角蛋白4过表达对喉癌细胞生物学行为的影响

目的 探讨角蛋白4(KRT4)过表达对喉癌细胞活力、增殖、迁移、侵袭和凋亡能力的影响。方法 构建KRT4过表达质粒,转染TU177喉癌细胞。实验共分 3 组:CON组(空白对照组,未转染),Oe-NC组(阴性对照组,转染对照质粒空载体),Oe-KRT4组(目的基因实验组,转染KRT4过表达质粒)。通过RT-qPCR法及Western blot法验证转染效率,通过CCK-8法、平板克隆实验、细胞划痕实验、Transwell小室侵袭实验和流式细胞术检测KRT4过表达对喉癌细胞活力、增殖、迁移、侵袭和凋亡能力的影响。结果 RT-qPCR法及Western blot法结果提示Oe-KRT4组KRT4 mRNA和KRT4蛋白表达水平较CON组与Oe-NC组显著升高,差异具有统计学意义(P＜0.000 1)。CCK-8法结果提示Oe-KRT4组细胞活力较CON组与Oe-NC组显著减弱,差异具有统计学意义(P＜0.000 1)。平板克隆实验结果提示Oe-KRT4组克隆数显著低于CON组与Oe-NC组,差异具有统计学意义(P＜0.000 1)。细胞划痕实验结果提示Oe-KRT4组迁移率显著低于CON组与Oe-NC组,差异具有统计学意义(P＜0.000 1)。Transwell小室侵袭实验结果提示Oe-KRT4组细胞穿膜数显著低于CON组与Oe-NC组,差异具有统计学意义(P＜0.000 1)。流式细胞术结果提示Oe-KRT4组细胞凋亡率较CON组与Oe-NC组显著增加,差异具有统计学意义(P＜0.000 1)。结论 KRT4过表达能显著抑制喉癌细胞的活力、增殖、迁移和侵袭,并促进喉癌细胞的凋亡,因此KRT4有望成为喉癌治疗的潜在生物标志物。     

范可尼贫血互补群B对丝裂霉素C诱导的293T细胞DNA损伤修复的研究

目的 研究丝裂霉素C诱导的DNA损伤的浓度和时间对293T细胞中范可尼贫血互补群B(FANCB),DNA损伤因子gammaH2AX,修复因子RAD51表达量的影响,探索FANCB在DNA损伤中的作用机理。方法 利用人293T细胞系作为研究载体,通过Western blot和qRT-PCR技术定量分析FANCB,gammaH2AX,RAD51在25 μM丝裂霉素C浓度作用下,在1、3、5 h不同作用时间点评估FANCB,gammaH2AX,RAD51蛋白和基因表达水平差异;分析细胞在25、35、45、60 μM 丝裂霉素C浓度下作用3 h后gammaH2AX蛋白表达水平;siRNA敲低FANCB表达后FANCB、gammaH2AX和RAD51蛋白和基因表达检测。结果 相比对照组,在蛋白水平,gammaH2AX表达在1、3 h对比0 h差异具有统计学意义(P均<0.05),而5 h对比0 h差异无统计学意义(P=0.223);FANCB表达在1、3、5 h对比0 h差异均具有统计学意义(P均<0.05); RAD51表达在1、3、5 h对比0 h差异均具有统计学意义(P均<0.05)。在基因水平,FANCB在1、3、5 h和RAD51在1、3、5 h相比对照组均具有统计学意义(P均<0.05);gammaH2AX蛋白表达水平与MMC浓度无明显关系。相比对照组,siRNA敲低组FANCB蛋白和基因表达下降,gammaH2AX蛋白表达上升,RAD51蛋白和基因表达下降。结论 在丝裂霉素C造成的293T DNA损伤模型中,FANCB在同源重组DNA修复途径中对DNA损伤具有潜在的调控功能。     

