Evidence map›Paper›PMID 14561327›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2003

Genetic epidemiology, genetic maps and positional cloning.

Newton E Morton

Open access · greenAbstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. 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

1 author at 1 institution in 1 country.

Newton E MortonUniversity of Southampton, Human Genetics Division, Duthie Building, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK. nem@soton.ac.uk
Southampton General Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic epidemiology developed in the middle of the last century, focused on inherited causes of disease but with methods and results applicable to other traits and even forensics. Early success with linkage led to the localization of genes contributing to disease, and ultimately to the Human Genome Project. The discovery of millions of DNA markers has encouraged more efficient positional cloning by linkage disequilibrium (LD), using LD maps and haplotypes in ways that are rapidly evolving. This has led to large international programmes, some promising and others alarming, with laws about DNA patenting and ethical guidelines for responsible research still struggling to be born.

Indexed as

Chromosome MappingGenetic MarkersGenetic Predisposition to DiseaseGenetic ResearchGenotypeHaplotypesHumansLinkage DisequilibriumResearch SubjectsGenetic Markers

Identifiers

PMID14561327
PMCPMC1693267
OpenAlexW2157638282

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.