Objective: To investigate the relationship between rs1053005 of signal conversion and transcription activator 3 (STAT3) and miR-452-3p, and the association between STAT3 gene polymorphism and noise-induced hearing loss (NIHL) . Methods: In December 2017, 1220 workers were selected from an automobile manufacturing factory, an energy company and a chemical fiber factory in Jiangsu Province who had occupational noise exposure and working age of more than 3 years. The workers with the mean hearing threshold of ≥26 dB (A) of the two ear high frequency (3000, 4000 and 6000 Hz) were defined as case group (n=609) , and the rest were control group (n=611) . Five single nucleotide polymorphism (SNP) sites of STAT3 (rs4796793, rs1053023, rs1053005, rs1053004 and rs3744483) were selected to explore the association between STAT3 gene polymorphism and NIHL by analyzing the points. The double luciferase reporter gene verified whether miR-452-3p was targeted to bind STAT3, and overexpressed miR-452-3p in HEI-OC1 cells to explore the mechanism of STAT3 expression regulation. Results: There was no significant difference in gender, age, smoking and drinking between the two groups (P>0.05) . Compared with the control group[ (15.58±4.76) dB], the mean hearing threshold of the case group [ (37.50±12.39) dB] was higher, and the difference were statistically significant (P<0.05) . Compared with the control group, the C alleles of rs1053023 and rs1053005 were higher in the case group (OR=1.367, 1.370, P<0.05) . The risk of NIHL in men with TC/CC genotype were 1.545 and 1.531 times higher than that in men with TT genotype (P<0.05) . Compared with the control group, the mRNA expression of STAT3 in the case group was significantly increased (P<0.05) . The STAT3 mRNA expression of miR-452-3p group cells was significantly decreased (P<0.05) . Conclusion: The rs1053023 and rs1053005 polymorphism of STAT3 are related to NIHL. The C alleles of rs1053023 and rs1053005 may be biomarkers of workers exposed to noise.

BACKGROUND:Obesity and metabolic syndrome frequently co-exist and define obese individuals into different obesity phenotypes, such as metabolically healthy obese (MHO), metabolically unhealthy obese (MUO) and metabolically unhealthy normal weight (MUNW). Growing evidence suggests that genetic predisposition and environmental factors can explain the heterogeneity among these phenotypes. METHODS:We conducted a case-control study including 130 MHO, 251 MUNW, 208 MUO and 336 health controls by genotyping 2 SNPs (rs2241766, rs1501299) in ADIPOQ to investigate possible associations between SNPs in the ADIPOQ gene with susceptibility to three obese phenotypes respectively in Chinese Han population. Unconditional logistic regressions were used to detect the association between ADIPOQ SNPs and MHO/MUNW/MUO risks. RESULTS:Variant G allele of rs2241766 was associated with a reduced odds of MUO (additive model: Adjusted OR = 0.55; 95% CI = 0.40-0.75; P < 0.001) and no evidence of any significant association between rs2241766 and MHO phenotype (additive model: Adjusted OR = 0.84; 95% CI = 0.61-1.16; P = 0.306) or MUNW phenotype (additive model: Adjusted OR = 0.95; 95% CI = 0.73-1.24; P = 0.720) was found. Minor allele T of rs1501299 were significantly associated with decreased risk of MHO (Adjusted OR = 0.53; 95% CI = 0.37-0.76; P < 0.001) and MUNW (Adjusted OR = 0.63; 95% CI = 0.48-0.83; P = 0.001) in additive genetic model after correction for multiple testing. CONCLUSIONS:The variant G allele of rs2241766 was negatively associated with risk of MUO and variant T allele of rs1501299 exhibited reduced odds for MHO and MUNW. Beyond that, future studies are warranted to validate and extend our findings.

Objectives: NIHL is a disease with irreversible damage caused by multi-factor interaction, and the STAT3 is an essential protein with signal transduction and transcription functions. This study is aimed to explore the effect of STAT3 polymorphism on individual susceptibility to NIHL individuals, and to further examine the interaction between lifestyles and NIHL in the dominant model .Methods: This study was designed a case-control study and included 609 NIHL cases and 611 healthy hearing controls from the Jiangsu province of China. By collecting the lifestyle and demographic information of the study participants, genotyping the collected blood samples, and performing Real-time Quantitative PCR (qRT-PCR) to analyze and investigate the potential association between STAT3 SNPs and NIHL.Results: Statistical analysis results show that individuals carrying the C allele of rs1053023 and rs1053005 were more likely to develop NIHL than individuals carrying the T allele (OR = 1.367, 95% CI = 1.148-1.628, P = 0.0001 and OR = 1.37, 95% CI = 1.147-1.636, P = 0.001). In the dominant model (TC/CC genotype and TT genotype), stratified analysis of lifestyle, we found that people who smoke regularly are more likely to suffer from NIHL than non-smokers or occasional smokers. Besides, the expression of STAT3 was higher in NIHL cases by real-time quantitative PCR.Conclusion: Gene polymorphisms, rs1053023 and rs1053005, from STAT3, are associated with NIHL and C alleles of rs1053023 and rs1053005 within STAT3 may become biomarkers for workers exposed to noise.

[This corrects the article DOI: 10.1155/2020/9589310.].

