Evidence map›Paper›PMID 38737102›Full record

ArticleOpen life sciences2024

Preliminary investigation into the genetic etiology of short stature in children through whole exon sequencing of the core family.

Jinshui He, Shuyun Zhang, Yueya Kang, Yugui Zhang, Zhugui Zheng, Minyi Ruan

Abstract read
In one paragraph

Article in Open life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. A novel homozygous variant in the POLR1A gene: a complicated hereditary spastic paraplegia (c-HSP) or a hypomyelinating leukodystrophy type-27 (HLD27) phenotype?Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Pooled it
  2. Article
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

6 authors.

Jinshui HeDepartment of Child Growth and Development, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou 363000, Fujian, China.
Shuyun ZhangDepartment of Child Growth and Development, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou 363000, Fujian, China.
Yueya KangDepartment of Child Growth and Development, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou 363000, Fujian, China.
Yugui ZhangDepartment of Child Growth and Development, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou 363000, Fujian, China.
Zhugui ZhengDepartment of Child Growth and Development, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou 363000, Fujian, China.
Minyi RuanDepartment of Ophthalmology, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A comprehensive survey was carried out to investigate the genetic etiology of short stature in children by whole exon sequencing of a core family cohort to find and study mutations in multiple genes to assess their potential correlations to low height in children. The study included 56 pediatric patients from the Department of Pediatrics at the Zhangzhou Affiliated Hospital of Fujian Medical University. The participants met strict inclusion criteria, including age, Han Chinese ethnicity, low height standard deviation score, and the absence of known causes for short stature. Core pedigrees were identified using exome sequencing. After sequencing, variations were categorized and interpreted according to a variety of factors, including inheritance, location, type, and disease-causing gene databases. Variants were verified by Sanger sequencing. Most of the 97 gene mutations were missense. ACAN, PHEX, and COL2A1 were the most common gene mutations. Copy number variations were identified, particularly associated with the PHEX gene. Protein functional studies revealed that the mutations had a considerable influence on disease-promoting damage. The chromosomal locations with the highest enrichment of these genes were chr12, chr5, and chr2. In conclusion, the study revealed numerous genetic changes that may substantially impact physiological processes and disease. These findings establish the basis for further investigations into their diagnostic and therapeutic capabilities.

Indexed as

gene mutationsgenetic etiologyshort staturewhole exon sequencing

Identifiers

PMID38737102
PMCPMC11087740

What Socratic 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 Socratic graph.