Evidence map›Paper›PMID 31553983›Full record

ArticleDevelopmental neuroscience2019

Administration of a 20-Hydroxyeicosatetraenoic Acid Synthesis Inhibitor Improves Outcome in a Rat Model of Pediatric Traumatic Brain Injury.

Shiyu Shu, Zhi Zhang, Dawn Spicer, Ewa Kulikowicz, Ke Hu, Savalan Babapoor-Farrokhran, Sujatha Kannan, Raymond C Koehler, Courtney L Robertson

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Developmental neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Shiyu ShuDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Zhi ZhangDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Dawn SpicerDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Ewa KulikowiczDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Ke HuDepartment of Ophthalmology, Retina Division, Wilmer Eye Institute, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Savalan Babapoor-FarrokhranDepartment of Ophthalmology, Retina Division, Wilmer Eye Institute, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Sujatha KannanDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Raymond C KoehlerDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.
Courtney L RobertsonDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA, crober48@jhmi.edu.
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Role of 20-HETE in Pediatric Traumatic Brain InjuryR01NS092747 · NINDS · JOHNS HOPKINS UNIVERSITY · PI ROBERTSON, COURTNEY L · 2016 to 2020
$1.8M
NINDS NIH HHS R01 NS092747
6 · The paper itself

Abstract

The arachidonic acid pathway metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) contributes to ischemia/reperfusion brain injury. Inhibition of 20-HETE formation can protect the developing brain from global ischemia. Here, we examined whether treatment with the 20-HETE synthesis inhibitor N-hydroxy-N-4-butyl-2-methylphenylformamidine (HET0016) can protect the immature brain from traumatic brain injury (TBI). Male rats at postnatal day 9-10 underwent controlled cortical impact followed by intraperitoneal injection with vehicle or HET0016 (1 mg/kg, 5 min and 3 h post-injury). HET0016 decreased the lesion volume by over 50% at 3 days of recovery, and this effect persisted at 30 days as the brain matured. HET0016 decreased peri-lesion gene expression of proinflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-1β [IL-1β]) at 1 day and increased reparative cytokine (IL-4, IL-10) expression at 3 days. It also partially preserved microglial ramified processes, consistent with less activation. HET0016 decreased contralateral hindlimb foot faults and improved outcome on the novel object recognition memory task 30 days after TBI. In cultured BV2 microglia, HET0016 attenuated the lipopolysaccharide-evoked increase in release of TNF-α. Our data show that HET0016 improves acute and long-term histologic and functional outcomes, in association with an attenuated neuroinflammatory response after contusion of an immature rat brain.

Indexed as

AmidinesAnimalsBrainBrain Injuries, TraumaticCytokinesDisease Models, AnimalHydroxyeicosatetraenoic AcidsInflammationMaleRats, Sprague-DawleyReperfusion Injury20-hydroxy-5,8,11,14-eicosatetraenoic acidAmidinesCytokinesHET0016Hydroxyeicosatetraenoic Acids20-Hydroxyeicosatetraenoic acidMicrogliaNeuroinflammationN-hydroxy-N-4-butyl-2-methylphenylformamidine

Identifiers

PMID31553983
PMCPMC7044071
OpenAlexW2976681202

What OpenQuestion holds

Textmetadata
LicenceTDM
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.