Evidence map›Paper›PMID 19812240›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2010

Role of late maternal thyroid hormones in cerebral cortex development: an experimental model for human prematurity.

P Berbel, D Navarro, E Ausó, E Varea, A E Rodríguez, J J Ballesta, M Salinas, E Flores, C C Faura, G Morreale de Escobar

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Reducing uncertainties in quantitative adverse outcome pathways by analysis of thyroid hormone in the neonatal rat brain.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 3 institutions in 1 country.

P BerbelInstituto de Neurociencias, Universidad Miguel Hernández and Consejo Superior de Investigaciones Científicas, Sant Joan d'Alacant, Alicante, Spain. pere.berbel@umh.es
D Navarro
E Ausó
E Varea
A E Rodríguez
J J Ballesta
M Salinas
E Flores
C C Faura
G Morreale de Escobar
Instituto de Neurociencias · ESConsejo Superior de Investigaciones Científicas · ESHospital Universitari Sant Joan D'Alacant · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypothyroxinemia affects 35-50% of neonates born prematurely (12% of births) and increases their risk of suffering neurodevelopmental alterations. We have developed an animal model to study the role of maternal thyroid hormones (THs) at the end of gestation on offspring's cerebral maturation. Pregnant rats were surgically thyroidectomized at embryonic day (E) 16 and infused with calcitonin and parathormone (late maternal hypothyroidism [LMH] rats). After birth, pups were nursed by normal rats. Pups born to LMH dams, thyroxine treated from E17 to postnatal day (P) 0, were also studied. In developing LMH pups, the cortical lamination was abnormal. At P40, heterotopic neurons were found in the subcortical white matter and in the hippocampal stratum oriens and alveus. The Zn-positive area of the stratum oriens of hippocampal CA3 was decreased by 41.5% showing altered mossy fibers' organization. LMH pups showed delayed learning in parallel to decreased phosphorylated cAMP response element-binding protein (pCREB) and phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) expression in the hippocampus. Thyroxine treatment of LMH dams reverted abnormalities. In conclusion, maternal THs are still essential for normal offspring's neurodevelopment even after onset of fetal thyroid function. Our data suggest that thyroxine treatment of premature neonates should be attempted to compensate for the interruption of the maternal supply.

Indexed as

AnimalsAnimals, NewbornBody PatterningBrainDevelopmental DisabilitiesDisease Models, AnimalDown-RegulationFemaleHippocampusHumansInfant, NewbornInfant, PrematureMaternal-Fetal ExchangeMossy Fibers, HippocampalNeurogenesisPregnancyThyroxine

Identifiers

PMID19812240
PMCPMC2871377
OpenAlexW2113004875

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.