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| 1 | 氨基糖苷类抗生素耳毒性研究显示文摘由于抗菌谱广和价格便宜等原因,氨基糖苷类抗生素被广泛应用于临床。然而氨基糖苷类抗生素的耳毒性和肾毒性却使其在临床应用中受到一定限制。氨基糖苷类抗生素在耳蜗毛细胞中的主要积聚部位是线粒体和溶酶体。氨基糖苷类抗生素引起的细胞内氧自由基活动增强是毛细胞损害的重要因素之一,因此局部或者全身应用氧自由基清除剂可以保护耳蜗免受氨基糖苷类抗生素的损害。钙激活的蛋白酶在氨基糖苷类抗生素引起的毛细胞破坏过程中同样扮演了重要的角色,因此抑制钙激活蛋白酶的活性也能有效保护耳蜗毛细胞。急性氨基糖苷类抗生素耳中毒引起的毛细胞破坏大都死于细胞凋亡,其凋亡原因主要是因为线粒体被药物特异性结合并破坏后,其内部的细胞色素C被释放到细胞质中,因而刺激了Caspase-9并激发其下游的Caspase-3,从而导致毛细胞的程序化死亡。与此不同的是,慢性氨基糖苷类抗生素耳中毒引起的毛细胞破坏不仅包括细胞凋亡而且涉及细胞坏死。在氨基糖苷类抗生素引起的毛细胞坏死过程中,溶酶体的超载破裂最终造成毛细胞自溶性坏死是其典型特征。氨基糖苷类抗生素对螺旋神经节没有直接的毒性作用,但是在耳蜗毛细胞被破坏之后,螺旋神经节往往由于缺乏神经营养因子而发生延迟性神经元死亡,应用转基因技术将神经营养因子基因片段转染到耳蜗支持细胞使之产生分泌神经营养因子的功能,可以有效减轻延迟性神经元死亡的发生率。 | 丁大连 Richard Salvi | 2007 | 中华耳科学杂志2007，5，2： | 46 |
| 2 | 顺铂及其耳毒性显示文摘顺铂是一种用于化疗的铂制剂,在临床上广泛应用于抗肿瘤治疗。然而由于顺铂所具有的肾毒性和耳毒性以及神经毒性等毒副作用,致使其临床应用受到一定的限制。顺铂损害耳蜗的三个主要靶目标分别是血管纹和毛细胞以及螺旋神经节,这三个靶目标在顺铂的作用下都以细胞凋亡的方式实现其程序化自我毁灭,因此顺铂耳中毒模型是一个典型的内耳细胞凋亡模型。顺铂造成的细胞内氧自由基活动增加和抗氧化酶类的活性丧失是产生细胞损害的重要因素之一,因而抗氧化治疗可有效降低顺铂对耳蜗中上述三个靶目标的破坏程度。顺铂在Caspase(半胱氨酸天冬氨酸蛋白酶)径路上激发的毛细胞凋亡是首先启动Caspase-8的活动,说明毛细胞膜表面的细胞死亡因子受体是顺铂诱导毛细胞凋亡的一根导火索;螺旋神经节细胞的凋亡却是被顺铂同时启动了Caspase-8和Caspase-9,因此螺旋神经节细胞的凋亡不但是因为细胞膜表面的死亡因子受体因受顺铂刺激而发出凋亡的信号,而且还会被从线粒体释放出的细胞色素C启动其凋亡自毁程序。肿瘤抑制基因p53是出现在顺铂耳中毒早期的一个促使细胞凋亡的重要'杀手',应用Superarray技术发现顺铂激发的耳蜗毛细胞和螺旋神经节凋亡基因主要涉及p53,肿瘤坏死因子家族,Death domain family(死亡结构域家族),Bcl-2family,Card family(Caspase相关的招募域家族),和GTP signal transdution(三磷酸鸟苷信号转导)等多条凋亡通路,其中p53信号通路是顺铂诱导毛细胞和螺旋神经节凋亡的主线,因此应用p53抑制剂-Pifithrinα可以通过有效阻止p53的活动而减轻顺铂诱导的毛细胞凋亡。分裂素激活的蛋白激酶在顺铂诱导的内耳细胞凋亡过程中也扮演了重要的角色,应用PD98059可以通过暂时抑制分裂素激活的蛋白激酶活性和p53磷酸化以及Caspase的活动延迟耳蜗毛细胞凋亡的起始阶段,但不能完全阻止病变的扩展,因而PD98059对顺铂引起的耳蜗毛细胞凋亡仅具有短期保护效应。 | 丁大连 亓卫东 张梅 王苹 蒋海燕 Richard Salvi | 2008 | 中华耳科学杂志2008，6，2： | 45 |
| 3 | 卡铂及其耳毒性显示文摘卡铂作为一种铂制剂广泛应用于临床抗肿瘤的化学治疗,其毒副作用主要包括耳毒性,肾毒性,神经毒性,和抑制骨髓造血系统等等。卡铂可以选择性破坏灰鼠的耳蜗内毛细胞和前庭I型毛细胞以及与之相联系的传入神经元。在卡铂引起的灰鼠单纯内毛细胞部分损害动物模型,动物具有正常的耳声发射和微音器电位以及听神经动作电位阈值,但总和电位和听神经动作电位的振幅却明显减小。在卡铂造成60%-90%的内毛细胞缺损的动物模型中,灰鼠在安静条件下对纯音的听觉条件反射阈可以保持正常,但在宽带或窄带噪声的掩蔽作用下,其纯音听觉反射阈值却明显提高,同时对听觉瞬时清晰度的辨别能力也明显降低。卡铂引起的内毛细胞和前庭I型毛细胞及其传入数据元的破坏过程往往伴随着钙激活蛋白酶的活动和Caspase-8的启动以及p53的过度调控从而引起细胞凋亡,同时可见琥珀酸脱氢酶,钠钾ATP酶,碱性磷酸酶和葡萄糖-6-磷酸酶活性的减弱以及钙激活ATP酶活性的增强。无论在灰鼠的活体动物实验还是离体培养条件下,卡铂都对灰鼠耳蜗内毛细胞和前庭I型毛细胞具有特殊的选择性破坏作用。卡铂对灰鼠听觉系统的损害除了导致内毛细胞和I型螺旋神经节凋亡之外,还会破坏耳蜗核神经元,但对下丘和听皮层的神经元却不造成致命性损坏。在耳蜗内毛细胞和I型螺旋神经节以及耳蜗核神经元被卡铂破坏之后,下丘和听皮层神经元对微弱的输入声刺激信号却表现出超乎寻常的敏感性提高,提示中枢神经元可能通过降低其某些抑制性神经递质的释放使神经元的活动代偿性增强,亦可能通过加强兴奋性神经递质的释放,或者通过神经元新长出的轴突和末梢而接受到更多的刺激信号,从而弥补了因周边听觉输入信号减弱而引起的听功能障碍,因此,卡铂耳中毒灰鼠模型还可成为一个研究听觉中枢重组现象或听神经病的理想实验动物模型。 | 丁大连 亓卫东 屈燕 蒋海燕 Richard Salvi | 2008 | 中华耳科学杂志2008，6，2： | 21 |
