Evidence map›Paper›PMID 8936357›Full record

ArticleJournal of neurology1996

Potential role of transforming growth factor-beta 1 in terminating the immune response in patients with Guillain-Barré syndrome.

E Sindern, K Schweppe, L M Ossege, J P Malin

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neurology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. A review of the role of genetic factors in Guillain-Barré syndrome.Journal of molecular neuroscience : MN · 2021
    Review
  4. Review
  5. Review
  6. Modelling neuroinflammatory phenotypes in vivo.Journal of neuroinflammation · 2004
    Article
  7. Article
  8. Article
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 at 2 institutions in 1 country.

E SindernNeurologische Klinik der Ruhr Universität, Bochum, Germany.
K Schweppe
L M Ossege
J P Malin
Ruhr University Bochum · DEBG University Hospital Bergmannsheil Bochum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-cell activation and proinflammatory cytokines seem to be important in promoting the disease activity in Guillain-Barré syndrome (GBS). Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional peptide with potent immunosuppressive activity, and can therefore be considered a putative disease-limiting cytokine. We determined levels of soluble TGF-beta 1 in the serum of 12 patients with GBS in serial investigations during the course of the disease, in 12 patients with other noninflammatory neurological diseases (OND), and in 12 healthy control subjects. Levels of biologically active and total TGF-beta 1 were significantly increased in patients with GBS compared with patients with OND and healthy controls. During the course of GBS, levels of TGF-beta 1 peaked in the plateau phase before onset of recovery. During the recovery phase levels of TGF-beta 1 decreased but still exceeded significantly the levels in patients with OND and healthy controls. The differences were more marked with biologically active than with total TGF-beta 1. The temporal relationship between increased serum levels of TGF-beta 1 and the end of the progressive phase indicates that TGF-beta 1 has a role in terminating the pathological immune response in GBS. These findings suggest that TGF-beta 1 may be important in recovery from GBS.

Indexed as

Antibody FormationCase-Control StudiesHumansImmune TolerancePolyradiculoneuropathySolubilityTransforming Growth Factor betaTransforming Growth Factor beta

Identifiers

PMID8936357
OpenAlexW2075932632

What OpenQuestion holds

Textmetadata
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.