Evidence map›Paper›PMID 28533743›Full record

ReviewFrontiers in cellular neuroscience2017

Neonatal Hypoxia Ischaemia: Mechanisms, Models, and Therapeutic Challenges.

Lancelot J Millar, Lei Shi, Anna Hoerder-Suabedissen, Zoltán Molnár

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed, 2 pooled it
41.4field-weighted citation impact, top 1% 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

167 citing papers in PubMed, 2 syntheses or guidelines pooled it, 341 citations in OpenAlex.

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107 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 4 countries.

Lancelot J MillarMolnár Group, Department of Physiology, Anatomy and Genetics, University of OxfordOxford, UK.
Lei ShiMolnár Group, Department of Physiology, Anatomy and Genetics, University of OxfordOxford, UK.
Anna Hoerder-SuabedissenMolnár Group, Department of Physiology, Anatomy and Genetics, University of OxfordOxford, UK.
Zoltán MolnárMolnár Group, Department of Physiology, Anatomy and Genetics, University of OxfordOxford, UK.
Oxford Research Group · GBJinan University · CN

Funding

Medical Research Council MR/N026039/1
6 · The paper itself

Abstract

Neonatal hypoxia-ischaemia (HI) is the most common cause of death and disability in human neonates, and is often associated with persistent motor, sensory, and cognitive impairment. Improved intensive care technology has increased survival without preventing neurological disorder, increasing morbidity throughout the adult population. Early preventative or neuroprotective interventions have the potential to rescue brain development in neonates, yet only one therapeutic intervention is currently licensed for use in developed countries. Recent investigations of the transient cortical layer known as subplate, especially regarding subplate's secretory role, opens up a novel set of potential molecular modulators of neonatal HI injury. This review examines the biological mechanisms of human neonatal HI, discusses evidence for the relevance of subplate-secreted molecules to this condition, and evaluates available animal models. Neuroserpin, a neuronally released neuroprotective factor, is discussed as a case study for developing new potential pharmacological interventions for use post-ischaemic injury.

Indexed as

encephalopathyhypoxia-ischemianeonatalneurodevelopmentneuroprotectionneuroserpinsubplate

Identifiers

PMID28533743
PMCPMC5420571
OpenAlexW2613618132

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.