Evidence map›Paper›PMID 10981038›Full record

ReviewCurrent hypertension reports

Linkage mapping for hypertension susceptibility genes.

N Kato, C Julier

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Genetic determinants of hypertension: an update.Current hypertension reports · 2008
    Review
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

2 authors.

N KatoDepartment of Internal Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8605, Japan.
C Julier

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several approaches based on linkage methods have been used to identify susceptibility genes for hypertension. Tests of candidate genes for essential hypertension have generally relied on the combination of linkage and association studies, and have given mostly negative or relatively conflicting results between studies. The detailed exploration of a candidate region, eg, a region of human homology to a principal quantitative trait locus for blood pressure variation in the rat, has led to the identification of linkage to a susceptibility locus for hypertension in humans. Studies of rare Mendelian forms of hypertension have enabled us to identify causative genes in several instances, and to detect mere linkages to chromosomal regions in other instances. Whether molecular variants at these genes are pathophysiologically involved in the common form of hypertension remains to be established. Finally, genome-wide linkage studies for essential hypertension are currently in progress. Confirming linkage to particular regions or genes with a high statistical significance in essential hypertension may prove difficult, therefore, other lines of evidence for a particular gene's role in hypertension susceptibility, derived from either studies in animal models, studies of Mendelian forms of hypertension, or from association studies, may prove to be crucial.

Indexed as

Chromosome MappingAnimalsGenetic MarkersGenetic Predisposition to DiseaseGenetic TestingHumansHypertensionRatsGenetic Markers

Identifiers

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.