ライフサイエンスコーパス: ototoxicity

1 tration of Lmo4 influences cisplatin-induced ototoxicity.

2 ularis, which are known targets of cisplatin ototoxicity.

3 ement in the identification of patients with ototoxicity.

4 ctivity can be dissected from aminoglycoside ototoxicity.

5 al ribosome (mitoribosome) in aminoglycoside ototoxicity.

6 also capable of regeneration after cisplatin ototoxicity.

7 o regenerate hair cells after aminoglycoside ototoxicity.

8 teria for identifying clinically significant ototoxicity.

9 useful strategy for prevention of cisplatin ototoxicity.

10 ve as a novel approach in treating cisplatin ototoxicity.

11 ationships between the different measures of ototoxicity.

12 acteristics on the incidence and severity of ototoxicity.

13 eventive strategy for iatrogenically induced ototoxicity.

14 seizure disorders, and 20% developed severe ototoxicity.

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

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

17 in the intact epithelium or after gentamicin ototoxicity.

18 ganglia of chinchillas following gentamicin ototoxicity.

19 ent of congenital deafness and prevention of ototoxicity.

20 redict this aspect of aminoglycoside-induced ototoxicity.

21 AR), protects against noise and drug-induced ototoxicity.

22 naptic ribbons in a mouse model of kanamycin ototoxicity.

23 nd showed meaningful reductions in cisplatin ototoxicity.

24 rugs that prevent hearing loss, and test for ototoxicity.

25 elosuppression, nephropathy, neuropathy, and ototoxicity.

26 follow-up are needed to evaluate late-onset ototoxicity.

27 ole of cochlear ion transport in hearing and ototoxicity.

28 an effective biomarker of cisplatin-induced ototoxicity.

29 by either trauma, genetic mutations, or drug ototoxicity.

30 ility is curtailed by its nephrotoxicity and ototoxicity.

31 teins in this pathway, thereby mitigating AG ototoxicity.

32 the UPR can be targeted to prevent cisplatin ototoxicity.

33 herapeutic targets for preventing AG-induced ototoxicity.

34 ss using an in vivo mouse model of cisplatin ototoxicity.

35 tion to platinum-based chemotherapy mediated ototoxicity.

36 ials for the prevention of cisplatin-induced ototoxicity.

37 n should not be altered as a means to reduce ototoxicity.

38 expression is related to cisplatin-mediated ototoxicity.

39 ficulties in children with treatment-related ototoxicity.

40 uced inflammatory response and the resulting ototoxicity.

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

42 therapeutic target for preventing cisplatin ototoxicity.

43 A repair in the protection against cisplatin ototoxicity.

44 R agonists could effectively treat cisplatin ototoxicity.

45 -dependent mechanism contributes to HPbetaCD ototoxicity.

46 ic target for attenuating cisplatin-mediated ototoxicity.

47 n of the vulnerability to cisplatin-mediated ototoxicity.

48 bution of DNA repair mechanisms to cisplatin ototoxicity.

49 ted with hypersusceptibility to drug-induced ototoxicity.

50 c protein synthesis inhibition to AG-induced ototoxicity.

51 cts in patients, including most prominently, ototoxicity.

52 everal potential therapeutic targets to stem ototoxicity.

53 pathologic conditions-such as presbycusis or ototoxicity.

54 rategies to prevent and treat aminoglycoside ototoxicity.

55 The incidence of ototoxicity (250-8,000 Hz) was 85.0% in placebo-treated

56 of sensory hair cells during aminoglycoside ototoxicity, a common cause of acquired hearing loss.

57 (9%) of 45 evaluable patients had grade 3-4 ototoxicity according to Pediatric Oncology Group ototox

58 Ototoxicity after cisplatin administration was significa

59 edisposes to profound aminoglycoside-induced ototoxicity (AIO).

60 S17 represents a novel mediator of cisplatin ototoxicity and a potential therapeutic target for treat

61 of individual C-subtypes and impurities for ototoxicity and antimicrobial activity.

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

63 (1%) patient receiving RS8 developed serious ototoxicity and ended treatment after 6 weeks.

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

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

66 nderscore the critical role of GABARAP in AG ototoxicity and highlight its potential as a therapeutic

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

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

69 afish lateral line as an in vivo readout for ototoxicity and kidney cell-based nephrotoxicity assay,

70 are at highest risk of developing AG-induced ototoxicity and may help prioritize patients for AG-spar

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

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

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

74 acrophage ablation against cisplatin-induced ototoxicity and nephrotoxicity is mediated by reduced pl

75 ties for cisplatin administration, including ototoxicity and nephrotoxicity, impact the clinical util

76 cer drug with notable side effects including ototoxicity and nephrotoxicity.

77 nt strategy for mitigating cisplatin-induced ototoxicity and nephrotoxicity.

78 teraction between caffeine and cisplatin for ototoxicity and suggest that caffeine consumption should

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

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

81 splatin alone had considerable hearing loss (ototoxicity) and kidney injury (nephrotoxicity).

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

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

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

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

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

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

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

89 clinical practice guidelines for monitoring ototoxicity are essential.

90 The cellular mechanisms underlying cisplatin ototoxicity are poorly understood.

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

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

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

94 ent tympanostomy tubes, without resulting in ototoxicity at up to 24 weeks.

