Noise-induced Hearing Loss Subjects Research Articles

Characteristics of brain glucose metabolism and metabolic connectivity in noise-induced hearing loss

The purpose of this study was to evaluate the differences in cerebral glucose metabolism and metabolic connectivity between noise-induced hearing loss (NIHL) subjects and normal subjects. Eighty-nine subjects who needed close observation for NIHL or were diagnosed with NIHL and 89 normal subjects were enrolled. After pre-processing of positron emission tomography images including co-registration, spatial normalization, and smoothing, a two-sample t-test was conducted to compare cerebral glucose metabolism between the two groups. To evaluate metabolic connectivity between two groups, BRAPH–BRain Analysis using graPH theory, a software package to perform graph theory analysis of the brain connectome was used. NIHL subjects showed hypometabolism compared to normal subjects in both insulae (x − 38, y − 18, z 4; × 42, y − 12, z 4) and right superior temporal gyrus (× 44, y 16, z − 20). No brain regions showed hypermetabolism in the NIHL subjects. In metabolic connectivity analysis, NIHL subjects showed decreased average strength, global efficiency, local efficiency, and mean clustering coefficient when compared with normal subjects. Decreased glucose metabolism and metabolic connectivity in NIHL subject might reflect decreased auditory function. It might be characteristic of sensorineural hearing loss.

Genome-wide association study identifies 7q11.22 and 7q36.3 associated with noise-induced hearing loss among Chinese population.

Noise‐induced hearing loss (NIHL) seriously affects the life quality of humans and causes huge economic losses to society. To identify novel genetic loci involved in NIHL, we conducted a genome‐wide association study (GWAS) for this symptom in Chinese populations. GWAS scan was performed in 89 NIHL subjects (cases) and 209 subjects with normal hearing who have been exposed to a similar noise environment (controls), followed by a replication study consisting of 53 cases and 360 controls. We identified that four candidate pathways were nominally significantly associated with NIHL, including the Erbb, Wnt, hedgehog and intraflagellar transport pathways. In addition, two novel index single‐nucleotide polymorphisms, rs35075890 in the intron of AUTS2 gene at 7q11.22 (combined P = 1.3 × 10−6) and rs10081191 in the intron of PTPRN2 gene at 7q36.3 (combined P = 2.1 × 10−6), were significantly associated with NIHL. Furthermore, the expression quantitative trait loci analyses revealed that in brain tissues, the genotypes of rs35075890 are significantly associated with the expression levels of AUTS2, and the genotypes of rs10081191 are significantly associated with the expressions of PTPRN2 and WDR60. In conclusion, our findings highlight two novel loci at 7q11.22 and 7q36.3 conferring susceptibility to NIHL.

Analysis of lncRNA-mRNA expression pattern in male textile workers with noise-induced hearing loss.

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. 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. 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). 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.

A predictive model of the association between gene polymorphism and the risk of noise-induced hearing loss caused by gunfire noise

Background Noise-induced hearing loss (NIHL) is one of the common diseases in otology. In general, we assume that most people who are exposed to loud noise constantly, e.g., soldiers, will suffer from hearing loss. Hearing loss is related to the gene polymorphisms, with the Wolfram syndrome type 1 gene (T2500C), interleukin-4 receptor α chain (Q576R) and chloride channel-Kb (T481S) polymorphisms being most related to NIHL. Methods We analyzed the association between the polymorphisms and the risk of NIHL in 119 subjects who were exposed to the same loud gunfire. In the current study, 39 persons with hearing loss and 80 with normal hearing were recruited from military officers and soldiers that were exposed to gunfire. Results The results showed that the genetic variation of Wolfram syndrome type 1 gene was a more crucial factor than other genes in causing hearing loss. There was a significant difference ( p = 0.027) in WFS1 (T2500C) polymorphism between NIHL subjects and controls. Conclusion In this study, we found that although loud noise could usually result in hearing damage, the clinical characteristics of hearing loss were irrelevant to gunfire noise. The gene polymorphisms provide predictors for us to evaluate the risk of NIHL prior to gunshot training.

Vestibular evoked myogenic potential in noise-induced hearing loss

Noise affects one's hearing as well as balance mechanism. The hearing mechanism of the noise-exposed individuals has been extensively studied. However, in view of the poor research focus on the sacculo-collic reflexes, especially in this study area, the present study was undertaken to examine the vestibular evoked myogenic potentials (VEMP) in subjects with noise-induced hearing loss (NIHL). A total of 30 subjects (55 ears) with NIHL participated in the present study within the age range of 30-40 years. VEMP recordings were done at 99 dBnHL using IHS instrument. The results indicated that as the average pure tone hearing threshold increased, the VEMP latencies were prolonged and peak to peak amplitude was reduced in NIHL subjects. Out of the 55 ears, VEMP was absent in 16 (29.0%) ears. The latency was prolonged and the peak to peak amplitude was reduced in 19 (34.6%) ears. VEMP results were normal in 20 (36.4%) ears. Therefore, VEMP was abnormal or absent in 67% of NIHL subjects in the present study. Hence it can be concluded that the possibility of vestibular dysfunction, specially the saccular pathway, is high in individuals with NIHL. VEMP, a non-invasive and user friendly procedure, can be employed in these individuals to assess sacculo-collic reflex.

Derived-Band Auditory Brain-Stem Response Estimates of Traveling Wave Velocity in Humans: II. Subjects With Noise-Induced Hearing Loss and Meniere’s Disease

Estimates of cochlear traveling wave velocity (TWV) were computed from derived-band auditory brain-stem response (ABR) latencies in subjects with noise-induced hearing loss (NIHL) or Meniére's disease (MD). ABR wave V latencies were determined for each of six derived frequency bands (unmasked-8 kHz, 8-4 kHz, 4-2 kHz, 2-1 kHz, 1 kHz-500 Hz, and 500-250 Hz). Representative frequencies were assigned to the derived bands by estimating their energy midpoints, and cochlear positions corresponding to these frequencies were determined using Greenwood's (1961) place-frequency function for humans. An exponential function of the form I = A + BeCd was fitted to each subject's latency-by-distance data using a least-squares algorithm, and a TWV function was generated by taking the reciprocal of the derivative of the latency function with respect to distance [v = 1/(BCeCd)]. Expected values for subjects' TWV functions were compared to normative data from Donaldson and Ruth (1993) at five cochlear loci. NIHL subjects' TWV estimates fell within normal limits at all cochlear loci, and no relation between severity of high-frequency hearing loss and TWV could be discerned. MD subjects with good low-frequency hearing sensitivity generally yielded normal TWV estimates, whereas MD subjects with low-frequency hearing loss yielded either normal or elevated TWVs. MD subjects' data generally support the hypothesis that endolymphatic hydrops results in increased TWV or, alternatively, a basalward shift in the peak of the traveling wave, in cochleas with presumed normal basilar membrane elasticity.