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hearing loss/hypoxia

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Pharmacokinetics of coenzyme Q10 in recovery of acute sensorineural hearing loss due to hypoxia.

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Coenzyme Q10 (CoQ10) has already been favorably evaluated in the clinical treatment of heart disease. In the otolaryngological field, it has been reported that CoQ10 is effective in promoting recovery from acute sudden deafness. However, the pharmakinetics of CoQ10 in the inner ear is not yet

Hypoxia induced hearing loss in animal models of the fetus in-utero.

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The human fetus in-utero has low arterial oxygen tension. It has, therefore, been suggested that at greater than 28 weeks gestational age, the fetus may have a sensori-neural hearing loss comparable to that seen in adult cats exposed to similar degrees of hypoxia. This is due to hypoxia induced

Perinatal hypoxia and auditory brainstem response thresholds: no evidence of permanent hearing loss.

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It has been suggested that pre-natal and or peri-natal hypoxia can cause permanent hearing loss as a result of interference with the generation of the endocochlear potential, especially if this interference occurs during the critical period of endocochlear potential development. This hypothesis was

Intrauterine hypoxia as a cause of hearing impairment in children.

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Among more than 10,000 mothers giving birth during 1974-1977, there were 20 known cases of severe placental insufficiency in connection with hypertensive disease during pregnancy. Well-documented signs of intrauterine hypoxia were observed in all the cases. In 50% of the fetuses intrauterine growth
Age-related hearing loss (ARHL) is the most common sensory disorder among the elderly, associated with aging and auditory hair cell death due to oxidative-stress-induced mitochondrial dysfunction. Although transgenic mice and long-term aging induction cultures have been used to study ARHL, there are
Anesthetized and artificially ventilated guinea pigs were exposed to broad-band noise of 95, 101, 106 or 115 dB SPL for 30 min and studied for 180 min after cessation of noise. The partial pressure of oxygen (pO2) in the perilymph, the cochlear blood flow (CoBF) and auditory-evoked potentials were

Successful treatment of noise-induced cochlear ischemia, hypoxia, and hearing loss.

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Cochlear blood flow (CoBF), perilymphatic partial pressure of oxygen (PL-pO2), cochlear microphonics (CMs), compound action potentials of the auditory nerve (CAPs), and auditory brainstem responses (ABRs) were studied in noise-exposed guinea pigs during and after the following treatments:

Roles of anoxia and noise-induced hearing loss in the postictal refractory period for audiogenic seizures in mice.

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The present series of experiments demonstrated a postictal refractory period for audiogenic seizures in DBA/2J mice, which was not related to hearing loss but apparently was related to anoxia. Unlike many previous studies, Experiment 1 controlled for the effects of noise exposure upon hearing

Mechanisms of noise-induced hearing loss potentiation by hypoxia.

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Potentiation of noise-induced permanent threshold shift (PTS) by hypoxia has been reported [Hear. Res. 172 (1-2) (2002) 186]. In this study in rats, effects of noise (110 dB SPL), hypoxia (10% O(2)), and their combination have been determined on different cochlear potentials and on the expression of

A model of peripherally developing hearing loss and tinnitus based on the role of hypoxia and ischemia.

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The incidence of sensorineural hearing loss often caused by direct damage to the cochlear hair cells is by far more frequent and more serious than disorders affecting the external ear or the middle ear. Mechanisms that are discussed to be relevant for the genesis of tinnitus and acquired hearing

Up-regulation of hypoxia-inducible factor-1 alpha by cobalt chloride prevents hearing loss in noise-exposed mice.

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Since hypoxia-inducible factor-1α (HIF-1α) is the key transcription factor that enables cells to survive in hypoxia, we have investigated whether an upregulation of HIF-1α prevents the noise-induced hearing loss in BALB/c hybrid mice, which were intraperitoneally injected with CoCl(2) (a HIF-1α
OBJECTIVE To investigate the incidence of neonatal hearing loss in well-baby populations and in a neonatal intensive care unit and to identify potential risk factors for hearing loss in a neonatal intensive care unit which the Joint Committee on Infant Hearing (JCIH) had not

Hearing loss of a central type secondary to anoxic anoxia.

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The effect of anoxic anoxia on the threshold sensitivity and amplitude of the responses from the auditory cortex, inferior colliculus and cochlea to acoustic stimuli in guinea pigs was studied. Decay of the amplitude of the responses from the auditory cortex and the inferior colliculus occurs faster

Sound-Induced Cochlear Ischemia/Hypoxia as a Mechanism of Hearing Loss.

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This review will briefly examine evidence supporting the hypothesis that sound causes changes in cochlear blood flow, intracochlear oxygen levels, and the morphology of cochlear blood vessels. A survey of the literature shows that traditional histopathological studies provided such evidence and that

Hearing impairment and hypoxia ischaemic encephalopathy: Incidence and associated factors.

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OBJECTIVE To establish the local incidence of hearing loss in newborns with Hypoxic Ischaemic Encephalopathy (HIE) and to identify associated risk factors. METHODS Retrospective Cohort Study. Neonatal Intensive Care Unit (NICU) dual stage hearing screening protocol, including automated otoacoustic
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