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 amplitudes from 1.5 to 8 kHz using an f2 to f1 rat

3 DPOAE amplitudes, SNRs and distribution of categories di

4 DPOAE and ABR exhibited an increasing threshold at high

5 DPOAE results correlated with age.

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

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

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

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

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

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

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

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

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

15 d partially recovered much like WT mice, but DPOAEs showed faster recovery.

16 Ongoing efforts aim to develop DPOAEs, which reflects the ear's health, into diagnostic

17 by distortion product otoacoustic emission (DPOAE) analysis.

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

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

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

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

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

23 wer distortion product otoacoustic emission (DPOAE) thresholds, increased cell survival rates, more r

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

25 ), Distortion Product Otoacoustic Emissions (DPOAE) amplitudes, Signal to Noise Ratios (SNRs) and dis

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

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

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

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

30 he distortion product otoacoustic emissions (DPOAEs) and the auditory brainstem responses (ABRs) acro

31 er distortion product otoacoustic emissions (DPOAEs) compared with HIV-negative controls, but the deg

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

33 at distortion product otoacoustic emissions (DPOAEs) recovered before EP.

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

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

36 Distortion product otoacoustic emissions (DPOAEs), a readout of active, MET-dependent, non-linear

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

38 ed distortion product otoacoustic emissions (DPOAEs), suggesting an improved electromechanical "ampli

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

40 s, distortion product otoacoustic emissions (DPOAEs), tympanometry, and word recognition scores.

41 nd distortion product otoacoustic emissions (DPOAEs).

42 ed distortion product otoacoustic emissions (DPOAEs).

43 as distortion-product otoacoustic emissions (DPOAEs).

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

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

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

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

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

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

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

51 .6-dB SPL (sound pressure level) decrease in DPOAE amplitude (95% CI: -2.6, -0.5; p = 0.003).

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

53 Variations in DPOAE amplitudes were noted, potentially indicating earl

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

55 ) to 3.8 dB (95% CI, 6.03 to -1.99 dB) lower DPOAE amplitudes at 6 and 8 kHz bilaterally and 0.28 muV

56 ults, CLWH had slightly, but reliably, lower DPOAEs and ABR wave V amplitudes than HIV-negative contr

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

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

59 mutant animals showed reduced inhibition of DPOAEs by contralateral noise, consistent with a weaker

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

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

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

63 w to moderate intensity, which suggests that DPOAEs may be used clinically to provide location-specif

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

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

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

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

68 The DPOAEs failed to accurately report the variation of coch

69 With IP injection, the DPOAEs recovered fully, whereas the EP was reduced, but

70 cts the region from which IDPs contribute to DPOAEs at low to moderate intensity, which suggests that

71 ledge on the cochlear extent contributing to DPOAEs.

72 onic (LCM), was measured simultaneously with DPOAE and EP while using intraperitoneal (IP) and intrav

73 -153 concentrations were not associated with DPOAEs at 45 months.