Evidence map›Paper›PMID 26507517›Full record

ArticleInternational archives of occupational and environmental health2016

Genetic variation in APE1 gene promoter is associated with noise-induced hearing loss in a Chinese population.

Huanxi Shen, Jianrui Dou, Lei Han, Ying Bai, Qian Li, Zhiqiang Hong, Jian Shi, Hengdong Zhang, Feng Zhang, Cheng Du and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in International archives of occupational and environmental health, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 45% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Integrating pharmacogenomics into clinical trials of hearing disorders.The Journal of the Acoustical Society of America · 2022
    Article
  4. Review
  5. Review
  6. Review
  7. 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

12 authors at 6 institutions in 2 countries.

Huanxi ShenKunshan Municipal Center for Disease Prevention and Control, Kunshan, China.
Jianrui DouYangzhou Center for Disease Prevention and Control, Yangzhou, China.
Lei HanDepartment of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing, China.
Ying BaiInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, 172 Jiangsu Road, Nanjing, 210009, China.
Qian LiThe First People's Hospital of Kunshan, Kunshan, China.
Zhiqiang HongInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, 172 Jiangsu Road, Nanjing, 210009, China.
Jian ShiKunshan Municipal Center for Disease Prevention and Control, Kunshan, China.
Hengdong ZhangInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, 172 Jiangsu Road, Nanjing, 210009, China.
Feng ZhangInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, 172 Jiangsu Road, Nanjing, 210009, China.
Cheng DuKunshan Municipal Center for Disease Prevention and Control, Kunshan, China.
Zhimin TongKunshan Municipal Center for Disease Prevention and Control, Kunshan, China.
Baoli ZhuDepartment of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing, China. zhubl@jscdc.cn.
Center for Disease Control · TWChinese Center For Disease Control and Prevention · CNJiangsu Provincial Center for Disease Control and Prevention · CNFirst People's Hospital of Kunshan · CNNanjing Medical University · CNYangzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate whether the apurinic/apyrimidinic endonuclease 1 (APE1) 1349 T>G and -656 T>G polymorphisms were associated with the risk of noise-induced hearing loss (NIHL) in a Chinese population.

methodsThe two APE1 polymorphisms were analyzed among 613 NIHL workers and 613 normal hearing workers using the minor groove binder TaqMan probe assay.

resultsWe found that the APE1 -656 TT genotype was associated with a increased risk of NIHL [adjusted odds ratio (OR) 1.46, 95% confidence interval (CI) 1.05-2.06]. This increased risk was more pronounced in the stratification analysis. Furthermore, we found that subjects with two risk genotypes (hOGG1 Cys/Cys, APE1 -656 TT) had a significantly increased risk of NIHL (adjusted OR 1.91, 95% CI 1.27-2.88).

conclusionOur study identified that the APE1 -656 T>G polymorphism may contribute to the susceptibility of NIHL.

Indexed as

AdultCase-Control StudiesChinaDNA-(Apurinic or Apyrimidinic Site) LyaseFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHearing Loss, Noise-InducedHumansMaleMiddle AgedNoise, OccupationalOccupational DiseasesPolymorphism, Single NucleotidePromoter Regions, GeneticAPEX1 protein, humanDNA-(Apurinic or Apyrimidinic Site) LyaseAPE1Noise-induced hearing loss susceptibilityPolymorphisms

Identifiers

PMID26507517
OpenAlexW1860240235

What OpenQuestion 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 OpenQuestion graph.