Macrophage-mediated immune response aggravates hearing disfunction caused by the disorder of mitochondrial dynamics in cochlear hair cells.

Mitochondrial dynamics is essential for maintaining the physiological function of the mitochondrial network, and its disorders lead to a variety of diseases. Our previous study identified mitochondrial dynamics controlled anti-tumor immune responses and anxiety symptoms. However, how mitochondrial dynamics affects auditory function in the inner ear remains unclear. Here, we show that the deficiency of FAM73a or FAM73b, two mitochondrial outer membrane proteins that mediate mitochondrial fusion, leads to outer hair cells (HCs) damage and progressive hearing loss in FVB/N mice. Abnormal mitochondrial fusion causes elevated oxidative stress and apoptosis of HCs in the early stage. Thereafter, the activation of macrophages and CD4+ T cell is found in the mutant mice with the increased expression of the inflammatory cytokines IL-12 and IFN-γ compared with control mice. Strikingly, a dramatically decreased number of macrophages by Clophosome®-A-Clodronate Liposomes treatment alleviates the hearing loss of mutant mice. Collectively, our finding highlights that FAM73a or FAM73b deficiency affects HCs survival by disturbing the mitochondrial function, and the subsequent immune response in the cochleae worsens the damage of HCs.

A novel microRNA signature predicts vascular invasion in hepatocellular carcinoma.

Vascular invasion (VI) in hepatocellular carcinoma (HCC) is an important clinical parameter to predict survival. In this study, we collected microRNA (miRNA) expression data from HCC patients using The Cancer Genome Atlas database and identified a novel miRNA signature associated with VI. First, we categorized HCC patients into groups with or without VI (VI+ and VI-). We identified three miRNAs (miRNA-210, miRNA-10b, and miRNA-9-1) that were associated with VI according to a Kaplan-Meier analysis. This three-miRNA signature exhibited good predictive ability for VI in patients with HCC according to a receiver operating characteristic curve analysis at 1, 3, and 5 years. Patients with HCC with a high risk score exhibited a trend toward worse outcomes as determined by multivariable Cox regression and stratified analyses. This three-miRNA signature provides an accurate prediction of VI and can be used as an independent prognostic indicator for predicting VI in HCC patients.

Rs1894720 polymorphism in MIAT increased susceptibility to age-related hearing loss by modulating the activation of miR-29b/SIRT1/PGC-1α signaling.

BACKGROUND: MIAT may be implicated in the pathogenesis of age-related hearing loss (AHL). This study aimed to clarify the effect of a MIAT signaling pathway on the risk of AHL. METHODS: Terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, auditory brainstem response (ABR) and quantitative hair cell counts were used to compare the hearing functions in different groups of mice. 5,5,6,6-Tetrachloro-1,1,3,3-tetraethylbenzimidazolylcarbocyanine iodide (JC-1) dye method was used to establish the potential association between mitochondrial dysfunction and aging. Real-time polymerase chain reaction, Western blot analysis, computational analysis, and luciferase assay were conducted to establish a myocardial infarction associated transcript (MIAT) signaling pathway, whose role in the pathogenesis of AHL was further validated by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay and flow cytometry. RESULTS: Aged C57BL/6 mice were associated with a more severe level of hair cell loss, while exhibiting a higher ABR threshold at various frequencies as well as a lower percentage of inner/outer hair cells. A reduced mitochondrial membrane potential in the cochleae of aged C57BL/6 mice indicated the presence of mitochondrial dysfunction in these mice. Relative expression of MIAT, Sirtuin1 (SIRT1), and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) was downregulated in aged mice, with microRNA-29b (miR-29b) being highly expressed. Also, MIAT binds to miR-29b, an inhibitor of SIRT1 expression. The regulatory relationship among MIAT, miR-29b, and SIRT1 was further validated by comparing the differentiated expression of these factors in cells treated with phosphate-buffered saline + H2 O2, a negative control + H2 O2, MIAT + H2 O2 , or H2 O2 + anti-miR-29b. CONCLUSION: MIAT could elevate the expression of SIRT1/PGC-1α via downregulating miR-29b. And the downregulated SIRT/PGC-1α increased the incidence of AHL via promoting the apoptosis of cochlear hair cells.

