Evidence map›Paper›PMID 25390897›Full record

ArticlePloS one2014

Role of recurrent hypoxia-ischemia in preterm white matter injury severity.

Matthew W Hagen, Art Riddle, Evelyn McClendon, Xi Gong, Daniel Shaver, Taasin Srivastava, Justin M Dean, Ji-Zhong Bai, Tania M Fowke, Alistair J Gunn and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
7.1field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

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  13. Transient Hypoxemia Disrupts Anatomical and Functional Maturation of Preterm Fetal Ovine CA1 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  14. Review
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  17. Transient Hypoxemia Chronically Disrupts Maturation of Preterm Fetal Ovine Subplate Neuron Arborization and Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
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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

15 authors at 3 institutions in 2 countries.

Matthew W HagenDepartment of Pediatrics, Oregon Health & Science University, Portland, Oregon, United States of America.
Art RiddleDepartment of Pediatrics, Oregon Health & Science University, Portland, Oregon, United States of America.
Evelyn McClendonDepartment of Pediatrics, Oregon Health & Science University, Portland, Oregon, United States of America.
Xi GongDepartment of Pediatrics, Oregon Health & Science University, Portland, Oregon, United States of America.
Daniel ShaverDepartment of Pediatrics, Oregon Health & Science University, Portland, Oregon, United States of America.
Taasin SrivastavaDepartment of Pediatrics, Oregon Health & Science University, Portland, Oregon, United States of America.
Justin M DeanDepartment of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.
Ji-Zhong BaiDepartment of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.
Tania M FowkeDepartment of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.
Alistair J GunnDepartment of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.
Daniel F JonesNew Zealand Genomics Ltd./Bioinformatics Institute, School of Biological Sciences, University of Auckland, Auckland, New Zealand.
Larry S ShermanDivision of Neuroscience, Oregon National Primate Research Center, Beaverton, Oregon, United States of America; Department of Cell and Developmental Biology, Oregon Health & Science University, Portland, Oregon, United States of America.
Marjorie R GrafeDepartment of Pathology, Oregon Health & Science University, Portland, Oregon, United States of America.
A Roger HohimerDepartment of Obstetrics and Gynecology, Oregon Health & Science University, Portland, Oregon, United States of America.
Stephen A BackDepartment of Pediatrics, Oregon Health & Science University, Portland, Oregon, United States of America; Department of Neurology, Oregon Health & Science University, Portland, Oregon, United States of America.
Oregon Health & Science University · USUniversity of Auckland · NZOregon National Primate Research Center · US

Funding

Role of Extracellular Matrix in Hypoxic-Ischemic Perinatal White Matter InjuryR01NS054044 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2006 to 2021
$4.8M
Cellular Mechanisms of Fetal White Matter InjuryR01NS045737 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2003 to 2019
$3.7M
Cellular mechanisms of fetal white matter injuryR37NS045737 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2007 to 2013
$2.7M
Cellular and molecular mechanisms of preterm white matter injuryF30NS066704 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI RIDDLE, ART · 2010 to 2013
$174k
NICHD NIH HHS P01HD03443NINDS NIH HHS 1F30NS066704NINDS NIH HHS 1R01NS054044NINDS NIH HHS F30 NS066704NINDS NIH HHS R01 NS045737NINDS NIH HHS R01 NS054044NINDS NIH HHS R37 NS045737NINDS NIH HHS R37NS045737-06S1/06S2
6 · The paper itself

Abstract

objectiveAlthough the spectrum of white matter injury (WMI) in preterm infants is shifting from cystic necrotic lesions to milder forms, the factors that contribute to this changing spectrum are unclear. We hypothesized that recurrent hypoxia-ischemia (rHI) will exacerbate the spectrum of WMI defined by markers of inflammation and molecules related to the extracellular matrix (hyaluronan (HA) and the PH20 hyaluronidase) that regulate maturation of the oligodendrocyte (OL) lineage after WMI.

methodsWe employed a preterm fetal sheep model of in utero moderate hypoxemia and global severe but not complete cerebral ischemia that reproduces the spectrum of human WMI. The response to rHI was compared against corresponding early or later single episodes of HI. An ordinal rating scale of WMI was compared against an unbiased quantitative image analysis protocol that provided continuous histo-pathological outcome measures for astrogliosis and microglial activation. Late oligodendrocyte progenitors (preOLs) were quantified by stereology. Analysis of hyaluronan and the hyaluronidase PH20 defined the progressive response of the extracellular matrix to WMI.

resultsrHI resulted in a more severe spectrum of WMI with a greater burden of necrosis, but an expanded population of preOLs that displayed reduced susceptibility to cell death. WMI from single episodes of HI or rHI was accompanied by elevated HA levels and increased labeling for PH20. Expression of PH20 in fetal ovine WMI was confirmed by RT-PCR and RNA-sequencing.

conclusionsrHI is associated with an increased risk for more severe WMI with necrosis, but reduced risk for preOL degeneration compared to single episodes of HI. Expansion of the preOL pool may be linked to elevated hyaluronan and PH20.

Indexed as

AnimalsAnimals, NewbornCell Adhesion MoleculesExtracellular MatrixFemaleFetusHyaluronic AcidHyaluronoglucosaminidaseHypoxia-Ischemia, BrainNecrosisOligodendrogliaSheepWhite MatterCell Adhesion MoleculesHyaluronic Acidhyaluronidase PH-20Hyaluronoglucosaminidase

Identifiers

PMID25390897
PMCPMC4229227
OpenAlexW2038353477

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.