ライフサイエンスコーパス: ototoxicity

1 ationships between the different measures of ototoxicity.

2 acteristics on the incidence and severity of ototoxicity.

3 eventive strategy for iatrogenically induced ototoxicity.

4 seizure disorders, and 20% developed severe ototoxicity.

5 herapy had less long-term renal toxicity and ototoxicity.

6 nancy, metastatic disease, renal disease, or ototoxicity.

7 in the intact epithelium or after gentamicin ototoxicity.

8 ganglia of chinchillas following gentamicin ototoxicity.

9 redict this aspect of aminoglycoside-induced ototoxicity.

10 A repair in the protection against cisplatin ototoxicity.

11 R agonists could effectively treat cisplatin ototoxicity.

12 -dependent mechanism contributes to HPbetaCD ototoxicity.

13 t interrupted for one dose, based on grade 1 ototoxicity.

14 ic target for attenuating cisplatin-mediated ototoxicity.

15 therapeutic target for preventing cisplatin ototoxicity.

16 bution of DNA repair mechanisms to cisplatin ototoxicity.

17 ted with hypersusceptibility to drug-induced ototoxicity.

18 c protein synthesis inhibition to AG-induced ototoxicity.

19 cts in patients, including most prominently, ototoxicity.

20 everal potential therapeutic targets to stem ototoxicity.

21 pathologic conditions-such as presbycusis or ototoxicity.

22 rategies to prevent and treat aminoglycoside ototoxicity.

23 tration of Lmo4 influences cisplatin-induced ototoxicity.

24 ularis, which are known targets of cisplatin ototoxicity.

25 ement in the identification of patients with ototoxicity.

26 ctivity can be dissected from aminoglycoside ototoxicity.

27 al ribosome (mitoribosome) in aminoglycoside ototoxicity.

28 also capable of regeneration after cisplatin ototoxicity.

29 o regenerate hair cells after aminoglycoside ototoxicity.

30 teria for identifying clinically significant ototoxicity.

31 useful strategy for prevention of cisplatin ototoxicity.

32 ve as a novel approach in treating cisplatin ototoxicity.

33 (9%) of 45 evaluable patients had grade 3-4 ototoxicity according to Pediatric Oncology Group ototox

34 n this report suggest that cisplatin-induced ototoxicity and cochlear uptake can be modulated by admi

35 te gene for susceptibility to aminoglycoside ototoxicity and for the autosomal dominant deafness gene

36 h a newly developed mouse model of cisplatin ototoxicity and found that preconditioning mouse inner e

37 ackground plays a role in the aminoglycoside ototoxicity and in the development of the deafness pheno

38 We retrospectively assessed the incidence of ototoxicity and its risk factors in children with retino

39 of toxicity data (CTCAE) has under-reported ototoxicity and minimized the significance of hearing lo

40 s anticipated that this regimen could reduce ototoxicity and nephrotoxicity compared with cisplatin-c

41 Concerns of aminoglycoside-induced ototoxicity and nephrotoxicity have led to studies of al

42 ctive of antibacterial activity with reduced ototoxicity and systemic toxicity, was greater for the e

43 ppression, vomiting, sensory neuropathy, and ototoxicity and were worse with cisplatin.

44 her toxicities, such as renal insufficiency, ototoxicity, and nausea and vomiting, and neuropathy wer

45 Nine of these 10 patients had grade 3 or 4 ototoxicity, and nine patients were less than 6 months o

46 useful, they exhibit high nephrotoxicity and ototoxicity, and their overuse has led to the developmen

47 via mechanotransducer channels would reduce ototoxicity, and therefore we synthesized 9 aminoglycosi

48 ivery system when side effects and potential ototoxicities appear during treatment.

49 d in the in vivo guinea pig model of chronic ototoxicity, apramycin causes only little hair cell dama

50 national standards for grading and comparing ototoxicity are essential to the success of prospective

51 denosine (R-PIA) inhibited cisplatin-induced ototoxicity, as measured by auditory brainstem responses

52 primary outcome was cumulative incidence of ototoxicity at 3 years, graded with the Pediatric Oncolo

53 Twelve patients (20%) developed ototoxicity at some time after treatment initiation; how

54 ponse to injury caused by acoustic trauma or ototoxicity, but the nature of the interaction between m

55 1 receptor (A1AR) protects against cisplatin ototoxicity by suppressing an inflammatory response init

56 aspirin to ameliorate the nephrotoxicity and ototoxicity caused by cisplatin.

57 for the delayed emergence of aminoglycoside ototoxicity, changes in lysosomal activities in cochlear

58 tives of our study were to compare different ototoxicity classification systems, to evaluate the feas

59 American Speech-Language-Hearing Association Ototoxicity Criteria (ASHA), Common Terminology Criteria

60 SIOP detected ototoxicity earlier than did the other scales.

61 doses of gentamicin cause nephrotoxicity and ototoxicity, entering the cell via the receptor megalin.

62 Their findings suggest a new way to reduce ototoxicity from therapeutic medications and raise large

63 verse Events, version 3.0 (CTCAE), and Brock Ototoxicity Grades (Brock).