| 4 | 全耳蜗毛细胞定量分析系统显示文摘目的介绍一种计算机辅助下的全耳蜗毛细胞定量分析系统。方法选取氨基糖甙类药物损伤、噪声性损伤以及老年性聋动物模型的耳蜗制备全耳蜗基底膜铺片,从蜗尖向蜗底逐个视野依次进行内外毛细胞计数,将采集的数据输入到计算机并用毛细胞定量分析系统制备成耳蜗图。结果氨基糖甙类药物耳蜗损害模型的耳蜗图显示毛细胞缺损自底回向顶回发展,外毛细胞的损伤比内毛细胞严重;强噪声引起的毛细胞破坏局限在与刺激声频率相对应的基底膜区域;6月龄C57BL/6J小鼠的耳蜗图显示老年性聋的早期损害起始于耳蜗底回的起始端,其中外毛细胞的破坏比内毛细胞严重。结论耳蜗毛细胞定量分析系统可清晰显示全耳蜗毛细胞在基底膜上不同部位的损失程度和破坏范围,并可对应到基底膜上各个频率敏感部位。将传统的耳蜗铺片与计算机技术相结合制备的耳蜗图,具有全面可靠、简便精确、规范等优点。 | 亓卫东 丁大连 蒋海燕 Richard J Salvi | 2007 | 听力学及言语疾病杂志2007，15，2： | 18 |
| 5 | 抗癌药紫杉醇的神经毒性和耳毒性显示文摘紫杉醇(Paclitaxel,商品名Tax01)是从红豆杉科红豆杉属植物中提取得到的二萜类化合物,分子式为C47H51N014。1963年,美国化学家瓦尼和沃尔从一种生长在美国西部大森林中的太平洋杉的树皮和木材中分离到紫杉醇粗提物,在筛选实验中发现其具有很强的抗肿瘤活性。1971年分离出紫杉醇单体成分、确定其化学结构,并正式命名为紫杉醇。从1989到1990年在完成了紫杉醇的Ⅱ期和Ⅲ期临床试验后, | 董杨 施建蓉 Richard Salvi 丁大连 | 2011 | 中华耳科学杂志2011，9，3： | 16 |
| 6 | Chloroplast Proteomics and the Compartmentation of Plastidial Isoprenoid Biosynthetic Pathways显示文摘proteomic 地里的最近的进展允许高产量的实验在叶绿体样品上被进行。许多 proteomic 调查集中了于整个叶绿体或 sub-plastidial 部分。迄今为止,植物蛋白质数据库(PPDB,阳光等, 2009 ) 介绍在网上可得到的最彻底的叶绿体 proteome。然而,在不同 sub-plastidial 分隔空间被识别的许多蛋白质的精确本地化仍然保持假想。为西班牙耶劳岛之旧称等。(2009 ) 去了进关于他们在由使用作为光谱的数知道的一条半量的 proteomic 途径的叶绿体以内的精确本地化的 Arabidopsis thaliana 叶绿体蛋白质的知识进一步的步。他们的 proteomic 策略基于精确的团和时间标签(AMT ) 数据库途径,他们建立了 AT_CHLORO,有 sub-plastidial 本地化的一个全面叶绿体 proteome 数据库和信封蛋白质的 curated 信息。比较这二个广泛的数据库,我们这里集中于涉及叶绿体特定的 isoprenoids 的合成的大约 100 酶。众所周知的小径(即甲基赤藻糖醇磷酸盐 biosynthetic 小径的分隔,在叶绿体以内的 tetrapyrroles 和叶绿素生合成和故障) 验证光谱基于计数的策略。一样的策略然后被用来在叶绿体以内识别类胡萝卜素和 prenylquinones 的生合成的精确本地化(即在信封膜,基质,或 thylakoids ) 那仍然保持不清楚直到现在。 | Jacques Joyard Myriam Ferro Christophe Masselon Daphne Seigneurin-Berny Daniel Salvi Jerome Garin Norbert Rolland | 2009 | Molecular Plant2009，2，6： | 15 |
| 7 | OTOTOXIC EFFECTS OF CARBOPLATIN IN ORGANOTYPIC CULTURES IN CHINCHILLAS AND RATS | DING Dalian JIANG Haiyan FU Yong Richard SALVI Shinichi SOMEYA Masaru TANOKURA | 2012 | Journal of Otology2012，7，2： | 14 |
| 8 | 基于改进微分进化算法的风光互补系统发电容量优化配置显示文摘为有效兼顾风光互补发电系统的可靠性与经济性,以年缺电负荷率最小及微网系统投资建设成本最低为目标函数,以储能电池充放电次数、微网功率平衡以及电池充放电上下限等为约束条件,搭建风光互补系统发电容量优化模型。针对缺电负荷率、系统成本2个目标函数相悖的特点,考虑将帕累托非劣排序操作引入至常规微分进化算法,并对常规算法中的变异策略进行了相应改进,使得改进后的算法在具备多目标寻优能力的同时,寻优速度也得到了较为显著的提升。最后,应用所提改进多目标微分进化算法对风光互补系统发电容量优化模型进行求解,算例结果验证了该文模型的合理性和所提算法的有效性。 | 陈天 蔡泽祥 谢鹏 Francois AUGER Salvy BOURGUET | 2017 | 电力科学与技术学报2017，32，3： | 13 |
| 9 | 钴的神经毒性及耳毒性显示文摘钴是参与维生素B12合成和许多生命活动中必不可少的微量元素,然而一旦机体细胞内的钴离子含量因职业暴露或因饮食摄取钴过量或因钴合金人工假体内源性释放超过安全标准,则可导致严重的金属沉着疾病,这种金属沉着病的症状主要包括感音神经性耳聋、神经性耳鸣、视觉缺陷、认知缺陷、心肌病、心衰、甲状腺疾病、皮肤感觉异常等,在上述病症中,感音神经性耳聋和视神经萎缩是最明显的钴中毒症状。钴中毒引起的细胞损害机制主要涉及细胞的氧化应激和缺氧性损害以及线粒体损害引起的细胞凋亡。因此,钴中毒引起的细胞损害模型尤其适用于听觉系统和视觉系统以及神经系统中因细胞内氧化/抗氧化失衡和细胞缺氧以及线粒体凋亡通路等方面的医学实验研究。 | 李鹏 丁大连 曾祥丽 Richard Salvi Jerome A.Roth | 2015 | 中华耳科学杂志2015，13，1： | 13 |
