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声损伤
相关语句
  acoustic trauma
     Expression of heat shock protein in guinea pig cochlea after acoustic trauma
     声损伤后豚鼠耳蜗热休克蛋白的表达
短句来源
     Objective:To observe the protective effects of MK-801, an antagonist of N-methyl-D-aspartate (NMDA) recepotor, against temporary (TTS) or permanent threshold shifts (PTS) in acoustic trauma.
     目的:观察N 甲基 D 天冬氨酸(NMDA)受体的非竞争性拮抗剂MK 801在声损伤中对暂时性阈 移(TTS)或永久性阈移(PTS)的保护作用。
短句来源
     2ATA hyperbaric air was not effective to prevent or to treat the acoustic trauma.
     2ATA的高压空气对内耳声损伤无预防或治疗作用。
短句来源
     Glu and its receptors played an important role in degeneration and death of SGN in acoustic trauma;
     结论:在声损伤中,Glu及其受体在SGN变性消亡中起着十分重要的作用;
短句来源
     An Investigation on the Effects of the Pathway of Glutamate-N-methyl-D-asparate-Nitric Oxide Synthase-Reactive Oxygen Species on Acoustic Trauma
     谷氨酸—N-甲基-D-天冬氨酸—一氧化氮合酶—活性氧通路在声损伤中的作用研究
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  “声损伤”译为未确定词的双语例句
     Conclusions (1)The ABR results of noise-induced hearing loss are correlated with a gradual pathological process from outer to inner hair cells, then to auditory nerve and brainstem auditory pathway.
     结论:(1)噪声性听损伤的ABR变化反映了声损伤始于外毛细胞,逐渐累及内毛细胞、听神经和脑干听觉通路的病变过程。
短句来源
     The HBO group (120 cases, 132 ears) were exposed to HBO(pure oxygen breathing at 025 MPa absolute for 40min×2 with a 10min air breathing break in the chamber) once a day;
     HBO组的声损伤患者120例(132耳),均在0.25MPa(2.5ATA)压力下吸纯氧40分钟2次,中间吸舱内压缩空气10分钟,每日1次;
短句来源
     ABR seems more sensitive to noise exposure duration than DPOAE.
     ABR比DPOAE更能体现声损伤时程的变化情况,是研究长期噪声暴露的敏感客观指标。
短句来源
     Result:The possible causes were identified in 11 children cases ( 52.4%) as 4 mumps, 3 upper respiratory tract infections, 2 ototoxicity from aminoglycoside antibiotics, 1 noise exposure and 1 genetic metabolic encephalopathy.
     结果 :儿童组中 11例 (5 2 .4 % )查到可能的病因 ,其中腮腺炎 4例 (19% )、上呼吸道感染 3例 (14 .3% )、耳毒性药物中毒 2例 (9.5 % )、声损伤和代谢性脑病各 1例 ; 对照组 19.4 %找到可疑的病因。
短句来源
     Anacoustictraumamodelforstudyoftherepairoftheauditoryepitheliawasestab-lishedinpostnatal8~14dayschicks. Theanimalswerecontinuouslyexposedtothewidebandnoiseat115dB(A)for72hours.
     为探讨听觉上皮修复过程的细胞生物学特点,用剂量为115dB(A)×72小时的宽带噪声建立8~14日龄鸡声损伤模型。
短句来源
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  相似匹配句对
     ACOUSTIC EMISSION TESTING OF WIRE ROPES FOR FATIGUE DAMAGE
     钢丝绳疲劳损伤发射测试
短句来源
     EXPLOSIVE ACOUSTIC TRAUMA AT BATTLEGROUND AND ITS PHYSICAL PROTECTION
     战场爆震性损伤及其防护
短句来源
     Duodenal injuries
     十二指肠损伤
短句来源
     EQUIVALENT DAMAGE CONVERSION
     当量损伤折算
短句来源
     Acoustic suspension phenomenon
     悬浮现象的研究
短句来源
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  acoustic trauma
The known etiologies of acquired sensorineural hearing loss include acoustic trauma, physical trauma, ototoxicity, genetic predisposition, infections, Meniere's disease, aging, and autoimmune disease.
      