95 Despite ototoxicity being a prevalent consequence of cisplatin c

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

97 he eukaryotic ribosomes appears to result in ototoxicity, but there is evidence that other effects ar

98 n calcium homeostasis, increases the risk of ototoxicity by 4.61 (95% CI: 3.04-7.02; N = 696, p < 0.0

99 esult, the effects of PBM against GM-induced ototoxicity by increasing ATP levels and mitochondrial m

100 superfamily, mediates reduction of cisplatin ototoxicity by removing 4-hydroxynonenal (4-HNE) in the

101 1 receptor (A1AR) protects against cisplatin ototoxicity by suppressing an inflammatory response init

102 capsaicin (TRPV1 agonist) prevents cisplatin ototoxicity by sustained increased activation of pro-sur

103 e data suggest that RGS17 mediates cisplatin ototoxicity by uncoupling cytoprotective GPCRs from thei

104 adverse effects due to treatment, including ototoxicity, cardiotoxicity, delayed growth, and seconda

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

106 Despite their severe ototoxicity, causing irreversible hearing loss in millio

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

108 Cisplatin (CisPt)-induced ototoxicity (CIO) is delineated as a consequence of CisP

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

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

111 SIOP detected ototoxicity earlier than did the other scales.

112 es through study design and sample size, and ototoxicity endpoints should be harmonised to enhance co

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

114 hesis was tested in a rat model of cisplatin ototoxicity following oral administration of caffeine.

115 ies, to evaluate the quality of evidence for ototoxicity following platinum-based chemotherapy and he

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

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

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

119 Audiograms were classified by the Chang Ototoxicity Grading Scale.

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

121 The different ototoxicity grading systems showed good overall agreemen

122 There is no consensus regarding optimal ototoxicity grading.

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

124 development to prevent or reverse cisplatin ototoxicity have largely focused on pathways of oxidativ

125 iotherapy, or both have an increased risk of ototoxicity (hearing loss, tinnitus, or both).

126 earing loss after treatment met criteria for ototoxicity in 17 of the 44 ears (38.6%), with 11 of the

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

128 investigated the effect of PBM in GM-induced ototoxicity in auditory cells.

129 line for the prevention of cisplatin-induced ototoxicity in children and adolescents with cancer, we

130 both untoward effects of nephrotoxicity and ototoxicity in cisplatin-treated patients, two potential

131 n contrast, they showed different degrees of ototoxicity in cochlear explants, with gentamicin C2b be

132 tivity of propylamycin, resulting in reduced ototoxicity in guinea pigs.

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

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

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

136 for studies documenting the genetic risk of ototoxicity in patients with cancer treated with cisplat

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

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

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

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

141 Ototoxicity is a common side effect of cisplatin therapy

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

143 Ototoxicity is a potential immune-related adverse event

144 Ototoxicity is an irreversible direct and late effect of

145 are safe and effective for cisplatin-induced ototoxicity is important, especially in children because

146 Ototoxicity is one of the major side-effects of platinum

147 Cisplatin-induced ototoxicity is the result of cochlear hair cell damage t

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

149 Although ototoxicity may be a tolerable side effect of anticancer

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

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

152 Cisplatin ototoxicity may result from oxidative stress, DNA damage

153 ility, and the secondary end points included ototoxicity measured by air conduction audiometry.

154 distortion product otoacoustic emissions for ototoxicity monitoring in children.

155 s the severity of accompanying late effects (ototoxicity, neurotoxicity, cardiovascular disease, seco

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

157 Ototoxicity occurred in one (2%) patient.

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

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

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

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

162 -concept of drug reformulation to minimizing ototoxicity of gentamicin in patients.

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

164 f fractalkine signaling after aminoglycoside ototoxicity or acoustic trauma.

165 No ototoxicity or nephrotoxicity was detected.

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

167 He had no symptoms of ototoxicity or peripheral neurotoxicity.

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

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

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

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

172 cochlear explants confirm the low levels of ototoxicity predicted on the basis of selectivity at the

173 tribute to sound detection and localization, ototoxicity prevention, and speech comprehension.

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

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

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

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

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

179 its intracellular mechanism(s) in GM-induced ototoxicity remain poorly understood.

180 of the mechanisms underlying aminoglycoside ototoxicity remains limited.

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

182 e involvement of GLAST in cisplatin-mediated ototoxicity remains unknown.

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

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

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

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

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

188 (International Society of Pediatric Oncology Ototoxicity Scale [SIOP] Grade >=2).

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

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

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

192 precipitous hearing loss and was related to ototoxicity severity.

193 An effective treatment for cisplatin ototoxicity, sodium thiosulfate (STS), while beneficial

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

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

196 in radiotherapy, and formulate and harmonise ototoxicity surveillance recommendations for CAYA cancer

197 An Ototoxicity Task Force was formed under the umbrella of

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

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

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

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

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

203 can result from an array of factors, such as ototoxicity, trauma, genetics, and ageing.

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

205 Ototoxicity was assessed using the American Speech-Langu

206 Ototoxicity was defined by American Speech-Language-Hear

207 Ototoxicity was evaluated by three different grading sys

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

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

210 A mouse model with cisplatin-induced ototoxicity was used in addition to human samples from t

211 Neutropenia and ototoxicity were dose-limiting.

212 Neurocognitive changes and ototoxicity were monitored over time.

213 iple doses of caffeine exacerbated cisplatin ototoxicity which was associated with damage to OHCs and

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

215 ixtures of C-subtypes demonstrated decreased ototoxicity while maintaining antimicrobial activity, th

216 in the C4'-C6' region on ring I that reduced ototoxicity while preserving antimicrobial activity, thu

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

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

219 OP pathway with ISRIB can mitigate cisplatin ototoxicity without reducing anti-cancer cell effects, s

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