| 10 | Land Surface Displacement Geohazards Monitoring Using Multi-temporal InSAR Techniques显示文摘China has been affected by some of the world’s most serious geological disasters and experiences high economic damage every year.Geohazards occur not only in remote areas but also in highly populated cities.In the framework of the Dragon-432365 Project,this paper presents the main results and the major conclusions derived from an extensive exploitation of Sentinel-1,ALOS-2(Advanced Land Observing Satellite 2),GF-3(Gao Fen Satellite 3),and latest launched SAR(Synthetic Aperture Radar),together with methods that allow the evaluation of their importance for various geohazards.Therefore,in the scope of this project,the great benefits of recent remote sensing data(wide spatial and temporal coverage)that allow a detailed reconstruction of past displacement events and to monitor currently occurring phenomena are exploited to study different areas and geohazards problems,including:surface deformation of mountain slopes;identification and monitoring of ground movements and subsidence;landslides;ground fissure;and building inclination studies.Suspicious movements detected in the different study areas were cross validated with different SAR sensors and truth data. | Guang LIU Perski ZBIGNIEW Salvi STEFANO Thiebes BENNI Lixin WU Jinghui FAN Shibiao BAI Lianhuan WEI Shiyong YAN Rui SONG Bignami CHRISTIAN Tolomei CRISTIANO Stefan SCHNEIDERBAUER Joao Sousa JOAQUIM 无 | 2021 | Journal of Geodesy and Geoinformation Science2021，4，1： | 13 |
| 11 | 对内耳氧化抗氧化失衡的反思显示文摘生物氧化是指生物细胞内通过对代谢物的一系列氧化一还原反应产生能量的化合过程,也被称之为细胞呼吸或组织呼吸,因此生物氧化可以说是生物存活须臾不可缺少的生命活动,一旦生物氧化终止则意味着生命的终结。伴随生物氧化过程所产生的活性氧自由基(reactiveoxygenspecies,ROs)是生命体活动中多种生化反应的正常中间代谢产物,作为机体的有效防御系统之一,自由基在维持能量供应、促进机体新陈代谢、剿灭细菌病原体、清除机体内毒素、调节机体内多种信号传递通路等许多方面都发挥着十分重要的积极作用。 | 王璐 丁大连 孙虹 Richard Salvi | 2013 | 临床耳鼻咽喉头颈外科杂志2013，27，17： | 12 |
| 12 | Ototoxic destruction by co-administration of kanamycin and ethacrynic acid in rats显示文摘It is well known that ethacrynic acid (EA) can potentiate the ototoxicity of aminoglycoside antibiotics (AmAn) such as kanamycin (KM),if they were applied at the same time.Currently,to create the model of EA-KMinduced cochlear lesion in rats,adult rats received a single injection of EA (75 mg/kg,intravenous injection),or followed immediately by KM (500 mg/kg,intramuscular injection).The hearing function was assessed by