Evidence map›Paper›PMID 29051615›Full record

ArticleScientific reports2017

Time-controllable Nkcc1 knockdown replicates reversible hearing loss in postnatal mice.

Takahisa Watabe, Ming Xu, Miho Watanabe, Junichi Nabekura, Taiga Higuchi, Karin Hori, Mitsuo P Sato, Fumiaki Nin, Hiroshi Hibino, Kaoru Ogawa and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  4. Oligodendrocytic NaNature communications · 2021
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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

12 authors at 6 institutions in 1 country.

Takahisa WatabeDepartment of Otolaryngology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
Ming XuDepartment of Neuropsychiatry, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
Miho WatanabeDepartment of Neurophysiology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu city, Shizuoka, 431-3192, Japan.
Junichi NabekuraDivision of Homeostatic Development, National Institute for Physiological Sciences, 38 Nishigonaka Myodaiji, Okazaki, Aichi, 444-8585, Japan.
Taiga HiguchiDepartment of Molecular Physiology, Niigata University School of Medicine, 757 Ichibancho, Asahimachi-dori, Chuo-ku, Niigata-shi, Niigata, 951-8510, Japan.
Karin HoriDepartment of Molecular Physiology, Niigata University School of Medicine, 757 Ichibancho, Asahimachi-dori, Chuo-ku, Niigata-shi, Niigata, 951-8510, Japan.
Mitsuo P SatoDepartment of Molecular Physiology, Niigata University School of Medicine, 757 Ichibancho, Asahimachi-dori, Chuo-ku, Niigata-shi, Niigata, 951-8510, Japan.
Fumiaki NinDepartment of Molecular Physiology, Niigata University School of Medicine, 757 Ichibancho, Asahimachi-dori, Chuo-ku, Niigata-shi, Niigata, 951-8510, Japan.
Hiroshi HibinoDepartment of Molecular Physiology, Niigata University School of Medicine, 757 Ichibancho, Asahimachi-dori, Chuo-ku, Niigata-shi, Niigata, 951-8510, Japan.ORCID 0000-0003-0688-1489
Kaoru OgawaDepartment of Otolaryngology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
Masatsugu MasudaDepartment of Otolaryngology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan. masoeur13@mac.com.
Kenji F TanakaDepartment of Neuropsychiatry, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan. kftanaka@keio.jp.
Niigata University · JPKeio University · JPHamamatsu University School of Medicine · JPKeio University Hospital · JPKyorin University · JPNational Institute for Physiological Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Identification of the causal effects of specific proteins on recurrent and partially reversible hearing loss has been difficult because of the lack of an animal model that provides reversible gene knockdown. We have developed the transgenic mouse line Actin-tTS::Nkcc1

Indexed as

AnimalsAnti-Bacterial AgentsAuditory PerceptionBrain StemCochleaDoxycyclineGene Expression RegulationGenotypeHearing LossIn Situ HybridizationMiceMice, KnockoutOrgan of CortiPhenotypeRepressor ProteinsSolute Carrier Family 12, Member 2Anti-Bacterial AgentsDoxycyclineRepressor ProteinsSlc12a2 protein, mouseSolute Carrier Family 12, Member 2tetracycline resistance-encoding transposon repressor protein

Identifiers

PMID29051615
PMCPMC5648887
OpenAlexW2764214946

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.