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1          Cisplatin is widely used but highly ototoxic.
2 b being the least and gentamicin C2 the most ototoxic.
3                          Persons who had had ototoxic (7 participants) or idiopathic (1 participant)
4                                   We used an ototoxic agent to produce complete vestibular receptor c
5                  Gentamicin is a widely used ototoxic agent.
6      Our results show that dose reduction of ototoxic agents is a safe, effective treatment for these
7             Prior work showed that uptake of ototoxic aminoglycosides (AG) into hair cells requires f
8 e models, such as systemic administration of ototoxic aminoglycosides, yield inconsistent and variabl
9 fe-threatening infections; however, they are ototoxic and cause irreversible damage to cochlear hair
10 y, with the lead compound N1MS 17 times less ototoxic and with reduced penetration of hair cell mecha
11 chloride, metabolites, and drugs such as the ototoxic anti-cancer drug cisplatin, and explore its phy
12 were cultured in media supplemented with the ototoxic antibiotic neomycin and selected pharmacologica
13 olecule tenascin and that treatment with the ototoxic antibiotic streptomycin results in a nearly com
14                           The addition of an ototoxic antibiotic to cultures, however, causes complet
15       In those studies, a laser microbeam or ototoxic antibiotics were used to damage the sensory epi
16                          Cisplatin is highly ototoxic but widely used.
17          Cisplatin is widely used and highly ototoxic, but patient-reported functional impairment bec
18 sensus reached was that children who receive ototoxic cancer treatment (platinum agents, cranial irra
19 onitoring in children undergoing potentially ototoxic cancer treatment.
20  suggest that EHF thresholds and DPOAEs show ototoxic changes before hearing loss is detected by conv
21 indow membrane niche for infusion of a known ototoxic compound (sodium salicylate) at 50 nL/min for 2
22 ateral line following the application of the ototoxic compound copper.
23 nhanced upon treatment with experimental and ototoxic compounds.
24 ly in the chicken auditory epithelium during ototoxic damage and hair cell regeneration.
25 dult human utricle and its early response to ototoxic damage using bulk and single-cell RNA-sequencin
26 ges consistent with a capacity to respond to ototoxic damage within 24 hours and potentially initiate
27                              Four days after ototoxic damage, we identified newly regenerated, nascen
28 ls but undergo robust regeneration following ototoxic damage.
29 tic stress caused consistent and synergistic ototoxic damage.
30 wth to new and repaired hair cells following ototoxic damage.
31 ty of auditory nerve synapses in response to ototoxic deafening and chronic electrical stimulation of
32 ination further suggests that the effects of ototoxic deafness are not identical to those of heredita
33      Kittens were bilaterally deafened by an ototoxic drug administered daily for 2 weeks immediately
34 the CN in adult cats deafened as neonates by ototoxic drug administration.
35 ed human embryonic kidney 293 cells with the ototoxic drug cisplatin markedly enhanced superoxide pro
36 s of age and under the administration of the ototoxic drug cisplatin.
37 tory function after hair cell loss caused by ototoxic drug damage or acoustic overstimulation, indica
38 its that commonly accompany aging, tinnitus, ototoxic drug exposure or noise damage.
39  SSNHL, intermediate in the noise-damage and ototoxic drug groups, and smallest in the ARHL group.
40                               It is the most ototoxic drug in clinical use, resulting in permanent he
41 tigations, such as the real-time tracking of ototoxic drug transport into the cochleae.
42 on of heat shock protein 70 (HSP70) inhibits ototoxic drug-induced hair cell death.
43 would induce HSPs in the cochlea and inhibit ototoxic drug-induced hearing loss.