64 Although both the Chang and CTCAE ototoxicity grades were significantly related to audiolo

65 Audiograms were classified by the Chang Ototoxicity Grading Scale.

66 We present a new ototoxicity grading system that has clearly defined and

67 The different ototoxicity grading systems showed good overall agreemen

68 There is no consensus regarding optimal ototoxicity grading.

69 Prevalence of platinum-related ototoxicity has ranged from 13% to 95% in previous repor

70 STS decreased carboplatin-induced ototoxicity in a guinea pig model, as determined by elec

71 ed for hearing aids (defined as >or= grade 3 ototoxicity in one ear) compared with a control group (n

72 hree (7%) of 45 patients developed grade 3-4 ototoxicity in one ear, although one later reverted to g

73 can significantly reduce the risk of severe ototoxicity in patients with AR medulloblastoma receivin

74 SHA, Brock, and CTCAE scales for classifying ototoxicity in pediatric patients who were treated with

75 e 32 children, 20 (62.5%) acquired bilateral ototoxicity in the conventional frequency range during c

76 audiometry results, 16 (94.1%) had bilateral ototoxicity in the EHF range.

77 f an influx copper transporter, CTR1, in the ototoxicity induced by cisplatin, a potent anticancer pl

78 Ototoxicity is a common side effect of cisplatin therapy

79 Ototoxicity is a main dose-limiting factor in the clinic

80 t the hypothesis that aminoglycoside-induced ototoxicity is, in part, an excitotoxic process involvin

81 Although ototoxicity may be a tolerable side effect of anticancer

82 l in vitro, suggesting that HPbetaCD-induced ototoxicity may involve disruption of this interaction.

83 cancer or antimicrobial therapy, even modest ototoxicity may not be acceptable in agents developed fo

84 Cisplatin ototoxicity may result from oxidative stress, DNA damage

85 distortion product otoacoustic emissions for ototoxicity monitoring in children.

86 Cisplatin-induced neurotoxicity and ototoxicity (NTX) are important adverse effects after ch

87 s that ranged from 324 to 660 mg/m2; grade 3 ototoxicity occurred in three patients at cumulative cis

88 Aminoglycoside ototoxicity occurs both in a sporadic dose-dependent and

89 Recent studies reported ototoxicity of 2-hydroxypropyl- beta-cyclodextrin (HPbet

90 Here, we show that the ototoxicity of DFMO may be mediated by alteration of the

91 region, implicating prestin's involvement in ototoxicity of HPbetaCD.

92 f fractalkine signaling after aminoglycoside ototoxicity or acoustic trauma.

93 No ototoxicity or nephrotoxicity was detected.

94 tion of platinum-associated neurotoxicity or ototoxicity or paclitaxel-associated neuropathy, prevent

95 He had no symptoms of ototoxicity or peripheral neurotoxicity.

96 No significant nephrotoxicity, ototoxicity, or cumulative neurologic toxicity was obser

97 nificantly fewer patients with any or severe ototoxicity ( P < .001 for both).

98 with CTCAE, SIOP detected significantly more ototoxicity ( P = .004), whereas Brock criteria detected

99 oped oliguric renal failure, hepatotoxicity, ototoxicity, peripheral neuropathy, blindness, and sever

100 studies have led to the hypothesis that the ototoxicity produced by aminoglycoside antibiotics invol

101 nt progressive neurodegeneration exacerbates ototoxicity, pulmonary toxicity and autophagy-based cell

102 f treatment, the prevalence of any degree of ototoxicity ranged from 40% to 56%, and severe ototoxici

103 otoxicity ranged from 40% to 56%, and severe ototoxicity ranged from 7% to 22%.

104 tially required to protect against cisplatin ototoxicity, relative to global genome repair-specific e

105 of the mechanisms underlying aminoglycoside ototoxicity remains limited.

106 Carboplatin-induced ototoxicity remains poorly defined but is of potential g

107 ostine-treated patients had at least grade 3 ototoxicity, requiring hearing aid in at least one ear.

108 me time after treatment initiation; however, ototoxicity resolved in two patients, and thus,10 patien

109 s in ACYP2 associated with cisplatin-related ototoxicity (rs1872328: P = 3.9 x 10(-8), hazard ratio =

110 rs, graded with the Pediatric Oncology Group ototoxicity scale (0-4), in the intention-to-treat popul

111 for Industrial and Organizational Psychology Ototoxicity Scale (SIOP).

112 xicity according to Pediatric Oncology Group ototoxicity scale in both ears at follow-up, and three (

113 he new internationally agreed-on SIOP Boston ototoxicity scale in current and future otoprotection tr

114 Pediatric Oncology Group hearing ototoxicity score at a follow-up of 5.0 years (IQR 2.9-6

115 precipitous hearing loss and was related to ototoxicity severity.

116 ted research toward autoimmune hearing loss, ototoxicity, spiral ganglion survival, and genetic forms

117 ocess when side effects or treatment-related ototoxicities start to occur, providing a novel and sali

118 stemic carboplatin had a higher incidence of ototoxicity than previously reported.

119 start of treatment) were more likely to have ototoxicity than were older patients.

120 of aminoglycoside antibiotics is limited by ototoxicity that can produce permanent hearing loss.

121 only used antineoplastic agent that produces ototoxicity that is mediated in part by increasing level

122 polychlorinated biphenyls (PCBs) may induce ototoxicity, though results of previous epidemiologic st

123 were analyzed to determine the incidence of ototoxicity using the American Speech-Language-Hearing A

124 Ototoxicity was evaluated by three different grading sys

125 rence of hematologic, renal, neurologic, and ototoxicity was evaluated.

126 Grade 3, reversible ototoxicity was the DLT in less-heavily pretreated patie

127 Neutropenia and ototoxicity were dose-limiting.

128 ated with nephrotoxicity, neurotoxicity, and ototoxicity, which has hindered its utility.

129 o represent clinical hearing loss induced by ototoxicity with regard to the impact on speech and lang

130 n, all 9 derivatives displayed no or reduced ototoxicity, with the lead compound N1MS 17 times less o

131 Reducing cisplatin and high-dose carboplatin ototoxicity without reducing efficacy is important.