auditory brainstem response (ABR) measurement in response to click and/or tone bursts at 4,8,12,16,20,24,and 32 kHz.The static microcirculation status in the stria vascularis after a single EA injection was evaluated with eosin staining.The pathological changes in cochlear and vestibular hair cells were also quantified after co-administration of EA and KM.After a single EA injection,blood flow in vessels supplying the stria vascularis rapidly diminished.However,the blood supply to the cochlear lateral wall partially recovered 5 h after EA treatment.Threshold changes in ABR were basically parallel to the microcirculation changes in stria vascularis after single EA treatment.Importantly,disposable co-administration of EA and KM resulted in a permanent hearing loss and severe damage to the cochlear hair cells,but spared the vestibular hair cells.Since the cochlear lateral wall is the important part of the blood-cochlea barrier,EA-induced anoxic damage to the epithelium of stria vascularis may enhance the entry of KM to the cochlea.Thus,experimental animal model of selective cochlear damage with normal vestibular systems can be reliably created through co-administration of EA and KM. | Hong LIU Da-lian D1NG Hai-yan JIANG Xue-wen WU Richard SALVI Hong SUN | 2011 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2011，12，10： | 10 |
| 13 | Modulation of copper transporters in protection against cisplatin-induced cochlear hair cell damage显示文摘Cisplatin belongs to platinum-based drugs and is widely used in cancer chemotherapy.Ototoxicity is one of the major dose limiting side-effects of cisplatin.For toxicity to occur cisplatin must first be transported from the bloodstream into cochlear cells.Three copper transporters are considered pathways for regulating the uptake and translocation of cisplatin into cells:Ctr1,ATP7A and ATP7B.Our recent study with cochlear organotypic cultures shows that cochlear hair cells can be destroyed by cisplatin at low concentrations from 10μm to 100μn.However,high doses of cisplatin cannot damage hair cells,maybe due to intrinsic feedback reactions that increase export of platinum by ATP7B when the platinum concentration is high in extracellular space.Cimitidine is a specific copper transporter inhibitor that can block the entrance of copper and platinum,and may prevent cisplatin-induced cochlear hair cell injury.To evaluate this hypothesis,we treated cochlear organotypic cultures with cisplatin (10 μm or 50 μm) alone,or cisplatin