Mitochondrial Regulation of Macrophages in Innate Immunity and Diverse Roles of Macrophages During Cochlear Inflammation.

Macrophages are essential components of the innate immune system and constitute a non-specific first line of host defense against pathogens and inflammation. Mitochondria regulate macrophage activation and innate immune responses in various inflammatory diseases, including cochlear inflammation. The distribution, number, and morphological characteristics of cochlear macrophages change significantly across different inner ear regions under various pathological conditions, including noise exposure, ototoxicity, and age-related degeneration. However, the exact mechanism underlying the role of mitochondria in macrophages in auditory function remains unclear. Here, we summarize the major factors and mitochondrial signaling pathways (e.g., metabolism, mitochondrial reactive oxygen species, mitochondrial DNA, and the inflammasome) that influence macrophage activation in the innate immune response. In particular, we focus on the properties of cochlear macrophages, activated signaling pathways, and the secretion of inflammatory cytokines after acoustic injury. We hope this review will provide new perspectives and a basis for future research on cochlear inflammation.

Identification of an immune-related signature as a prognostic classifier for patients with early-stage head and neck squamous cell carcinoma.

Background: Head and neck squamous cell carcinoma (HNSCC) is the most common type and accounts for 90% of all head and neck cancer cases. Despite advances in early diagnosis and treatment strategies-chemotherapy, surgical resection, and radiotherapy-5-year survival remains grim. For patients with early-stage HNSCC, accurately predicting clinical outcomes is challenging. Considering the pivotal role of the immune system in HNSCC, we developed a reliable immune-related gene signature (IRGS) and explored its predictive accuracy in patients with early-stage HNSCC. Methods: We examined immune gene expression profiles and clinical information from 230 early-stage HNSCC specimens, including 100 cases from The Cancer Genome Atlas (TCGA), 49 cases from the Gene Expression Omnibus (GEO; GSE65858), and 81 cases from an independent clinical cohort. The prognostic signature was constructed using Kaplan-Meier analysis and the least absolute shrinkage and selection operator (LASSO) Cox algorithm. We also explored the IRGS-related biological pathways and immune landscape using bioinformatics analysis. Results: A nine-immune-gene signature was generated to significantly stratify patients into high and low-risk groups. High risk patients exhibited shorter survival time [hazard ratio (HR) =13.795, 95% confidence interval (CI): 3.275-58.109, P<0.001]. The signature demonstrated robust prognostic ability in the training and validation sets and could independently predict overall survival (OS) and relapse-free survival (RFS). Subsequently, the receiver operating characteristic (ROC) curve and C-index confirmed the signature's predictive accuracy compared to clinical parameters. Additionally, cases classified as low risk showed more immune cell infiltration than high-risk cases. Conclusions: Our novel IRGS is a reliable and robust classifier for accurate patient stratification and prognostic evaluation. Future studies will attempt to affirm the signature's clinical application to early-stage HNSCC.

Contrast-Enhanced Computed Tomography-Based Machine Learning Radiomics Predicts IDH1 Expression and Clinical Prognosis in Head and Neck Squamous Cell Carcinoma.