MMP-2和MMP-9及胃蛋白酶对喉鳞状细胞癌侵袭作用的机制研究

目的探讨基质金属蛋白酶2(MMP-2)、基质金属蛋白酶9(MMP-9)及胃蛋白酶(Pepsin)对喉鳞状细胞癌局部侵袭的作用。方法收集2020年10月—2022年3月柳州市人民医院耳鼻咽喉科住院手术并经病理确诊的32例喉鳞状细胞癌患者的癌组织及其癌旁组织新鲜标本,通过实时荧光定量PCR(qRT-PCR)分别检测MMP-2、MMP-9及Pepsin mRNA在上述组织标本中的表达情况,结合临床资料分析。结果喉癌组织中MMP-2、MMP-9及Pepsin mRNA表达高于癌旁组织,差异具有统计学意义(P＜0.05);Ⅲ、Ⅳ期组表达水平高于Ⅰ、Ⅱ期组(P＜0.05),淋巴结转移组高于无转移组(P＜0.05);MMP-2、MMP-9 mRNA在中-低分化鳞状细胞癌组的表达高于高分化组(P＜0.05);Pepsin mRNA在60岁及以上喉癌组中表达高于60岁以下组(P＜0.05)。结论MMP-2、MMP-9和Pepsin在喉鳞状细胞癌的局部侵袭过程中发挥协同促进作用,预防和治疗咽喉反流是防止喉癌局部侵袭的重要环节。     

敲低蛋白磷酸酶2A的癌性抑制因子表达对下咽癌细胞增殖、迁移的影响

目的 通过shRNA敲低下咽癌FaDu细胞（简称FaDu细胞）蛋白磷酸酶2A(protein phosphatase 2A,PP2A)的癌性抑制因子（cancerous inhibitor of protein phosphatase 2A,CIP2A）的表达,了解其在下咽癌发生发展中的作用。方法 设计特异性shRNA序列,包装慢病毒并转染FaDu细胞,特异性敲低CIP2A的表达,分别通过RT-PCR和Western blot检测CIP2A mRNA和CIP2A蛋白的表达情况。结果 （1）shRNA敲低FaDu细胞中CIP2A后,实验组CIP2AmRNA和CIP2A蛋白的表达量均较空白组显著降低。（2）细胞克隆和CCK8实验结果显示,实验组细胞较空白组细胞增殖能力明显下降（t=50.86,P<0.01;t=12.406,P<0.001）。细胞划痕实验结果显示,实验组细胞横向迁移能力较空白组细胞明显下降。Transwell实验结果显示,实验组细胞纵向迁移能力较空白组细胞明显下降（t=40.038,P<0.01;t=12.247,P<0.001）。结论 敲低FaDu...     

HARS2基因突变致以耳聋为表现的Perrault综合征机制的研究

目的 研究耳聋家系HARS2基因突变位点对HARS2蛋白的影响,为研究HARS2基因突变致Perrault综合征的发病机制奠定基础。方法 检测并验证该家系成员样本DNA的HARS2基因。使用软件对蛋白质建模,分析预测Asp117Asn和Leu303Pro突变对HARS2蛋白结构稳定性的影响。转染含野生型HARS2基因和HARS2基因Asp117Asn突变、Leu303Pro突变的慢病毒重组质粒以及空载体至HEK 293T细胞(人胚肾细胞)中,分别获得WT细胞组(转染野生型的HEK293T细胞)、Asp117Asn细胞组(转染Asp117Asn突变的HEK293T细胞)、Leu303Pro细胞组(转染Leu303Pro突变的HEK293T细胞)、NC细胞组(转染空病毒载体的HEK293T细胞)。Northern blot检测线粒体tRNAHis氨酰化水平;Western blot检测HARS2蛋白的表达;免疫荧光测定HARS2蛋白表达部位。结果 ①先证者及其哥哥为耳聋患者,为HARS2 c.349G>A(p.Asp117Asn)和c.908T>C(p.Leu303Pro)复合杂合突变;其父亲为HARS2 c.908T>C(p.Leu303Pro)杂合突变;其外婆、母亲、舅舅为HARS2 349G>A(p.Asp117Asn)杂合突变;②突变可能导致HARS2蛋白稳定性下降;③WT细胞组线粒体tRNAHis氨酰化水平高于其余3组(P<0.05);Asp117Asn细胞组较Leu303Pro细胞组线粒体tRNAHis氨酰化水平高(P=0.016);④HARS2蛋白均于线粒体表达;⑤HARS2蛋白在NC细胞组中无明显表达;WT细胞组HARS2蛋白表达与Asp117Asn细胞组无明显差异(P=0.356),高于Leu303Pro细胞组(P=0.000)。结论 ①明确了HARS2基因2个新突变位点c.349G>A和c.908T>C;②该突变可能通过降低HARS2蛋白氨酰化能力和/或表达,导致线粒体tRNAHis氨酰化能力降低,进而出现线粒体功能障碍,从而导致听力损失。     

