Evidence map›Paper›PMID 15745103›Full record

ArticleDigestive diseases and sciences2005

Genotypic and phenotypic stability of Helicobacter pylori markers in a nine-year follow-up study of patients with noneradicated infection.

Anders Gustavsson, Magnus Unemo, Björn Blomberg, Dan Danielsson

Abstract read
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Article in Digestive diseases and sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. An enzymatic ruler modulates Lewis antigen glycosylation of Helicobacter pylori LPS during persistent infection.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  6. 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.

Anders GustavssonDepartment of Medicine, Division of Gastroenterology, Orebro University Hospital, Orebro, Sweden.
Magnus Unemo
Björn Blomberg
Dan Danielsson

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cagA gene, alleles of the vacA gene,random amplified polymorphic DNA (RAPD), and neutrophil activating capacity (HpNAC) were used to examine paired H. pylori isolates from 10 noneradicated individuals 9 years apart. Paired isolates from each patient were indistinguishable with regard to vacA alleles, RAPD, and HpNAC. Isolates from nine patients showed concordance for the cagA gene, which was not detected in the recent isolate of the tenth patient. Antibodies to CagA were, however, demonstrated in the serum specimens 9 years apart and were also present in two other patients whose paired isolates were cagA-, indicating the existence of both cagA+ and cagA-organisms, with the latter predominating in some patients. The present study suggests a greater stability of phenotypic and genotypic markers of H. pylori than previously regarded. This might be true for a community with low infection and transmission rates. Complementary techniques like microarrays might, however, disclose evolutionary changes not identified here.

Indexed as

AdultAntigens, BacterialBacterial ProteinsEnzyme-Linked Immunosorbent AssayFemaleFollow-Up StudiesGenes, BacterialGenotypeHelicobacter InfectionsHelicobacter pyloriHumansImmunoglobulin AImmunoglobulin GLuminescent MeasurementsMaleMiddle AgedAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriImmunoglobulin AImmunoglobulin Gneutrophil-activating protein A, Helicobacter pyloriVacA protein, Helicobacter pylori

Identifiers

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Registered trials

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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.