ArticleImmunogenetics1990
Genetic control of avian scleroderma.
Article in Immunogenetics, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- Avian models with spontaneous autoimmune diseases.Advances in immunology · 2006Review
- Animal models for scleroderma: an update.Current rheumatology reports · 2002Review
- Altered procollagen mRNA expression during the progression of avian scleroderma.Molecular medicine (Cambridge, Mass.) · 1997Article
- Endothelial cell apoptosis is a primary pathogenetic event underlying skin lesions in avian and human scleroderma.The Journal of clinical investigation · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The inheritance of avian scleroderma, a fibrotic autoimmune disease of chickens resembling human scleroderma, was investigated. Comb inflammations and lesions were used to determine the state of disease of 4-week-old chickens. All line 200 males and 60% of female line 200 chicks showed abnormalities. Crosses (F1) between line 200 and eight partially inbred lines of chickens maintained at the University of California at Davis were all normal. Backcrosses of F1 cocks to line 200 hens showed a higher incidence of scleroderma in males than in females for all lines. The incidence of affected birds varied between backcrosses from a low of 42% for backcross line 217 males derived from a New Hampshire line, to 88% for males of backcross line 213 derived from a partially inbred Leghorn line, demonstrating the presence of genes modifying the penetrance of presumed major genes causing the disease. Backcross genotypes segregating for haplotypes of the major histocompatibility complex (MHC) derived from inbred lines showed consistently lower penetrance of scleroderma than homozygotes carrying the line 200 haplotype. Thus B3Bs (lines 211 and 215), B14Bs (line 217), and B15Bs (lines 212, 213, 216, and 218) all had fewer affected individuals than BsBs homozygotes from the same families.
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What OpenQuestion holds
Registered trials
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.