ライフサイエンスコーパス: overstimulation

1 on and protecting the cochleae from acoustic overstimulation.

2 ve process of the cochlea following acoustic overstimulation.

3 olamine stimulation to simulate neurohumoral overstimulation.

4 mpared at 6, 12, and 24 weeks after acoustic overstimulation.

5 ents were mild and associated with transient overstimulation.

6 tion and protects central immune organs from overstimulation.

7 cing hearing loss due to aminoglycosides and overstimulation.

8 in the chick basilar papilla after acoustic overstimulation.

9 f seconds) may protect the ear from acoustic overstimulation.

10 uld help protect receptor-bearing cells from overstimulation.

11 Chronic sympathetic overstimulation, a hallmark of heart failure (HF), induc

12 Chronic beta-adrenergic receptor (beta-AR) overstimulation, a hallmark of heart failure, is associa

13 e receptor partial activation usually avoids overstimulation and also minimizes desensitization.

14 ing ligand and recently suggested to control overstimulation and deletion of iNKT cells in alpha-gala

15 ting from aging, ototoxic drugs, infections, overstimulation and other causes is irreversible and lea

16 ll function and prevents chronic immune cell overstimulation and proliferation.

17 regulation of cochlear responses to acoustic overstimulation and that the modulation of MMP activity

18 ing TSHR antibodies are the cause of thyroid overstimulation and were originally called long-acting t

19 thelium, defined miRNA responses to acoustic overstimulation, and explored potential mRNA targets of

20 could inhibit Cox-2 expression during noise overstimulation; and could attenuate noise-induced heari

21 pression signature indicative of chronic TPO overstimulation as the underlying causative mechanism, d

22 an important role in protecting neurons from overstimulation by excitatory neurotransmitters.

23 urring elsewhere in the nephron, there being overstimulation by inappropriately elevated aldosterone

24 Cardiac overstimulation by the sympathetic nervous system (SNS)

25 that the toxic effects of glutamate receptor overstimulation can be accounted for solely by calcium i

26 Noise overstimulation can induce loss of synaptic ribbons asso

27 approximately 1.27 octaves at 6 weeks after overstimulation decreases substantially to DeltaCF appro

28 nism may underlie the development of beta-AR overstimulation-dependent cardiac dysfunction.

29 ons degenerate after injuries resulting from overstimulation, drugs, genetic mutations, and aging.

30 PD-1 in preserving TEX cell populations from overstimulation, excessive proliferation, and terminal d

31 ion of pro-apoptotic cytochrome c after NMDA overstimulation in cultured hippocampal neurons.

32 mal function, suggesting a possible role for overstimulation in diseases of accumulation.

33 that counterbalance the deleterious beta1AR overstimulation in heart failure.

34 es in humans have found associations between overstimulation in infancy via excessive television view

35 ckers administered to counteract sympathetic overstimulation in patients with congestive heart failur

36 stimulated at 4:00 A.M., suggesting chronic overstimulation in vivo.

37 s caused by ototoxic drug damage or acoustic overstimulation, indicating that mechanisms exist to ree

38 e preconditioning reduced glutamate receptor overstimulation-induced neuronal injury/death.

39 Herein, we propose that CB overstimulation is involved in the etiology of IR and HT

40 wever, recent data revealed that sympathetic overstimulation is strongly related to mortality, and bl

41 al mechanism of hearing loss due to acoustic overstimulation is the generation of reactive oxygen spe

42 is via N-methyl-D-aspartate (NMDA) receptor overstimulation, leading to excess calcium influx and ox

43 Both aminoglycoside treatment and acoustic overstimulation led to the loss of hair cells as well as

44 The overstimulation makes Env-specific T lymphocytes more su

45 In sepsis, prolonged, sympathetic overstimulation may lead to vasopressor-refractory hypot

46 lumns to a synchronized state upon temporary overstimulation of a single column and/or randomization