RATIONALE AND OBJECTIVES: Isocitrate dehydrogenase 1 (IDH1) is a potential therapeutic target across various tumor types. Here, we aimed to devise a radiomic model capable of predicting the IDH1 expression levels in patients with head and neck squamous cell carcinoma (HNSCC) and examined its prognostic significance. MATERIALS AND METHODS: We utilized genomic data, clinicopathological features, and contrast-enhanced computed tomography (CECT) images from The Cancer Genome Atlas and the Cancer Imaging Archive for prognosis analysis and radiomic model construction. The selection of optimal features was conducted using the intraclass correlation coefficient, minimum redundancy maximum relevance, and recursive feature elimination algorithms. A radiomic model for IDH1 prediction and radiomic score (RS) were established using a gradient-boosting machine. Associations between IDH1 expression, RS, clinicopathological variables, and overall survival (OS) were determined using univariate and multivariate Cox proportional hazards regression analyses and Kaplan-Meier curves. RESULTS: IDH1 emerged as a distinct predictive factor in patients with HNSCC (hazard ratio [HR] 1.535, 95% confidence interval [CI]: 1.117-2.11, P = 0.008). The radiomic model, built on eight optimal features, demonstrated area under the curve values of 0.848 and 0.779 in the training and validation sets, respectively, for predicting IDH1 expression levels. Calibration and decision curve analyses validated the model's suitability and clinical utility. RS was significantly associated with OS (HR=2.22, 95% CI: 1.026-4.805, P = 0.043). CONCLUSION: IDH1 expression is a significant prognostic marker. The developed radiomic model, derived from CECT features, offers a promising approach for diagnosing and prognosticating HNSCC.

AAV-mediated Gpm6b expression supports hair cell reprogramming.

Irreversible damage to hair cells (HCs) in the cochlea leads to hearing loss. Cochlear supporting cells (SCs) in the murine cochlea have the potential to differentiate into HCs. Neuron membrane glycoprotein M6B (Gpm6b) as a four-transmembrane protein is a potential regulator of HC regeneration according to our previous research. In this study, we found that AAV-ie-mediated Gpm6b overexpression promoted SC-derived organoid expansion. Enhanced Gpm6b prevented the normal decrease in SC plasticity as the cochlea develops by supporting cells re-entry cell cycle and facilitating the SC-to-HC transformation. Also, overexpression of Gpm6b in the organ of Corti through the round window membrane injection facilitated the trans-differentiation of Lgr5+ SCs into HCs. In conclusion, our results suggest that Gpm6b overexpression promotes HC regeneration and highlights a promising target for hearing repair using the inner ear stem cells combined with AAV.

An immune checkpoint-based signature predicts prognosis and chemotherapy response for patients with small cell lung cancer.

BACKGROUND: Therapeutic options for small cell lung cancer (SCLC), a particularly lethal malignancy, remain limited. Members of the B7-CD28 family are compelling targets for immune checkpoint blockade strategies, which involve activating, inhibiting, and fine-tuning the T cell immune response. However, their clinical features and significance have not been explored comprehensively. METHOD: We enrolled 228 patients with an initial diagnosis of SCLC, including 77 cases from Cbioportal and a validation cohort of 151 cases with qPCR data. Kaplan-Meier analysis and LASSO Cox model were used to identify a signature based on the B7-CD28 family, which was applied for accurate prediction of chemotherapy benefit and prognosis for SCLC patients. In addition, we applied bioinformatics analysis to explore potential signature-related molecular mechanisms and the immune landscape. RESULTS: The mutation profiles of healthy tissues and SCLC tissues were distinct. A signature consisting of seven genes (CD86, ICOSLG, CD276, CD28, CTLA-4, PDCD1, and TMIGD2) was identified and applied to group patients based on risk level (high-risk and low-risk), producing two groups for which survival outcomes differed significantly (HR = 3.81, 95% CI: 2.16-6.74, P < 0.001). The immune checkpoint-based signature accurately predicted patient outcomes for the selected training and validation sets. Notably, low-risk patients were more likely to benefit from chemotherapy and showed greater immune activation. Additionally, time-dependent ROC curves and C-index analysis confirmed that the immune checkpoint-based signature has excellent predictive power for prognosis and chemotherapy benefit compared to clinically recognized parameters. Finally, multivariate analysis confirmed the identified signature as an independent risk factor for prognosis and chemotherapeutic response. CONCLUSION: We systematically obtained a comprehensive molecular profile for B7-CD28 family members in SCLC patients, from which we produced a reliable and robust prognostic immune checkpoint-based signature with the potential to improve prognostic stratification and therapy strategies for SCLC patients.