BACKGROUND:Extracellular long non-coding RNA (lncRNA) has attracted increasing attention as a potential biomarker to indicate disease status and physiological process. It plays a unique role in pathogenesis, and may be a new potential biomarker, especially for chronic hearing loss. Early screening of NIHL susceptible population is of great significance in reducing the incidence of NIHL.METHODS:The expression profiles of lncRNAs and mRNAs in serum of noise-induced hearing loss (NIHL) and exposure groups were detected by microarray technique in serum. The differentially expressed mRNAs was analyzed by GO and KEGG to identify related biological functions and signaling pathways. The top up-regulated and down regulated lncRNAs were identified by qRT-PCR.RESULTS:A total of 2,072 differentially expressed lncRNAs (889 up-regulated and 1,183 down-regulated) were included in NIHL subjects compared to exposed group by using microarrays. GO enrichment and KEGG pathway analysis showed that the expression pattern of mRNAs in serum of NIHL was associated with noise exposure. LncRNAs were verified by qRT-PCR, namely, LOC101928211, LOC101928804, and BANCR. The expression of LOC101928211 and LOC101928804 in the NIHL group was significantly higher than that in the exposed group, while the expression of BANCR was obviously decreased (P<0.001).CONCLUSIONS:In this study, lncRNAs and mRNAs expression profile in NIHL was preliminarily investigated in silico. The newly discovered lncRNAs might be involved in the pathological process of hearing loss and may serve as potential biomarkers to indicate long-term noise exposure-induced hearing loss.

Occupational noise is among the most common risks associated with the wellbeing of employees.Occupational exposure to noise causes disabling hearing loss in 16% of adults worldwide [1] .It has been acknowledged that noise-induced hearing loss（NIHL） is a m ultifactorial disease,having both genetic and environmental factors.NIHL continues to be permanent as well as irreversible,but NIHL can be prevented.As demonstrated by the latest research,

Objectives This study investigated the hearing loss characteristics among occupational noise exposure workers with hypertension and the link between hypertension and hearing loss when exposed to occupational noise. Methods A total of 267,766 occupational noise-exposed workers were enrolled, including 29,868 workers with hypertension and 240,165 without hypertension. Hypertension was diagnosed according to WHO criteria. Hypertension was classified into four grades based on blood pressure. Assessment of hearing was performed through measurement of an unadulterated tone threshold at different frequencies, which ranged between 250 and 8,000 Hz. Results A substantial link was observed to exist between hypertension and the increment in the hearing limit. The increase in the hearing threshold was substantially higher among those having grade 2 hypertension. Conclusion The current investigation suggested patients with hypertension exhibit a substantial rise in hearing loss in comparison with patients without hypertension. The rise in hearing loss was significant in patients with grade 2 hypertension. Efficient and practicable measures are required to decrease the hearing loss in workers with hypertension and work-related noise exposure.

Noise-induced hearing loss (NIHL), one of the most widespread occupational health risks worldwide, is a kind of complex disorder resulting from both genetic and environmental factors. KCNQ4 channels are crucial to the internal ear potassium recycling. To explore whether KCNQ4 polymorphism is associated with individual susceptibility to NIHL, we performed this genetic association study on 571 NIHL cases and 639 normal hearing controls selected from about 2700 Chinese noise-exposed workers. General information and audiometric data were obtained through questionnaires and pure-tone audiometry (PTA). DNA samples were collected and genotyping for three selected SNPs (rs709688, rs2769256 and rs4660468) was performed. Significant differences were observed between cases and controls for the genotype frequency and allele frequency in rs4660468, suggesting that rs4660468 CT/TT genotype and T allele may be risk factors for NIHL. In subjects exposed to noise for more than 16 years (OR = 1.23, 95% CI = 1.09-1.53) and those who exposed to noise > 92 dB (OR = 1.29, 95% CI = 1.08-1.69), increased risks of NIHL were found after stratified analysis for rs4660468. Our results suggest that rs4660468 T allele of KCNQ4 involves with a higher risk of NIHL and could be one biomarker of susceptibility for Chinese noise exposed workers.

OBJECTIVE:To detect single nucleotide polymorphisms (SNPs) of the myocilin (MYOC) gene and to investigate their associations with primary open-angle glaucoma (POAG).METHODS:One hundred and fifty-seven sporadic patients with POAG and 155 unrelated control subjects without POAG were recruited from staff and visitors to the Prince of Wales Hospital between 1998 and 2000. All study subjects are ethnic Chinese living in Hong Kong. The two populations were matched in frequencies of gender and age. The SNPs of the MYOC gene in POAG patients and control subjects were screened and identified by high throughout conformation sensitive gel electrophoresis and fluorescent labeling automated sequencing. The genotype frequencies of each SNP in the two groups were compared by the Chi2 test or Fisher's exact 2-tailed test.RESULTS:A total of seventeen SNPs were identified from 2172 bp long of the MYOC gene, including all 3 exons and adjacent non-coding regions. The identified SNPs were 1-83G --> A, G12R, P16L, A17S, R46X, R76K, R91X, T123T, D208E, L215P, 730+35A --> G, A260A, I288I, E300K, T353I, Y471C and 1515+73G --> C, respectively. Of these, R91X, E300K and Y471C were found only in POAG patients. A significant difference between POAG patients and control subjects was found in the genotype frequencies of 1515+73G --> C. The frequency of the heterozygote (CG) was 0.6% in POAG patients, significantly less than the 4.5% in control subjects (Fisher's exact 2-tailed test, P=0.036, OR=0.136, 95%CI=0.022-0.828). No significant difference was found between the two populations in genotype frequencies of all other SNPs.CONCLUSION:The polymorphisms of the MYOC gene may be related to POAG.