Evidence map›Paper›PMID 37762352›Full record

ArticleInternational journal of molecular sciences2023

Treatment of Status Epilepticus after Traumatic Brain Injury Using an Antiseizure Drug Combined with a Tissue Recovery Enhancer Revealed by Systems Biology.

Natallie Kajevu, Anssi Lipponen, Pedro Andrade, Ivette Bañuelos, Noora Puhakka, Elina Hämäläinen, Teemu Natunen, Mikko Hiltunen, Asla Pitkänen

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

Article in International journal of molecular sciences, 2023. 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
0.6field-weighted citation impact, top 29% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Review
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 1 institution in 1 country.

Natallie KajevuA. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
Anssi LipponenA. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.ORCID 0000-0002-4403-9084
Pedro AndradeA. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.ORCID 0000-0001-9118-8341
Ivette BañuelosA. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
Noora PuhakkaA. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
Elina HämäläinenA. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
Teemu NatunenInstitute of Biomedicine, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
Mikko HiltunenInstitute of Biomedicine, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.ORCID 0000-0003-3566-4096
Asla PitkänenA. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.ORCID 0000-0002-8163-5416
University of Eastern Finland · FI

Funding

European union Marie Sklodowska-Curie grant agreement No 740264Medical Research Council of the Academy of Finland Grant 272249Medical Research Council of the Academy of Finland Grant 273909Medical Research Council of the Academy of Finland Grant 317203Medical Research Council of the Academy of Finland Grant 338182Sigrid Juselius Foundation A.P, M.H
6 · The paper itself

Abstract

We tested a hypothesis that in silico-discovered compounds targeting traumatic brain injury (TBI)-induced transcriptomics dysregulations will mitigate TBI-induced molecular pathology and augment the effect of co-administered antiseizure treatment, thereby alleviating functional impairment. In silico bioinformatic analysis revealed five compounds substantially affecting TBI-induced transcriptomics regulation, including calpain inhibitor, chlorpromazine, geldanamycin, tranylcypromine, and trichostatin A (TSA). In vitro exposure of neuronal-BV2-microglial co-cultures to compounds revealed that TSA had the best overall neuroprotective, antioxidative, and anti-inflammatory effects. In vivo assessment in a rat TBI model revealed that TSA as a monotherapy (1 mg/kg/d) or in combination with the antiseizure drug levetiracetam (LEV 150 mg/kg/d) mildly mitigated the increase in plasma levels of the neurofilament subunit pNF-H and cortical lesion area. The percentage of rats with seizures during 0-72 h post-injury was reduced in the following order: TBI-vehicle 80%, TBI-TSA (1 mg/kg) 86%, TBI-LEV (54 mg/kg) 50%, TBI-LEV (150 mg/kg) 40% (

Indexed as

AnticonvulsantsBrain Injuries, TraumaticStatus EpilepticusSystems BiologyAnimalsDisease Models, AnimalDrug Therapy, CombinationHydroxamic AcidsLevetiracetamMaleMicrogliaNeuroprotective AgentsRatsRats, Sprague-DawleyTranscriptomeAnticonvulsantsHydroxamic AcidsLevetiracetamNeuroprotective Agentstrichostatin Abiomarkerelectroencephalographyfluid-percussion injurygene expressionin siliconeuronal cultureneuroprotectionoxidative stresspost-traumatic epilepsyseizure

Identifiers

PMID37762352
PMCPMC10531083
OpenAlexW4386748421

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.