Evidence map›Paper›PMID 38649481›Full record

ArticleCommunications biology2024

Intranasal oxytocin suppresses seizure-like behaviors in a mouse model of NGLY1 deficiency.

Yukimasa Makita, Makoto Asahina, Reiko Fujinawa, Hiroshi Yukitake, Tadashi Suzuki

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2024. 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
1.9field-weighted citation impact, top 15% 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. Review
  2. 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

5 authors at 2 institutions in 2 countries.

Yukimasa MakitaTakeda-CiRA Joint Program, 26-1, Muraoka-Higashi 2-chome, Fujisawa, Kanagawa, 251-8555, Japan.ORCID 0000-0002-9566-8286
Makoto AsahinaTakeda-CiRA Joint Program, 26-1, Muraoka-Higashi 2-chome, Fujisawa, Kanagawa, 251-8555, Japan.
Reiko FujinawaGlobal Advanced Platform, R&D Research, Takeda Pharmaceutical Co., Ltd. 26-1, Muraoka-Higashi 2-chome, Fujisawa, Kanagawa, 251-8555, Japan.
Hiroshi YukitakeTakeda-CiRA Joint Program, 26-1, Muraoka-Higashi 2-chome, Fujisawa, Kanagawa, 251-8555, Japan.
Tadashi SuzukiGlobal Advanced Platform, R&D Research, Takeda Pharmaceutical Co., Ltd. 26-1, Muraoka-Higashi 2-chome, Fujisawa, Kanagawa, 251-8555, Japan. tsuzuki_gm@riken.jp.ORCID 0000-0003-1030-7631
Takeda (Japan) · JPPioneer (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NGLY1 deficiency is a genetic disease caused by biallelic mutations of the Ngly1 gene. Although epileptic seizure is one of the most severe symptoms in patients with NGLY1 deficiency, preclinical studies have not been conducted due to the lack of animal models for epileptic seizures in NGLY1 deficiency. Here, we observed the behaviors of male and female Ngly1

Indexed as

Congenital Disorders of GlycosylationOxytocinPeptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine AmidaseSeizuresAdministration, IntranasalAnimalsBehavior, AnimalDisease Models, AnimalFemaleHypothalamusMaleMiceMice, Inbred C57BLMice, KnockoutOxytocinPeptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine Amidase

Identifiers

PMID38649481
PMCPMC11035592
OpenAlexW4395002357

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.