老龄豚鼠耳蜗微循环与SOD变化

[目的]研究老龄豚鼠血管纹微循环与脑SOD含量变化在豚鼠老年聋发生过程中的作用。[方法]根据21只26月龄雄性豚鼠,8只3月龄豚鼠的听性脑干诱发电位(ABR)测量结果,将动物分成老龄组、老年聋组、正常组。比较各组豚鼠血管纹微血管面积与脑组织超氧化物歧化酶(SOD)含量的关系。[结果]老龄组与老年聋组豚鼠的血管纹微血管面积均比正常3月龄豚鼠减少,SOD含量亦明显减少,相关性检验表明老年聋豚鼠血管纹微血管面积与脑组织超氧化物歧化酶(SOD)含量有显著性相关。[结论]随增龄的微循环障碍不是导致老年聋发生的唯一决定因素。缺血再灌注可能产生了更多的自由基,对组织的损害更严重。自由基的清除障碍可能对听觉神经传导具有一定的影响。     

老年人听力与高尿酸血症的相关性分析

目的：探讨高尿酸血症对老年人听力的影响。方法：选择2013年9月—2016年3月高尿酸血症患者100例（199耳）与100例（199耳）同年龄组相对健康老年人,分为疾病组和对照组,对两组进行纯音听力和高刺激率听觉脑干反应（ABR）测试,并对结果统计分析。结果：疾病组纯音听力各频率均显著高于对照组（P＜0.01）;疾病组ABR测试I、III、V波潜伏期和I–III、I–V波间期均较对照组显著延长（P＜0.01）,III–V波间期较对照组比较无显著差异（P＞0.05）,疾病组V波阈值较对照组显著增加（P＜0.05）。结论：高尿酸血症对老年人的外周和脑干听觉中枢均可造成损害,使患者听阈增加,导致听力下降,预防和治疗高尿酸血症是防止和延缓老年性耳聋的重要措施之一。     

Effect of Hypertension on Hearing Function,LDH and ChE of the Cochlea in Older Rats

Hypertensionisconsideredasanimportantriskfactorinmanypathologicalprocesses,includingtheagingprocessofthehearingorgan However ,itspre cisemechanismisunclear Inthepresentstudy ,weselectedspontaneouslyhypertensiveratstroke prone(SHRSP)astheanimalmodelwhichcanmimictheprocessofhumanhypertension Electrophysiologicandhistochemicalmethodswereappliedtoobservethechangesinhearing ,thetransformationofcochleapathologyandtheeffectofhypertensiononinnerearfunction ,aimedtoexplainthepathogenesisofhear inglos…     

Associations between Age-Related Hearing Loss and Dietary Assessment Using Data from Korean National Health and Nutrition Examination Survey

Age-related hearing loss (ARHL) is a major and rapidly growing public health problem that causes disability, social isolation, and socioeconomic cost. Nutritional status is known to cause many aging-related problems, and recent studies have suggested that there are interaction effects between ARHL and dietary factors. We aimed to investigate the association between ARHL and dietary assessment using data from the fifth Korean National Health and Nutrition Examination Survey, which is a nationwide cross-sectional survey that included 5201 participants aged ≥50 years from 2010 to 2012. All participants had normal findings on otoscopic examination and symmetric hearing thresholds of <15 dB between both sides. Nutritional survey data included food consumption and nutrient intake using the 24 h recall method. Data were analyzed using multiple regression models with complex sampling adjusted for confounding factors, such as age, sex, educational level, and history of diabetes. Higher intake of seeds and nuts, fruits, seaweed, and vitamin A were positively associated with better hearing. Our findings suggest that dietary antioxidants or anti-inflammatory food may help reduce ARHL.     

438名离休干部耳鼻咽喉检查结果分析

我们对４３８例离休干部进行耳鼻咽喉检查，结果发现耳鼻咽喉患病者占受检人数的４３％（１８８／４３８），尤其各种耳病较为突出占患病总数的５２％（９７／１８８），其中老年聋占５５．７％（５４／９７），其发病年龄多在６１－８０岁之间其病因可能与血脂增高有关。     

豚鼠线粒体DNA4568缺失与老年性聋的关系

目的 探讨豚鼠听觉器官中线粒体DNA(mitochondrial DNA, mtDNA)4568缺失与老年性聋的关系.方法 将44只豚鼠分为两组A组青年豚鼠22只;B组老年豚鼠22只.再将B组分为B1组(老年听力正常组6只)和B2组(老年聋组16只).应用听觉脑干反应(auditory brainstem response, ABR)测试豚鼠听力阈值,以左耳听阈为评判标准,并提取耳蜗螺旋器、听神经、大脑颞叶组织和外周血中的DNA,采用PCR技术检测mtDNA4568大片段缺失的情况,并与耳聋程度作比较. 结果 老年聋组(B2)豚鼠的ABR平均听阈值为(57.33±4.65)dBSPL,明显高于老年听力正常组B1[(23.00±1.43)dBSPL]和青年组[A组(15.90±1.05)dBSPL];老年组不同器官组织中mtDNA4568缺失率均明显高于青年组;老年聋组耳蜗螺旋器组织和听神经组织中mtDNA4568缺失率明显高于老年听力正常组;而大脑颞叶组织mtDNA4568缺失率在两组间差异无统计学意义;血液中仅极少数存在mtDNA缺失,未纳入统计分析.结论 豚鼠mtDNA4568缺失的发生与老龄有关;与听觉有关的耳蜗螺旋器组织和听神经组织中mtDNA4568缺失与老年性聋有关;大脑颞叶组织和外周血中mtDNA4568缺失与老年性聋的关系尚待进一步研究.     

