Evidence map›Paper›PMID 34367251›Full record

ArticleFrontiers in genetics2021

Multi-Level Analyses of Genome-Wide Association Study to Reveal Significant Risk Genes and Pathways in Neuromyelitis Optica Spectrum Disorder.

Ting Li, He Li, Yue Li, Shu-An Dong, Ming Yi, Qiu-Xia Zhang, Bin Feng, Li Yang, Fu-Dong Shi, Chun-Sheng Yang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 11 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

10 authors at 4 institutions in 2 countries.

Ting LiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
He LiDepartment of Neurology, Tianjin Huanhu Hospital, Tianjin, China.
Yue LiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Shu-An DongDepartment of Anesthesiology, Tianjin Hospital of Integrated Traditional Chinese and Western Medicine, Tianjin, China.
Ming YiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Qiu-Xia ZhangDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Bin FengDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Li YangDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Fu-Dong ShiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Chun-Sheng YangDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Tianjin Medical University General Hospital · CNSt. Joseph's Hospital and Medical Center · USTianjin Hospital · CNTianjin Huanhu Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuromyelitis optica spectrum disorder (NMOSD) is an inflammatory disease of the central nervous system and it is understandable that environmental and genetic factors underlie the etiology of NMOSD. However, the susceptibility genes and associated pathways of NMOSD patients who are AQP4-Ab positive and negative have not been elucidated.

methodsSecondary analysis from a NMOSD Genome-wide association study (GWAS) dataset originally published in 2018 (215 NMOSD cases and 1244 controls) was conducted to identify potential susceptibility genes and associated pathways in AQP4-positive and negative NMOSD patients, respectively (132 AQP4-positive and 83 AQP4-negative).

resultsIn AQP4-positive NMOSD cases, five shared risk genes were obtained at chromosome 6 in AQP4-positive NMOSD cases by using more stringent

conclusionThe potential molecular mechanism underlying NMOSD may be related to proteins encoded by these novel genes in complements, antigen presentation, and immune regulation. The new results may represent an improved comprehension of the genetic and molecular mechanisms underlying NMOSD.

Indexed as

gene differential expressiongene setsGenome-wide association studyNeuromyelitis optica spectrum disorderpathway

Identifiers

PMID34367251
PMCPMC8335167
OpenAlexW3186212326

What Socratic holds

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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 Socratic graph.