Evidence map›Paper›PMID 26063194›Full record

ReviewArchives of disease in childhood. Fetal and neonatal edition2015

New horizons for newborn brain protection: enhancing endogenous neuroprotection.

K Jane Hassell, Mojgan Ezzati, Daniel Alonso-Alconada, Derek J Hausenloy, Nicola J Robertson

2 registry-linked trialsOpen access · bronzeAbstract readReview
In one paragraph

Review in Archives of disease in childhood. Fetal and neonatal edition, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 108 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 7 pooled it
35.1field-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.

NCT03806816 naunknown statusnot on this mapstarted 2018, after this paper: background citation

Use of Melatonin for Neuroprotection in Term Infants With Hypoxic-ischaemic Encephalopathy

TypeinterventionalSponsorUniversity Hospital of FerraraRan2018 to 2022Enrolled100ConditionsHypoxic-Ischemic Encephalopathy, Cell Damage, Asphyxia PerinatalArmsMelatonin, PLACEBO group
NCT03897101 unknown statusnot on this mapstarted 2019, after this paper: background citation

Autophagy, Mitophagy, Inflammation and Plasmatic Concentration of Melatonin in Newborn With Metabolic Acidosis at Birth

Typeobservational_patient_registrySponsorUniversity Hospital of FerraraRan2019 to 2020Enrolled150ConditionsNeonatal Encephalopathy, Cell Damage, Metabolic Acidosis, Inflammation
3 · Its place in the literature

Who cites it

108 citing papers in PubMed, 7 syntheses or guidelines pooled it, 203 citations in OpenAlex.

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  19. Peculiarities of melatonin levels in preterm infants.Wiener klinische Wochenschrift · 2024
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48 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

5 authors at 2 institutions in 1 country.

K Jane HassellInstitute for Women's Health, University College London, London, UK.
Mojgan EzzatiInstitute for Women's Health, University College London, London, UK.
Daniel Alonso-AlconadaInstitute for Women's Health, University College London, London, UK.
Derek J HausenloyThe Hatter Cardiovascular Institute, Institute of Cardiovascular Science, NIHR University College London Hospitals Biomedical Research Centre, University College London Hospital & Medical School, London, UK.
Nicola J RobertsonInstitute for Women's Health, University College London, London, UK.
University College London · GBUCL Biomedical Research Centre · GB

Funding

British Heart Foundation FS/10/039/28270Department of HealthMedical Research Council MR/J00457X/1
6 · The paper itself

Abstract

Intrapartum-related events are the third leading cause of childhood mortality worldwide and result in one million neurodisabled survivors each year. Infants exposed to a perinatal insult typically present with neonatal encephalopathy (NE). The contribution of pure hypoxia-ischaemia (HI) to NE has been debated; over the last decade, the sensitising effect of inflammation in the aetiology of NE and neurodisability is recognised. Therapeutic hypothermia is standard care for NE in high-income countries; however, its benefit in encephalopathic babies with sepsis or in those born following chorioamnionitis is unclear. It is now recognised that the phases of brain injury extend into a tertiary phase, which lasts for weeks to years after the initial insult and opens up new possibilities for therapy.There has been a recent focus on understanding endogenous neuroprotection and how to boost it or to supplement its effectors therapeutically once damage to the brain has occurred as in NE. In this review, we focus on strategies that can augment the body's own endogenous neuroprotection. We discuss in particular remote ischaemic postconditioning whereby endogenous brain tolerance can be activated through hypoxia/reperfusion stimuli started immediately after the index hypoxic-ischaemic insult. Therapeutic hypothermia, melatonin, erythropoietin and cannabinoids are examples of ways we can supplement the endogenous response to HI to obtain its full neuroprotective potential. Achieving the correct balance of interventions at the correct time in relation to the nature and stage of injury will be a significant challenge in the next decade.

Indexed as

Asphyxia NeonatorumBrainCannabinoidsErythropoietinHumansHypothermia, InducedHypoxia-Ischemia, BrainInfant, NewbornMelatoninNeuroprotectionNeuroprotective AgentsCannabinoidsErythropoietinMelatoninNeuroprotective AgentsBirth asphyxiaMelatoninNeonatal encephalopathyNeuroprotectionPost Conditioning

Identifiers

PMID26063194
PMCPMC4680177
OpenAlexW2217900354

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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.