[Cochleo-vestibular lesions and prognosis in patients with profound sudden sensorineural hearing loss: a comparative analysis].

Objective: To investigate the characteristics of cochleo-vestibular dysfunction in patients with profound sudden deafness, and the prognosis of inner ear hemorrhage. Methods: From January 2017 to December 2018, 92 inpatients with profound sudden sensorineural hearing loss were enrolled in the Department of Otorhinolaryngology, First Affiliated Hospital of Sun Yat-sen University. Our studied patients included 47 males and 45 females, aged 20-78 (39.3±6.1) years. According to the results of inner ear magnetic resonance imaging (MRI), the patients were divided into two groups: inner ear hemorrhage group and non-inner ear hemorrhage group. The clinical features, vestibular tests and audiological examination results during follow up were compared between the two groups. SPSS 22.0 software was used for statistical analysis. Results: The inner ear hemorrhage group consisted of 32 cases (34.8%, 32/92), all of whom complained of vertigo (100%, 32/32). Simultaneous vertigo attack and hearing loss occurred in 78.1% of this group (24/32). Neither semicircular canals function, nor cervical vestibular evoked myogenic potential (c-VEMP), nor ocular vestibular evoked myogenic potential (o-VEMP) in the affected side was normal (100%, 32/32). The rates of benign paroxysmal positional vertigo (BPPV) and disequilibrium were 37.5% (12/32) and 25.0% (8/32) respectively. Hearing improved in 28.1% (9/32) two weeks after treatment, and became stable at one month's follow up. In 60 cases without inner ear hemorrhage, 58.3% of them (35/60) experienced vertigo, which occurred simultaneously with hearing loss in 21 patients (60%, 21/35). The abnormal rates of semicircular canals function, c-VEMP and o-VEMP were 71.6% (43/60), 78.3% (47/60) and 66.7% (40/60), respectively. The incidence of BPPV was 16.7% (10/60) and 8.3% (5/60) in cases with disequilibrium. Hearing improved in 58.3% (35/60) two week after treatment, and became stable at three months' follow up. Significant difference was found in either vertigo rate, or simultaneous vertigo/hearing loss rate, or abnormal c-VEMP/o-VEMP rates, or accompanying BPPV, or disequilibrium rates between the two groups (P<0.05 each). Moreover, we observed better hearing recovery in non-inner ear hemorrhage group in the two weeks, one month, three months and six months' follow up, when compared with those in inner ear hemorrhage groups (P<0.05 each). Conclusions: Inner ear hemorrhage is associated with more severe cochlea-vestibular lesion and poorer prognosis, in comparison to the non-inner ear hemorrhage,in patients with profound sudden sensorineural hearing loss.

[Clinical characteristics and etiological analysis of sudden deafness patients with vertigo].

