Evidence map›Paper›PMID 2066099›Full record

ArticleHuman genetics1991

Screening for a prevalent LDL receptor mutation in patients with severe hypercholesterolaemia.

M J Savolainen, T Korhonen, K Aalto-Setälä, K Kontula, Y A Kesäniemi

Abstract read
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In one paragraph

Article in Human genetics, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

0 citing papers in PubMed, 10 citations in OpenAlex.

No citing paper in PubMed yet.

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

5 authors at 2 institutions in 1 country.

M J SavolainenBiocenter Oulu, University of Oulu, Finland.
T Korhonen
K Aalto-Setälä
K Kontula
Y A Kesäniemi
University of Oulu · FIUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A rapid new method for the diagnosis of familial hypercholesterolaemia (FH) detects the deletion extending from intron 15 to exon 18 in the low density lipoprotein (LDL) receptor gene, i.e. the FH-Helsinki mutation responsible for a major portion of FH in Finland. Amplification of the DNA sequences flanking the deletion in the mutant allele generated an abnormal 391-bp product that could be detected by photographing the ethidium-bromide-stained agarose gel after electrophoresis. Up to 50 samples can be analysed in about 8 h. The method was validated by comparison with a routine Southern blot technique. The deletion was found in 23 out of 37 patients with a clinical diagnosis of FH (62%) and in 2 out of 73 with primary hypercholesterolaemia without a clinical diagnosis of FH within a series of 110 consecutive patients with severe hypercholesterolaemia (serum cholesterol greater than 8 mmol/l). The data indicate that DNA techniques may provide a supplementary aid for the routine diagnosis of FH and suggest that the polymerase chain reaction in particular may offer major advantages because of its simplicity and rapidity.

Indexed as

Chromosome DeletionAdultBase SequenceCholesterolCholesterol, HDLCholesterol, LDLElectrophoresis, Agar GelFemaleGenetic TestingHumansHypercholesterolemiaMaleMiddle AgedMolecular Sequence DataOligonucleotide ProbesPolymerase Chain ReactionCholesterolCholesterol, HDLCholesterol, LDLOligonucleotide ProbesReceptors, LDLTriglycerides

Identifiers

PMID2066099
OpenAlexW1990395287

What OpenQuestion holds

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Registered trials

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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.