Evidence map›Paper›PMID 23959780›Full record

ReviewCurrent allergy and asthma reports2013

New approaches to modulating idiopathic pulmonary fibrosis.

Richard H Gomer

Abstract readReview
In one paragraph

Review in Current allergy and asthma reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. 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.

Richard H Gomer

Funding

Regulating fibrocyte differentiation in fibrosisR01HL083029 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI GOMER, RICHARD H · 2006 to 2009
$1.5M
NHLBI NIH HHS R01 HL083029
6 · The paper itself

Abstract

Until recently, idiopathic pulmonary fibrosis (IPF) has been a devastating and generally fatal disease with no effective therapeutic. New developments in understanding the biology of the disease include a growing consensus that the lesions are mainly composed of cells that originated from resident fibroblasts. New developments in therapeutics include recommendations against several treatment regimes that have been previously used. On a positive note, the orally available drug pirfenidone has been approved for use in IPF in China, Japan, India, and the European Union, but not yet in the United States. Other possibilities for managing IPF include managing gastrointestinal reflux, and limiting excessive salt intake. A variety of potential therapeutics for IPF are in clinical trials; for instance, in a Phase 1b trial, intravenous injections of a recombinant version of the normal human serum protein Serum Amyloid P (SAP, also known as PTX2) improved lung function in IPF patients.

Indexed as

AnimalsDiagnosis, DifferentialGastrointestinal TractHumansIdiopathic Pulmonary FibrosisLungMacrophagesSerum Amyloid P-ComponentSerum Amyloid P-Component

Identifiers

PMID23959780
PMCPMC3947240

What OpenQuestion holds

Textmetadata
LicenceTDM
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.