Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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.
Cole C JohnsonThe Russell H. Morgan Department of Radiology and Radiological Science, Division of Cancer Imaging Research, Johns Hopkins University, Baltimore, MD, USA.
Caitlin M TresslerThe Russell H. Morgan Department of Radiology and Radiological Science, Division of Cancer Imaging Research, Johns Hopkins University, Baltimore, MD, USA.
Kristine GlundeThe Russell H. Morgan Department of Radiology and Radiological Science, Division of Cancer Imaging Research, Johns Hopkins University, Baltimore, MD, USA.ORCID http://orcid.org/0000-0002-5067-2724
Rida AliThe Michael V. Johnston Center for Developmental Neuroscience, Kennedy Krieger Institute, Baltimore, MD, USA.
Michael J WolfgangDepartment of Physiology, Pharmacology & Therapeutics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID http://orcid.org/0000-0003-2349-8414
Susanna ScafidiDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. sscafid2@jhmi.edu.ORCID http://orcid.org/0000-0002-1229-8778
Joseph ScafidiThe Michael V. Johnston Center for Developmental Neuroscience, Kennedy Krieger Institute, Baltimore, MD, USA. Scafidi@kennedykrieger.org.
Funding
Sleep and Circadian Dysfunction, Brain and Neurobehavioral Development in AutismP50HD103538 · NICHD · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI Stewart H Mostofsky · 2020 to 2026
$9.9M
Bioenergetic Failure Underlies Cerebral Dysmaturity After Perinatal Brain InjuryR01NS099461 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI SCAFIDI, JOSEPH · 2017 to 2021
$1.9M
Coordination of fatty acid metabolism following neonatal brain injury from preterm birthR01NS125653 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI Joseph Scafidi, Susanna Scafidi · 2022 to 2026
$1.9M
Role of fatty acid oxidation after pediatric head injuryR01NS110808 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SCAFIDI, SUSANNA · 2019 to 2023
$1.8M
Mechanisms of metabolic adaptation after traumatic brain injuryR01NS111230 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SCAFIDI, SUSANNA · 2019 to 2023
$1.8M
NICHD NIH HHS P50 HD103538NINDS NIH HHS R01 NS099461NINDS NIH HHS R01 NS110808NINDS NIH HHS R01 NS111230NINDS NIH HHS R01 NS125653U.S. Department of Health & Human Services | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) P50HD103538U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) NS099461U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) NS110808U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) NS111230U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) NS125653
6 · The paper itself
Abstract
The brain is a lipid-rich organ that experiences rapid growth and development after birth in a period hallmarked by extensive lipid synthesis. We still lack a fundamental understanding of lipid metabolism during this critical time of brain development and how these dynamics occur in infants born extremely preterm (<28 weeks of gestation) suffering from brain injuries. Using an established model of neonatal brain injury due to intermittent hypoxemia, we recapitulate hippocampal-dependent cognitive impairments and examine the extent of changes in the brain's lipid profile. Our results show changes in hippocampal lipid composition and abnormal fatty acid profile. Furthermore, we provide evidence of an increase in mitochondrial fatty acid β-oxidation, a process that is not classically thought of occurring in the developing brain. We find that a specific alternative fuel, acetate, spares fatty acids from mitochondrial β-oxidation. Here, we show that treatment with acetate in vivo in the form of glycerol-triacetate promotes functional recovery and restores hippocampal fatty acid profile after neonatal brain injury.
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.
Dysregulated hippocampal fatty acid metabolism following intermittent hypoxemia-induced neonatal brain injury is rescued by treatment with acetate. · full record | OpenQuestion