Evidence map›Paper›PMID 27555091›Full record

ArticleEpilepsia2016

Early cardiac electrographic and molecular remodeling in a model of status epilepticus and acquired epilepsy.

Amy L Brewster, Kyle Marzec, Alexandria Hairston, Marvin Ho, Anne E Anderson, Yi-Chen Lai

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

Article in Epilepsia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
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 2 institutions in 1 country.

Amy L BrewsterDepartment of Psychological Sciences, Purdue University, West Lafayette, Indiana, U.S.A.
Kyle MarzecDepartment of Psychological Sciences, Purdue University, West Lafayette, Indiana, U.S.A.
Alexandria HairstonDepartment of Psychological Sciences, Purdue University, West Lafayette, Indiana, U.S.A.
Marvin HoDepartment of Pediatrics, Baylor College of Medicine, Houston, Texas, U.S.A.
Anne E AndersonDepartment of Pediatrics, Baylor College of Medicine, Houston, Texas, U.S.A.
Yi-Chen LaiDepartment of Pediatrics, Baylor College of Medicine, Houston, Texas, U.S.A.
Baylor College of Medicine · USPurdue University West Lafayette · US

Funding

Signaling pathway dysregulation in epilepsyR01NS081053 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI ANDERSON, ANNE E · 2013 to 2016
$1.4M
PARP-1 activation in seizures and status epilepticusK08NS063117 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI LAI, YI-CHEN · 2009 to 2013
$861k
Cardiac dysfunction in epilepsy: a candidate mechanism in sudden unexpected deathR21NS077028 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI ANDERSON, ANNE E · 2011 to 2012
$446k
NINDS NIH HHS K08 NS063117NINDS NIH HHS R01 NS081053NINDS NIH HHS R21 NS077028
6 · The paper itself

Abstract

objectivesA myriad of acute and chronic cardiac alterations are associated with status epilepticus (SE) including increased sympathetic tone, rhythm and ventricular repolarization disturbances. Despite these observations, the molecular processes underlying SE-associated myocardial remodeling remain to be identified. Here we determined early SE-associated myocardial electrical and molecular alterations using a model of SE and acquired epilepsy.

methodsWe performed electrocardiography (ECG) assessments in rats beginning at 2 weeks following kainate-induced SE, and calculated short-term variability (STV) of the corrected QT intervals (QTc) as a marker of ventricular stability. Using western blotting, we quantified myocardial β1-adrenergic receptors (β1-AR) and ventricular gap junction protein connexin 43 (Cx43) levels as makers of increased sympathetic tone. We determined the activation status of three kinases associated with sympathetic stimulation and their downstream ion channel targets: extracellular signal-regulated kinase (ERK), protein kinase A (PKA), Ca

resultsCompared with the sham group, SE animals exhibited higher heart rate, longer QTc interval, and higher STV beginning at 2 weeks following SE. Concurrently, the myocardium of SE rats showed lower β1-AR and higher Cx43 protein levels, higher levels of phosphorylated ERK, PKA, and CamKII along with decreased HCN2 and Kv SIGNIFICANCE: SE triggers early molecular alterations in the myocardium consistent with increased sympathetic tone and altered Ca

Indexed as

ElectrocardiographyAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Connexin 43Disease Models, AnimalExcitatory Amino Acid AgonistsExtracellular Signal-Regulated MAP KinasesGene Expression RegulationHeartHeart RateKainic AcidMaleMyocardiumPotassium Channels, Voltage-GatedRatsRats, Sprague-DawleyCalcium-Calmodulin-Dependent Protein Kinase Type 2Connexin 43Excitatory Amino Acid AgonistsExtracellular Signal-Regulated MAP KinasesGja1 protein, ratKainic AcidPotassium Channels, Voltage-GatedReceptors, Adrenergic, beta-1Cardiac remodelingEpilepsyIntracellular signalingIon channelopathyStatus epilepticus

Identifiers

PMID27555091
PMCPMC5545890
OpenAlexW2509446763

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.