Evidence map›Paper›PMID 7714835›Full record

ArticleThe Journal of physiology1995

The genetic advantage hypothesis in cystic fibrosis heterozygotes: a murine study.

A W Cuthbert, J Halstead, R Ratcliff, W H Colledge, M J Evans

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 74 citations in OpenAlex.

  1. Trial
  2. Article
  3. Mechanisms by which the cystic fibrosis transmembrane conductance regulator may influence SARS-CoV-2 infection and COVID-19 disease severity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  4. Article
  5. Lessons in aging from Myc knockout mouse models.Frontiers in cell and developmental biology · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Hypoxia inducible factor-1 (HIF-1)-mediated repression of cystic fibrosis transmembrane conductance regulator (CFTR) in the intestinal epithelium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009
    Article
  11. Evaluating candidate agents of selective pressure for cystic fibrosis.Journal of the Royal Society, Interface · 2007
    Article
  12. Lung infections associated with cystic fibrosis.Clinical microbiology reviews · 2002
    Review
  13. Article
  14. Article
  15. Article
  16. delta F508 in cystic fibrosis: willing but not able.Archives of disease in childhood · 1997
    Review
  17. Article
  18. A mouse model for the delta F508 allele of cystic fibrosis.The Journal of clinical investigation · 1995
    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

5 authors at 1 institution in 1 country.

A W CuthbertDepartment of Pharmacology, University of Cambridge, UK.
J Halstead
R Ratcliff
W H Colledge
M J Evans
University of Cambridge · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

1. The delta F508 mutation of the cystic fibrosis (CF) gene is of high frequency in man (1 in 25) and in homozygotes causes cystic fibrosis. It is suggested that cystic fibrosis heterozygotes withstand secretory diarrhoea better than normal individuals and so are genetically advantaged. This hypothesis has been examined by measuring electrogenic chloride secretion in gut epithelia of normal and heterozygous CF mice. 2. Chloride secretory responses of normal and heterozygous colonic epithelia to forskolin, vasoactive intestinal polypeptide (VIP), isoprenaline, cholera toxin, heat-stable enterotoxin (STa), guanylin, carbachol and lysylbradykinin were examined. No significant differences in responses of tissues of the two genotypes were found. 3. Responses of normal and heterozygous ileal epithelia to forskolin and glucose were investigated. Heterozygous tissues responded as well as normal tissues. 4. Frusemide (furosemide) caused virtually identical inhibition of the chloride secretory responses to forskolin in colonic epithelia of both genotypes. 5. No evidence to support the genetic advantage hypothesis in ileal or colonic epithelia of the null CF mouse has been found, at least for acute responses. If the hypothesis is true then either (a) other non-cystic fibrosis transmembrane conductance regulator (non-CFTR) transport processes are involved, (b) prolonged exposure to secretagogues is required, or (c) delta F508 CFTR is responsible for the protective effect.

Indexed as

Gastrointestinal HormonesAnimalsBacterial ToxinsCalciumCarbacholChloride ChannelsCholera ToxinColforsinColonCyclic AMPCystic FibrosisEnterotoxinsEpitheliumEscherichia coli ProteinsFurosemideGlucoseBacterial ToxinsCalciumCarbacholChloride ChannelsCholera ToxinColforsinCyclic AMPEnterotoxinsEscherichia coli ProteinsFurosemideGastrointestinal HormonesGlucoseguanylinheat stable toxin (E coli)IsoproterenolKallidinNatriuretic PeptidesPeptidesVasoactive Intestinal Peptide

Identifiers

PMID7714835
PMCPMC1157742
OpenAlexW2084619830

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.