变应性鼻炎特异性病毒应答相关基因的生物信息学分析

目的 变应性鼻炎（AR）患者感染鼻病毒后病情及气道炎症加重,但其分子机制尚未完全阐明。本研究通过生物信息学方法分析双链RNA （dsRNA）刺激后AR鼻黏膜上皮细胞中特异的基因表达特征。方法 基于GEO数据库的GSE51392数据集,利用R语言的Limma函数筛选出dsRNA刺激后AR上皮细胞特异性差异表达基因（DEGs）。通过GO和KEGG进行通路富集分析,以确定这些基因参与的生物学过程及功能。此外,通过STRING数据库构建蛋白质相互作用（PPI）网络,并使用Cytoscape寻找AR特异性的hub基因和集簇。结果 共筛选出545个上调和400个下调的AR特异性DEGs,包括上调基因PPBP/CXCL7和下调基因IL20、BLNK、CEBPD、LY96。通过GO和KEGG分析,我们发现dsRNA刺激后AR与健康对照受试者（HC）上皮相比具有不同的功能和信号通路。此外,AR特异性的DEGs构建了由791个节点和603条连线组成的PPI网络。并利用MCODE从该PPI网络中筛选出PPBP/CXCL7等16个hub基因和5个重要集簇。结论 本研究通过生物信息学对数据进行挖掘并筛选出dsRNA刺激后AR特异性病毒应答相关基因,提示上调的hub基因以及下调的IL20、BLNK、CEBPD和LY96可能是鼻病毒诱发AR加重的重要因素。为下一步的研究提供参考。     

ECRG4基因甲基化在喉鳞状细胞癌中的表达及其临床意义

目的 探讨喉鳞状细胞癌(LSCC)中ECRG4的mRNA和蛋白表达以及其在LSCC肿瘤组织中的甲基化水平,分析其临床意义。方法 从人类蛋白图谱(HPA)以及基因表达谱交互分析(GEPIA)数据库分析ECRG4在头颈部肿瘤中的表达,收集15例原发LSCC患者的组织样本及癌旁正常组织样本,实时荧光定量PCR(RT-qPCR)检测样本中的ECRG4 mRNA表达,Western blot检测组织中的蛋白表达,甲基化特异性PCR(MSP)及测序分析检测ECRG4启动子甲基化水平,比较ECRG4mRNA表达及甲基化水平与LSCC患者临床病理特征之间的相关性。结果 HPA和GEPIA分析结果发现ECRG4在头颈部鳞状细胞癌中表达下降。与癌旁正常组织相比,RT-qPCR和Western blot实验结果表明LSCC患者肿瘤组织中的ECRG4 mRNA和蛋白表达较低(P<0.001),测序分析结果指出LSCC肿瘤组织中ECRG4启动子甲基化水平明显升高(P<0.001)。ECRG4 mRNA高表达水平与LSCC患者Ⅲ、Ⅳ期、存在淋巴转移、复发以及G2、G3期相关(P<0.05),而Ⅲ、Ⅳ期、复发以及G2、G3期的LSCC患者肿瘤组织中的ECRG4启动子甲基化水平升高更明显(P<0.05)。结论 ECRG4在LSCC中表达水平下降,甲基化水平升高,在Ⅲ、Ⅳ期、复发以及G2、G3期的患者中变化更明显,为LSCC后续研究提供理论基础。     