47 This work suggests that overstimulation of acetylcholine receptors could disrupt

48 Our results indicate that overstimulation of alpha1BAR leads to apoptotic neurodeg

49 Overstimulation of CD14 by LPS can cause the often fatal

50 adds support to current theories which link overstimulation of cell-mediated immunity and exposure t

51 dopaminergic transmission by DAT blockers or overstimulation of D(2) receptors in normal mice have si

52 sed to explain findings that both under- and overstimulation of dopamine (DA) receptors in medial pre

53 Thus, overstimulation of ENaC by metabolic abnormalities in ob

54 Excitotoxicity resulting from overstimulation of glutamate receptors is a major cause

55 Excitoxicity caused by overstimulation of glutamate receptors is a major cause

56 practice, reduces neuronal injury caused by overstimulation of glutamate receptors.

57 Our findings establish that overstimulation of immune responses that are normally ne

58 lutamate-induced excitotoxicity, mediated by overstimulation of N-methyl-D-aspartate (NMDA) receptors

59 Neurotoxicity induced by overstimulation of N-methyl-D-aspartate (NMDA) receptors

60 ordingly, homocysteine neurotoxicity through overstimulation of N-methyl-D-aspartate receptors may co

61 While overstimulation of N-methyl-d-aspartate-type glutamate r

62 In this paper, we show that pathological overstimulation of neurons by glutamate plus carbachol d

63 ulating self antigen, it remains unclear how overstimulation of NKT cells is avoided.

64 , which in neurons subjected to pathological overstimulation of NMDA receptors (NMDARs) increased the

65 Here we show that overstimulation of NMDA receptors by relatively low conc

66 Given that overstimulation of NMDA receptors can cause cell death,

67 Overstimulation of NMDA receptors may increase intracell

68 Taken together, our studies show that overstimulation of NMDARs reduces AMPAR functions in cor

69 With a constraining wall near the orifice, overstimulation of regurgitant flow rates was noted and

70 onsistent with our previous observation that overstimulation of the activity of endogenous members of

71 s over the past 20 years to show how and why overstimulation of the amiloride-sensitive epithelial Na

72 e toxin TSST-1 act as superantigens to cause overstimulation of the host immune system, leading to th

73 d to the undesirable effects associated with overstimulation of the immune system, whereas too weak a

74 racellular glutamate accumulation leading to overstimulation of the ionotropic glutamate receptors me

75 l6, Ccl2, and Tnfalpha, which depends on the overstimulation of the JNK1/c-Jun pathway by saturated f

76 that flat affect in schizophrenia relates to overstimulation of the limbic system.

77 otransmitter of the ine transporter and thus overstimulation of the motor neuron by this neurotransmi

78 Overstimulation of the N-methyl-D-aspartate (NMDA) recep

79 mitter acetylcholine, potentially leading to overstimulation of the nervous system and death.

80 rimarily by massive Ca2+ influx arising from overstimulation of the NMDA subtype of glutamate recepto

81 Mechanical overstimulation of the patch or the cell from excessive

82 ra-deficient mice is probably due to chronic overstimulation of the proinflammatory pathway via IL-1,

83 ustrial, military, and recreational auditory overstimulation on hearing disability.

84 pensatory effect of repeated endocannabinoid overstimulation or an enduring trait-like feature.

85 avidity that enter a refractory state due to overstimulation or low avidity that are only partially s

86 portant therapies for disorders arising from overstimulation or overexpression of individual nitric o

87 e with detrimental effects produced by NMDAR overstimulation, persistent elevation of D-aspartate lev

88 he brain and Ang II receptor type 1 (AT(1)R) overstimulation produces vasoconstriction and inflammati

89 rdiac myocytes, which may protect cells from overstimulation under high concentrations of catecholami

90 Immediately after acoustic overstimulation, WDR1 mRNA was seen in supporting cells.

91 We developed and tested a mouse model of overstimulation whereby p10 mice were subjected to audio