Evidence map›Paper›PMID 15170041›Full record

ReviewThorax2004

Alpha1-antitrypsin deficiency. 4: Molecular pathophysiology.

D A Lomas, H Parfrey

Open access · bronzeAbstract readReview
In one paragraph

Review in Thorax, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 148 citations in OpenAlex.

  1. Article
  2. HeterozygousInternational journal of molecular sciences · 2024
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Intrapleural Gene Therapy for Alpha-1 Antitrypsin Deficiency-Related Lung Disease.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2018
    Article
  15. Article
  16. Observational
  17. Gene Therapy for Alpha-1 Antitrypsin Deficiency Lung Disease.Annals of the American Thoracic Society · 2016
    Review
  18. Review
  19. Article
  20. The βγ-crystallins: native state stability and pathways to aggregation.Progress in biophysics and molecular biology · 2014
    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 1 institution in 1 country.

D A LomasRespiratory Medicine Unit, Department of Medicine, University of Cambridge, Cambridge Institute for Medical Research, Cambridge CB2 2XY, UK. dal16@cam.ac.uk
H Parfrey
Wellcome Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular basis of alpha(1)-antitrypsin deficiency is reviewed and is shown to be due to the accumulation of mutant protein as ordered polymers within the endoplasmic reticulum of hepatocytes. The current goals are to determine the cellular response to polymeric alpha(1)-antitrypsin and to develop therapeutic strategies to block polymerisation in vivo.

Indexed as

alpha 1-Antitrypsinalpha 1-Antitrypsin DeficiencyHumansLiver DiseasesLung DiseasesMutationPolymersalpha 1-AntitrypsinPolymers

Identifiers

PMID15170041
PMCPMC1747018
OpenAlexW2130880533

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.