Piezoelectric biomaterials for neural tissue engineering.

Nerve injury caused by trauma or iatrogenic trauma can lead to loss of sensory and motor function, resulting in paralysis of patients. Inspired by endogenous bioelectricity and extracellular matrix, various external physical and chemical stimuli have been introduced to treat nerve injury. Benefiting from the self-power feature and great biocompatibility, piezoelectric biomaterials have attracted widespread attention in biomedical applications, especially in neural tissue engineering. Here, we provide an overview of the development of piezoelectric biomaterials for neural tissue engineering. First, several types of piezoelectric biomaterials are introduced, including inorganic piezoelectric nanomaterials, organic piezoelectric polymers, and their derivates. Then, we focus on the in vitro and in vivo external energy-driven piezoelectric effects involving ultrasound, mechanical movement, and other external field-driven piezoelectric effects. Neuroengineering applications of the piezoelectric biomaterials as in vivo grafts for the treatment of central nerve injury and peripheral nerve injury are also discussed and highlighted. Finally, the current challenges and future development of piezoelectric biomaterials for promoting nerve regeneration and treating neurological diseases are presented.

Mitochondrial dysfunction in hearing loss: Oxidative stress, autophagy and NLRP3 inflammasome.

Sensorineural deafness becomes an inevitable worldwide healthy problem, yet the current curative therapy is limited. Emerging evidences demonstrate mitochondrial dysfunction plays a vital role of in the pathogenesis of deafness. Reactive oxygen species (ROS)-induced mitochondrial dysfunction combined with NLRP3 inflammasome activation is involved in cochlear damage. Autophagy not only clears up undesired proteins and damaged mitochondria (mitophagy), but also eliminate excessive ROS. Appropriate enhancement of autophagy can reduce oxidative stress, inhibit cell apoptosis, and protect auditory cells. In addition, we further discuss the interplays linking ROS generation, NLRP3 inflammasome activation, and autophagy underlying the pathogenesis of deafness, including ototoxic drugs-, noise- and aging-related hearing loss.

Advances in nerve guidance conduits for peripheral nerve repair and regeneration.

Peripheral nerve injury (PNI) can cause partial or total motor and sensory nerve function, leading to physical disability and nerve pain that severely affects patients' quality of life. Autologous nerve transplantation is currently the clinically recognized gold standard, but due to its inherent limitations, researchers have been searching for alternative treatments. Nerve guidance conduits (NGCs) have attracted much attention as a favorable alternative to promote the repair and regeneration of damaged peripheral nerves. In this review, we provide an overview of the anatomy of peripheral nerves, peripheral nerve injury and repair, and current treatment methods. Importantly, different design strategies of NGCs used for the treatment of PNI and their applications in PNI repair are highlighted. Finally, an outlook on the future development and challenges of NGCs is presented.

Circular RNA ciRS-7 promotes laryngeal squamous cell carcinoma development by inducing TGM3 hypermethylation via miR-432-5p/DNMT3B axis.