combined with cimitidine at concentrations ranging from 10-2000 μm for 48 hours.cisplatin at 10 μm damaged about 20% hair cells.In contrast,when cimitidine (10 μm,100 μm and 2000 μm) was added to the culture,near 100% cochlear hair cell survived.At higher concentration (50 μm),cisplatin destroyed about 80% of cochlear hair cells.However,100 μmcimitidine rescued about 50% hair cells from cisplatin damage,and 2000μm cimitidine protected about 80% hair cells.The data of western blot showed that CTR1 and ATP7B expressions were increased in cisplatin treated cochlear tissue,but cimitidine significantly reduced CTR1 and ATP7B.In addition,ATP7A expression was depressed a little after cisplatin treatment.Considering that Ctr1 is involved in copper and platinum influx,but the ATP7A and ATP7B are copper export transporters,the results suggest that cimitidine can effectively block the entrance by copper transporters and stop the influx of cisplatin. | Richard Salvi | 2011 | Journal of Otology2011，6，2： | 10 |
| 14 | Gene expression in cisplatin ototoxicity and protection with p53 inhibitor显示文摘Cisplatin damages cochlear hair cells and spiral ganglion neurons through cell death signaling pathways that are not fully understood. We used focused apoptosis gene microarrays to study early changes in gene expres- sion in cochlear cultures from P3 neonatal rats treated with cisplatin (0.2 mM). After 12 hours of cisplatin treat- ment, more than 50% of the 96 genes on the array showed a significant decrease in expression, consistent with widespread cell death. However, after 3 hours of cisplatin treatment, 10 genes showed significant increase in ex- pression in total cochlear tissue. In experiments with subsets of cochlear tissues, at 3h, cisplatin induced increased expression of 12 genes in the cochlear sensory epithelium (basilar membrane) and 11 genes in the spiral ganglion (tissue of Rosenthal's canal, containing the spiral ganglion). These included pro- and anti-apoptotic genes in- volved in the p53 signaling pathway, TNF receptor family, NF-kappaB pathway, death domain family, death effec- tor domain family, Bcl-2 family, CARD family, TRAF family, and GTP signal transduction. Although the changes in gene expression showed an overlap between basilar membrane and spiral ganglion, other changes, which may reflect the unique response of each tissue, were also observed. Pifithrin-α blocked cisplatin-induced up-regulation of genes in the p53 signaling pathway when assayed by both superarray and real time PCR. The data add to our understanding of the involvement of p53 in cisplatin-induced ototoxicity and otoprotection, conferred by the p53 inhibitor Pifithrin-α. | Donald Coling Richard Salvi | 2009 | Journal of Otology2009，4，2： | 9 |