长链非编码RNA核富集转录体1促进喉鳞状细胞癌细胞迁移和侵袭的机制研究

目的 探究长链非编码RNA(lncRNA)核富集转录体1(NEAT1)NEAT1对喉鳞状细胞癌(LSCC)细胞迁移和侵袭的影响,并进一步分析miR-429/锌指E-盒结合同源异形盒1(ZEB1)轴在其中发挥的作用。方法 慢病毒转染建立稳定敲减lncRNA NEAT1的LSCC细胞,通过RT-qPCR检测细胞lncRNA NEAT1表达以验证转染效率,通过Transwell实验检测细胞迁移和侵袭能力,通过Western blot检测细胞上皮-间充质转化(EMT)相关蛋白N-cadherin、Vimentin、Slug和Snail表达。通过生物信息学分析miR-429与lncRNA NEAT1和ZEB1 mRNA间的潜在结合位点,并通过双荧光素酶报告基因实验验证miR-429与lncRNA NEAT1以及miR-429与ZEB1 mRNA结合。将miR-429抑制剂转染敲减lncRNA NEAT1的LSCC细胞,通过Western blot检测细胞ZEB1表达。进一步检查敲减ZEB1对抑制miR-429的敲减lncRNA NEAT1的LSCC细胞迁移、侵袭和EMT的影响。结果 敲减lncRNA NEAT1降低LSCC细胞lncRNA NEAT1表达,抑制细胞迁移和侵袭并下调细胞N-cadherin、Vimentin、Slug和Snail表达。miR-429与lncRNA NEAT1和ZEB1 mRNA间存在潜在结合位点,且miR-429与lncRNA NEAT1以及miR-429与ZEB1 mRNA结合。抑制miR-429逆转了敲减lncRNA NEAT1对LSCC细胞ZEB1表达的抑制作用。此外,敲减ZEB1逆转了抑制miR-429对敲减lncRNA NEAT1的LSCC细胞迁移和侵袭的促进作用及EMT相关蛋白N-cadherin、Vimentin、Slug和Snail表达的上调作用。结论 lncRNA NEAT1促进LSCC细胞迁移和侵袭,其机制可能与海绵化miR-429上调ZEB1表达促进LSCC细胞EMT有关。     

RNA干扰DJ-1基因抑制喉癌细胞的增殖

目的 探讨RNA干扰(RNAi)抑制喉癌Hep-2细胞DJ-1基因的表达及观察其细胞效应.方法 设计合成3对特异性针对人DJ-1基因的小干扰RNA(siRNA),脂质体法转染Hep-2细胞,实验分为4组:瞬时转染非特异性siRNA对照组及转染特异性siRNA 3组(siRNA1、siRNA2、siRNA3).采用RT-PCR检测DJ-1 mRNA,蛋白免疫印迹法检测DJ-1蛋白,流式细胞仪检测细胞凋亡及四甲基偶氮唑蓝(MTT)比色法检测特异性siRNA1组对Hep-2细胞效应.结果 本实验设计合成的3对特异性siRNA均不同程度地抑制DJ-1基因表达,其中特异性siRNA1组抑制效果最佳.M1Tr比色法结果显示特异性siRNAl组(终浓度50 nmo~L、100 nmolZL)对Hep-2细胞增殖具有抑制作用.流式细胞仪检测结果最示特异性siRNA1组能诱导Hep-2细胞凋亡,转染特异性siRNA1组凋亡率为(15.7±4.8)%,非特异性siRNA对照组凋亡率为(4.5±0.4)%,非特异性siRNA对照组与特异性siRNA1组凋亡率比较差异有统计学意义(t=4.736,P<0.01).结论 转染特异性siRNA组能有效抑制Hep-2细胞增殖,诱导Hep-2细胞凋亡.     

