ArticleBioscience reports2019
Rare copy number variants in the genome of Chinese female children and adolescents with Turner syndrome.
Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Systematic mapping and in silico reevaluation of genomic copy number variations in primary ovarian insufficiency.The Journal of clinical endocrinology and metabolism · 2026Pooled it
- Integrative Bioinformatics Analyses Reveal X Chromosome Inactivation Escape Genes Dosage Dysregulation Is the Primary Contributor to Turner Syndrome.Iranian journal of biotechnology · 2026Article
- Genome-wide Mendelian randomization identifies drugs associated with body height.Translational pediatrics · 2024Article
- DNA Hypermethylation and a Specific Methylation Spectrum on the X Chromosome in Turner Syndrome as Determined by Nanopore Sequencing.Journal of personalized medicine · 2022Article
- Article
- Capacitive interdigitated system of high osteoinductive/conductive performance for personalized acting-sensing implants.NPJ Regenerative medicine · 2021Article
- TheFrontiers in molecular neuroscience · 2021Article
- Effect of Hormone Replacement Therapy on Bone Mineral Density and Body Composition in Chinese Adolescent and Young Adult Turner Syndrome Patients.Frontiers in endocrinology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Turner syndrome (TS) is a congenital disease caused by complete or partial loss of one X chromosome. Low bone mineral status is a major phenotypic characteristic of TS that can not be fully explained by X chromosome loss, suggesting other autosomal-linked mutations may also exist. Therefore, the present study aimed to detect potential genetic mutations in TS through examination of copy number variation (CNV). Seventeen patients with TS and 15 healthy volunteer girls were recruited. Array-based comparative genomic hybridization (a-CGH) was performed on whole blood genomic DNA (gDMA) from the 17 TS patients and 15 healthy volunteer girls to identify potential CNVs. The abnormal CNV of one identified gene (
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Registered trials
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