| 15 | 三甲基锡的神经毒性和耳毒性显示文摘有机锡化合物环境污染对人类健康造成很大的危害。众多有机锡化合物中三甲基锡(TMT)对人体有较强的神经毒性和耳毒性。TMT神经毒性可选择性破坏大脑边缘结构尤其是海马神经元以及听神经系统的神经元。TMT之所以选择性损害某些敏感神经元,其原因是因为这些神经元富含一种被称为Stannin的蛋白质,而Stannin蛋白正是TMT攻击的特异性靶目标。由于这种蛋白同样存在于线粒体,因此富含线粒体的细胞比线粒体贫乏的细胞更容易遭受有机锡化合物的攻击。TMT与Stannin产生不可逆性结合之后进而破坏线粒体的结构和功能,最终导致线粒体损害,细胞色素C释放,从而启动细胞凋亡程序。TMT耳毒性主要表现在用药后迅速发生的高频听力损失,其最早期功能改变表现为听神经动作电位的反应阈升高,随后逐渐出现耳蜗微音器电位振幅的降低。因此,TMT对听觉系统的急性损伤部位很可能最早是发生在从内毛细胞到I型螺旋神经节的听神经末梢及其神经纤维,随着用药后时间的延长才会逐渐累及外毛细胞。TMT对周边听觉系统的损害作用包括兴奋性氨基酸毒性,氧化应激,细胞内钙超载,线粒体破坏,神经纤维脱髓鞘病变等多重损害机制,因此TMT模型可能有助于模拟和研究听神经病的多重损害模式。 | 于进涛 丁大连 孙虹 殷善开 Richard Salvi | 2013 | 中华耳科学杂志2013，11，4： | 9 |
| 16 | OTOTOXIC MODEL OF OXALIPLATIN AND PROTECTION FROM NICOTINAMIDE ADENINE DINUCLEOTIDE显示文摘Oxaliplatin,an anticancer drug commonly used to treat colorectal cancer and other tumors,has a number of serious side effects,most notably neuropathy and ototoxicity.To gain insights into its ototoxic profile,oxaliplatin was applied to rat cochlear organ cultures.Consistent with it neurotoxic propensity,oxaliplatin selectively damaged nerve fibers at a very low dose 1μM.In contrast,the dose required to damage hair cells and spiral ganglion neurons was 50 fold higher(50μM).Oxailiplatin-induced cochlear lesions initially increased with dose,but unexpectedly decreased at very high doses.This non-linear dose response could be related to depressed oxaliplatin uptake via active transport mechanisms.Previous studies have demonstrated that axonal degeneration involves biologically active processes which can be greatly attenuated by nicotinamide adenine dinucleotide(NAD+).To determine if NAD+would protect spiral ganglion axons and the hair cells from oxaliplatin damage,cochlear cultures were treated with oxaliplatin alone at doses of 10μM or 50μM respectively as controls or combined with 20 mM NAD+.Treatment with 10μM oxaliplatin for 48 hours resulted in minor damage to auditory nerve fibers,but spared cochlear hair cells.However,when cochlear cultures were treated with 10μM oxaliplatin plus 20 mM NAD+,most auditory nerve fibers were intact.50μM oxaliplatin destroyed most of spiral ganglion neurons and cochlear hair cells with apoptotic characteristics of cell fragmentations.However,50μM oxaliplatin plus 20 mM NAD+treatment