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1 e amount of change in the distortion product otoacoustic emission (at 2f(1)-f(2)) just after onset of
2  functionally assessed by distortion product otoacoustic emission (DPOAE) analysis.
3 function was evaluated by distortion product otoacoustic emission (DPOAE) and auditory brainstem resp
4 cally tuned effect on the distortion product otoacoustic emission (DPOAE) and the cochlear whole-nerv
5                           Distortion product otoacoustic emission (DPOAE) assay and acoustic brainste
6                   We used distortion product otoacoustic emission (DPOAE) measurements to monitor coc
7                           Distortion product otoacoustic emission (DPOAE) testing was performed on 97
8 ponse (ABR) wave I, lower distortion product otoacoustic emission (DPOAE) thresholds, increased cell
9 as assessed through the contralateral evoked otoacoustic emission (EOAE) amplitude attenuation effect
10     Neonatal hearing test results, including otoacoustic emission (OAE) data, were sought for all neo
11 ening was performed using transiently evoked otoacoustic emission (TEOAE) and automated auditory brai
12 se -- ABR thresholds, and distortion-product otoacoustic emission -- DPOAE magnitudes), and were clus
13                           Distortion product otoacoustic emission amplitudes of Coch(G88E/G88E) mice
14               Tone-evoked distortion product otoacoustic emission and auditory brainstem response mea
15 itory brainstem response, distortion product otoacoustic emission and cochlear microphonics tests, an
16 t with large reduction in distortion product otoacoustic emission and severe hearing loss at high fre
17 However, the fundamental question of how the otoacoustic emission exits the cochlea remains unanswere
18                          Electrically evoked otoacoustic emission is a manifestation of reverse trans
19 n auditory threshold, and distortion product otoacoustic emission measurements indicate that this mil
20  hearing screening was performed by means of otoacoustic emission testing and auditory brain stem res
21       Real-time shifts in distortion product otoacoustic emission thresholds and amplitudes were meas
22 lity to amplify sound, as distortion product otoacoustic emission thresholds were not affected in age
23 esponse (ABR) thresholds, distortion product otoacoustic emission thresholds, or ABR wave I amplitude
24 and how the inner ear-generated sound, i.e., otoacoustic emission, exits the cochlea, we created a so
25 anical activity in hair cells is spontaneous otoacoustic emission, the unprovoked emanation of sound
26 g, compressive nonlinearity, and spontaneous otoacoustic emission.
27 y, compressive nonlinearity, and spontaneous otoacoustic emission.
28 sholds (0.25-16 kHz), and distortion product otoacoustic emissions (1-16 kHz) were utilized for the r
29                                 Click-evoked otoacoustic emissions (CEOAEs) are echo-like waveforms e
30 eption thresholds (SRTs), Distortion Product Otoacoustic Emissions (DPOAE) amplitudes, Signal to Nois
31 with the cubic 2f(1)-f(2) distortion product otoacoustic emissions (DPOAE) at the start of the study
32       Here we used 2f1-f2 distortion product otoacoustic emissions (DPOAE) measurements to refine the
33 ainstem response (ABR) or distortion product otoacoustic emissions (DPOAE) or is being challenged by
34 instem response (ABR) and distortion product otoacoustic emissions (DPOAE) to assess hearing recovery
35 sure were observed in the distortion product otoacoustic emissions (DPOAEs) and the auditory brainste
36 iving with HIV have lower distortion product otoacoustic emissions (DPOAEs) compared with HIV-negativ
37 teral suppression (CS) of distortion product otoacoustic emissions (DPOAEs) in humans and CBA mice.
38 bly reduce EP showed that distortion product otoacoustic emissions (DPOAEs) recovered before EP.
39 (0.5 to 8 kHz) and evoked distortion product otoacoustic emissions (DPOAEs) were conducted for 32 pat
40 stem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) were unaffected by loss o
41                           Distortion product otoacoustic emissions (DPOAEs), a readout of active, MET
42 hlear status, assessed by distortion product otoacoustic emissions (DPOAEs), and to further clarify t
43  mice, displayed enhanced distortion product otoacoustic emissions (DPOAEs), suggesting an improved e
44 audiometry, tympanometry, distortion-product otoacoustic emissions (DPOAEs), transient otoacoustic em
45 ded pure tone thresholds, distortion product otoacoustic emissions (DPOAEs), tympanometry, and word r
46 table in the ear canal as distortion-product otoacoustic emissions (DPOAEs).