昆明小鼠耳蜗内脂肪酸转运蛋白4的表达与分布

目的 探索昆明小鼠耳蜗组织中脂肪酸转运蛋白4 (FATP4)的表达与分布。方法 选取健康成年(10周)昆明小鼠8只(16耳),其中2只(4耳)用于免疫荧光染色,6只(12耳)用于Western blot蛋白检测。通过耳蜗石蜡切片免疫荧光染色检测FATP4在耳蜗内各组织中的表达分布,Western blot蛋白检测耳蜗组织FATP4的表达水平。结果 耳蜗石蜡切片免疫荧光染色提示FATP4主要分布于耳蜗螺旋神经节、蜗轴、支持细胞、内毛细胞、外毛细胞、血管纹的中间细胞,Western blot蛋白检测结果进一步验证了FATP4在昆明小鼠耳蜗表达。结论 本研究初步揭示了FATP4在成年昆明小鼠耳蜗中的表达具有一定的特异性,为进一步研究耳蜗内脂肪酸代谢提供了理论依据。     

High mobility group box 1 (HMGB1) is upregulated by the Epstein-Barr virus infection and promotes the proliferation of human nasopharyngeal carcinoma cells

Conclusion: The current study confirmed the significant high mobility group box 1 (HMGB1) was promoted in human nasopharyngeal carcinoma (NPC) tissues by Epstein-Barr virus (EBV) infection, in association with the malignant status of NPC, and promoted the proliferation NPC cells RAGE-dependently. Objectives: The present study was to examine the association of HMGB1 over-expression in human NPC with the EBV-positivity and to determine the regulatory role of HMGB1 on the proliferation of NPC cells in vitro. Methods: Real-time PCR and Western blotting were utilized to examine the HMGB1 expression. EBV infection in CNE-2 cells was performed to investigate the HMGB1 promotion by EBV infection. RNA interference technology was utilized for the RAGE knockout. Results: It was demonstrated that HMGB1 was significantly higher in both mRNA and protein levels in the EBV-positive NPC tissues, in marked association with the malignant status of NPC, and with the LMP1 DNA level in EBV-positive NPC samples. In addition, the MTT assay, growth curve, and the colony forming assay confirmed the promotion by HMGB1 to the proliferation of CNE-2 cells, depending on RAGE.     

慢性噪声暴露对大鼠听皮层及海马脑区胰岛素样生长因子－1表达的影响

目的：观察慢性噪声暴露后大鼠听皮层及海马脑区胰岛素样生长因子－1（insulin－like growth fac-tor－1,IGF－1）的表达,探讨其在长期噪声性中枢神经系统损伤中的作用。方法成年健康雄性 Wistar 大鼠16只,随机分为噪声组和对照组各8只,噪声组暴露于100 dB SPL 白噪声28天,每天4小时,制成慢性噪声暴露模型,对照组不予任何处理。造模结束后检测两组大鼠 ABR 反应阈,并采用免疫组织化学染色方法检测 IGF－1在听皮层和海马的表达。结果噪声组造模结束后 ABR 反应阈（80．62±4．58 dB SPL）较对照组（38．75±3．54 dB SPL）明显升高（P＜0．05）,听皮层及海马脑区 IGF－1阳性神经元数目和表达强度均较对照组显著增加（P＜0．05）。结论慢性噪声暴露可以使听皮层及边缘系统海马脑区 IGF－1表达增高,这可能与其对中枢神经系统噪声性损伤的保护作用有关。     

SMARCB1(INI-1)缺失性鼻腔鼻窦癌的诊疗进展

SMARCB1(INI-1)缺失性鼻腔鼻窦癌(SDSC)是一类罕见的鼻腔鼻窦恶性肿瘤,具有高度侵袭性。免疫组化染色检测细胞核中INI-1蛋白表达缺失是诊断SDSC最具价值的方法,由于临床表现的非特异性,大多数患者被确诊为该疾病时已处于晚期,极大程度地降低了患者的生存率及生存质量。手术完整切除肿物、术后辅以放/化疗的综合治疗模式是目前临床工作中的主要治疗手段,但仍有较高的复发率及死亡率。而新辅助治疗以及靶向治疗对于该疾病的有效性仍处于临床试验阶段。因此,早期诊断及探索最佳的治疗策略对患者至关重要。本文就SDSC的诊断及治疗进展进行综述,以助于提高对此类罕见肿瘤类型的临床认知。     

Inhibitory effect of N-acetyl cysteine and ascorbic acid on the development of myringosclerosis: An experimental study

Objectives

This study investigated the effects of ascorbic acid and N-acetyl cysteine (NAC) antioxidants on the development of myringosclerosis (MS) in an experimental model.

