Evidence map›Paper›PMID 9038658›Full record

ArticleGut1996

Increased production of interleukin 1 beta and hepatocyte growth factor may contribute to foveolar hyperplasia in enlarged fold gastritis.

Y Yasunaga, Y Shinomura, S Kanayama, Y Higashimoto, M Yabu, Y Miyazaki, S Kondo, Y Murayama, H Nishibayashi, S Kitamura and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 82 citations in OpenAlex.

  1. Trial
  2. World journal of gastroenterology · 2023
    Review
  3. [Clinical Application of the Kyoto Classification of Gastritis].The Korean journal of helicobacter and upper gastrointestinal research · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Endoscopic Kyoto classification ofWorld journal of gastroenterology · 2020
    Review
  10. Article
  11. Nodular gastritis in association with gastric cancer development before and afterJGH open : an open access journal of gastroenterology and hepatology · 2018
    Article
  12. Interleukin-1B signalling leads to increased survival of gastric carcinoma cells through a CREB-C/EBPβ-associated mechanism.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2016
    Article
  13. Article
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  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Y YasunagaSecond Department of Internal Medicine, Osaka University Medical School, Japan.
Y Shinomura
S Kanayama
Y Higashimoto
M Yabu
Y Miyazaki
S Kondo
Y Murayama
H Nishibayashi
S Kitamura
Y Matsuzawa
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsIt has been reported that eradication of Helicobacter pylori improves fold width in H pylori associated enlarged fold gastritis. The aim of this study was to clarify the mechanism of fold thickening in this condition. PATIENTS AND

methodsIn eight patients with enlarged fold gastritis and 13 patients without enlarged folds, the presence of H pylori infection, inflammatory infiltrates, mucosal plasia, and epithelial cell proliferation in the body mucosa were investigated, and production of transforming growth factor alpha (TGF alpha), hepatocyte growth factor (HGF), and interleukin 1 beta (IL 1 beta) was determined by a competitive reverse transcription/polymerase chain reaction method and in vitro short-term culture of biopsy specimens.

resultsIn the patients with enlarged fold gastritis, inflammatory infiltrates including macrophages increased with H pylori colonisation in the body. Foveolar thickness and proliferating cell nuclear antigen (PCNA) labelling index were increased. Messenger RNA levels of HGF, but not TGF alpha, were increased, and release of HGF and IL 1 beta was increased. HGF release, which was positively correlated with IL 1 beta release and foveolar thickness, decreased in the presence of IL 1 receptor antagonist. After eradication of H pylori, inflammatory infiltrates, IL 1 beta and HGF release decreased with concomitant decreases in PCNA labelling index, foveolar thickness and fold width.

conclusionsIncreased IL 1 beta and HGF production caused by H pylori infection may contribute to fold thickening of the stomach by stimulating epithelial cell proliferation and foveolar hyperplasia in patients with enlarged fold gastritis.

Indexed as

Helicobacter pyloriAdultAgedBiomarkersEpitheliumFemaleGastric MucosaGastritis, HypertrophicHelicobacter InfectionsHepatocyte Growth FactorHumansInterleukin-1MaleMiddle AgedPolymerase Chain ReactionProliferating Cell Nuclear AntigenBiomarkersHepatocyte Growth FactorInterleukin-1Proliferating Cell Nuclear AntigenRNA, MessengerTransforming Growth Factor alpha

Identifiers

PMID9038658
PMCPMC1383448
OpenAlexW2006921696

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.