OBJECTIVE: This work is to explore the mechanism by which circular RNA ciRS-7 affects laryngeal squamous cell carcinoma (LSCC). METHODS: ciRS-7 expression in LSCC tissues was detected by qRT-PCR, and the association between ciRS-7 with clinicopathological features of LSCC patients was evaluated. HN-4 and UM-SCC-10A cells were transfected or cotransfected with si-ciRS-7, miR-432-5p inhibitor, LV-DNMT3B or si-TGM3. Then, the viability and aggressive nature of the cells were tested. The binding site between ciRS-7 and miR-432-5p or between miR-432-5p and DNMT3B was predicted and the targeting relationship was identified. The specific binding between ciRS-7 and miR-432-5p was further verified by AGO2 RIP assay. HN-4 cells transfected with si-ciRS-7 was injected into nude mice to induce xenograft tumors. RESULTS: Higher ciRS-7 expression in LSCC tissues was closely associated with higher clinical stage, and exacerbated infiltration and lymph node metastasis in LSCC patients. Silencing ciRS-7 inhibited LSCC cell viability, epithelial-mesenchymal transition (EMT), and promoted the apoptosis. When miR-432-5p was inhibited or DNMT3B was overexpressed, the growth and EMT of LSCC cells were stimulated despite ciRS-7 silencing. Downregulation of ciRS-7 restrained the growth of xenograft tumors in vivo. CONCLUSION: ciRS-7 promotes the progression of LSCC through increasing TGM3 methylation via miR-432-5p/DNMT3B axis.

Genome-wide methylation profiling identify hypermethylated HOXL subclass genes as potential markers for esophageal squamous cell carcinoma detection.

BACKGROUND: Numerous studies have revealed aberrant DNA methylation in esophageal squamous cell carcinoma (ESCC). However, they often focused on the partial genome, which resulted in an inadequate understanding of the shaped methylation features and the lack of available methylation markers for this disease. METHODS: The current study investigated the methylation profiles between ESCC and paired normal samples using whole-genome bisulfite sequencing (WGBS) data and obtained a group of differentially methylated CpGs (DMC), differentially methylated regions (DMR), and differentially methylated genes (DMG). The DMGs were then verified in independent datasets and Sanger sequencing in our custom samples. Finally, we attempted to evaluate the performance of these genes as methylation markers for the classification of ESCC. RESULTS: We obtained 438,558 DMCs, 15,462 DMRs, and 1568 DMGs. The four significantly enriched gene families of DMGs were CD molecules, NKL subclass, HOXL subclass, and Zinc finger C2H2-type. The HOXL subclass homeobox genes were observed extensively hypermethylated in ESCC. The HOXL-score estimated by HOXC10 and HOXD1 methylation, whose methylation status were then confirmed by sanger sequencing in our custom ESCC samples, showed good ability in discriminating ESCC from normal samples. CONCLUSIONS: We observed widespread hypomethylation events in ESCC, and the hypermethylated HOXL subclass homeobox genes presented promising applications for the early detection of esophageal squamous cell carcinoma.

Association Between the Number of Intratympanic Steroid Injections and Hearing Recovery in Sudden Sensorineural Hearing Loss.

The frequency of intratympanic (IT) steroid injection varies from once daily to once weekly or less among studies and does not reach a uniform standard. This study investigated the potential association between the number of IT steroid injections and hearing recovery to determine the optimal number in sudden sensorineural hearing loss (SSNHL) patients. A retrospective study involving 233 SSNHL patients receiving IT steroids plus batroxobin within 7 days of onset was performed. Patients were followed up for 3 months. More than 15 dB of HL improvement in the pretreatment pure tone average (PTA) was defined as effective. The effective group had a higher IT injection numbers than the ineffective group (≥ 6 times: 84.6 vs. 61.1, p < 0.001). Regardless of the unadjusted model or adjusted model, patients who received more frequent IT steroid injections seemed more likely to recover hearing (unadjusted model, OR, 95% CI: 1.25, 1.06-1.48; p = 0.007; adjusted model, OR, 95% CI: 1.21, 1.01-1.45; p = 0.044). Six IT injections had the highest rate of hearing recovery (79.1%). In conclusion, IT injection number was an independent factor that was positively associated with hearing recovery, and the optimal number of IT steroid injections was 6. Batroxobin plus higher number of IT steroid injections showed more effective for treating SSNHL.

Association Between Hearing Characteristics/Prognosis and Vestibular Function in Sudden Sensorineural Hearing Loss With Vertigo.

