ライフサイエンスコーパス: DPOAE

1 DPOAE amplitudes and CS of DPOAEs were collected for C57

2 DPOAE and ABR exhibited an increasing threshold at high

3 DPOAE results correlated with age.

4 decreased neural responses without affecting DPOAEs (at low frequencies).

5 At 45 months of age, DPOAEs were assessed at 11 frequencies in both ears.

6 changes in Aqp4 gene expression and ABR and DPOAE hearing status in the cochlea and auditory midbrai

7 ocedure with or without the canalostomy, and DPOAE thresholds were elevated reversibly during the sal

8 Screening with otoscopy, tympanometry, and DPOAE is an efficient and sensitive way to identify pati

9 At high frequencies, both ABRs and DPOAEs were attenuated by loss of M2 and/or M4, and the

10 een PCB concentrations at different ages and DPOAEs, adjusting for potential confounders.

11 EHF audiometry and DPOAEs have the potential to reveal earlier changes in a

12 Pilot data suggest that EHF thresholds and DPOAEs show ototoxic changes before hearing loss is dete

13 by distortion product otoacoustic emission (DPOAE) analysis.

14 by distortion product otoacoustic emission (DPOAE) and auditory brainstem response (ABR) thresholds

15 the distortion product otoacoustic emission (DPOAE) and the cochlear whole-nerve action potential (CA

16 Distortion product otoacoustic emission (DPOAE) assay and acoustic brainstem evoked response (ABR

17 sed distortion product otoacoustic emission (DPOAE) measurements to monitor cochlear activity during

18 Distortion product otoacoustic emission (DPOAE) testing was performed on 97.4% of ears.

19 d distortion-product otoacoustic emission -- DPOAE magnitudes), and were clustered into four groups b

20 2) distortion product otoacoustic emissions (DPOAE) at the start of the study (baseline) and at time-

21 f2 distortion product otoacoustic emissions (DPOAE) measurements to refine the hearing loss phenotype

22 or distortion product otoacoustic emissions (DPOAE) or is being challenged by a noise exposure.

23 nd distortion product otoacoustic emissions (DPOAE) to assess hearing recovery in FVB/nJ mice exposed

24 of distortion product otoacoustic emissions (DPOAEs) in humans and CBA mice.

25 ed distortion product otoacoustic emissions (DPOAEs) were conducted for 32 patients age 8 months to 2

26 nd distortion product otoacoustic emissions (DPOAEs) were unaffected by loss of Gq-coupled receptors

27 by distortion product otoacoustic emissions (DPOAEs), and to further clarify the critical periods in

28 y, distortion-product otoacoustic emissions (DPOAEs), transient otoacoustic emissions, and the hearin

29 nd distortion product otoacoustic emissions (DPOAEs).

30 n [distortion product otoacoustic emissions (DPOAEs)].

31 cy distortion-product-otoacoustic-emissions (DPOAEs), and passive basilar membrane (BM) responses.

32 gnificantly younger than patients who failed DPOAE (60.0 +/- 16.6 yrs, p <.0001).

33 quantitative trait locus (QTL), Tmc1m1, for DPOAE amplitude on chromosome 2 in [(C/B)F1xC]N2-Tmc1Bth

34 For DPOAEs, the E+P group presented with lower (worse) level

35 the Cx26 cKO desensitizes mid-high-frequency DPOAEs and active BM responses and sensitizes low-mid-fr

36 However, DPOAE analysis reveals that some function is preserved i

37 .6-dB SPL (sound pressure level) decrease in DPOAE amplitude (95% CI: -2.6, -0.5; p = 0.003).

38 t, and 26 (81.3%) had bilateral decreases in DPOAE amplitudes and dynamic range.

39 d vulnerability in D2 knock-outs was seen in DPOAEs, suggesting a role for dopamine in the outer hair

40 ration of outer hair cells and diminution of DPOAE amplitudes but no difference in degeneration of in

41 DPOAE amplitudes and CS of DPOAEs were collected for C57s from 6 to 40 weeks of age

42 The mean age of passed DPOAE (44.2 +/- 16.2 yrs) was significantly younger than

43 s of age were associated with lower (poorer) DPOAE amplitudes.

44 measured levels of the auditory processing: DPOAE levels differed significantly between periods of v

45 current-level-dependent but less so for the DPOAE.

46 th small effects on isolated portions of the DPOAE spectrum.

47 trains and performed linkage analysis on the DPOAE data obtained from the second-generation populatio

48 By partitioning the DPOAE data into frequency subsets, we determined that Hf

49 -153 concentrations were not associated with DPOAEs at 45 months.