Evidence map›Paper›PMID 37215868›Full record

ArticleHeliyon2023

A model of traumatic brain injury in rats is influenced by neuroprotection of diurnal variation which improves motor behavior and histopathology in white matter myelin.

R J Martínez-Tapia, F Estrada-Rojo, T G López-Aceves, S García-Velasco, V Rodríguez-Mata, E Pulido-Camarillo, A Pérez-Torres, E Y López-Flores, P Ugalde-Muñiz, R Noriega-Navarro and 1 more

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

11 authors at 3 institutions in 1 country.

R J Martínez-TapiaLaboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico.
F Estrada-RojoLaboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico.
T G López-AcevesLaboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico.
S García-VelascoLaboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico.
V Rodríguez-MataDepartamento de Biología Celular y Tisular, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico.
E Pulido-CamarilloDepartamento de Biología Celular y Tisular, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico.
A Pérez-TorresDepartamento de Biología Celular y Tisular, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico.
E Y López-FloresResidente de Anatomía Patológica, CMN "20 de Noviembre", ISSSTE, Ciudad de México, Mexico.
P Ugalde-MuñizLaboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico.
R Noriega-NavarroLaboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico.
L NavarroLaboratory of Neuroendocrinology, Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, México City, Mexico.
Universidad Nacional Autónoma de México · MXAutonomous University of Sinaloa · MXInstitute for Social Security and Services for State Workers · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) represents a significant public health concern and has been associated with high rates of morbidity and mortality. TBI generates two types of brain damage: primary and secondary. Secondary damage originates a series of pathophysiological processes, which include metabolic crisis, excitotoxicity, and neuroinflammation, which have deleterious consequences for neuronal function. However, neuroprotective mechanisms are also activated. The balance among these tissue responses, and its variations throughout the day determines the fate of the damage tissue. We have demonstrated less behavioral and morphological damage when a rat model of TBI was induced during the light hours of the day. Moreover, here we show that rats subjected to TBI in the dark lost less body weight than those subjected to TBI in the light, despite no change in food intake. Besides, the rats subjected to TBI in the dark had better performance in the beam walking test and presented less histological damage in the corpus callosum and the cingulum bundle, as shown by the Klüver-Barrera staining. Our results suggest that the time of day when the injury occurs is important. Thus, this data should be used to evaluate the pathophysiological processes of TBI events and develop better therapies.

Indexed as

Diurnal variationMyelinNeuroprotectionTraumatic brain injuryWhite matter

Identifiers

PMID37215868
PMCPMC10196591
OpenAlexW4377565072

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.