Hearing sensitivity in older adults: associations with cardiovascular risk factors in the health, aging and body composition study

OBJECTIVES: To examine the association between cardiovascular disease (CVD) and its risk factors and age‐associated hearing loss in a cohort of older black and white adults. DESIGN: Cross‐sectional cohort study. SETTING: The Health, Aging, and Body Composition (Health ABC) Study, a community‐based cohort study of older adults from Pittsburgh, Pennsylvania, and Memphis, Tennessee. PARTICIPANTS: Two thousand forty‐nine well‐functioning adults (mean age 77.5; 37% black). MEASUREMENTS: Pure‐tone audiometry measurement and history of clinical CVD were obtained at the fourth annual follow‐up visit. Pure‐tone averages in decibels reflecting low (250, 500, and 1,000 Hz), middle (500, 1,000, and 2,000 Hz), and high (2,000, 4,000, and 8,000 Hz) frequencies were calculated for each ear. CVD risk factors, aortic pulse‐wave velocity (PWV), and ankle–arm index (AAI) were obtained at study baseline. RESULTS: In sex‐stratified models, after adjustment for age, race, study site, and occupational noise exposure, risk factors associated with poorer hearing sensitivity in men included high triglyceride levels, high resting heart rate, and history of smoking. In women, poor hearing sensitivity was associated with high body mass index, high resting heart rate, fast PWV, and low AAI. CONCLUSION: Modifiable risk factors for CVD may play a role in the development of age‐related hearing loss.     

Cochlear mitochondrial DNA3867bp deletion in aged mice

目的　探讨老龄小鼠耳蜗mtDNA缺失情况 ,明确老龄小鼠耳蜗mtDNA缺失的位置。方法　应用套式PCR和DNA测序技术对不同月龄 12 9/CD1杂交小鼠耳蜗 31个 (2月龄 7个 ,7- 10月龄 16个 ,17- 19月龄 8个 )进行定性及定量检测。结果　 1 小鼠耳蜗mtDNA386 7bp大片缺失 ,缺失发生在nt910 3-nt12 970之间 ,其两侧nt90 89-nt910 3和nt12 95 6-nt12 970为核苷酸完全相同的 15bp重复序列。 2 随着小鼠月龄的增加 ,耳蜗mtDNA386 7bp缺失发生率有明显增加的趋势 ,2月龄小鼠未发现缺失 (0 /7) ;17- 19月龄小鼠 (7/8)明显高于 7- 10月龄小鼠 (4/16 ) (P <0 0 1)。 3 缺失mtDNA/总mtDNA比值 ,17- 19月龄小鼠明显高于 7- 10月龄小鼠 (P <0 0 1)。结论　老龄小鼠耳蜗出现mtDNA386 7bp大片缺失可能与老年性聋发生相关     

复聪片对老年大鼠蜗内神经结构影响的实验研究

为探讨复聪片防治老年性聋的机制,以老年大鼠疆孔内神经纤维和螺旋神经为观察指标,发现复聪能有效支持上述蜗内神经结构。提示蜗内神经结构的退变可能是老年性聋的主要病理基础。复聪片支持蜗内神经结构可能基于如下途径：１）促进神经生长因了与其受体的结合;（２）通过保护毛细胞,间接促进神经生长因子的产生。     

年龄相关性听力减退大鼠听皮层、蜗核、耳蜗组织中SOD、MDA的变化

目的探讨年龄相关性听力减退大鼠听觉系统抗氧化能力随月龄增长的变化。方法采用硫代巴比妥酸(Thibabituric Acid,TBA)法、黄嘌呤氧化酶法测定3月龄和18月龄大鼠听皮层、蜗核及耳蜗组织中的丙二醛(MDA)、超氧化物歧化酶(SOD)。结果18月龄大鼠听皮层、蜗核及耳蜗组织中的SOD活性较3月龄大鼠显著降低,MDA含量显著升高,两组比较差异有显著性(P<0.01)。结论年龄相关性听力减退与听觉系统抗氧化能力下降密切相关。     

