ライフサイエンスコーパス: ototoxic

1 Cisplatin is widely used but highly ototoxic.

2 We used an ototoxic agent to produce complete vestibular receptor c

3 Gentamicin is a widely used ototoxic agent.

4 Prior work showed that uptake of ototoxic aminoglycosides (AG) into hair cells requires f

5 y, with the lead compound N1MS 17 times less ototoxic and with reduced penetration of hair cell mecha

6 were cultured in media supplemented with the ototoxic antibiotic neomycin and selected pharmacologica

7 olecule tenascin and that treatment with the ototoxic antibiotic streptomycin results in a nearly com

8 The addition of an ototoxic antibiotic to cultures, however, causes complet

9 In those studies, a laser microbeam or ototoxic antibiotics were used to damage the sensory epi

10 suggest that EHF thresholds and DPOAEs show ototoxic changes before hearing loss is detected by conv

11 wth to new and repaired hair cells following ototoxic damage.

12 ty of auditory nerve synapses in response to ototoxic deafening and chronic electrical stimulation of

13 ination further suggests that the effects of ototoxic deafness are not identical to those of heredita

14 Kittens were bilaterally deafened by an ototoxic drug administered daily for 2 weeks immediately

15 the CN in adult cats deafened as neonates by ototoxic drug administration.

16 ed human embryonic kidney 293 cells with the ototoxic drug cisplatin markedly enhanced superoxide pro

17 s of age and under the administration of the ototoxic drug cisplatin.

18 tory function after hair cell loss caused by ototoxic drug damage or acoustic overstimulation, indica

19 its that commonly accompany aging, tinnitus, ototoxic drug exposure or noise damage.

20 on of heat shock protein 70 (HSP70) inhibits ototoxic drug-induced hair cell death.

21 would induce HSPs in the cochlea and inhibit ototoxic drug-induced hearing loss.

22 o preparation allows for detailed studies of ototoxic-drug-induced hair cell death in an adult mammal

23 Two major classes of ototoxic drugs are cisplatin and the aminoglycoside anti

24 who are receiving concomitantly administered ototoxic drugs are particularly at risk for developing h

25 Ototoxic drugs include the aminoglycoside antibiotics an

26 gets, the inner hair cells (IHCs): following ototoxic drugs or acoustic overexposure, IHC death is ra

27 For example, following exposure to noise, ototoxic drugs or age, it would be highly desirable to a

28 Hair cells die after acoustic trauma, ototoxic drugs or aging diseases, leading to progressive

29 Ototoxic drugs stimulate cell proliferation in adult rat

30 erapies against hair cell damage (e.g., from ototoxic drugs) through targeted stimulation of S1PR2.

31 tion of the organ of Corti, acoustic trauma, ototoxic drugs, and hereditary deafness.

32 nts should be urged to avoid noise exposure, ototoxic drugs, and other factors that further damage he

33 onditioning protects against both classes of ototoxic drugs, and they suggest that sound therapy hold

34 tem, sensory cell loss resulting from aging, ototoxic drugs, infections, overstimulation and other ca

35 Ototoxic drugs, such as platinum-based chemotherapeutics

36 hen HCs are irreversibly damaged by noise or ototoxic drugs, surrounding SCs seal the epithelial surf

37 l of IHC loss that does not involve noise or ototoxic drugs.

38 variety of insults like acoustic trauma and ototoxic drugs.

39 cells are susceptible to acoustic trauma and ototoxic drugs.

40 ing loss and balance problems in response to ototoxic drugs.

41 oustic over-stimulation or administration of ototoxic drugs.

42 Cisplatin-induced ototoxic effects are an important complication that affe

43 ed with protection against cisplatin-induced ototoxic effects in 2 independent cohorts (combined coho

44 c variants associated with cisplatin-induced ototoxic effects in adult testicular cancer patients.

45 The mechanism for the ototoxic effects of DFMO remains uncertain.

46 Our data additionally suggest that ototoxic effects of organotins can derive from their dis

47 results point to new biology underlying the ototoxic effects of platinum agents.

48 Cisplatin-induced ototoxic effects were independently diagnosed by 2 audio

49 inhibitor, prevents murine cisplatin-induced ototoxic effects, the findings from this study have impo

50 vidence has suggested that heavy metals have ototoxic effects, yet few epidemiological studies have i

51 16A5 in the development of cisplatin-induced ototoxic effects.

52 nd potentially lead to strategies to prevent ototoxic effects.

53 atin remains severely limited because of its ototoxic effects.

54 ants that were significantly associated with ototoxic effects.

55 g variation in SLC16A5 and cisplatin-induced ototoxic effects.

56 Cisplatin-induced ototoxic effects.

57 lls, is their ability to survive in a highly ototoxic environment.

58 This ototoxic hair cell death is prevented by broad-spectrum

59 we observed no recovery of hair cells after ototoxic injury caused by cisplatin.

60 or caspase activation in hair cell death and ototoxic injury that can be reduced by concurrent treatm

61 beta-tectorin and SCA--is reduced following ototoxic injury.

62 tibular organs of birds can regenerate after ototoxic injury.

63 sory hair cells die after acoustic trauma or ototoxic insults, but the signal transduction pathways t

64 erapeutic value in hair cell protection from ototoxic insults.

65 w-up, and audiologic testing for potentially ototoxic investigational agents.

66 Following ototoxic lesion with the aminoglycoside gentamicin, the

67 f organ of Corti explants challenged with an ototoxic level of an inflammatory cytokine modulates NFk

68 hearing impairment, such as noise exposure, ototoxic medication use, and smoking (adjusted odds rati

69 Risk factors include hearing loss, ototoxic medication, head injury, and depression.

70 ical or accidental trauma, administration of ototoxic medications, local or systemic infections, vasc

71 umour necrosis factor alpha (TNFalpha) as an ototoxic molecule and fibroblast growth factor 2 (FGF2)

72 of mature birds regenerate hair cells after ototoxic or acoustic insult.

73 obramycin was not associated with detectable ototoxic or nephrotoxic effects or with accumulation of

74 nthesis, which in turn correlates with their ototoxic potential in both murine cochlear explants and

75 inase (JNK) pathway correlated well with its ototoxic potential.

76 Therapeutic drugs with ototoxic side effects cause significant hearing loss for

77 eath from exposure to therapeutic drugs with ototoxic side effects, including aminoglycoside antibiot

78 ycoside antibiotics, such as kanamycin, have ototoxic side effects, which often result in degeneratio

79 ys initiated by neurotrophin-deprivation and ototoxic stress (e.g., CDDP) have been shown to be diffe

80 unlikely primary cause of hair cell death in ototoxic stress situations.