Evidence map›Paper›PMID 15760595›Full record

ReviewCurrent rheumatology reports2005

Animal models in scleroderma.

Stephen H Clark

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Is scleroderma a vasculopathy?Current rheumatology reports · 2009
    Review
  4. Article
  5. Fibrosis in systemic sclerosis.Rheumatic diseases clinics of North America · 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

1 author.

Stephen H ClarkUniversity of Connecticut Health Center, Farmington, CT 06030, USA. sclark@nso2.uchc.edu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Scleroderma or systemic sclerosis is an insidious connective tissue disease with no known cure. A hallmark feature of scleroderma is the excess synthesis and deposition of collagen resulting in a fibrotic state. In scleroderma, fibrosis is not confined only to the skin but impacts internal organs as well. In an effort to better understand the pathophysiology of this disease, researchers have developed a variety of animal models that display features of the human condition. This paper focuses on mouse models of scleroderma and summarizes work conducted with these experimental paradigms that is focused on understanding the cellular and molecular events associated with the onset and maintenance of fibrosis.

Indexed as

Disease Models, AnimalScleroderma, SystemicAnimalsGenetic EngineeringMiceRodent Diseases

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.