Degeneration of spiral ganglion neurons (SGNs) and hair cells in the cochlea induced by aging, injury, ototoxic drugs, acoustic trauma, and various diseases is the major cause of hearing loss.
      
A fan-in projection of the dendritic system revealed no changes in the radial growth of basal dendrites resulting from the early acoustic trauma.
      
Posttraumatic stimulation is one of the factors which markedly potentiate the regressive effect of acoustic trauma.
      
Acoustic trauma effects from doubling the exposure time
      
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  acoustic injury
On macroscopic examination only limited thermal and acoustic injury was found in crater adjacent tissue structures.
      
The present study examines the role of CCL2 and CCR2 in acoustic injury.
      
Acoustic injury to cetaceans may occur within a radius of 2km of pile-driving activity.
      
Both obser vations probably are the result of considerable thermal and/or acoustic injury of the arterial wall during the TABLE 3.
      


This paper is to report the results of the experimental study on the effects of the explosion sound waves on the hearing power and the activities of succinic dehydrogenase (SDH) and malic dehydrogenase (MDH) of the cochlea tissues in guinea pigs. The alterations of the hearing power and the activities of the two enzymes were monitored with auditory physiological and histochemical methods respectively. The results of the experiment were as follows:The activities of both SDH and MDH decreased significantly (P<0.01)...

This paper is to report the results of the experimental study on the effects of the explosion sound waves on the hearing power and the activities of succinic dehydrogenase (SDH) and malic dehydrogenase (MDH) of the cochlea tissues in guinea pigs. The alterations of the hearing power and the activities of the two enzymes were monitored with auditory physiological and histochemical methods respectively. The results of the experiment were as follows:The activities of both SDH and MDH decreased significantly (P<0.01) after the impact of the explosion sound waves since it brought about a disturbance of the oxidation metabolism of the inner ear paricularly of the out hair cells of the first and second loops of the cochlea.The severity of the hearing impairment after the sound impact was in positive correlation with the reduction of SHD and MDH activities. If the normal activities of the two enzymes can be preserved, then hearing power can be protected from being injured.If the hearing impairment can be kept withing 40 dB.no permanent hearing loss will be resulted since the reduction of the,SDH and MDH activities is reversible. If hearing impairment exceeds 40 dB and no effective measures are taken to reverse the lowered activities of the two enzymes, then therapeutic results would be disappointing and permanent hearing loss is most likely to occur.

本实验采用听生理方法和耳蜗组织化学方法观察了爆震对豚鼠听力和耳蜗琥珀酸脱氢酶、苹果酸脱氢酶的影响。结果表明:(1)爆震使豚鼠耳蜗内琥珀酸脱氢酶、苹果酸脱氢酶活性下新;(2)爆震引起的听力学改变,与耳蜗内SDH、MDH活性呈负相关。如果是这样,那末,在考虑声损伤的防治时,就可以从维持上述两种酶的活性来看手;(3)若听力损失限制在40dB以内,因酶活性下降和听力损失是可逆的,故可避免战位人员的永久性听力损失;听力损失超过40dB,若无有效措施使酶的活性逆转,则会遗留永久性听力损失,治疗效果可能欠佳。

Four groups of guinea pigs were exposed to loud sound ( 3h, 1KHz, 125 dB SPL ) .One group inhaling air as control (C-group),the other groups inhaling 2ATA hyperbaric oxygen ( HBO ) for 30 minutes each time.These three groups were. "Prevention group" ( P-group ) inhaling HBO once before exposure; "Treatment group" ( T-group ) inhaling HBO daily for 14 days after exposure; "Prevention-treatment group" ( PT-group ) inhaling HBO once before exposure and daily for 14 days after exposure.After exposure, the cortical...