47 nses (ABRs) and decreased distortion product otoacoustic emissions (DPOAEs).
48 instem response (ABR) and distortion product otoacoustic emissions (DPOAEs).
49 outer hair cell function [distortion product otoacoustic emissions (DPOAEs)].
50                                              Otoacoustic emissions (OAEs) are faint sounds generated
51                                      We used otoacoustic emissions (OAEs) as a method to quantify the
52                                              Otoacoustic emissions (OAEs) provide information about t
53 on push-pull amplification must contend with otoacoustic emissions (OAEs), whose existence implies th
54 tone audiometry (CPA) and distortion product otoacoustic emissions (OAEs).
55                           Stimulus-frequency otoacoustic emissions (SFOAEs) are a potentially powerfu
56                           Stimulus-frequency otoacoustic emissions (SFOAEs) provide a noninvasive alt
57              Furthermore, stimulus-frequency otoacoustic emissions (SFOAEs), sounds emitted by the ea
58                                  Spontaneous otoacoustic emissions (SOAEs) are weak sounds that emana
59 lf-sustained oscillations called spontaneous otoacoustic emissions (SOAEs) can often be measured in t
60                 We also observed spontaneous otoacoustic emissions (SOAEs) in 70% of the homozygous m
61 e pharmacological sensitivity of spontaneous otoacoustic emissions (SOAEs) in a lizard, the Tokay gec
62 ivity can be measured using Transient-Evoked Otoacoustic Emissions (TEOAE), which assess the cochlea'
63 mutants show only minimal distortion product otoacoustic emissions and 70-80 dB threshold shifts in a
64 function was assessed via distortion product otoacoustic emissions and auditory brainstem responses (
65 function was assessed via distortion product otoacoustic emissions and auditory brainstem responses,
66 function was assessed via distortion product otoacoustic emissions and auditory brainstem responses.
67              However, previous recordings of otoacoustic emissions and cochlear microphonic potential
68                 They lack distortion product otoacoustic emissions and cochlear microphonic responses
69 ddle ear muscle reflexes, distortion product otoacoustic emissions and cochlear microphonics, as well
70 ferent function measures (distortion product otoacoustic emissions and contralateral suppression) wer
71 ms, to evaluate the feasibility of including otoacoustic emissions and extended high frequency audiom
72                        Distortion product of otoacoustic emissions and immunohistochemistry in the ra
73 in the presence of normal distortion product otoacoustic emissions and normal audiometric thresholds.
74                       Since the discovery of otoacoustic emissions and outer hair cell (OHC) motility
75  not involved in the backward propagation of otoacoustic emissions and that sounds exit the cochlea p
76 sed on the measurement of stimulus-frequency otoacoustic emissions and, unlike previous noninvasive p
77 und by 6-7 months, whilst distortion product otoacoustic emissions are no different to control animal
78 stem evoked responses and distortion product otoacoustic emissions are, for most frequencies, normal
79 oscopy, tympanometry, and distortion product otoacoustic emissions as near the time of admission as w
80 r, the olivocochlear efferents, by examining otoacoustic emissions created by the normal ear, which c
81 se-induced suppression of distortion product otoacoustic emissions derived from outer hair cell trans
82 -frequency audiometry and distortion product otoacoustic emissions for ototoxicity monitoring in chil
83 aneous (SOAE) and stimulus-frequency (SFOAE) otoacoustic emissions from a bird (barn owl, Tyto alba)
84 afness by P25 and reduced distortion product otoacoustic emissions from P15 onward.
