Evidence map›Paper›PMID 7706484›Full record

ArticleThe Journal of clinical investigation1995

Population and family studies of three disease-related polymorphic genes in systemic lupus erythematosus.

D F Huang, K A Siminovitch, X Y Liu, T Olee, N J Olsen, C Berry, D A Carson, P P Chen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

7 citing papers in PubMed, 30 citations in OpenAlex.

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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

8 authors at 3 institutions in 2 countries.

D F HuangDepartment of Medicine, University of California, San Diego, La Jolla 92093-0663, USA.
K A Siminovitch
X Y Liu
T Olee
N J Olsen
C Berry
D A Carson
P P Chen
University of California San Diego · USScripps Research Institute · USUniversity of Toronto · CA

Funding

VALIDATION OF SELF ADMINISTERED QUALITY OF WELL BEING SCALE IN ARTHRITISP60AR040770 · NIAMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SILVERMAN, GREGG JOSHUA · 1991 to 2000
$787k
MOLECULAR GENETICS OF AUTOANTIBODIES IN HUMANSR01AI032243 · NIAID · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI CHEN, POJEN P · 1991 to 2000
$275k
RHEUMATOID FACTOR: GENETICS, PATHOGENESIS, &MODULATIONR01AR025443 · NIAMS · SCRIPPS CLINIC AND RESEARCH FOUNDATION · PI CARSON, DENNIS A · 1986 to 1988
–
RHEUMATOID FACTOR: GENETICS, PATHOGENESIS AND MODULATIONR37AR025443 · NIAMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI CARSON, DENNIS A · 1989 to 1998
–
NIAID NIH HHS AI-32243NIAMS NIH HHS AR-25443NIAMS NIH HHS AR-40770
6 · The paper itself

Abstract

The contribution to systemic lupus erythematosus (SLE) of three lupus-associated polymorphisms (involving the C4A2 complement component, Humhv3005 and the T cell antigen receptor alpha chain gene) are investigated in 81 individuals from 14 multiplex SLE families, 41 unrelated lupus patients, and 88 unrelated healthy controls. The results show a strong association between C4A deletion and SLE in these families. While the current study confirms the previously reported association between hv3005 deletion and sporadic SLE, the study fails to support this association in familial SLE patients. Moreover, no correlation is detected between the occurrence of hv3005 deletion and C4A null alleles in lupus patients, suggesting that the effects of these genetic polymorphisms on predisposition to lupus are independent. The previously reported lupus-associated T cell receptor (TCR) alpha chain polymorphism is not detected in any of the individuals studied here. The combined data suggest that C4A null alleles predispose strongly to development of lupus, whereas the influence of hv3005 deletion is relatively weak. The results also suggest that contributions of weak susceptibility genes such as hv3005 to disease predisposition may be obscured by the effects of stronger genetic factors and thus need to be examined in patients lacking these factors.

Indexed as

Polymorphism, Restriction Fragment LengthBase SequenceCanadaComplement C4aFemaleGene DeletionGenetics, PopulationGenome, HumanHumansImmunoglobulin Variable RegionLupus Erythematosus, SystemicMaleMolecular Sequence DataPedigreeReceptors, Antigen, T-Cell, alpha-betaRisk FactorsComplement C4aImmunoglobulin Variable RegionReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID7706484
PMCPMC295700
OpenAlexW2045144441

What OpenQuestion holds

Textmetadata
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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.