Evidence map›Paper›PMID 11686872›Full record

ReviewRespiratory research2001

Using single nucleotide polymorphisms as a means to understanding the pathophysiology of asthma.

L J Palmer, W O Cookson

Open access · goldAbstract readReview
In one paragraph

Review in Respiratory research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. An understanding of the genetic basis of asthma.The Indian journal of medical research · 2011
    Review
  3. Article
  4. Pharmacogenomics of pediatric asthma.Indian journal of human genetics · 2010
    Article
  5. Article
  6. Article
  7. Th2 cytokines and asthma: an introduction.Respiratory research · 2001
    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 at 2 institutions in 2 countries.

L J PalmerChanning Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. lyle.palmer@channing.harvard.edu
W O Cookson
Brigham and Women's Hospital · USCentre for Human Genetics · GB

Funding

ADMINISTRATIVE/EDUCATION CENTER FOR INNATE IMMUNITY PGAU01HL066795 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI WEISS, SCOTT T · 2000 to 2004
$1.9M
NHLBI NIH HHS U01 HL066795NHLBI NIH HHS U01-HL66795
6 · The paper itself

Abstract

Asthma is the most common chronic childhood disease in the developed nations, and is a complex disease that has high social and economic costs. Studies of the genetic etiology of asthma offer a way of improving our understanding of its pathogenesis, with the goal of improving preventive strategies, diagnostic tools, and therapies. Considerable effort and expense have been expended in attempts to detect specific polymorphisms in genetic loci contributing to asthma susceptibility. Concomitantly, the technology for detecting single nucleotide polymorphisms (SNPs) has undergone rapid development, extensive catalogues of SNPs across the genome have been constructed, and SNPs have been increasingly used as a method of investigating the genetic etiology of complex human diseases. This paper reviews both current and potential future contributions of SNPs to our understanding of asthma pathophysiology.

Indexed as

Polymorphism, Single NucleotideAnimalsAsthmaChromosome MappingGenetic Predisposition to DiseaseGenotypeHumansPolymorphism, Restriction Fragment Length

Identifiers

PMID11686872
PMCPMC59575
OpenAlexW2103872546

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.