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1 uld help protect receptor-bearing cells from overstimulation.
2 to elevated sound levels and protection from overstimulation.
3 ified to be efficient or dampened to prevent overstimulation.
4 eir daily environments to reduce feelings of overstimulation.
5 ways, a common occurrence following acoustic overstimulation.
6 ful to hair cells themselves during cochlear overstimulation.
7 togenesis reduce cortical activity following overstimulation.
8 l's cuticular plate and protecting them from overstimulation.
9 in protecting the mu-opioid receptor against overstimulation.
10 ating the deleterious effects of sympathetic overstimulation.
11 olamine stimulation to simulate neurohumoral overstimulation.
12 cing hearing loss due to aminoglycosides and overstimulation.
13 on and protecting the cochleae from acoustic overstimulation.
14 ve process of the cochlea following acoustic overstimulation.
15 mpared at 6, 12, and 24 weeks after acoustic overstimulation.
16 ents were mild and associated with transient overstimulation.
17 tion and protects central immune organs from overstimulation.
18 in the chick basilar papilla after acoustic overstimulation.
19 f seconds) may protect the ear from acoustic overstimulation.
21 Chronic beta-adrenergic receptor (beta-AR) overstimulation, a hallmark of heart failure, is associa
22 ubtle stimuli, and greater susceptibility to overstimulation, all of which may impact well-being and
23 d MEN-associated tumors, but rather that RET overstimulation alone is enough to cause both phenotypes
25 ing ligand and recently suggested to control overstimulation and deletion of iNKT cells in alpha-gala
26 ting from aging, ototoxic drugs, infections, overstimulation and other causes is irreversible and lea
29 regulation of cochlear responses to acoustic overstimulation and that the modulation of MMP activity
30 iac stress-induction, one with isoproterenol overstimulation and the other with 5/6 nephrectomy-induc
31 ing TSHR antibodies are the cause of thyroid overstimulation and were originally called long-acting t
32 thelium, defined miRNA responses to acoustic overstimulation, and explored potential mRNA targets of
33 could inhibit Cox-2 expression during noise overstimulation; and could attenuate noise-induced heari
34 pression signature indicative of chronic TPO overstimulation as the underlying causative mechanism, d
37 urring elsewhere in the nephron, there being overstimulation by inappropriately elevated aldosterone
40 that the toxic effects of glutamate receptor overstimulation can be accounted for solely by calcium i
43 approximately 1.27 octaves at 6 weeks after overstimulation decreases substantially to DeltaCF appro
46 ons degenerate after injuries resulting from overstimulation, drugs, genetic mutations, and aging.
48 PD-1 in preserving TEX cell populations from overstimulation, excessive proliferation, and terminal d
49 eading to beta-adrenergic receptor (beta-AR) overstimulation in cardiac myocytes, is a key mechanism
52 s between SPS, triggers, and fluctuations of overstimulation in everyday life were examined using an
53 at the right place and time, to avoid toxic overstimulation in healthy tissues or incorrect programm
55 es in humans have found associations between overstimulation in infancy via excessive television view
56 ckers administered to counteract sympathetic overstimulation in patients with congestive heart failur
60 s caused by ototoxic drug damage or acoustic overstimulation, indicating that mechanisms exist to ree
66 wever, recent data revealed that sympathetic overstimulation is strongly related to mortality, and bl
67 al mechanism of hearing loss due to acoustic overstimulation is the generation of reactive oxygen spe
68 is via N-methyl-D-aspartate (NMDA) receptor overstimulation, leading to excess calcium influx and ox
69 Both aminoglycoside treatment and acoustic overstimulation led to the loss of hair cells as well as
72 lumns to a synchronized state upon temporary overstimulation of a single column and/or randomization
76 adds support to current theories which link overstimulation of cell-mediated immunity and exposure t
77 dopaminergic transmission by DAT blockers or overstimulation of D(2) receptors in normal mice have si
78 sed to explain findings that both under- and overstimulation of dopamine (DA) receptors in medial pre
86 lutamate-induced excitotoxicity, mediated by overstimulation of N-methyl-D-aspartate (NMDA) receptors
87 ordingly, homocysteine neurotoxicity through overstimulation of N-methyl-D-aspartate receptors may co
89 In this paper, we show that pathological overstimulation of neurons by glutamate plus carbachol d
92 , which in neurons subjected to pathological overstimulation of NMDA receptors (NMDARs) increased the
97 se-induced damage, however, is determined by overstimulation of primary auditory receptors, upstream
99 With a constraining wall near the orifice, overstimulation of regurgitant flow rates was noted and
100 is thought to bind to TRPV channels causing overstimulation of sensory neurons in the aphid feeding
101 ced exhaustion program serves to prevent the overstimulation of T cells and activation-induced cell d
103 isease-causing mutation, Kv3.3-G592R, causes overstimulation of Tank Binding Kinase 1 (Tbk1) in the c
104 onsistent with our previous observation that overstimulation of the activity of endogenous members of
105 s over the past 20 years to show how and why overstimulation of the amiloride-sensitive epithelial Na
106 of HIGM2 naive B cells result from premature overstimulation of the B-cell receptor prior to the germ
108 e toxin TSST-1 act as superantigens to cause overstimulation of the host immune system, leading to th
109 d to the undesirable effects associated with overstimulation of the immune system, whereas too weak a
110 racellular glutamate accumulation leading to overstimulation of the ionotropic glutamate receptors me
111 l6, Ccl2, and Tnfalpha, which depends on the overstimulation of the JNK1/c-Jun pathway by saturated f
113 otransmitter of the ine transporter and thus overstimulation of the motor neuron by this neurotransmi
116 rimarily by massive Ca2+ influx arising from overstimulation of the NMDA subtype of glutamate recepto
118 ra-deficient mice is probably due to chronic overstimulation of the proinflammatory pathway via IL-1,
122 ctivated through the cAMP signaling pathway, overstimulation of which during cholera leads to CFTR-me
125 avidity that enter a refractory state due to overstimulation or low avidity that are only partially s
126 portant therapies for disorders arising from overstimulation or overexpression of individual nitric o
127 e with detrimental effects produced by NMDAR overstimulation, persistent elevation of D-aspartate lev
128 he brain and Ang II receptor type 1 (AT(1)R) overstimulation produces vasoconstriction and inflammati
129 B subunit-containing NMDA receptors prevents overstimulation, resulting in neuroprotective effects.
130 these mechanisms are downregulated, so that overstimulation results in synaptic strengthening and el
131 unds, which may constitute a form of sensory overstimulation (SOS) that leads to cognitive and behavi
132 ponse to elevated activity driven by sensory overstimulation, then test how plasticity changes with a
133 n differentiates five distinct types, namely overstimulation (type alpha), hypersensitivity or immuno
134 rdiac myocytes, which may protect cells from overstimulation under high concentrations of catecholami
136 sitive individuals reported higher levels of overstimulation when auditory and visual stimuli were ra
137 We developed and tested a mouse model of overstimulation whereby p10 mice were subjected to audio
138 nsitive individuals reported lower levels of overstimulation with momentary pleasant auditory and vis
139 ing but becomes detrimental upon chronic JNK overstimulation, with important implications for chronic