Evidence map›Paper›PMID 18937363›Full record

ArticleBirth defects research. Part A, Clinical and molecular teratology2008

Wnt signaling in caudal dysgenesis and diabetic embryopathy.

Gabriela Pavlinkova, J Michael Salbaum, Claudia Kappen

Open access · greenAbstract read
In one paragraph

Article in Birth defects research. Part A, Clinical and molecular teratology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The status of diabetic embryopathy.Upsala journal of medical sciences · 2016
    Review
  7. Article
  8. Article
  9. TGFβ and Wnt in cardiac outflow tract defects in offspring of diabetic pregnancies.Birth defects research. Part B, Developmental and reproductive toxicology · 2014
    Article
  10. Modeling anterior development in mice: diet as modulator of risk for neural tube defects.American journal of medical genetics. Part C, Seminars in medical genetics · 2013
    Review
  11. Article
  12. Responses of the embryonic epigenome to maternal diabetes.Birth defects research. Part A, Clinical and molecular teratology · 2012
    Article
  13. Article
  14. Strain-specific modifier genes governing craniofacial phenotypes.Birth defects research. Part A, Clinical and molecular teratology · 2012
    Article
  15. Diabetic embryopathy: a role for the epigenome?Birth defects research. Part A, Clinical and molecular teratology · 2011
    Review
  16. Article
  17. Neural tube defect genes and maternal diabetes during pregnancy.Birth defects research. Part A, Clinical and molecular teratology · 2010
    Article
  18. 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

3 authors at 2 institutions in 1 country.

Gabriela PavlinkovaDepartment of Pediatrics, University of Nebraska Medical Center, Omaha, Nebraska, USA.
J Michael Salbaum
Claudia Kappen
Louisiana State University System · USUniversity of Nebraska Medical Center · US

Funding

TRANSGENIC EXPRESSION ANALYSIS OF MIRNA-144P20RR018788 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI NYSTUEN, ARNE M · 2003 to 2011
$16.5M
MOLECULAR MECHANISMS IN DIABETIC EMBRYOPATHYR01HD037804 · NICHD · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI KAPPEN, CLAUDIA T · 1998 to 2010
$2.5M
NCRR NIH HHS P20 RR018788NICHD NIH HHS R01 HD037804NICHD NIH HHS R01-HD37804NICHD NIH HHS R01-HD37804-S1
6 · The paper itself

Abstract

backgroundCongenital defects are a major complication of diabetic pregnancy, and the leading cause of infant death in the first year of life. Caudal dysgenesis, occurring up to 200-fold more frequently in children born to diabetic mothers, is a hallmark of diabetic pregnancy. Given that there is also an at least threefold higher risk for heart defects and NTDs, it is important to identify the underlying molecular mechanisms for aberrant embryonic development.

methodsWe have investigated gene expression in a transgenic mouse model of caudal dysgenesis, and in a pharmacological model using situ hybridization and quantitative real-time PCR.

resultsWe identified altered expression of several molecules that control developmental processes and embryonic growth.

conclusionsThe results from our models point towards major implication of altered Wnt signaling in the pathogenesis of developmental anomalies associated with embryonic exposure to maternal diabetes.

Indexed as

Pregnancy in DiabeticsSignal TransductionAnimalsDiabetes Mellitus, ExperimentalDisease Models, AnimalEmbryo, MammalianFemaleFetal DiseasesMiceMice, TransgenicNeural Tube DefectsPregnancyWnt ProteinsWnt Proteins

Identifiers

PMID18937363
PMCPMC2963627
OpenAlexW2023643048

What OpenQuestion holds

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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.