Methods

Myringotomies were performed in the ears of 15 guinea pigs, and Spongostan^® pieces were placed on the perforated regions of the tympanic membrane. The subjects were divided randomly into three groups and treated with three different solutions on the Spongostan—group 1: (control, 0.9% saline), group 2 (ascorbic acid), and group 3 (NAC). On day 15 after treatment, specimens from the tympanic membranes were obtained and examined via light microscopy. Sclerosis and inflammation scores and the tympanic membrane thicknesses were evaluated. Immunohistochemical methods were used to evaluate the expression of VEGF, TGF-β, iNOS, and IL1-β in all groups.

Results

Lower sclerosis and inflammation scores and reduced tympanic membrane thicknesses were observed in groups treated with NAC or ascorbic acid compared with the control group. Immunohistochemical studies revealed significantly less expression of VEGF, TGF-β, and iNOS in groups 2 and 3 compared with group 1. Additionally, IL1-β expression was significantly less in group 3 than in group 1. Compared with group 1, group 2 animals exhibited reduced inflammation in the lamina propria, fewer active fibroblasts, less leukocyte infiltration, and decreased thickness of the vessels; group 3 animals exhibited decreased numbers of active fibroblasts and collagen fibers in the lamina propria.

Conclusions

Inflammation scores, cellular infiltration, and expression of VEGF, TGF-β, and iNOS were reduced by ascorbic acid and/or NAC treatments, thereby decreasing MS development. Decreased expression of IL1-β was observed only in animals treated with NAC.     

MBL,P2X7, and SLC11A1 gene polymorphisms in patients with oropharyngeal tularemia

Conclusion: A significant association was found of oropharyngeal tularemia with SLC11A1 allele polymorphism (INT4?G/C) and MBL2 C?+?4T (P/Q). These results indicate C allele and Q allele might be a risk factor for the development of oropharyngeal tularemia.

Aim: This study aimed to investigate the relationship of SLC11A1, MBL, and P2X₇ gene polymorphism with oropharyngeal tularemia.

Methods: The study included totally 120 patients who were diagnosed with oropharyngeal tularemia. Frequencies of polymorphisms in the following genes were analyzed both in the patient and control groups in the study: SLC11A1 (5’(GT)_n Allele 2/3, Int4?G/C, 3’ UTR, D543N G/A), MBL (MBL2 C?+?4T (P/Q), and P2X₇ (?762 C/T and 1513 A/C).

Results: Among all polymorphisms that were investigated in this study, SLC11A1 gene showed a significance in the distriburtion of polymorphism allelle frequency at the INT4 region. Frequency of C allele was 54 (28%) in patients with oropharyngeal tularemia, and 31 (13%) in the control group (p?=?0.006 and OR = 1.96 (1.21–3.20)). An association was detected between MBL2 C?+?4T (P/Q) gene polymorphism and oropharyngeal tularemia (p?7 (?762 C/T and 1513 A/C) gene polymorphism and oropharyngeal tularemia in this study (p?>?0.05).     