Sudden sensorineural hearing loss (SSNHL) patients with vertigo have a poorer prognosis. However, the factors associated with hearing recovery remain uncertain. This retrospective study was to evaluate the association between hearing characteristics/hearing recovery and the patterns of vestibulocochlear lesions in SSNHL patients with vertigo. Patients were classified into groups according to the patterns of vestibular dysfunction. We not only compared hearing characteristics and prognosis among subgroups but also determined the potential association between vestibular lesion location and hearing recovery. The shapes of the audiogram differed significantly between patients with normal vestibular function and patients with vestibular dysfunction (p = 0.022). Patients whose audiogram indicated profound hearing loss were 3.89 times more likely to have vestibular dysfunction than those whose audiogram shape indicated low-frequency hearing loss (95% CI, 1.02-14.86, p = 0.047). Patients who had saccule dysfunction were 0.11 times as likely to have hearing recovery than those who had normal saccule function (95% CI, 0.11-0.31, p = 0.001). When adjusted for sex and age, patients who had saccule dysfunction were 0.07 times as likely to have hearing recovery than those who had normal saccule function (95% CI, 0.02-0.22, p = 0.001). Abnormal results following cVEMP testing may be a potential predictive factor for poor hearing recovery.

Specific clinical and immune features of CD68 in glioma via 1,024 samples.

BACKGROUND: There is a growing recognition that tumor-associated macrophages (TAMs) are recruited to the glioma environment, facilitating tumor proliferation and migration by creating an immunosuppressive microenvironment. CD68 has been widely reported as a specific marker of TAMs in cancer. PURPOSE: To clarify the role of CD68 in glioma, we investigated its function at the transcriptome level and relationship with clinical practice. PATIENTS AND METHODS: In total, 325 RNA-seq data from Chinese Glioma Genome Atlas (CGGA) and 697 RNA-seq data from The Cancer Genome Atlas (TCGA) network were enrolled in this study. CD68-specific findings were further analyzed with R language, and the prognostic impacts were validated through analyzing the overall survival (OS). RESULTS: CD68 showed a positive correlation with the WHO grade of malignancy in glioma. Meanwhile, CD68 was predominantly expressed in IDH wide type and mesenchymal subtype. Gene ontology (GO) analysis revealed that CD68-related genes were closely related to inflammatory response and immune response. Moreover, seven cultures of metagenes further confirmed that CD68 was a specific marker for macrophages in inflammatory response and played an important role in suppressing T-cell-mediated immunity. The Pearson correlation test suggested that CD68 showed robust correlation with other markers of macrophages and immune checkpoints, including PD-1 and TIM-3. Clinically, a high expression level of CD68 in tumors exhibited a poor survival in glioma patients. CONCLUSION: Our results demonstrated that CD68 acted as an immune suppressor and contributed to glioma progression in the tumor microenvironment. These findings may expand our understanding of CD68-specific clinical and immune features in glioma.

[The application of Tb-ABR and ASSR in pediatric hearing assessment].

OBJECTIVE: To observe the correlation between the threshold of tone burst auditory brain stem response (Tb-ABR) and ASSR (auditory steady-state response) and the threshold of BA (behavioral audiometry). To investigate the accuracy and clinical value of Tb-ABR and ASSR in pediatric hearing assessment. METHOD: From January, 2014 to December, 2014, 76 children (123 ears) recieved hearing examination in the First Affiliated Hospital of Zhengzhou University. They were classified into three groups according to the hearing level: 23 children (46 ears) with normal hearing ability in group A, 27 children (32 ears) with slightly-moderate sensorineural deafness in group B and 26 children (45 ears) with severe-profound sensorineural deafness in group C. Tb-ABR, ASSR, BA in 4 frequencies (0.5, 1.0, 2.0, 4.0 kHz) were tested and the results were statistically analyzed. RESULT: (1) At the 4 frequencies (0.5-4.0 kHz), we obtained 132 thresholds of Tb-ABR, 144 of ASSR, 152of BA. And 166 thresholds were obtained in Tb-ABR+ASSR+BA in total . (2) The thresholds of Tb-ABR, ASSR and those of BA in all 3 groups had linear relations at 0.5-4.0 kHz. The correlation coefficients of group A were 0.76, 0.82, 0.87 and 0.91; 0.52, 0.57, 0.67 and 0.64. Those of Group B were 0.89, 0.95, 0.98 and 0.95; 0.74, 0.82, 0.87 and 0.90. Those of Group C were 0.91, 0.90, 0.92 and 0.89; 0.93, 0.95, 0.95 and 0.91. CONCLUSION: (1) Both ASSR and Tb-ABR can allow reasonably accurate predictions for the pediatric hearing assessment. The correlation between Tb-ABR threshold and BA threshold is higher in normal hearing children and slightly-moderate sensorineural deafness children. The correlation between ASSR threshold and BA threshold is higher in severe-profound sensorineural deafness children. (2) The hearing test combination can evaluate the residual hearing ability for children with severe hearing loss.

