Evidence map›Paper›PMID 34153467›Full record

ArticleNeurobiology of disease2021

Neutrophil-specific deletion of Syk results in recruitment-independent stabilization of the barrier and a long-term improvement in cognitive function after traumatic injury to the developing brain.

Alpa Trivedi, Kayleen G Tercovich, Amy Jo Casbon, Jacob Raber, Clifford Lowell, Linda J Noble-Haeusslein

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

Article in Neurobiology of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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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

6 authors at 3 institutions in 1 country.

Alpa TrivediDepartments of Laboratory Medicine, University of California San Francisco, San Francisco, CA 94143, USA; Departments of Neurological Surgery, University of California San Francisco, San Francisco, CA 94143, USA. Electronic address: alpa.mahuvakar@ucsf.edu.
Kayleen G TercovichDepartments of Neurological Surgery, University of California San Francisco, San Francisco, CA 94143, USA.
Amy Jo CasbonDepartments of Anatomy, University of California San Francisco, San Francisco, CA 94143, USA.
Jacob RaberDepartments of Behavioral Neuroscience, Neurology, and Radiation Medicine, ONPRC, Oregon Health & Science University, Portland, OR 97239, USA; Division of Neuroscience, ONPRC, Oregon Health & Science University, Portland, OR 97239, USA. Electronic address: raberj@ohsu.edu.
Clifford LowellDepartments of Laboratory Medicine, University of California San Francisco, San Francisco, CA 94143, USA. Electronic address: clifford.lowell@ucsf.edu.
Linda J Noble-HaeussleinDepartments of Neurological Surgery, University of California San Francisco, San Francisco, CA 94143, USA; Departments of Neurology and Psychology, The Dell Medical School and the College of Liberal Arts, University of Texas, Austin, TX 78712, USA. Electronic address: linda.noble@austin.utexas.edu.
University of California, San Francisco · USNeurological Surgery · USOregon Health & Science University · US

Funding

Signaling by Cytoplasmic Tyrosine Kinases in LeukocytesR01AI068150 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2006 to 2016
$3.4M
Regulation of Innate Immune Signaling by Lyn KinaseR01AI113272 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOWELL, CLIFFORD A · 2015 to 2019
$2.0M
Determinants of vulnerability and recovery after trauma to the developing brainR01NS077767 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NOBLE, LINDA J. · 2012 to 2016
$1.7M
NIAID NIH HHS R01 AI068150NIAID NIH HHS R01 AI113272NINDS NIH HHS R01 NS077767
6 · The paper itself

Abstract

While traumatic brain injury (TBI) is the leading cause of death and disability in children, we have yet to identify those pathogenic events that determine the extent of recovery. Neutrophils are best known as "first responders" to sites of infection and trauma where they become fully activated, killing pathogens via proteases that are released during degranulation. However, this activational state may generate substantial toxicity in the young brain after TBI that is partially due to developmentally regulated inadequate antioxidant reserves. Neutrophil degranulation is triggered via a downstream signaling pathway that is dependent on spleen tyrosine kinase (Syk). To test the hypothesis that the activational state of neutrophils is a determinant of early pathogenesis and long-term recovery, we compared young, brain-injured conditional knockouts of Syk (syk

Indexed as

CognitionAnimalsBlood-Brain BarrierBrainBrain Injuries, TraumaticLearningMiceMice, KnockoutMorris Water Maze TestNeuronsNeutrophil InfiltrationNeutrophilsReactive Oxygen SpeciesRecovery of FunctionSpatial MemorySyk KinaseReactive Oxygen SpeciesSyk KinaseSyk protein, mouseAnxietyBarrierLearningMemoryNeutrophilsOxidative stressSpleen tyrosine kinase

Identifiers

PMID34153467
PMCPMC11302380
OpenAlexW3176271538

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.