Four groups of guinea pigs were exposed to loud sound ( 3h, 1KHz, 125 dB SPL ) .One group inhaling air as control (C-group),the other groups inhaling 2ATA hyperbaric oxygen ( HBO ) for 30 minutes each time.These three groups were. "Prevention group" ( P-group ) inhaling HBO once before exposure; "Treatment group" ( T-group ) inhaling HBO daily for 14 days after exposure; "Prevention-treatment group" ( PT-group ) inhaling HBO once before exposure and daily for 14 days after exposure.After exposure, the cortical auditory potential threshold evoked by click rose in all animals. The hearing loss of C-group was severest, up to 70 dB; while P-group and PT-group were 53 and 5ldB respectively ( P<0.01, compared with C-group ) ; T-group was 68.5dB.Similar findings resulted from measurement by tone burst. The above phenomena remained 21 days until these animals were killed. The average trauma length in organ of Corti was 527μm in C-group; 142μm and 106μm in P-group and PT-group respectively ( P<0.05 ) ; and 295μm in T-group. From the findings, we consider HBO plays markable preventive role on sound-induced auditory damage. The prevention mechanism and treament effect of the HBO were discussed.

将四组豚鼠在125dBSPL,1KHz强声中暴露3小时。一组动物于声暴露前后吸空气作为对照组。其余三组动物吸2ATA高压氧(HBO),每次30分钟。其中于声暴露前吸1次者为预防组;于声暴露后连续吸14天次者为治疗组;于声暴露前吸1次,声后吸14天次者为HBO防治组。声暴露后,各组动物短声诱发皮层听区电位听阈上升。对照组听力损失最重,达70dB;预防组和防治组仅损失53dB和51dB(同对照组比P<0.01);治疗组损失68.5dB。短纯音测昕结果与此类似。对照组耳蜗病理损伤长度平均为527μm;预防组和防治组分别为142μm和106μm(P<0.05);治疗组为295μm。由此可以认为HBO对声损伤具有显著的预防作用。 文中讨论了高压氧的预防机理及其治疗作用

The effects of hyperbaric oxygen (HBO) before and after sound exposure on the hair cell loss rate, the succinic dehydrogenase (SDH) activity, and the cortical evoked potental threshold in guinea pigs were observed. After exposure, in the HBO preventive groups of different exposure intensities, the hair cell losses were less significant, the SDH activities were protected, the temporal threshold shift (TTS) was reduced or the persistent threshold shift (PTS) was turned to TTS, or the PTS was reduced Over 10dB....

The effects of hyperbaric oxygen (HBO) before and after sound exposure on the hair cell loss rate, the succinic dehydrogenase (SDH) activity, and the cortical evoked potental threshold in guinea pigs were observed. After exposure, in the HBO preventive groups of different exposure intensities, the hair cell losses were less significant, the SDH activities were protected, the temporal threshold shift (TTS) was reduced or the persistent threshold shift (PTS) was turned to TTS, or the PTS was reduced Over 10dB. The therapeutic effect of HBO could also be seen from the rate of hair cell losses and the degree of SDH aetivity reductions among the groups. But the mean hearing of animals was not improved in the therapeufic group. The machanism is still unknown. 2ATA hyperbaric air was not effective to prevent or to treat the acoustic trauma.

以豚鼠为实验对象,以外毛细胞缺失率、琥珀酸脱氢酶(SDH)活性和皮层听区诱发电位反应阈为指标,观察高压氧对不同程度声损伤的预防和治疗效 果。结果表明,高压氧具有预防内耳声损伤的作用,可以减少毛细胞缺失,保护SDH,降低暂时性阈移(TTS),使永久性阈移(PTS)转变为TTS,或使PTS降低10dB以上。高压氧治疗也有一定的作用,可以减少毛细胞缺失,保护SDH,但未能改善皮层听区诱发反应阈。2ATA的高压空气对内耳声损伤无预防或治疗作用。

 
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