Evidence map›Paper›PMID 27766954›Full record

ArticleBMC medical genetics2016

Identification of novel genetic variations affecting osteoarthritis patients.

Mamdooh Abdullah Gari, Mohammed AlKaff, Haneen S Alsehli, Ashraf Dallol, Abdullah Gari, Muhammad Abu-Elmagd, Roaa Kadam, Mohammed F Abuzinadah, Mazin Gari, Adel M Abuzenadah and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC medical genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

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  10. Atopic Eczema: Genetic Analysis ofBioMed research international · 2019
    Article
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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

13 authors at 3 institutions in 1 country.

Mamdooh Abdullah GariSheikh Salem Bin Mahfouz Scientific Chair for Treatment of Osteoarthritis by Stem Cells, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia. mgari@kau.edu.sa.
Mohammed AlKaffSheikh Salem Bin Mahfouz Scientific Chair for Treatment of Osteoarthritis by Stem Cells, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Haneen S AlsehliSheikh Salem Bin Mahfouz Scientific Chair for Treatment of Osteoarthritis by Stem Cells, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Ashraf DallolCenter of Innovation in Personalized Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Abdullah GariCenter of Innovation in Personalized Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Muhammad Abu-ElmagdCentre of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Roaa KadamCentre of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Mohammed F AbuzinadahCenter of Innovation in Personalized Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Mazin GariCenter of Innovation in Personalized Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Adel M AbuzenadahCenter of Innovation in Personalized Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Kalamegam GauthamanSheikh Salem Bin Mahfouz Scientific Chair for Treatment of Osteoarthritis by Stem Cells, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Heba AlkhatabiCentre of Excellence in Genomic Medicine Research, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Mohammed M AbbasSheikh Salem Bin Mahfouz Scientific Chair for Treatment of Osteoarthritis by Stem Cells, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
King Abdulaziz University · SAKing Abdulaziz Medical City · SAKing Abdulaziz Hospital · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteoarthritis (OA) is a progressive joint disease characterized by gradual degradation of extracellular matrix (ECM) components in the cartilage and bone. The ECM of cartilage is a highly specified structure that is mainly composed of type II collagen and provides tensile strength to the tissue via aggrecan and proteoglycans. However, changes in the ECM composition and structure can lead to loss of collagen type II and network integrity. Several risk factors have been correlated with OA including age, genetic predisposition, hereditary factors, obesity, mechanical injuries, and joint trauma. Certain genetic association studies have identified several genes associated with OA using genome-wide association studies (GWASs).

resultsWe identified several novel genetic variants affecting genes that function in several candidate causative pathways including immune responses, inflammatory and cartilage degradation such as SELP, SPN, and COL6A6.

conclusionsThe approach of whole-exome sequencing can be a promising method to identify genetic mutations that can influence the OA disease.

Indexed as

Genetic VariationAgedCartilageCollagen Type IICollagen Type VIExomeGenome-Wide Association StudyHumansLeukosialinMiddle AgedOsteoarthritisPolymorphism, Single NucleotideP-SelectinRisk FactorsCOL2A1 protein, humanCOL6A6 protein, humanCollagen Type IICollagen Type VILeukosialinP-SelectinSELP protein, humanSPN protein, humanOsteoarthritisSingle nucleotide variantsWhole-exome sequencing

Identifiers

PMID27766954
PMCPMC5073985
OpenAlexW2531805509

What OpenQuestion holds

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Registered trials

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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.