Objective: To explore the possible causes and mechanisms of sudden deafness with vertigo. Methods: Between August 2016 and December 2017, 74 patients with sudden deafness and vertigo were hospitalized in the Department of Otolaryngology, First Affiliated Hospital of Sun Yat-sen University. Among them, 36 were male and 38 were female, aged 18-75 (40.5±6.5) years. According to the results of magnetic resonance imaging (MRI), the patients were divided into two groups: internal ear hemorrhage (IEH) and non-IEH (NIEH). The characteristics of deafness, vertigo, laboratory examination and follow-up results were compared between the two groups. Results: In IEH group, deafness and vertigo occurred simultaneously in 22 cases (84.6%), abnormalities of semicircular canal function, cervical vestibular evoked myogenic potential (C-VEMP), ocular vestibular evoked myogenic potential (O-VEMP) in 26 cases (100%) and benign paroxysmal positional vertigo (BPPV) in 10 cases (38.5%). The total effective rate was 19.2% (5/26) after 14 days of treatment, and 11 cases (42.3%) appeared disturbance after 180 days of treatment. The abnormal rate of lateral vestibular function, C-VEMP and O-VEMP was 69.2% (18/26), 53.8% (14/26) and 57.7% (15/26) respectively. The improvement of hearing threshold was (28.6±9.7) dB. In NIEH group, deafness and vertigo occurred simultaneously in 25 cases (52.1%). The abnormalities of semicircular canal function, C-VEMP and O-VEMP happened in 37 cases (77.1%), 34 cases (70.8%), 26 cases (54.2%), respectively, and 6 cases (12.5%) were of BPPV. The total effective rate was 52.1% (25/48) after 14 days of treatment. After 180 days of treatment, 8 cases (16.7%) were out of balance, and the abnormal rate of lateral vestibular function, C-VEMP and O-VEMP were 31.2% (15/48), 25.0% (12/48) and 20.8% (10/48) respectively. The improvement of hearing threshold was (42.5±10.3) dB. The incidence of stimulantous deafness and vertigo, vestibular dysfunction rate, BPPV incidence rate and the total effective rate after 14 days of treatment were significantly different between the two groups (all P<0.05). The vestibular and cochlear dysfunction in IEH group was more serious than that in NIEH group. After 180 days of treatment, the vestibular dysfunction rate, imbalance rate and improvement of hearing threshold in NIEH group were significantly higher than that in IEH group (all P<0.05). The recovery of vestibular and cochlear function in NIEH group was better than that in IEH group. Conclusions: Sudden deafness with vertigo can cause vestibular and cochlear dysfunction. Different etiologies may lead to different clinical features and prognosis. The vestibular and cochlear function damage caused by inner ear hemorrhage was more serious and the recovery effect was poor.

[Clinical study of inner ear hemorrhage-associated sudden deafness and vertigo].

Objective: To analyze the clinical features and possible pathogenesis of sudden deafenss and vertigo induced by inner ear hemorrhage. Methods: Clinical data of 30 patients with inner ear hemorrhage, from the first affiliated hospital of Sun Yat-sen university during Jan 2016 to May 2017, were retrospectively analyzed. Results: Vergito and profound deafness were seen in all patients. The duration of vertigo ranged from 24 hours to three days in 11 cases, three to 14 days in the remaining 19 cases. Simultaneous occurrence of vergito and deafenss were seen in 24 patients. Semicircular canal hypofunction and abnormal cervical vestibular evoked myogenic potentials(C-VEMP)/ocular vestibular evoked myogenic potentials(O-VEMP) were detected in all cases. Ten patients had benign paroxysmal positional vertigo(BPPV) simultaneously. Hearing recovered in 20% of the cohort posttreatment. Dizziness and balance disturbance disappeared 1 to 2 months after therapy in 16 cases. Long term (6 months) follow up revealed poor hearing outcome and vestibular rehabilitation. Conclusion: Vestibular vertigo and profound sensorineural hearing loss, with unsatisfactory clinical prognosis, constituted the characters of inner ear hemorrhage-associated sudden deafness.

MiR-144-3p inhibits the proliferation and metastasis of pediatric Wilms' tumor cells by regulating Girdin.

OBJECTIVE: The aim of this study was to investigate the role of miR-144-3p in the proliferation and metastasis capacity of pediatric Wilms' tumor (WT) cells and to explore the underlying mechanism. PATIENTS AND METHODS: The quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) was performed to measure the expression level of miR-144-3p in pediatric WT tissues and cell lines (G401). A bioinformatics software was utilized to predict the interaction between miR-144-3p and Girdin. Subsequently, the interaction was further verified by dual luciferase reporter (DLR) gene assay and Western blot. The proliferation and colony formation ability of G401 cells were examined by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and colony formation assay, respectively. Finally, the effect of miR-144-3p on cell invasion and migration was analyzed by transwell assay. RESULTS: In the current study, we found that the expression level of miR-144-3p was significantly reduced in pediatric WT tissues and cells, whereas Girdin expression was upregulated. On-line target gene prediction software was applied to screen Girdin, which was considered as a downstream target gene of miR-144-3p. The interaction between miR-144-3p and Girdin was further verified by dual Luciferase reporter gene assay and Western blot. Subsequent experiments demonstrated that the proliferation and metastasis ability of cells was remarkably suppressed after up-regulating the expression of miR-144-3p. However, an addition of Girdin could reverse the effect of miR-144-3p. CONCLUSIONS: MiR-144-3p, which was up-regulated in pediatric WT, might inhibit the proliferation and metastasis of the cells by directly targeting Girdin. This further indicated that miR-144-3p could be a potential therapeutic target for the treatment of pediatric WT.

