Evidence map›Paper›PMID 28536923›Full record

ArticleJournal of molecular neuroscience : MN2017

Single Nucleotide Polymorphisms in SLC19A1 and SLC25A9 Are Associated with Childhood Autism Spectrum Disorder in the Chinese Han Population.

Jun Liu, Weiming Mo, Zengyu Zhang, Hong Yu, Aiping Yang, Fei Qu, Pingfang Hu, Zhuo Liu, Shihu Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Association between Genetic Variants inBehavioural neurology · 2021
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. A Latent Gaussian Copula Model for Mixed Data Analysis in Brain Imaging Genetics.IEEE/ACM transactions on computational biology and bioinformatics
    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

9 authors at 4 institutions in 2 countries.

Jun LiuDepartment of Clinical Laboratory, Zhejiang Xiaoshan Hospital, Hangzhou, Zhejiang, 311202, China. 18967167212@163.com.ORCID http://orcid.org/0000-0003-4132-4450
Weiming MoDepartment of Clinical Laboratory, Zhejiang Xiaoshan Hospital, Hangzhou, Zhejiang, 311202, China.
Zengyu ZhangDepartment of Pediatrics, Xiaoshan First Affiliated Hospital of HangzhouNormal University, Hangzhou, Zhejiang, 311201, China.
Hong YuDepartment of Child and Adolescent Mental Health, Zhejiang Xiaoshan Hospital, Hangzhou, Zhejiang, 311202, China.
Aiping YangDepartment of Clinical Laboratory, Zhejiang Xiaoshan Hospital, Hangzhou, Zhejiang, 311202, China.
Fei QuDepartment of Clinical Laboratory, Zhejiang Xiaoshan Hospital, Hangzhou, Zhejiang, 311202, China.
Pingfang HuDepartment of Clinical Laboratory, Zhejiang Xiaoshan Hospital, Hangzhou, Zhejiang, 311202, China.
Zhuo LiuDepartment of Internal Medicine, Zhejiang Xiaoshan Hospital, Hangzhou, Zhejiang, 311202, China.
Shihu WangDepartment of Cancer Biology, Wake Forest School of Medicine, Winston Salem, NC, 27157, USA.
Affiliated Hospital of Hangzhou Normal University · CNThe First People's Hospital of Xiaoshan District, Hangzhou · CNWake Forest University · USZhejiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic variants have been implicated in the development of autism spectrum disorder (ASD). Recent studies suggest that solute carriers (SLCs) may play a role in the etiology of ASD. This purpose of this study was to determine the association between single nucleotide polymorphisms (SNPs) in SLC19A1 and SLC25A12 genes with childhood ASD in a Chinese Han population. A total of 201 autistic children and 200 age- and gender-matched healthy controls were recruited. A TaqMan probe-based real-time PCR approach was used to determine genotypes of SNPs corresponding to rs1023159 and rs1051266 in SLC19A1, and rs2056202 and rs2292813 in SLC25A12. Our results showed that both the T/T genotype of rs1051266 (odds ratio (OR) = 1.85, 95% confidence interval (CI) = 1.06-3.23, P = 0.0301) and the T allele (OR = 1.77, 95% CI = 1.07-2.90, P = 0.0249) of rs2292813 were significantly associated with an increased risk of childhood ASD. In addition, the G-C haplotype of rs1023159-rs1051266 in SCL19A1 (OR = 0.71, 95% CI = 0.51-0.98, P = 0.0389) and C-C haplotype of rs2056202-rs2292813 in SLC25A12 (OR = 0.58, 95% CI = 0.35-0.96, P = 0.0325) were associated with decreased risks of childhood ASD. There was no significant association between genotypes and allele frequencies with the severity of the disease. Our study suggests that these genetic variants of SLC19A1 and SLC25A12 may be associated with risks for childhood ASD.

Indexed as

Polymorphism, Single NucleotideAdolescentAutism Spectrum DisorderCase-Control StudiesChildChild, PreschoolChinaFemaleGene FrequencyHaplotypesHumansMaleReduced Folate Carrier ProteinUncoupling Protein 3Reduced Folate Carrier ProteinSLC19A1 protein, humanUCP3 protein, humanUncoupling Protein 3Autism spectrum disorder (ASD)Single nucleotide polymorphisms (SNPs)SLC19A1, SLC25A12

Identifiers

PMID28536923
OpenAlexW2618103155

What Socratic holds

Textmetadata
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.