The effect of intratympanic oxytocin treatment on rats exposed to acoustic trauma.

OBJECTIVE: To investigate whether oxytocin can prevent ototoxicity related to acoustic trauma. METHODS: Twenty-eight rats were divided into four groups: noise (group 1), control (group 2), noise plus oxytocin (group 3), and oxytocin (group 4). Intratympanic oxytocin was administered on days 1, 2, 4, 6, 8 and 10 in groups 3 and 4. Groups 1 and 3 were exposed to acoustic trauma. Distortion product otoacoustic emission and auditory brainstem response testing were performed in all groups. RESULTS: In group 1, auditory brainstem response thresholds increased significantly after acoustic trauma. In group 3, auditory brainstem response thresholds increased significantly on day 1 after acoustic trauma, but there were no significant differences between thresholds at baseline and on the 7th and 21st days. In group 1, significant differences were observed between distortion product otoacoustic emission signal-to-noise ratios measured before and on days 1, 7 and 21 after acoustic trauma. In group 3, no significant differences were observed between the distortion product otoacoustic emission signal-to-noise ratios measured before and on days 7 and 21 after acoustic trauma. CONCLUSION: Oxytocin had a therapeutic effect on rats exposed to acoustic trauma in this experiment.

Expression of a disintegrin and metalloproteinase-33 protein in vocal fold polyps.

BACKGROUND: This study aimed to evaluate the association of a disintegrin and metalloproteinase-33 protein ('ADAM-33') expression in vocal polyp formation and to determine its correlation with clinical characteristics. METHODS: Medical charts and histological sections of 32 patients diagnosed with vocal polyps who underwent surgery were analysed. Controls were histopathologically normal vocal fold tissues obtained from 36 patients who underwent surgery for laryngeal squamous cell carcinoma. Immunohistochemical staining was performed to detect ADAM-33 expression in epithelial cells, stroma and vessels. RESULTS: All epithelial, stromal and vascular staining scores were significantly greater in polyp tissue than in controls (p < 0.001). Stromal ADAM-33 staining scores were higher in vocal polyp patients with a symptom duration of less than six months (p < 0.05). Vocal overuse or the presence of reflux symptoms, sinonasal symptoms or allergy did not affect ADAM-33 immunostaining scores (p = 0.05). CONCLUSION: In this study, ADAM-33 immunostaining was significantly increased in vocal polyps. Therefore, over-expression of this protein may be associated with vocal polyp pathogenesis.

Expression of disintegrin and metalloproteinase family proteins 10, 12 and 17 in cholesteatoma.

OBJECTIVE: Proteases of the disintegrin and metalloproteinase family (also known as ADAM proteins) are involved in various physiological and pathological processes. This study assessed the expression of disintegrin and metalloproteinase family proteins 10, 12 and 17 in cholesteatoma. MATERIALS AND METHODS: The study evaluated cholesteatoma specimens from 19 patients, and external ear canal skin samples from 7 of the same patients (as controls), for the expression of disintegrin and metalloproteinase family proteins 10, 12 and 17, using immunohistochemical methods. RESULTS AND ANALYSIS: The study observed over-expression of proteins 10 and 17 in blood vessels, and over-expression of proteins 12 and 17 in cholesteatoma stroma. Immunostaining scores for proteins 10, 12 and 17 in epithelial and inflammatory cells from cholesteatoma specimens versus control specimens showed no statistically significant differences. CONCLUSION: Over-expression of disintegrin and metalloproteinase family proteins 10, 12 and 17 in cholesteatoma may be related to cholesteatoma pathogenesis. These proteins deserve further study as they may represent potential targets for cholesteatoma treatment.

Expression of "a disintegrin and metalloproteinase-33" (ADAM-33) protein in laryngeal squamous cell carcinoma.

OBJECTIVE: A disintegrin and metalloproteinase domain containing protein 33 (also known as ADAM-33) is a member of a matrix metalloproteinase family which mediates extracellular matrix remodelling and changes in cellular adhesion. This study aimed to evaluate expression of this protein in laryngeal squamous cell carcinoma, and to determine its correlation with patients' clinicopathological characteristics. SUBJECTS AND METHODS: Forty paraffin blocks of laryngeal carcinoma underwent immunohistochemical staining to detect "a disintegrin and metalloproteinase-33" expression. Case records were reviewed to determine patient characteristics. RESULTS: All epithelial, vascular and stromal staining scores were significantly increased in tumour tissue compared with controls (p < 0.001). However, patients' clinical characteristics at the time of diagnosis, and their disease extent, did not correlate significantly with the immunohistochemical staining scores. CONCLUSION: This study suggests that increased expression of "a disintegrin and metalloproteinase-33" may play a role in the pathogenesis of laryngeal carcinoma.

Evaluation of vestibular evoked myogenic potentials during benign paroxysmal positional vertigo attacks; neuroepithelial degeneration?

OBJECTIVE: Recent studies show that benign paroxysmal positional vertigo (BPPV) may also affect the macula of the saccule. We investigated vestibular evoked myogenic potential (VEMP) results in patients with BPPV. MATERIALS AND METHODS: The study group included 31 patients (31 ears) diagnosed with posterior canal BPPV and the control group included 23 healthy volunteers (46 ears) with no neurotologic symptoms. After VEMP recordings were performed, mean latency values for p13 of the study and control groups were compared. RESULTS: VEMP responses were elicited in all controls (46 ears). In the study group, responses were normal in 19, delayed in 5, and absent in 7 ears. There was a significant difference between abnormal VEMP rates for patients versus controls (p < 0.001). Although VEMP responses were elicited in all non-affected ears of patients, there was a delayed response in 6 (19%) non-affected ears. This was statistically significant when compared with controls (p = 0.002). There was no correlation between abnormal VEMPs and the number of canalith reposition maneuvers required (p = 0.392). CONCLUSION: Our findings suggest the prolongation of mean latency values for p13 of VEMP in patients with BPPV might signify neuronal degeneration in the macula of the saccule, and the absence of VEMP waves might represent the extent of damage. Also, high latency values for p13 in non-affected ears of patients might indicate bilateral neural degeneration in BPPV.

A founder TMIE mutation is a frequent cause of hearing loss in southeastern Anatolia.

Using Affymetrix 10K arrays, we searched for regions of homozygosity in 51 Turkish families including at least three members with either congenital or prelingual autosomal recessive non-syndromic sensorineural hearing loss (ARNSSNHL), and identified four families whose deafness mapped to the DFNB6 locus on 3p21 containing the TMIE gene. Mutation analysis revealed the p.R84W mutation in all four families. Screening of this mutation in 254 families with ARNSSNHL, without GJB2 mutations, revealed four additional affected families. A novel mutation was found in a non-complementary marriage between a deaf couple who were homozygous for p.R84W and p.W57X, respectively with two affected children who were compound heterozygotes. Six of the TMIE families originated from southeastern Anatolia, making p.R84W a common cause of hearing loss in that region with a relative frequency of 10.3% (95% CI is 2.5-18.1%). The overall prevalence of the p.R84W mutation in ARNSSNHL in Turkey is 2.4% (95% CI is 0.7-4.0%). Genotyping of single-nucleotide polymorphisms flanking the TMIE gene revealed a conserved haplotype, suggesting a single origin for p.R84W from a common ancestor 1250 years ago (95% CI is 650-2500 years). We conclude that p.R84W could be a common mutation in other Middle Eastern populations and should be included in mutation screening offered to individuals with ARNSSNHL.