Evidence map›Paper›PMID 16222037›Full record

ReviewProceedings of the American Thoracic Society2005

Genetic determinants and ethnic disparities in sepsis-associated acute lung injury.

Kathleen C Barnes

Abstract readReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-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

16 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Healthcare disparities in critical illness.Critical care medicine · 2013
    Review
  7. Article
  8. Article
  9. Article
  10. Endothelial dysfunction and claudin 5 regulation during acrolein-induced lung injury.American journal of respiratory cell and molecular biology · 2011
    Article
  11. Article
  12. Review
  13. Article
  14. Recent advances in genetic predisposition to clinical acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2009
    Review
  15. Article
  16. 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

1 author at 1 institution in 1 country.

Kathleen C BarnesDivision of Johns Hopkins Allergy and Clinical Immunology, Johns Hopkins University, Baltimore, MD 21224, USA. kbarnes@jhmi.edu
Johns Hopkins University · US

Funding

VENTILATOR ASSOCIATED LUNG INJURY: MOLECULAR APPROACHESP50HL073994 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BROWER, ROY G. · 2003 to 2007
$21.3M
NHLBI NIH HHS P50 HL073994NHLBI NIH HHS P50HL07399401
6 · The paper itself

Abstract

Acute lung injury (ALI) is a common and devastating illness that occurs in the context of sepsis and other systemic inflammatory disorders. In systemic illnesses like sepsis, only a subset of patients develops ALI even when pathologic stimuli are apparently equivalent, suggesting that there are genetic features that may influence its onset. Considerable obstacles in defining the exact nature of the pathogenesis of ALI include substantial phenotypic variance, incomplete penetrance, complex gene-environment interactions and a strong potential for locus heterogeneity. Moreover, ALI arises in a critically ill population with diverse precipitating factors and appropriate controls that best match the reference population have not been agreed upon. The sporadic nature of ALI precludes conventional approaches such as linkage mapping for the elucidation of candidate genes, but tremendous progress has been made in combining robust, genomic tools such as high-throughput, expression profiling with case-control association studies in well characterized populations. Similar to trends observed in common, complex traits such as hypertension and diabetes, some of these studies have highlighted differences in allelic variant frequencies between European American and African American ALI patients for novel genes which may explain, in part, the complex interplay between ethnicity, sepsis and the development of ALI. In trying to understand the basis for contemporary differences in allelic frequency, which may lead to differences in susceptibility, the potential role of positive selection for genetic variants in ancestral populations is considered.

Indexed as

Black or African AmericanBlack PeopleGene Expression ProfilingGene FrequencyGenetic Predisposition to DiseaseHumansRespiratory Distress SyndromeRisk FactorsSepsisWhite People

Identifiers

PMID16222037
PMCPMC2713318
OpenAlexW2099243786

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.