Evidence map›Paper›PMID 16556512›Full record

ReviewAutonomic neuroscience : basic & clinical2006

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases.

Paul L R Andrews, Charles C Horn

Open access · greenAbstract readReview
In one paragraph

Review in Autonomic neuroscience : basic & clinical, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 3 pooled it
19.9field-weighted citation impact, top 1% 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

116 citing papers in PubMed, 3 syntheses or guidelines pooled it, 250 citations in OpenAlex.

  1. Pooled it
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  7. Article
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  12. Article
  13. Review
  14. Sensory signals for nausea.Trends in neurosciences · 2025
    Review
  15. Article
  16. Review
  17. Endocannabinoid signaling in stress, nausea, and vomiting.Neurogastroenterology and motility · 2025
    Review
  18. Article
  19. Article
  20. Article

56 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Paul L R AndrewsDivision of Basic Medical Sciences, St George's University of London, Cranmer Terrace, London, SW 17 0RE, UK. pandrews@sgul.ac.uk
Charles C Horn
Monell Chemical Senses Center · USSt George's, University of London · GB

Funding

Neural basis of learned food aversion and nauseaR01DK065971 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HORN, CHARLES CHRISTOPHER · 2004 to 2009
$1.2M
NIDDK NIH HHS DK065971NIDDK NIH HHS R01 DK065971
6 · The paper itself

Abstract

Nausea and vomiting are amongst the most common symptoms encountered in medicine as either symptoms of diseases or side effects of treatments. In a more biological setting they are also important components of an organism's defences against ingested toxins. Identification of treatments for nausea and vomiting and reduction of emetic liability of new therapies has largely relied on the use of animal models, and although such models have proven invaluable in identification of the anti-emetic effects of both 5-hydroxytryptamine(3) and neurokinin(1) receptor antagonists selection of appropriate models is still a matter of debate. The present paper focuses on a number of controversial issues and gaps in our knowledge in the study of the physiology of nausea and vomiting including: The choice of species for the study of emesis and the underlying behavioural (e.g. neophobia), anatomical (e.g. elongated, narrow abdominal oesophagus with reduced ability to shorten) and physiological (e.g. brainstem circuitry) mechanisms that explain the lack of a vomiting reflex in certain species (e.g. rats); The choice of response to measure (emesis[retching and vomiting], conditioned flavour avoidance or aversion, ingestion of clay[pica], plasma hormone levels[e.g. vasopressin], gastric dysrhythmias) and the relationship of these responses to those observed in humans and especially to the sensation of nausea; The stimulus coding of nausea and emesis by abdominal visceral afferents and especially the vagus-how do the afferents encode information for normal postprandial sensations, nausea and finally vomiting?; Understanding the central processing of signals for nausea and vomiting is particularly problematic in the light of observations that vomiting is more readily amenable to pharmacological treatment than is nausea, despite the assumption that nausea represents "low" intensity activation of pathways that can evoke vomiting when stimulated more intensely.

Indexed as

Disease Models, AnimalAnimalsHumansNauseaResearch DesignSpecies SpecificityVomiting

Identifiers

PMID16556512
PMCPMC2658708
OpenAlexW2012053734

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.