不同周龄小鼠耳蜗组织中Otos的表达及其意义

目的：观察Otos在不同周龄年龄相关性听力损失（AHL）小鼠耳蜗组织中的表达和分布,探讨其与AHL的关系。方法：40只SPF级C57BL/6Cnc小鼠按鼠龄分成4、16、32和48周龄组,每组10只。各组小鼠行听性脑干反应（ABR）检查后取出耳蜗,免疫荧光法检测各组小鼠耳蜗组织中Otospiralin蛋白的表达量和分布,qRT-PCR法检测各组小鼠耳蜗组织中Otos mRNA表达水平,Western blotting法检测各组小鼠耳蜗组织中Otospiralin蛋白表达水平。结果：Otospiralin蛋白在小鼠耳蜗组织中主要表达于螺旋韧带且在5种纤维细胞中均有表达;与4周龄组比较,16、32和48周龄小鼠耳蜗组织中Otospiralin蛋白表达量明显降低（P<0.01）。与4周龄组比较,16、32和48周龄组小鼠ABR平均阈值均明显升高（P<0.01）,耳蜗组织中Otos mRNA和Otospiralin蛋白表达水平均明显降低（P<0.01）;与16周龄组比较,32和48周龄组小鼠ABR平均阈值均明显升高（P<0.01）,耳蜗组织中Otos mRNA和Otospiralin蛋白表达水平均明显降低（P<0.01）;与32周龄组比较,48周龄组小鼠ABR平均阈值明显升高（P<0.01）,耳蜗组织中Otos mRNA和Otospiralin蛋白表达水平均明显降低（P<0.01）。结论：随着AHL小鼠鼠龄的增加其听觉功能逐渐减退,其耳蜗组织中Otos mRNA和Otospiralin蛋白表达水平也逐渐减少。Otos的这种改变可能参与AHL的发生发展。     

Predictive model for progression of hearing loss: meta‐analysis of multi‐state outcome

Rationale, aims and objectives To develop a multi‐state Markov model to predict multi‐state progression of age‐related hearing loss (ARHL). Method A systematic searching of literature from Medline (1966–2005) was performed. The disease process for hearing loss was modelled as a four‐state continuous‐time Markov process. We estimated the progression rates for each study separately, then calculated weighted averages over all studies across age groups, weighting for each study by the inverse of variance. The pooled estimates were obtained and transition probabilities between states were illustrated. Results The progression of hearing loss increased with the ascending frequencies across all age groups. Men had significantly faster progression rates in all frequencies and age groups except for the age group of 90 years or older. In comparison between ears, the progression of hearing would be slightly faster in left ears initially in early elder life and did not show any difference in further ageing and later hearing declines. With the pooled estimates of progression rates, the probabilities of hearing deterioration could be obtained. Conclusions The multi‐state model can quantify the nature course of hearing progression in ARHL. Predictions of hearing status can be simulated either at population or individual level with this model.     

高血黏和血脂对老年人听力影响的观察

目的探讨高血黏和高血脂对老年人听力的影响。方法按血清检测结果分组，对照组87例，高黏血症组68例，高血脂症组82例，进行纯音听阈测试。结果纯音听阈高黏血症组、高血脂症组各频率均值均显著高于对照组。结论高黏血症、高血脂症对老年人的听觉系统可造成损害，预防和治疗高黏血症、高血脂症是预防和延缓老年性耳聋的重要措施之一。     

Auditory efferent feedback system deficits precede age-related hearing loss: contralateral suppression of otoacoustic emissions in mice

The C57BL/6J mouse has been a useful model of presbycusis, as it displays an accelerated age-related peripheral hearing loss. The medial olivocochlear efferent feedback (MOC) system plays a role in suppressing cochlear outer hair cell (OHC) responses, particularly for background noise. Neurons of the MOC system are located in the superior olivary complex, particularly in the dorsomedial periolivary nucleus (DMPO) and in the ventral nucleus of the trapezoid body (VNTB). We previously discovered that the function of the MOC system declines with age prior to OHC degeneration, as measured by contralateral suppression (CS) of distortion product otoacoustic emissions (DPOAEs) in humans and CBA mice. The present study aimed to determine the time course of age changes in MOC function in C57s. DPOAE amplitudes and CS of DPOAEs were collected for C57s from 6 to 40 weeks of age. MOC responses were observed at 6 weeks but were gone at middle (15-30 kHz) and high (30-45 kHz) frequencies by 8 weeks. Quantitative stereological analyses of Nissl sections revealed smaller neurons in the DMPO and VNTB of young adult C57s compared with CBAs. These findings suggest that reduced neuron size may underlie part of the noteworthy rapid decline of the C57 efferent system. In conclusion, the C57 mouse has MOC function at 6 weeks, but it declines quickly, preceding the progression of peripheral age-related sensitivity deficits and hearing loss in this mouse strain.