44 o preparation allows for detailed studies of ototoxic-drug-induced hair cell death in an adult mammal
45 neural hearing loss (SSNHL), (5) exposure to ototoxic drugs (carboplatin and/or cisplatin, vancomycin
46                         Two major classes of ototoxic drugs are cisplatin and the aminoglycoside anti
47 who are receiving concomitantly administered ototoxic drugs are particularly at risk for developing h
48                                              Ototoxic drugs include the aminoglycoside antibiotics an
49 gets, the inner hair cells (IHCs): following ototoxic drugs or acoustic overexposure, IHC death is ra
50    For example, following exposure to noise, ototoxic drugs or age, it would be highly desirable to a
51        Hair cells die after acoustic trauma, ototoxic drugs or aging diseases, leading to progressive
52                                              Ototoxic drugs stimulate cell proliferation in adult rat
53 erapies against hair cell damage (e.g., from ototoxic drugs) through targeted stimulation of S1PR2.
54 tion of the organ of Corti, acoustic trauma, ototoxic drugs, and hereditary deafness.
55 nts should be urged to avoid noise exposure, ototoxic drugs, and other factors that further damage he
56 onditioning protects against both classes of ototoxic drugs, and they suggest that sound therapy hold
57 ng loss are common results of treatment with ototoxic drugs, including the widely used aminoglycoside
58 alance deficits that arise when loud sounds, ototoxic drugs, infections, and aging cause hair cell lo
59 deficits.SIGNIFICANCE STATEMENT Loud sounds, ototoxic drugs, infections, and aging kill sensory hair
60 tem, sensory cell loss resulting from aging, ototoxic drugs, infections, overstimulation and other ca
61                                              Ototoxic drugs, such as platinum-based chemotherapeutics
62 hen HCs are irreversibly damaged by noise or ototoxic drugs, surrounding SCs seal the epithelial surf
63 tested in animals after exposure to noise or ototoxic drugs, which can cause deficits beyond synaptop
64 ding loud noise, aging, genetic defects, and ototoxic drugs.
65  variety of insults like acoustic trauma and ototoxic drugs.
66 l of IHC loss that does not involve noise or ototoxic drugs.
67 cells are susceptible to acoustic trauma and ototoxic drugs.
68 ing loss and balance problems in response to ototoxic drugs.
69 oustic over-stimulation or administration of ototoxic drugs.
70 ed with a decreased risk of platinum-induced ototoxic effects among patients treated with platinum-in
71                             Platinum-induced ototoxic effects are a significant issue because platinu
72                            Cisplatin-induced ototoxic effects are an important complication that affe
73                     Relative risks (RRs) for ototoxic effects development and hemopoietic event devel
74 ng platinum-based chemotherapy that compared ototoxic effects development between patients who receiv
75 tatistically significantly decreased risk of ototoxic effects during the course of platinum-based che
76 ed with protection against cisplatin-induced ototoxic effects in 2 independent cohorts (combined coho
77 c variants associated with cisplatin-induced ototoxic effects in adult testicular cancer patients.
78                        The mechanism for the ototoxic effects of DFMO remains uncertain.
79           Our data additionally suggest that ototoxic effects of organotins can derive from their dis
80  results point to new biology underlying the ototoxic effects of platinum agents.
81 t that concurrent STS for protection against ototoxic effects should be considered for patients indic
82 ctant for the prevention of platinum-induced ototoxic effects that functions by binding the platinum-
83                            No nephrotoxic or ototoxic effects were detected after intravenous gentami
84                            Cisplatin-induced ototoxic effects were independently diagnosed by 2 audio
85 n patients' skin and assessments for safety (ototoxic effects, nephrotoxic effects, and autoimmune re
86   All 5 patients completed the study, and no ototoxic effects, nephrotoxic effects, or anti-laminin 3
87 inhibitor, prevents murine cisplatin-induced ototoxic effects, the findings from this study have impo
88 vidence has suggested that heavy metals have ototoxic effects, yet few epidemiological studies have i
89 rapeutic agent cisplatin is renowned for its ototoxic effects.
90 16A5 in the development of cisplatin-induced ototoxic effects.