老年性聋病人血浆SOD及MDA含量的检测

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2种钾离子转运蛋白在血管纹性老年性聋发病中的作用(不同基因型小鼠的听觉生理研究)

目的 探讨Na-K-2Cl联合转运子1(Na-K-2Cl cotransporter 1,NKCC1)和α2Na,K-ATP酶(α2Na,K-ATPase)在血管纹性老年性聋(strial presbycusis)发病过程中的作用. 方法分别以不同基因型的NKCC1小鼠(杂合子和野生型)和α2Na,K-ATPase小鼠(杂合子和野生型)为实验对象,检测小鼠生长过程不同阶段的听性脑干反应(auditory brainstem response,ABR)和耳蜗内电位(endocochlear potential,EP),以观察NKCC1和α2Na,K-ATPase基因缺陷与血管纹性老年性聋的关系. 结果听性脑干反应检测结果显示,与NKCC1+/+野生型小鼠相比较,NKCC1+/-杂合子小鼠的ABR阈值在所有周龄组的各测试频率均升高,差异均有统计学意义(均P＜0.05).NKCC1+/-杂合子小鼠的听力随鼠龄增长而下降,与低龄小鼠相比,老龄小鼠的ABR阈值显著升高(均P＜0.05).NKCC1+/-小鼠的EP也随年龄增长而呈下降趋势,老龄小鼠的EP值与低龄小鼠相比明显降低(P＜0.05).α2Na,K-ATPase+/-杂合子小鼠的听力及EP低于同周龄组野生型小鼠,其听力随鼠龄增长而下降,高龄小鼠的ABR阈值与其低龄时相比明显升高(P＜0.05).结论 只携带1个NKCC1或α2Na,K-ATPase等位基因的小鼠(杂合子)可呈现伴EP下降的年龄相关性听力下降,耳蜗侧壁的NKCC1和α2Na,K-ATPase基因缺陷可能在血管纹性老年性聋的发病中起一定作用.     

脑干听觉诱发电位检测老年性聋

目的探讨老年性聋患者脑干听觉诱发电位的改变及其临床意义。方法对30例老年性聋患者行脑干听觉诱发电位（ABR）检测,观察ABR各波出现率、潜伏期值及波间期,并以正常健康老年人为对照。结果老年聋组ABR除Ⅴ波外,两组各主波出现率差异均非常显著（P<0.01）。老年聋组的Ⅰ、Ⅲ、Ⅳ波的潜伏期较对照组的Ⅰ、Ⅲ、Ⅳ波的潜伏期明显延长,均值有显著性差异（P<0.05）,波Ⅴ潜伏期均值有极显著性差异（P<0.01）。老年聋组与对照组相比Ⅰ～Ⅲ、Ⅰ～Ⅴ波间潜伏期明显延长,均值有极显著性差异（P<0.01）。结论老年性聋患者不仅有耳蜗功能的损害,脑干传导通路也可发生病损。     

Mutations in the mitochondrial 12S rRNA gene in elderly Chinese people

Conclusion: Our data indicate that the mitochondrial 12S rRNA gene, and particularly the A827G mutation, may be associated with susceptibility to age-related hearing loss. Objective: Hearing loss associated with aging is common among elderly persons. In all genetic backgrounds, mitochondrial DNA (mtDNA) mutations may be one of the most important factors contributing to aging and age-related hearing loss. The mitochondrial 12S rRNA is a hot spot for deafness-associated mutations in Chinese populations. The purpose of the present study was to elucidate the relationship of 12S rRNA gene polymorphisms and age-related hearing loss. Methods: The 12S rRNA gene polymorphisms were detected by direct sequencing. Statistical analyses were performed to assess the associations between age-related hearing loss and 12S rRNA gene variants. Results: We report here a systematic mutational screening of the mitochondrial 12S rRNA gene in 662 elderly subjects from the general population with various hearing threshold levels (211 controls and 451 age-related hearing loss subjects). Mutational screening of the mitochondrial 12S rRNA gene identified 55 nucleotide changes, including 4 mutations localized at highly conserved sites and 51 known variants. Of the known deafness-associated mutations in the mitochondrial 12S rRNA gene, the incidence of the A1555G mutation was 0.15%, A827G was 4.38%, T1095C was 0.45%, and T1005C was 3.78%. The incidence of the other known variants was 0.15–99.85%. We found statistically significant differences in the proportions of subjects with the A827G mutation among the various age-related hearing loss groups and normal controls.