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1 propagates toward the CNS, thus shaping the pain sensation.
2 iving increasing attention as a modulator of pain sensation.
3 ey it to supraspinal brain regions to induce pain sensation.
4 pain pathway that lead to persistence of the pain sensation.
5 RPalpha have long been thought important for pain sensation.
6 nsory cortex represent the ongoing status of pain sensation.
7 ng ion conduction, and resulting in elevated pain sensation.
8 plays little role in either acute or chronic pain sensation.
9 g noxious stimuli, is crucial in determining pain sensation.
10 ning, fear behaviors, neurodegeneration, and pain sensation.
11 crobiota is required for the normal visceral pain sensation.
12 r loss of function as the basis for impaired pain sensation.
13 n regulate spinal nociceptive processing and pain sensation.
14 hannels mediate temperature transduction and pain sensation.
15 pivotal for TRPV1 activation and subsequent pain sensation.
16 ic with the maladaptive coping of the PAG to pain sensation.
17 performance of PANs with significantly less pain sensation.
18 d subsequent neuronal activation, leading to pain sensation.
19 TRPA1 and TRPV1 are ion channels crucial for pain sensation.
20 ical variables, including blood pressure and pain sensation.
21 t mechanical stimuli that generate touch and pain sensation.
22 r paddle of NaV1.7, the subtype critical for pain sensation.
23 he complex molecular processes that underlie pain sensation.
24 therapy in CP to attenuate both fibrosis and pain sensation.
25 V1) channels, membrane receptors involved in pain sensation.
26 neurodegeneration after ischemic stroke, and pain sensation.
27 pathetic neurons underlies distinct types of pain sensation.
28 for probing molecular mechanisms underlying pain sensation.
29 proton-gated channels that are important for pain sensation.
30 contrast retain normal touch and mechanical pain sensation.
31 ctively participate in acute temperature and pain sensation.
32 ands such as capsaicin, leading to a burning pain sensation.
33 e role voltage-gated sodium channels play in pain sensation.
34 n the nociceptive system, leading to reduced pain sensation.
35 ved in processing the affective component of pain sensation.
36 nsory neurons, mediates inflammatory thermal pain sensation.
37 hat described in somatic pathways regulating pain sensation.
38 uli or to low pH to mediate normal touch and pain sensation.
39 ed in modulating moderate- to high-intensity pain sensation.
40 led to VR1 being considered as important for pain sensation.
41 n catastrophizing is an exaggerated focus on pain sensations.
42 Nav1.8 is crucial for pain sensations.
43 apeutic target for the treatment of aberrant pain sensations.
44 olecules are important for modality specific pain sensations.
45 ations versus those with predominantly acute pain sensations.
46 oupings of scans associated with deqi versus pain sensations.
47 sential first step for eliciting thermal and pain sensations.
48 on channel that plays a key role in enhanced pain sensation after inflammation, but directly blocking
49 volumes within brain regions associated with pain sensation and affective processing, which may refle
50 NT Despite their critical role in both acute pain sensation and chronic pain, little is known of the
51 frequent infections, attributed to a lack of pain sensation and failure to seek care for minor injuri
52 VR1 is essential for selective modalities of pain sensation and for tissue injury-induced thermal hyp
53 chomotor behaviors, anxiety, depression, and pain sensation and in the rewarding effects of alcohol a
54 irectly stimulate sensory neurons leading to pain sensation and modulation of immune system have high
55 All patients tested had alterations of cold pain sensation and tactile sensation, as measured by von
56 a nonselective cation channel that mediates pain sensations and is commonly activated by a wide vari
57 into contact with the body, evoking touch or pain sensations and possibly triggering an approach or e
58 sory and sympathetic neurons abolishes these pain sensations and recapitulates the pain-free phenotyp
60 ss of VGLUT3 specifically impairs mechanical pain sensation, and in particular the mechanical hyperse
61 heat-sensitive ion channel also involved in pain sensation, and is the receptor for capsaicin, the a
62 l roles, involving fear behaviors, learning, pain sensation, and neurodegeneration after stroke, make
66 s is highlighted by their roles in touch and pain sensation as well as in cardiovascular and respirat
67 confirms the involvement of this channel in pain sensation, as well as in hypersensitivity to noxiou
68 1.7 is believed to be a critical mediator of pain sensation based on clinical genetic studies and pha
69 ot appear to play a major role in mechanical pain sensation, because the stimulus-response function o
73 0 as a critical regulator of nociception and pain sensation by modulating TRP channels expression in
74 reatly assist pain-sensitive human to reduce pain sensation by normalizing hyperexcitable central neu
78 t, capsaicin, which evokes a mix of itch and pain sensations, enhances both excitatory and inhibitory
79 ical situations such as learning and memory, pain sensation, fear and anxiety, substance abuse and ce
81 nately deqi sensation grouping and the acute pain sensation grouping (deqi>pain contrast), only negat
83 physiological processes, including touch and pain sensation, hearing, and blood pressure regulation.
84 rimental focal neuritis produces neuropathic pain sensations (heat- and mechano-hyperalgesia, and col
85 fic antagonist, TAK-242, attenuated visceral pain sensation in animals with functional TLR4 when admi
86 gated sodium channel, Nav1.7, is critical to pain sensation in mammals, pharmacological inhibitors of
87 ociceptive responses are used as measures of pain sensation in newborn humans, as they are in animals
88 the cardiovascular and immune systems and in pain sensation in peripheral systems through their inter
89 ciceptors showed a defect in nociception and pain sensation in response to thermal, mechanical and in
90 acetylation of genes that regulate visceral pain sensation in the peripheral nervous system of rats.
91 y, in a spinal cord-injured patient who lost pain sensation in the right leg, proprioception and sngc
93 better match the psychophysics of mechanical pain sensations in humans than the discharge of the HPC
94 bditis elegans As capsaicin elicits heat and pain sensations in mammals, transgenic TRPV1 worms exhib
95 imulus intensity and alters the magnitude of pain sensations in the direction of the trend of increas
96 e mammalian capsaicin receptor implicated in pain sensation; in AWC olfactory neurons, ODR-3 may inte
97 cal studies show serial interactions between pain sensation intensity, pain unpleasantness, and secon
99 uli are applied to primate hairy skin, first pain sensation is mediated by type-II A-fibre nociceptor
102 sociated with physiological and pathological pain sensation, making presynaptic P2X receptors a possi
103 ains unresolved whether changes in one's own pain sensation may affect empathic responding to others'
105 esses, including mindful reinterpretation of pain sensations, nonreactivity, savoring, positive atten
109 -expressed sodium channel with a key role in pain sensation, shows strong protection against migraine
110 trahydrocannabinol (delta-9-THC), may reduce pain sensation, studies of humans have produced inconsis
111 ium channels (Navs) can cause alterations in pain sensation, such as chronic pain diseases like inher
112 uides avoidance of ingestion of toxins while pain sensations, such as noxious heat, signal adverse co
113 e for a genotype-dependent influence on cold pain sensation suggesting that carriers of the reduced m
114 ain levels of anandamide and display reduced pain sensation that is reversed by the CB(1) antagonist
115 amygdala in the processing and modulation of pain sensation, the experience of which involves a consi
118 hich inflammatory cytokines promote itch and pain sensations to coordinate host-protective behavioral
119 viously known as VR1, has been implicated in pain sensation under both physiological and pathological
121 efore, may give rise to acute post-traumatic pain sensation via a yet elusive molecular mechanism.
122 logical functions from prosocial behavior to pain sensation via central projection in the brain.