Evidence map›Paper›PMID 16105888›Full record

ArticleGut2006

Serum from achalasia patients alters neurochemical coding in the myenteric plexus and nitric oxide mediated motor response in normal human fundus.

S Bruley des Varannes, J Chevalier, S Pimont, J-C Le Neel, M Klotz, K-H Schafer, J-P Galmiche, M Neunlist

Open access · greenAbstract read
In one paragraph

Article in Gut, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Achalasia.Nature reviews. Disease primers · 2022
    Review
  3. Article
  4. Review
  5. Review
  6. An Overview of Achalasia and Its Subtypes.Gastroenterology & hepatology · 2017
    Article
  7. Review
  8. Article
  9. Observational
  10. Review
  11. Review
  12. Chronic constipation: no more idiopathic, but a true neuropathological entity.Gastroenterology and hepatology from bed to bench · 2011
    Review
  13. Review
  14. Article
  15. Article
  16. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

S Bruley des VarannesINSERM U539, University Hospital Hôtel Dieu, Place Alexis Ricordeau, 44035 NANTES Cedex, France.
J Chevalier
S Pimont
J-C Le Neel
M Klotz
K-H Schafer
J-P Galmiche
M Neunlist
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsAchalasia is a disease of unknown aetiology. An immune mechanism has been suggested on the basis of previous morphological observations. The objective of this study was to test whether the serum of achalasia patients could reproduce the phenotype and functional changes that occur with disease progression in an ex vivo human model.

methodsSpecimens of normal human fundus were maintained in culture in the presence of serum from patients with achalasia, gastro-oesophageal reflux disease (GORD), or healthy subjects (controls). Immunohistochemical detection of choline acetyltransferase (ChAT), neurone specific enolase (NSE), vasoactive intestinal polypeptide (VIP), nitric oxide synthase (NOS), and substance P was carried out in whole mounts of gastric fundus myenteric plexus. In addition, the effects of achalasia serum on electrical field stimulation (EFS) induced contractions were measured in circular muscle preparations.

resultsSerum from achalasia patients did not affect the number of myenteric neurones. Tissues incubated with serum from achalasia patients showed a decrease in the proportion of NOS (-26% of NSE positive neurones; p=0.016) and VIP (-54%; p=0.09) neurones, and a concomitant increase in ChAT neurones (+16%; p<0.001) compared with controls. In contrast, GORD serum did not modify the phenotype of myenteric neurones. Area under the curve of EFS induced relaxations (abolished by N-nitro-L-arginine methyl ester) was significantly decreased following incubation with serum from achalasia patients compared with controls (-7.6 (2.6) v -14.5 (5.0); p=0.036).

conclusionsSerum from achalasia patients can induce phenotypic and functional changes which reproduce the characteristics of the disease. Further identification of putative seric factors and mechanisms involved could lead to the development of novel diagnostic and/or therapeutic strategies in achalasia.

Indexed as

AdultAgedAged, 80 and overCholine O-AcetyltransferaseDisease ProgressionElectric StimulationEsophageal AchalasiaFemaleGangliaGastric FundusGastroesophageal RefluxHumansMaleMiddle AgedMyenteric PlexusNitrergic NeuronsCholine O-AcetyltransferaseNitric OxideNitric Oxide SynthaseVasoactive Intestinal Peptide

Identifiers

PMID16105888
PMCPMC1856095
OpenAlexW2134048332

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.