's Hospital Medical School, Tooting, London, UK. daviesdc@sghms.ac.uk
St George's Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Septic encephalopathy is associated with breakdown of the blood-brain barrier and cerebral oedema. These features are also common properties of brain tumours. Perimicrovessel oedema, disruption of associated astrocyte end feet and neuronal injury occur in a porcine model of acute septic encephalopathy. The adrenergic system has been implicated in the inflammatory response to sepsis and may play a role in controlling blood-brain barrier permeability, since the beta2-adrenoceptor agonist dopexamine inhibits perimicrovessel oedema formation whereas the alpha1-adrenoceptor agonist methoxamine provokes it. Electron microscopy revealed tight junction opening in high-grade astrocytoma microvessels. Expression of the tight junction protein occludin is reduced in these microvessels and this reduction is inversely correlated with the degree of cerebral oedema. Normal astrocytes secrete factors that induce barrier properties in endothelial cells, whereas high-grade astrocytomas secrete vascular endothelial growth factor, which stimulates angiogenesis, down regulates occludin and increases endothelial cell permeability. The water channel protein aquaporin-4 is normally expressed in astrocyte foot processes around cerebral microvessels. Its expression is massively up-regulated in high-grade astrocytoma and around metastatic adenocarcinoma. There is a significant correlation between aquaporin-4 expression and the degree of cerebral oedema, but it is not clear whether increased aquaporin-4 expression enhances oedema formation or clearance. These results suggest that the pathophysiology of brain oedema is multifactorial, but that there may be common processes operating regardless of the aetiology.

Indexed as

Blood-Brain BarrierAquaporin 4AquaporinsAstrocytomaBrain EdemaBrain NeoplasmsEndothelium, VascularHumansMembrane ProteinsOccludinSepsisTight JunctionsAQP4 protein, humanAquaporin 4AquaporinsMembrane ProteinsOccludinOCLN protein, human

Identifiers

PMID12162731
PMCPMC1570752
OpenAlexW2015387729

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.