Evidence map›Paper›PMID 32405349›Full record

ArticleIranian journal of basic medical sciences2020

Neuronal injury and death following focal mild brain injury: The role of network excitability and seizure.

Tahereh Ghadiri, Ali Gorji, Gelareh Vakilzadeh, Vahid Hajali, Fariba Khodagholi, Mohammad Sharifzadeh

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In one paragraph

Article in Iranian journal of basic medical sciences, 2020. 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
1.1field-weighted citation impact, top 19% 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, 13 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

6 authors at 2 institutions in 1 country.

Tahereh GhadiriDepartment of Neurosciences, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
Ali GorjiShefa Neuroscience Research Center, Khatamolanbia Hospital, Tehran , Iran.
Gelareh VakilzadehShefa Neuroscience Research Center, Khatamolanbia Hospital, Tehran , Iran.
Vahid HajaliQuchan Higher Health Education Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Fariba KhodagholiNeuroscience Research Center , Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad SharifzadehFaculty of Pharmacy, Department of Toxicology, Tehran University of Medical Sciences, Tehran, Iran.
Mashhad University of Medical Sciences · IRTabriz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesWhile traumatic brain injury (TBI) is a predisposing factor for development of post-traumatic epilepsy (PTE), the occurrence of seizures following brain trauma can infuriate adverse consequences of brain injury. However, the effect of seizures in epileptogenesis after mild TBI cannot yet be accurately confirmed. This study was designed to investigate the histopathological and molecular modifications induced by seizures on traumatized brain. MATERIALS AND

methodsUsing a new method, head was traumatized and seizures were evoked by sub-convulsive dose of pentylenetetrazole (PTZ) fifteen days after induction of focal mild TBI. Convulsion assessments were performed one hour after PTZ injection and was followed by histopathological and molecular evaluations.

resultsA significantly higher score and longer duration of seizure attacks as well as higher number of epileptiform discharges were observed in the TBI+PTZ group compared to sham and TBI groups. An elevated number of apoptotic cells was observed in the TBI+PTZ group compared to sham and TBI rats. Molecular investigations revealed higher levels of Bax/Bcl2 ratio, Caspase 3, and NF-κB in the TBI+PTZ group compared to the other animal groups. The value of Nrf2 did not change after mild TBI compared to sham and PTZ control groups. Occurrence of seizures after TBI, however, significantly decreased the level of Nrf2.

conclusionOur data indicated that seizure occurrence following mild TBI aggravates cell injury and death via activation of neuroinflammatory processes and may increase the risk of PTE. Additionally, our results suggest a potential protective role of Nrf2 after chemically evoked PTE.

Indexed as

ApoptosisConvulsiveHippocampusNeuroinflammationPost-traumaticSeizure

Identifiers

PMID32405349
PMCPMC7206845
OpenAlexW3007556133

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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.