Evidence map›Paper›PMID 36105588›Full record

ArticleiScience2022

Resolving primary pathomechanisms driving idiopathic-like spinal curvature using a new

Anne Meyer-Miner, Jenica L M Van Gennip, Katrin Henke, Matthew P Harris, Brian Ciruna

Open access · goldAbstract read
In one paragraph

Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

6 citing papers in PubMed, 16 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

5 authors at 2 institutions in 2 countries.

Anne Meyer-MinerProgram in Developmental & Stem Cell Biology, The Hospital for Sick Children, 686 Bay Street, Toronto, ON M5G 0A4, Canada.
Jenica L M Van GennipProgram in Developmental & Stem Cell Biology, The Hospital for Sick Children, 686 Bay Street, Toronto, ON M5G 0A4, Canada.
Katrin HenkeDepartment of Orthopedic Research, Boston Children's Hospital, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Matthew P HarrisDepartment of Orthopedic Research, Boston Children's Hospital, Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Brian CirunaProgram in Developmental & Stem Cell Biology, The Hospital for Sick Children, 686 Bay Street, Toronto, ON M5G 0A4, Canada.
University of Toronto · CABoston Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic scoliosis (IS) refers to abnormal spinal curvatures that occur in the absence of vertebral or neuromuscular defects. IS accounts for 80% of human spinal deformity, afflicts ∼3% of children worldwide, yet pathogenic mechanisms are poorly understood. A key role for cerebrospinal fluid (CSF) homeostasis in zebrafish spine development has been identified. Specifically, defects in cilia motility of brain ependymal cells (EC), CSF flow, and/or Reissner fiber (RF) assembly are observed to induce neuroinflammation, oxidative stress, abnormal CSF-contacting neuron activity, and urotensin peptide expression, all associating with scoliosis. However, the functional relevance of these observations to IS remains unclear. Here we characterize zebrafish

Indexed as

Model organismMolecular biology experimental approachMolecular genetics

Identifiers

PMID36105588
PMCPMC9464966
OpenAlexW4293577655

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.