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。     

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.     

Metabolic changes in the auditory cortex in presbycusis demonstrated by MR spectroscopy

In humans, aging is accompanied by the deterioration of the hearing function — presbycusis. The major etiology for presbycusis is the loss of hair cells in the inner ear; less well known are changes in the central auditory system. Therefore, we used 1 H magnetic resonance spectroscopy at 3 T tomograph to examine metabolite levels in the auditory cortex of three groups of subjects: young healthy subjects less than 30 years old and subjects older than 65 years either with mild presbycusis corresponding to their age or with expressed presbycusis. Hearing function in all subjects was examined by pure tone audiometry (125–16000 Hz). Significant differences were found in the concentrations of glutamate and N-acetylaspartate, with lower levels in aged subjects. Lactate was particularly increased in subjects with expressed presbycusis. Significant differences were not found in other metabolites, including GABA, between young and elderly subjects. The results demonstrate that the age-related changes of the inner ear are accompanied by a decrease in the excitatory neurotransmitter glutamate as well as a lactate increase in the auditory cortex that is more expressed in elderly subjects with large hearing threshold shifts.     

JNK信号通路在老年大鼠耳蜗细胞凋亡中的作用

目的探讨c-Jun氨基末端激酶(c-Juna mino-terminal kinase,JNK)信号通路在老年大鼠耳蜗细胞凋亡中的作用,为老年性聋的预防和治疗提供更多的切入点。方法Wistar大鼠24只,其中12只为对照组(3～4月龄),12只为自然衰老组(22～24月龄);听性脑干反应(auditory brainstem response,ABR)检测听力学改变;采用透射电镜观察老年大鼠耳蜗的超微病理变化;用免疫组化及Western blotting方法检测p-JNK和p-c-Jun蛋白的表达。结果老年组大鼠听力〔(72.083±13.345)dBSPL〕较对照组〔(32.083±3.878)dBSPL〕明显下降,差异具有统计学意义(P<0.01);透射电镜下可见外毛细胞有凋亡样改变,螺旋神经节细胞内大量脂褐素沉着;在耳蜗石蜡切片中可观察到p-JNK和p-c-Jun免疫反应阳性细胞,定位于细胞核,老年组与对照组相比,差异具有统计学意义(P<0.05);Western blotting结果显示老年组内耳组织p-JNK和p-c-Jun的蛋白表达明显高于对照组,差异有统计学意义(P<0.05)。结论在大鼠老年性聋的发生过程中,各种损伤因素可能通过激活JNK信号通路而促使耳蜗细胞的凋亡。     

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.     

固肾培元方治疗老年性聋临床观察

目的:观察固肾培元方治疗老年性聋的临床疗效。方法:67例老年性聋患者,随机分为两组。对照组口服金施尔康和达纳康,治疗组在口服金施尔康和达纳康的基础上,给予固肾培元方治疗,用药结束后进行疗效观察。结果:治疗组总有效率62.9%,对照组总有效率53.1%。两组总有效率比较无显著性意义(P>0.05),但治疗组总有效率高于对照组。结论:固肾培元方治疗老年性耳聋总有效率优于对照组,提示补肾活血通窍中药可能通过改善内耳局部微循环,促进内耳毛细胞功能恢复,从而起到提高听力的作用。     

From the Cover: Age-related hearing loss in C57BL/6J mice is mediated by Bak-dependent mitochondrial apoptosis

Age-related hearing loss (AHL), known as presbycusis, is a universal feature of mammalian aging and is the most common sensory disorder in the elderly population. The molecular mechanisms underlying AHL are unknown, and currently there is no treatment for the disorder. Here we report that C57BL/6J mice with a deletion of the mitochondrial pro-apoptotic gene Bak exhibit reduced age-related apoptotic cell death of spiral ganglion neurons and hair cells in the cochlea, and prevention of AHL. Oxidative stress induces Bak expression in primary cochlear cells, and Bak deficiency prevents apoptotic cell death. Furthermore, a mitochondrially targeted catalase transgene suppresses Bak expression in the cochlea, reduces cochlear cell death, and prevents AHL. Oral supplementation with the mitochondrial antioxidants α-lipoic acid and coenzyme Q₁₀ also suppresses Bak expression in the cochlea, reduces cochlear cell death, and prevents AHL. Thus, induction of a Bak-dependent mitochondrial apoptosis program in response to oxidative stress is a key mechanism of AHL in C57BL/6J mice.     

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。     

Sensorineural Hearing Loss and Neural Correlates of Temporal Acuity in the Inferior Colliculus of the C57bl/6 Mouse

Perception of complex sounds depends on the encoding of the dynamic and static structures within the ongoing stimulus by the auditory system. Aging has been associated with deficits in both areas, thus, the difficulty that the elderly have in speech comprehension could due to hearing loss, or to a loss of temporal sensitivity, or some combination of both. We investigated the effects of sensorineural hearing loss (SNHL) on neural correlates of temporal resolution by recording the responses of inferior colliculus neurons to a gap detection paradigm. We used C57BL/6 (C57) strain of laboratory mouse, which carries the Ahl deafness gene that initiates a progressive high frequency SNHL beginning at about 2 months of age and rapidly progresses to total deafness by 18 months. We compared gap encoding from inferior collicular neurons from young, normal-hearing C57 mice and middle-aged, hearing-impaired, C57 mice, quantifying minimal gap threshold, and recovery functions. The proportion of unit types, spontaneous rates and degree of monotonicity were comparable between young and middle-aged C57 mice. As expected, single unit thresholds were elevated by 30–40 dB in middle-aged C57 mice. However, no significant differences in mean minimal gap thresholds or in the slopes of the gap recovery functions were found between the two age groups. Thus, the results suggest that moderate high frequency SNHL does not affect temporal processing as measured by the gap detection paradigm.