Evidence map›Paper›PMID 31898392›Full record

ArticleGenes, brain, and behavior2020

A mouse model for benign paroxysmal positional vertigo with genetic predisposition for displaced otoconia.

Amiel A Dror, Shahar Taiber, Eyal Sela, Ophir Handzel, Karen B Avraham

Open access · greenAbstract read
In one paragraph

Article in Genes, brain, and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Natural Mutations Affect Structure and Function of gC1q Domain of Otolin-1.International journal of molecular sciences · 2021
    Article
  9. Article
  10. 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 1 country.

Amiel A DrorDepartment of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.
Shahar TaiberDepartment of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0002-0787-4216
Eyal SelaDepartment of Otolaryngology-Head and Neck Surgery, Galilee Medical Center, Nahariya, Israel.
Ophir HandzelDepartment of Otolaryngology Head and Neck Surgery and Maxillofacial Surgery, Tel-Aviv Sourasky Medical Center, Tel Aviv, Israel.ORCID 0000-0002-6905-3034
Karen B AvrahamDepartment of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0002-4913-251X
Tel Aviv University · ILBar-Ilan University · IL

Funding

Genomic Approaches to Discovery and Characterization of Genes for Inherited Hearing LossR01DC011835 · NIDCD · TEL AVIV UNIVERSITY · PI AVRAHAM, KAREN B., KANAAN, MOIEN · 2011 to 2022
$3.5M
NIDCD NIH HHS R01 DC011835
6 · The paper itself

Abstract

Abnormal formation of otoconia, the biominerals of the inner ear, results in balance disorders. The inertial mass of otoconia activates the underlying mechanosensory hair cells in response to change in head position primarily during linear and rotational acceleration. Otoconia associate exclusively with the two gravity receptors, the utricle and saccule. The cristae sensory epithelium is associated with an extracellular gelatinous matrix known as cupula, equivalent to otoconia. During head rotation, the inertia of endolymphatic fluids within the semicircular canals deflects the cupula of the corresponding crista and activates the underlying mechanosensory hair cells. It is believed that detached free-floating otoconia particles travel ectopically to the semicircular canal and cristae and are the culprit for benign paroxysmal positional vertigo (BPPV). The Slc26a4 mouse mutant harbors a missense mutation in pendrin. This mutation leads to impaired transport activity of pendrin and to defects in otoconia composition and distribution. All Slc26a4

Indexed as

AnimalsBenign Paroxysmal Positional VertigoFemaleGenetic Predisposition to DiseaseHomozygoteMaleMiceMutationOtolithic MembraneSulfate TransportersSlc26a4 protein, mouseSulfate TransportersbalancedeafnesshearingSLC26A4vertigo

Identifiers

PMID31898392
PMCPMC7286769
OpenAlexW2997877379

What OpenQuestion holds

Textmetadata
LicenceTDM
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.