Epstein-Barr virus (EBV) latent membrane protein 1 induces interleukin-8 through the nuclear factor-kappa B signaling pathway in EBV-infected nasopharyngeal carcinoma cell line

BACKGROUND/OBJECTIVES: Nasopharyngeal carcinoma (NPC) is a highly invasive and metastatic malignant tumor and is associated with Epstein-Barr virus (EBV) infection that exhibits type II latency. Angiogenesis is essential for tumor growth, invasion, and metastasis. Our previous studies have indicated that interleukin (IL)-8 was over-expressed in many NPC tissues and was found to be significantly correlated with angiogenesis by immunohistochemistry. STUDY DESIGN: In vitro design. METHODS: The influence of the EBV genome for IL-8 gene expression was studied using the EBV-genome-positive and -negative epithelial/NPC hybrid cell line NPC-KT. The EBV-positive and -negative clones were selected by polymerase chain reaction and in situ hybridization. RESULTS: EBV-positive clones expressed abundant IL-8 mRNA compared with EBV-negative clones. This result indicated that over-expression of IL-8 depended on the presence of EBV genomes in NPC-KT cells. Two encoded genes, latent membrane protein (LMP)1 and EBV-encoded small RNAs (EBERs), expressed in NPC were transfected in EBV-negative NPC-KT cells. LMP1 transactivated the IL-8 promoter, whereas EBERs did not. Moreover, the nuclear factor (NF)-kappa B binding site in the IL-8 promoter was essential for the response to LMP1, and the activator protein (AP)-1 binding site played only a partial role. CONCLUSIONS: LMP1 induces IL-8 mainly through the activation of NF-kappa B and partly through AP-1 in NPC model cell lines, NPC-KT, and this suggests that LMP1 plays an important role in the angiogenesis of NPC.     

Assessment of cochlear implant candidacy in patients with cochlear nerve deficiency using the P1 CAEP biomarker

Abstract

Objective

The goal of this report was to ascertain the efficacy of the P1 cortical auditory evoked potential (CAEP) biomarker as an objective tool to assist in the evaluation of cochlear implant (CI) candidacy in children with a radiological diagnosis of cochlear nerve deficiency (CND).

Methods

Retrospective case study review of audiological and radiological findings was performed in four pediatric patients identified with CND and severe-to-profound sensorineural hearing loss. Cortical auditory evoked potential testing was conducted, and the presence and latency of the P1 component were analyzed.

Results

Three out of four children demonstrated robust P1 CAEP responses, indicating activation of the central auditory pathways by auditory stimulation, despite the diagnosis of CND. These children were considered good candidates for cochlear implantation.

Discussion

Although cochlear implantation in children is a fairly routine procedure, cases exist for which implant candidacy is questionable. Among these cases are children with CND. In these children, cochlear implantation may be contraindicated due to the likelihood that the implant electrodes may not stimulate the VIII nerve adequately. Magnetic resonance imaging (MRI) is considered the gold standard in the assessment of CND, but this measure is not always sufficient to determine CI candidacy in cases of CND. The addition of the P1 CAEP measurement to the usual electrophysiological, audiometric, and radiological test battery may prove to be useful in determining CI options for children with CND.     

前庭代偿过程中Ⅰ组代谢性谷氨酸受体亚型在前庭内侧核中的变化

目的观察单侧迷路破坏术后前庭内侧核(medialvestibular nuclei,MVN)内I组代谢性谷氨酸受体亚型(group I metabotropic glutamate receptors,mGluR1)的表达变化。方法成年雄性Wistar大鼠28只,分为迷路破坏组(20只)和对照组(8只),前者破坏单侧迷路,对照组手术方式相同但保持迷路完好。单侧迷路破坏术后,通过免疫组织化学、原位杂交组织化学法检测不同存活时间(术后12h、36h、7d、30d)两组动物MVN内mGluR1的表达变化。结果单侧迷路破坏术后可诱导同侧MVN区I组代谢性谷氨酸受体亚型mGluR1减少,术后12h最少,术后36h开始增加,至术后7d和30d后和对照组差异无统计学意义;对侧和术侧的变化趋势相同。结论单侧迷路破坏术后可诱导MVN区I组代谢性谷氨酸受体亚型mGluR1减少。初级前庭传入或中枢前庭神经元的静息放电降低可能与I组代谢性谷氨酸受体亚型mGluR1减少有关,但其在前庭代偿中的作用尚有待研究。