Evidence map›Paper›PMID 24929209›Full record

ArticleBrain research2014

Alpha II Spectrin breakdown products in immature Sprague Dawley rat hippocampus and cortex after traumatic brain injury.

Michelle E Schober, Daniela F Requena, Lizeth J Davis, Ryan R Metzger, Kimberly S Bennett, Denise Morita, Christian Niedzwecki, Zhihui Yang, Kevin K W Wang

Abstract read
In one paragraph

Article in Brain research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  14. Dysfunction of the β2-spectrin-based pathway in human heart failure.American journal of physiology. Heart and circulatory physiology · 2016
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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.

Michelle E SchoberDepartment of Pediatrics, Division of Critical Care, University of Utah School of Medicine, Salt Lake City, UT 84132, United States. Electronic address: michelle.schober@hsc.utah.edu.
Daniela F RequenaDepartment of Pediatrics, Division of Neonatology, University of Utah, Salt Lake City, UT 84132, United States.
Lizeth J DavisDepartment of Pediatrics, Division of Neonatology, University of Utah, Salt Lake City, UT 84132, United States.
Ryan R MetzgerDepartment of Surgery, University of Utah, Salt Lake City, UT 84132, United States.
Kimberly S BennettDepartment of Pediatrics, Division of Critical Care, University of Utah School of Medicine, Salt Lake City, UT 84132, United States.
Denise MoritaDepartment of Pediatrics, Division of Neurology, University of Utah, Salt Lake City, UT 84132, United States.
Christian NiedzweckiDepartment of Pediatrics, Division of Physical Medicine and Rehabilitation, University of Utah, Salt Lake City, UT 84132, United States.
Zhihui YangDepartment of Pediatrics, Center for Neuroproteomics & Biomarker Research, Department of Psychiatry, University of Florida, Gainsville, FL 32611, United States.
Kevin K W WangDepartment of Pediatrics, Center for Neuroproteomics & Biomarker Research, Department of Psychiatry, University of Florida, Gainsville, FL 32611, United States.
University of Utah · USUniversity of Florida · US

Funding

Genetic /Developmental Mechanisms of Pediatric DiseasesK12HD001410 · NICHD · UNIVERSITY OF UTAH · PI CLARK, EDWARD BOWERSOX · 2003 to 2012
$4.3M
NICHD NIH HHS K12 HD001410NICHD NIH HHS K12HD001410
6 · The paper itself

Abstract

After traumatic brain injury (TBI), proteolysis of Alpha II Spectrin by Calpain 1 produces 145 Spectrin breakdown products (SBDPs) while proteolysis by Caspase 3 produces 120 SBDPs. 145 and 120 SBDP immunoblotting reflects the relative importance of caspase-dependent apoptosis or calpain-dependent excitotoxic/necrotoxic cell death in brain regions over time. In the adult rat, controlled cortical impact (CCI) increased 120 SBDPs in the first hours, lasting a few days, and increased 145 SBDPs within the first few days lasting up to 14 days after injury. Little is known about SBDPs in the immature brain after TBI. Since development affects susceptibility to apoptosis after TBI, we hypothesized that CCI would increase 145 and 120 SBDPs in the immature rat brain relative to SHAM during the first 3 and 5 days, respectively. SBDPs were measured in hippocampi and cortices at post injury days (PID) 1, 2, 3, 5, 7 and 14 after CCI or SHAM surgery in the 17 day old Sprague Dawley rat. 145 SBDPs increased in both brain tissues ipsilateral to injury during the first 3 days, while changes in contralateral tissues were limited to PID2 cortex. 145 SBDPs elevations were more marked and enduring in hippocampus than in cortex. Against expectations, 120 SBDPs only increased in PID1 hippocampus and PID2 cortex. 145 SBDPs elevations occurred early after CCI, similar to previous studies in the adult rat, but resolved more quickly. The minimal changes in 120 SBDPs suggest that calpain-dependent, but not caspase-dependent, cell death predominates in the 17 day old rat after CCI.

Indexed as

AnimalsBrain InjuriesCell DeathCerebral CortexDisease Models, AnimalFunctional LateralityHippocampusImmunoblottingMaleRandom AllocationRats, Sprague-DawleySpectrinTime FactorsSpectrinApoptosisCell deathControlled cortical impactDevelopmentalExcitotoxicity

Identifiers

PMID24929209
PMCPMC4131452
OpenAlexW2012968561

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.