MiR-429 regulates the proliferation and apoptosis of nephroblastoma cells through targeting c-myc.

OBJECTIVE: We explored the regulation of miR-429 in nephroblastoma cells, investigating the mechanisms by which miR-429 influenced the proliferation and apoptosis of nephroblastoma. PATIENTS AND METHODS: The quantitative reverse transcription polymerase chain reaction (qRT-PCR) was conducted to detect the expression of miR-429 in nephroblastoma tissues and cell lines (G401). The interaction between miR-429 and c-myc was confirmed by qRT-PCR, Western blotting and luciferase assays, respectively. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and clone formation assay were used to detect the effect of miR-429 on the proliferation and clone formation ability of G401 cells. Cell cycle and apoptosis of G401 cells were measured by flow cytometry and TUNEL staining, respectively. RESULTS: miR-429 was down-regulated in nephroblastoma tissues and cells. On-line target gene prediction software was applied to screen c-myc, the potential downstream target gene of miR-429. The expression of c-myc was negatively regulated by miR-429. Subsequent experiments demonstrated that overexpression of miR-429 inhibited the proliferation ability and arrested cell cycle of G401 cells in G0/G1 phase. Besides, the number of apoptotic cells was increased in miR-429 intervened group. However, c-myc could reverse the biological effects of miR-429 on proliferation, apoptosis, clone formation and cell cycle of G401 cells. CONCLUSIONS: MiR-429 can regulate the proliferation, clone formation, cell cycle and apoptosis of nephroblastoma cells through targeting c-myc, indicating miR-429 may function as a potential therapeutic target for the treatment of nephroblastoma.

MicroRNA-613 attenuates the proliferation, migration and invasion of Wilms' tumor via targeting FRS2.

OBJECTIVE: Wilms' tumor is the most common malignant tumor in children worldwide. Considering the poor therapeutic effect on Wilms' tumor, we determined the effects of microRNA-613 on cell proliferation and metastasis in vitro, providing therapeutic targets for the treatment of Wilms' tumor. PATIENTS AND METHODS: Quantitative real-time PCR (qRT-PCR) was employed to identify the expression level of miR-613. CCK8 and colony formation assays were incorporated to assess cell viability and proliferation capacity. Cell migration and invasion assays were performed to investigate the metastasis capacity of Wilms' tumor cells. Flow cytometry was used to detect cell cycle distribution and cell apoptosis. Protein levels were assessed by western blotting assay. The target gene was predicted and verified by bioinformatics analysis and luciferase assay. RESULTS: The expression of miR-613 was downregulated in Wilms' tumor tissues compared with adjacent normal tissues (n=32). Overexpression of miR-613 could attenuate Wilms' tumor cell viability, proliferation, invasion, and migration capacity, as well as induce cell cycle arrest at the G0/G1 phase. FRS2 was chosen as the target of miR-613 by bioinformatics analysis and a luciferase reporter assay. MiR-613 expression was inversely correlated with FRS2 in Wilms' tumor tissues. Moreover, restoration of FRS2 rescued the tumor suppressive role of miR-613 in Wilms' tumor cell growth and metastasis. CONCLUSIONS: MiR-613 had a tumor-suppressive effect on Wilms' tumor progression and metastasis via targeting FRS2 in vitro, which provided an innovative and candidate target for the diagnosis and treatment of Wilms' tumor.