[Incidence of facial nerve dehiscence in mastoidectomy].

OBJECTIVE: To describe the incidence and location of the facial nerve dehiscence (FND) in chronic suppurative otitis media patients with and without cholesteatoma. METHODS: 360 patients (370 ears) who received canal wall down tympanomastoidectomy due to otitis media(145 ears without cholesteatoma and 225 ears with cholesteatoma) were analyzed retrospectively, in which the incidence and locations of FND was studied, and the relevance for FND, clinical features (age, disease duration, preoperative facial paralysis) and intraoperative findings (state of FND and lateral semicircular canal fistula), were analyzed. RESULTS: The presence of FND was 31.6% of total surgical procedures and the locations of FND were the tympanic segment. The dehiscence was detected 28.4% (94/334) in adults, but 61.1% (22/36) in the patients 18 years and younger, the differences were statistical significance (P < 0.05). The dehiscence rate was 37.1% (104/280) and 14.4% (13/90) respectively, in the cases of disease duration more than and less than 5 years, with significant difference (P < 0.05). Facial nerve dehiscence was detected in 29 patients (20.0%) and 89(39.1%) in cases without and with cholesteatoma respectively (P < 0.05). Facial nerve prolapse over the oval window was 11.4% (42/370), with FND of 83.3% (35/42). The incidence of lateral semicircular canal fistula was 7.8% (29/370), with FND of 65.5% (19/29). The presence of preoperative facial paralysis with FND was 75.0% (18/24), and that without FND was 28.6% (99/346), the differences were statistical significance (P < 0.05). CONCLUSIONS: The incidence of FND most commonly located at the tympanic segment. The facial nerves should be taken much care in mastoidectomy for patients with cholesteatoma, preoperative facial paralysis and lateral semicircular canal fistula, as well as long disease duration.

[The relationship between ossicular status and conductive hearing loss in cholesteatoma].

OBJECTIVE: To investigate and analyze the characteristic of destructive ossicular chain and it's impact on air-bone gap (ABG) among patients with cholesteatoma. METHOD: Data from 204 cases (213 ears) undergoing an initial surgery for cholesteatoma were retrospectively reviewed to evaluate the relationships between preoperative pure tone audiometry data and intraoperative assessment of individual ossicular destruction. RESULT: Incus was the most significantly affected ossicle. Furthermore, the destruction of malleus and stapes was often accompanied by the destruction of incus. A partially eroded incus caused significantly increase in ABG from that of an intact incus with cholesteatoma abutting (P < 0.05). A partially eroded incus and a partially eroded stapes caused significantly increase in ABG compared to a partially eroded incus (P < 0.05). A completely eroded incus caused significantly increase in ABG compared to a partially eroded incus (P < 0.05). False fibre-connected would significantly influence on ABG in some ossicular chain erosion patterns (P < 0.05). Cholesteatoma abutting an intact ossicle significantly altered average ABG compared to a normal ossicle (P < 0 01). CONCLUSION: Different ossicular chain erosion pattern caused different degrees of ABG.