Evidence map›Paper›PMID 8101041›Full record

ArticleAmerican journal of human genetics1993

Meiotic crossing-over in nondisjoined chromosomes of children with trisomy 21 and a congenital heart defect.

C M Howard, G E Davies, M J Farrer, L M Cullen, M M Coleman, R Williamson, R K Wyse, R Palmer, A M Kessling

Abstract read
In one paragraph

Article in American journal of human genetics, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

3 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Down syndrome phenotypes: the consequences of chromosomal imbalance.Proceedings of the National Academy of Sciences of the United States of America · 1994
    Article
  3. 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

9 authors at 1 institution in 1 country.

C M HowardDepartment of Biochemistry and Molecular Genetics, St. Mary's Hospital Medical School, London, England.
G E Davies
M J Farrer
L M Cullen
M M Coleman
R Williamson
R K Wyse
R Palmer
A M Kessling
St. Mary's Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have used DNA polymorphisms to study meiotic crossovers of chromosome 21q in 27 nuclear families. Each family had a child with Down syndrome and a congenital heart defect. Twenty DNA polymorphisms on chromosome 21 were used to determine parental and meiotic origin of nondisjunction and to identify crossovers. Twenty-four cases were of maternal origin, and three were of paternal origin. Twenty-two unequivocal crossover events were identified. Sixteen crossovers were observed in 22 chromosome pairs nondisjoining at the second meiotic division. Fifty percent of crossover events in MI nondisjunction are detectable by molecular genetic means. Thus, the results suggest that, in this sample, each nondisjoined chromosome 21 pair has been involved in at least one crossover event.

Indexed as

Crossing Over, GeneticNondisjunction, GeneticAdolescentChildChild, PreschoolChromosomes, Human, Pair 21Down SyndromeFathersFemaleGenotypeHeart Defects, CongenitalHumansMaleMeiosisMothersPolymorphism, Restriction Fragment Length

Identifiers

PMID8101041
PMCPMC1682344
OpenAlexW1510344557

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.