Evidence map›Paper›PMID 33731549›Full record

ArticleExperimental animals2021

Repair of brain damage size and recovery of neurological dysfunction after ischemic stroke are different between strains in mice: evaluation using a novel ischemic stroke model.

Yasuki Matano, Yuuto Nojiri, Mizuki Nomura, Akira Masuda, Yuuki Moriike, Yasuhiro Suzuki, Kazuo Umemura, Nobuo Nagai

Open access · diamondAbstract read
In one paragraph

Article in Experimental animals, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

4 citing papers in PubMed, 4 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

8 authors at 3 institutions in 1 country.

Yasuki MatanoLaboratory of Animal Physiology, Division of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura, Nagahama, Shiga 526-0829, Japan.
Yuuto NojiriLaboratory of Animal Physiology, Division of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura, Nagahama, Shiga 526-0829, Japan.
Mizuki NomuraLaboratory of Animal Physiology, Division of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura, Nagahama, Shiga 526-0829, Japan.
Akira MasudaLaboratory of Animal Physiology, Division of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura, Nagahama, Shiga 526-0829, Japan.
Yuuki MoriikeLaboratory of Animal Physiology, Division of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura, Nagahama, Shiga 526-0829, Japan.
Yasuhiro SuzukiSchool of Pharmaceutical Sciences, Faculty of Pharmacy, Ohu University, 31-1 Sankaku-do, Tomita-cho, Kohriyama, Fukushima 963-8611, Japan.
Kazuo UmemuraDepartment of Pharmacology, Hamamatsu University School of Medicine, 1-20-1 Handa-yama, Higashi-ku, Hamamatsu, Shizuoka 431-3125, Japan.
Nobuo NagaiLaboratory of Animal Physiology, Division of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura, Nagahama, Shiga 526-0829, Japan.
Nagahama Institute of Bio-Science and Technology · JPHamamatsu University School of Medicine · JPOhu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the current study, we established a novel murine ischemic brain damage model using a photochemical reaction to evaluate the recovery of neurological dysfunction and brain repair reactions. In this model, reproducible damage was induced in the frontal lobe of the cortex, which was accompanied by neurological dysfunction. Sequential changes in damage size, microglial accumulation, astrocyte activation, and neurological dysfunction were studied in C57BL/6J and BALB/c mouse strains. Although the initial size of damage was comparable in both strains, the extent of damage was later reduced to a greater extent in C57BL/6J mice than that in BALB/c mice. In addition, C57BL/6J mice showed later edema clearance until day 7, less microglial accumulation, and relatively more astrocyte activation on day 7. Neurologic dysfunction was evaluated by three behavioral tests: the von Frey test, the balance beam test, and the tail suspension test. The behavioral abnormalities evaluated by these tests were remarkable following the induction of damage and recovered by day 21 in both strains. However, the abnormalities were more prominent and the recovery was later in C57BL/6J mice. These findings demonstrate that our novel ischemic stroke model is useful for evaluating brain repair reactions and the recovery of neurological dysfunction in mice with different genetic backgrounds. In addition, we found that both the brain repair reactions and the recovery of neurological dysfunction after comparable ischemic brain damage varied between strains; in that, they both occurred later in C57BL/6J mice.

Indexed as

AnimalsBrain IschemiaDisease Models, AnimalIschemic StrokeMaleMiceMice, Inbred BALB CMice, Inbred C57BLSpecies Specificityedemaischemic strokemicroglianeurological dysfunctionstrains

Identifiers

PMID33731549
PMCPMC8390305
OpenAlexW3138749225

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.