Evidence map›Paper›PMID 29343614›Full record

ArticleDisease models & mechanisms2018

Suppressor of cytokine signaling 2 (

Ross Dobie, Vicky E MacRae, Chloe Pass, Elspeth M Milne, S Faisal Ahmed, Colin Farquharson

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

6 authors at 2 institutions in 1 country.

Ross DobieDivision of Developmental Biology, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Roslin, Midlothian, Edinburgh EH25 9RG, UK.
Vicky E MacRaeDivision of Developmental Biology, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Roslin, Midlothian, Edinburgh EH25 9RG, UK.
Chloe PassDivision of Developmental Biology, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Roslin, Midlothian, Edinburgh EH25 9RG, UK.
Elspeth M MilneDivision of Developmental Biology, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Roslin, Midlothian, Edinburgh EH25 9RG, UK.
S Faisal AhmedSchool of Medicine, University of Glasgow, Royal Hospital for Children, Govan Road, Glasgow G51 4TF, UK.
Colin FarquharsonDivision of Developmental Biology, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Roslin, Midlothian, Edinburgh EH25 9RG, UK colin.farquharson@roslin.ed.ac.uk.ORCID 0000-0002-4970-4039
Roslin Institute · GBRoyal Hospital for Children · GB

Funding

Biotechnology and Biological Sciences Research Council BB/J004316/1Medical Research Council MR/N003403/1
6 · The paper itself

Abstract

Individuals with inflammatory bowel disease (IBD) often present with poor bone health. The development of targeted therapies for this bone loss requires a fuller understanding of the underlying cellular mechanisms. Although bone loss in IBD is multifactorial, the altered sensitivity and secretion of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) in IBD is understood to be a critical contributing mechanism. The expression of suppressor of cytokine signaling 2 (SOCS2), a well-established negative regulator of GH signaling, is stimulated by proinflammatory cytokines. Therefore, it is likely that SOCS2 expression represents a critical mediator through which proinflammatory cytokines inhibit GH/IGF-1 signaling and decrease bone quality in IBD. Using the dextran sodium sulfate (DSS) model of colitis, we reveal that endogenously elevated GH function in the

Indexed as

Gene DeletionAnimalsBody WeightBone and BonesCancellous BoneColonCortical BoneDextran SulfateInflammatory Bowel DiseasesInsulin-Like Growth Factor IMice, Inbred C57BLPhenotypeRNA, MessengerSuppressor of Cytokine Signaling ProteinsTibiaDextran SulfateInsulin-Like Growth Factor IRNA, MessengerSocs2 protein, mouseSuppressor of Cytokine Signaling ProteinsBoneGrowth hormoneIBDInflammatory bowel diseaseSOCS2

Identifiers

PMID29343614
PMCPMC5818069
OpenAlexW2776160409

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.