Evidence map›Paper›PMID 17943142›Full record

ArticleGenes and immunity2008

An autosomal genome-wide screen for celiac disease in Bedouin families.

Y C Ding, Z Weizman, B Yerushalmi, K Elbedour, C P Garner, S L Neuhausen

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Genes and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 31% 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.

  1. Pooled it
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

6 authors at 2 institutions in 2 countries.

Y C DingDepartment of Epidemiology, University of California Irvine, Irvine, CA 92697-7550, USA.
Z Weizman
B Yerushalmi
K Elbedour
C P Garner
S L Neuhausen
Soroka Medical Center · ILUniversity of California, Irvine · US

Funding

MAPPING OF NON-HLA LOCI FOR GLUTEN SENSITIVE ENTEROPATHYR01DK050678 · NIDDK · UNIVERSITY OF UTAH · PI NEUHAUSEN, SUSAN L. · 1996 to 2005
$2.7M
GENOTYPING FOR LOCATING HUMAN DISEASE GENESN01HG065403 · NHGRI · JOHNS HOPKINS UNIVERSITY · PI VALLE, DAVID L · 1996 to 2000
$1.7M
NHGRI NIH HHS N01-HG-65403NIDDK NIH HHS DK50678
6 · The paper itself

Abstract

Celiac disease is a common, familial autoimmune disease caused by exposure to gliadin in wheat, and related prolamins in barley and rye. The prevalence of the disease is approximately 1:133. Celiac disease can cause significant morbidity. The only treatment is a gluten-free diet. A genome-wide search of 405 microsatellite markers was performed on samples from 18 Bedouin families with a minimum of two cases of celiac disease. Non-parametric and parametric (including both dominant and recessive models of inheritance) linkage analyses were performed. The most significant genome-wide linkage evidence was at chromosome 3p26 with an HLod of 3.21, under the dominant model. The only other HLod or NPL greater than 2 was at 4q35, with an HLod of 2.15 under a dominant model. The region at 3p26, previously reported in two linkage analyses, harbors interleukin receptor genes, plausible candidates for celiac disease.

Indexed as

FamilyGenetic TestingGenome, HumanArabsCeliac DiseaseChromosomes, Human, Pair 3Chromosomes, Human, Pair 4Genes, DominantGenes, RecessiveGenetic HeterogeneityGenetic LinkageGenetic MarkersHaplotypesHumansLod ScoreMicrosatellite RepeatsGenetic Markers

Identifiers

PMID17943142
OpenAlexW2058109237

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.