85 y brainstem responses and distortion product otoacoustic emissions from these mice displayed wild-typ
86 fails to produce adaptation of MET-dependent otoacoustic emissions in vivo in the Tecta/Tectb(-/-) mi
87 le the exact mechanism for the production of otoacoustic emissions is not known, active motion of ind
88 und AN responses by 40-70% without impacting otoacoustic emissions or behavioral tone sensitivity in
89                                              Otoacoustic emissions or OAEs (reflections of cochlear e
90                              We suggest that otoacoustic emissions originate from phase coherence in
91 and the relatively robust distortion product otoacoustic emissions that are found in elderly subjects
92     The morphology of sensory hair cells and otoacoustic emissions that depend on the integrity of ha
93 surement of auditory brainstem responses and otoacoustic emissions to assess cochlear presynaptic and
94                                              Otoacoustic emissions were absent in patients with a mod
95                           Distortion product otoacoustic emissions were also monitored.
96                                              Otoacoustic emissions were not impaired pointing to norm
97                           Distortion product otoacoustic emissions were not recordable from Clrn1(-/-
98 rve action potential, and stimulus frequency otoacoustic emissions were recorded from 12 days after b
99 ochlear receptor outer hair cell activities (otoacoustic emissions) and absent or abnormally delayed
100 mpound action potentials, distortion product otoacoustic emissions) during efferent fiber activation,
101 r functions (auditory brainstem response and otoacoustic emissions).
102 r microphonic potentials, distortion product otoacoustic emissions, and basilar membrane motion indic
103 tory brainstem responses, distortion product otoacoustic emissions, and number of hair cell synapses.
104 ct otoacoustic emissions (DPOAEs), transient otoacoustic emissions, and the hearing-in-noise test (HI
105 ry brainstem response and distortion-product otoacoustic emissions, and was accompanied by cochlear h
106                                 Such sounds, otoacoustic emissions, are widely used for diagnosis of
107 iological tests including distortion product otoacoustic emissions, auditory brainstem responses, env
108                     Two possible sources for otoacoustic emissions, both localized within individual
109 es were unrelated to the modest variation in otoacoustic emissions, cochlear tuning, or the residual
110 or tympanometry, acoustic reflex thresholds, otoacoustic emissions, hearing sensitivity, speech recep
111 se thresholds and reduced distortion-product otoacoustic emissions, in the presence of normal endococ
112 roperties, as measured by distortion product otoacoustic emissions, neither before nor after noise ex
113                                              Otoacoustic emissions, sounds generated by the inner ear
114                                 Furthermore, otoacoustic emissions, sounds generated inside the cochl
115 e mice, mutant mice showed reduced or absent otoacoustic emissions, suggesting cochlear outer hair ce
116 e mice progressively lost distortion product otoacoustic emissions, suggesting defects in outer hair
117 hearing revealed subtle differences in their otoacoustic emissions, suggesting that the expression of
118 r hair cell function (cochlear microphonics, otoacoustic emissions, summating potentials) and auditor
119                            These spontaneous otoacoustic emissions, the most striking manifestation o
120 bly modulated by drugs that affect mammalian otoacoustic emissions, the salicylates and the aminoglyc
121 the recovery of odd-order distortion product otoacoustic emissions.
122 itive, sharply tuned hearing and spontaneous otoacoustic emissions.
123 t of middle-ear immittance, and recording of otoacoustic emissions.
124 athways compared with previous studies using otoacoustic emissions.
125 s recordings of ear canal distortion product otoacoustic emissions.
126 conduction as well as numerous properties of otoacoustic emissions.
127 earing, sounds that are known as spontaneous otoacoustic emissions.
128  of the sensory input as well as spontaneous otoacoustic emissions.
129  stimulus, the inner ear emits sounds called otoacoustic emissions.
130 y brainstem responses and distortion product otoacoustic emissions.
131 oscillations that might underlie spontaneous otoacoustic emissions.
132 oltage, low-mid-frequency distortion-product-otoacoustic-emissions (DPOAEs), and passive basilar memb
133 computed tomography scans and ophthalmic and otoacoustic evaluations at the time of this investigatio
134                                          The otoacoustic measurements indicate that at low sound leve
135 a birth cohort in eastern Slovakia underwent otoacoustic testing at 45 months of age.
136 s were associated with poorer performance on otoacoustic tests at age 45 months.

 
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