Evidence map›Paper›PMID 33931083›Full record

ArticleMolecular brain2021

Ablation of interleukin-19 improves motor function in a mouse model of amyotrophic lateral sclerosis.

Hiroyasu Komiya, Hideyuki Takeuchi, Yuki Ogawa, Kosuke Suzuki, Akihiro Ogasawara, Keita Takahashi, Yasu-Taka Azuma, Hiroshi Doi, Fumiaki Tanaka

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

Article in Molecular brain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

0 citing papers in PubMed, 4 citations in OpenAlex.

No citing paper in PubMed yet.

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 2 institutions in 1 country.

Hiroyasu KomiyaDepartment of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Hideyuki TakeuchiDepartment of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan. htake@yokohama-cu.ac.jp.ORCID 0000-0001-5912-7581
Yuki OgawaDepartment of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Kosuke SuzukiDepartment of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Akihiro OgasawaraDepartment of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Keita TakahashiDepartment of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Yasu-Taka AzumaLaboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, Osaka, 598-9531, Japan.
Hiroshi DoiDepartment of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Fumiaki TanakaDepartment of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan. ftanaka@yokohama-cu.ac.jp.
Yokohama City University · JPOsaka Prefecture University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammation by activated microglia and astrocytes plays a critical role in progression of amyotrophic lateral sclerosis (ALS). Interleukin-19 (IL-19) is a negative-feedback regulator that limits pro-inflammatory responses of microglia in an autocrine and paracrine manner, but it remains unclear how IL-19 contributes to ALS pathogenesis. We investigated the role of IL-19 in ALS using transgenic mice carrying human superoxide dismutase 1 with the G93A mutation (SOD1

Indexed as

Gene DeletionAmyotrophic Lateral SclerosisAnimalsAstrocytesCytokinesDisease Models, AnimalGlial Cell Line-Derived Neurotrophic FactorInflammation MediatorsInterleukinsLongevityLumbar VertebraeMiceMice, Inbred C57BLMice, TransgenicMicrogliaMotor ActivityCytokinesGlial Cell Line-Derived Neurotrophic FactorIl19 protein, mouseInflammation MediatorsInterleukinsNeuroprotective AgentsReceptors, InterleukinSuperoxide DismutaseTumor Necrosis Factor-alphaAmyotrophic lateral sclerosisAstrocyteInterleukin-19Microglia

Identifiers

PMID33931083
PMCPMC8086093
OpenAlexW3158989690

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.