RESUMO
Hypothesis: Cochlear microphonic recorded at ear canal (CM-EC) can be a substitute for the one recorded at round window (CM-RW). Background: Almost all clinics do not measure tone-burst evoked CM due to technical difficulty although it can provide more information than click evoked CM. Moreover, clinicians like the CM-EC more than that measured at CM-RW because CM-EC is non-invasive. There is difference between CM-RW and CM-EC, for example, CM-EC is less prominent than CM-RW, therefore, studying tone-burst evoked CM-EC and its relationship with CM-RW are highly significant and can promote the clinical application of CM-EC. Method: Nine guinea pigs were randomly allocated into three groups, group 1 was not exposed to noise, called normal control. group 2 and group 3 were exposed to the low- (0.5-2 kHz) and high-frequency band-noise (6-8 kHz) at 120 dB SPL for 1 h, respectively. It was difficulty to record low-frequency CM due to severe environmental interruption, in current study the recording technology of tone-burst evoked CM was optimized so that tone-burst evoked CM was measured across full speech frequency (0.5-8 kHz) in the presence of normal hearing and noise induced hearing loss (NIHL). Results: CM-RW and CM-EC were successfully recorded across speech frequency. Significant reduction in CM amplitude was observed at 0.5 and 2 kHz in group 2, at 6 and 8 kHz in group 3 as compared to group 1, p < .05, indicating that CM amplitude was sensitive to band-noise exposure. Significant correlation between CM-RW and CM-EC was also verified, p < .05. Conclusion: CM-EC is a useful objective test for evaluation of hearing function; the result of current study supports the clinical application of non-invasive CM-EC.
RESUMO
Long noncoding RNA (lncRNA) LINC00461 (LINC00461) is reported to be related to glioma progression. However, the mechanism of LINC00461 in glioma remains unclear. Expression of LINC00461, miRNA (miR)-216a, and aquaporin 4 (AQP4) was detected using real-time quantitative PCR (RT-qPCR) and western blotting. Proliferation, temozolomide (TMZ) resistance, migration, and invasion were assessed by MTT, colony formation, and transwell assays, respectively. The target binding among miR-216a, LINC00461, and AQP4 was confirmed by the luciferase reporter assay. The tumor growth was monitored in the xenograft experiment. LINC00461 was upregulated, and miR-216a was downregulated in glioma tissues and cells, and LINC00461 upregulation was correlated with large tumor size, higher WHO grade and recurrence, and poor overall survival. LINC00461 knockdown suppressed cell viability, abilities of cell cloning and migration and invasion, and TMZ resistance in glioma. Mechanically, LINC00461 was confirmed to sponge miR-216a to affect AQP4 expression. Rescue assays verified that miR-216a downregulation or AQP4 upregulation abrogated the inhibitory effect of LINC00461 knockdown on cell proliferation, migration, invasion, and TMZ resistance in vitro. Moreover, LINC00461 downregulation blocked the glioma tumor growth in vivo. In conclusion, LINC00461 knockdown inhibits glioma cell proliferation, migration, invasion, and TMZ resistance through miR-216a/AQP4 axis, suggesting LINC00461 as an oncogene in glioma progression.