91 nd potentially lead to strategies to prevent ototoxic effects.
92 ants that were significantly associated with ototoxic effects.
93 g variation in SLC16A5 and cisplatin-induced ototoxic effects.
94                            Cisplatin-induced ototoxic effects.
95 atin remains severely limited because of its ototoxic effects.
96 lls, is their ability to survive in a highly ototoxic environment.
97 s responded similarly to mice > 3 weeks from ototoxic exposure with decreased levels of prestin in th
98 his ototoxin alters the sensitivity to other ototoxic exposures later in life.
99 isk factors for HL in patients with multiple ototoxic exposures.
100 challenged by damage from a variety of other ototoxic factors, including loud noise, aging, genetic d
101                                         This ototoxic hair cell death is prevented by broad-spectrum
102  we observed no recovery of hair cells after ototoxic injury caused by cisplatin.
103 or caspase activation in hair cell death and ototoxic injury that can be reduced by concurrent treatm
104 he utricles of neonatal or mature mice after ototoxic injury.
105  beta-tectorin and SCA--is reduced following ototoxic injury.
106 tibular organs of birds can regenerate after ototoxic injury.
107 sory hair cells die after acoustic trauma or ototoxic insults, but the signal transduction pathways t
108 uildup is thought to sensitize hair cells to ototoxic insults, including the antibiotic neomycin.
109 erapeutic value in hair cell protection from ototoxic insults.
110 w-up, and audiologic testing for potentially ototoxic investigational agents.
111                                    Following ototoxic lesion with the aminoglycoside gentamicin, the
112 f organ of Corti explants challenged with an ototoxic level of an inflammatory cytokine modulates NFk
113  hearing impairment, such as noise exposure, ototoxic medication use, and smoking (adjusted odds rati
114           Risk factors include hearing loss, ototoxic medication, head injury, and depression.
115 loss cases were among those with exposure to ototoxic medications (19.6 million [range 12.6 million-2
116 tabolic causes of pulsatile tinnitus include ototoxic medications and systemic causes of high cardiac
117  that is attributable to disease sequelae or ototoxic medications contributes substantially to the gl
118 ical or accidental trauma, administration of ototoxic medications, local or systemic infections, vasc
119 nital rubella syndrome, cytomegalovirus, and ototoxic medications, specifically aminoglycosides, plat
120 umour necrosis factor alpha (TNFalpha) as an ototoxic molecule and fibroblast growth factor 2 (FGF2)
121  of mature birds regenerate hair cells after ototoxic or acoustic insult.
122 obramycin was not associated with detectable ototoxic or nephrotoxic effects or with accumulation of
123 nthesis, which in turn correlates with their ototoxic potential in both murine cochlear explants and
124 inase (JNK) pathway correlated well with its ototoxic potential.
125 onstrate the efficacy of a 6-week subchronic ototoxic protocol in inducing transient and partial vest
126 , in order to identify additional markers of ototoxic risk associated with platinum-based chemotherap
127  helps reassure patients about the immediate ototoxic risks while highlighting the need for continued
128                       Therapeutic drugs with ototoxic side effects cause significant hearing loss for
129 eath from exposure to therapeutic drugs with ototoxic side effects, including aminoglycoside antibiot
130 ycoside antibiotics, such as kanamycin, have ototoxic side effects, which often result in degeneratio
131 lycoside antibiotic whose use is hampered by ototoxic side-effects.
132 ys initiated by neurotrophin-deprivation and ototoxic stress (e.g., CDDP) have been shown to be diffe
133 unlikely primary cause of hair cell death in ototoxic stress situations.
134  the need to investigate factors beyond age, ototoxic substances, and recreational noise- factors aff
135 nnel, with the stronger the binding the less ototoxic the compound.
136 nic and can be cytotoxic, nephrotoxic and/or ototoxic, which has limited their clinical development.

 
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