greatly reduced neuronal degenerations and hair cell missing.The results suggested that NAD+provides significant protection against oxaliplatin-induced neurotoxicity and ototoxicity,which may be due to its actions of antioxidant,antiapoptosis,and energy supply. | DING Dalian JIANG Haiyan FU Yong LI Yongqi Richard Salvi Shinichi Someya Masaru Tanokura | 2013 | Journal of Otology2013，8，1： | 9 |
| 17 | 镉中毒及其耳毒性显示文摘1镉污染概述
重金属是指比重大于5的金属,即密度大于每立方厘米4.5克的金属。重金属的种类有45种,这些重金属属于过渡元素,所谓过渡金属的概念是指元素周期表中d区的一系列金属元素,镉便是其中一种毒性较高的过渡金属。 | 刘洪 孙虹 Richard Salvi 丁大连 | 2011 | 中华耳科学杂志2011，9，1： | 8 |
| 18 | 缺氧性内耳损害显示文摘1缺氧对人类听觉的损害缺氧对听觉的影响是勿庸置疑的。但是在自然环境高海拔地区所存在的缺氧环境对听觉的影响却微乎其微。虽然早在1949年Wever等就报道了气压变化可导致听觉迟钝[1]。 | 丁大连 曲雁 亓卫东 蒋海燕 Richard Salvi | 2008 | 中华耳科学杂志2008，6，4： | 8 |
| 19 | Lead neurotoxicity in rat cochlear organotypic cultures显示文摘Lead is a major environmental toxicant throughout the world.Lead can induce severe neurotoxicity including irreversible hearing impairment.Many in vivo studies have shown that lead damages the auditory nervous system,but has little or no effect on cochlear sensory hair cells.To gain insights on lead ototoxic and neurotoxic effects in vitro,lead acetate (LA) was applied to postnatal day 3-4 rat cochlear organotypic cultures for 24 or 72 h with doses of 0.1,0.5,1,2 or 4 mM.After 24 or 72 h treatment with lead acetate,nearly all of cochlear sensory hair cells were intact.However,after 72 h treatment,the peripheral auditory nerve fibers projecting to the hair cells and the spiral ganglion neurons (SGN) were damaged when lead concentration exceeded 2 mM.Our results indicated that 72 h treatment with only the high doses (> 2 mM) of lead actate damaged SGNs and peripheral nerve fibers;hair cells remained structurally intact even after 4 mM treatment.These results show that lead primarily damages cochlear nerve fibers andSGNratherthanhaircells. | Richard Salvi | 2011 | Journal of Otology2011，6，2： | 7 |
| 20 | 噪声影响下纯音诱发听性脑干反应的改变显示文摘目的观察噪声影响下纯音诱发听性脑干反应(ABR)的改变。方法将10只成年南美栗鼠随机平均分为两组,分别暴露强度为105dB SPL窄带噪声,中心频率4kHz,2h或5h。噪声暴露前、后1h、2周及4周,测试动物对短纯音声音刺激(1、2、4、8、12以及16kHz)诱发的听神经复合动作电位(CAP)和ABR,并结合耳蜗毛细胞的损害程度和范围进行分析。结果 2h和5h的窄带噪声暴露造成南美栗鼠不同程度和范围的耳蜗毛细胞损害。与毛细胞损害部位相对应频率的CAP及ABR阈值在暴露噪声后均出现不同程度的提高。噪声暴露后4周,尽管某些动物的CAP已经发生了不可逆性永久阈移,但在某些短纯音频率诱发的ABR阈值却呈现部分恢复,甚至在个别动物的CAP测试波形中引出了低于CAP阈值的ABR波形成分。结论中枢听觉功能的重组在一定条件下可能促进脑干听觉神经元提高感知因周边耳蜗损害而引起微弱听觉输入信号的敏感性。 | 吴学文 丁大连 蒋海燕 刘洪 Ed Lobarinas 孙虹 Richard Salvi | 2011 | 中国眼耳鼻喉科杂志2011，11，2： | 7 |
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