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1 Freund's Adjuvant)-induced inflammation and thermal hyperalgesia.
2 V1 receptors may play a role in inflammatory thermal hyperalgesia.
3 cation channel required for certain types of thermal hyperalgesia.
4 gion in spinal lamina II, leading to reduced thermal hyperalgesia.
5 dly exhibit deficits in inflammation-induced thermal hyperalgesia.
6 l allodynia but no significant reductions in thermal hyperalgesia.
7 TRPV1, or PKC may abrogate protease-induced thermal hyperalgesia.
8 M-1 also blocked neutrophil accumulation and thermal hyperalgesia.
9 th the development of morphine tolerance and thermal hyperalgesia.
10 e development of both morphine tolerance and thermal hyperalgesia.
11 but blocked prostaglandin E2 (PGE2)-induced thermal hyperalgesia.
12 nt of both morphine tolerance and associated thermal hyperalgesia.
13 ical allodynia and inflammatory pain but not thermal hyperalgesia.
14 the endogenous amino acid L-cysteine, induce thermal hyperalgesia.
15 itivity to noxious heat, a phenomenon termed thermal hyperalgesia.
16 atic nerve produces mechanical allodynia and thermal hyperalgesia.
17 ein structure of gp120 blocked gp120-induced thermal hyperalgesia.
18 (48 nmol) completely blocked the SP-induced thermal hyperalgesia.
19 Trk inhibitor GNF-5837 prevented C5a-induced thermal hyperalgesia.
20 pain sensation and for tissue injury-induced thermal hyperalgesia.
21 and thus provides a mechanism for peripheral thermal hyperalgesia.
22 to highly noxious stimuli and mechanical and thermal hyperalgesia.
23 1 receptors (CRFR1s) reduces stress-induced thermal hyperalgesia.
24 duced apoptosis mice abolished C5a-dependent thermal hyperalgesia.
25 s and may be critical in the pathogenesis of thermal hyperalgesia.
26 ay an impaired sensation of noxious heat and thermal hyperalgesia.
27 P causes sensitization of TRPV1 and produces thermal hyperalgesia.
28 (FeTMPyP(5+)) dose-dependently reversed this thermal hyperalgesia.
29 gesia and allodynia as well as taxol-induced thermal hyperalgesia.
30 exhibited symptoms of tactile allodynia and thermal hyperalgesia.
31 the TRPV1 channel, and contributes to acute thermal hyperalgesia.
32 rawal to radiant heat in mice, indicative of thermal hyperalgesia.
33 urons, and thereby sensitizes TRPV1 to cause thermal hyperalgesia.
36 (ED(50) approximately 100 mg/kg, i.p.), and thermal hyperalgesia after intraplantar complete Freund'
38 nM to 1microM) affected tactile allodynia or thermal hyperalgesia after SNL, but it increases cold al
39 econdary, but not primary, mechanical and/or thermal hyperalgesia after topical mustard oil applicati
40 f C5a into the mouse hindpaw produced strong thermal hyperalgesia, an effect that was absent in TRPV1
41 show that epinephrine-induced mechanical and thermal hyperalgesia and acetic acid-associated hyperalg
43 ose-dependent inhibition of mGluR-1-mediated thermal hyperalgesia and by colocalization of the antibo
45 significantly inhibited carrageenan-induced thermal hyperalgesia and indomethicin inhibited paw infl
47 = 10-15 micromolkg s.c.) in attenuating both thermal hyperalgesia and mechanical allodynia after chro
48 and DM (15 mg/kg) effectively reversed both thermal hyperalgesia and mechanical allodynia although e
49 of these neurons resulted in a reduction of thermal hyperalgesia and mechanical allodynia associated
50 sation through TRPV1, and enduringly reduced thermal hyperalgesia and mechanical allodynia caused by
51 -/-) mice, and this correlated with enhanced thermal hyperalgesia and mechanical allodynia in Pap(-/-
52 ganglion (DRG) neurons and the responses to thermal hyperalgesia and mechanical allodynia in strepto
54 egulation by PD98059 resulted in exacerbated thermal hyperalgesia and mechanical allodynia reversible
55 eloped a rat model of NGF-induced persistent thermal hyperalgesia and mechanical allodynia to determi
59 e development of neuropathic pain behaviors (thermal hyperalgesia and mechanical allodynia) induced b
64 (i.th.) administration of ligand 14 reversed thermal hyperalgesia and mechanical hypersensitivity in
65 l group II mGluRs inhibits forskolin-induced thermal hyperalgesia and nociceptor heat sensitization,
66 n and morphine were able to block or reverse thermal hyperalgesia and normalize gait in the CARR mode
68 , but it significantly prevented progressive thermal hyperalgesia and prevented C-fiber atrophy, dege
70 MHC-II in myelinating Schwann cells reduces thermal hyperalgesia and, to a lesser extent, also dimin
71 in response thresholds to both heat stimuli (thermal hyperalgesia) and light tactile stimuli (mechani
72 Both lowering of thermal pain threshold (thermal hyperalgesia) and lowering of response threshold
73 oTx elicits nonneurogenic inflammatory pain, thermal hyperalgesia, and mechanical allodynia, of which
74 d in the development of analgesic tolerance, thermal hyperalgesia, and tactile allodynia in response
75 P acting at the NK1 receptor causes chronic thermal hyperalgesia, and that the reduced opioid effica
77 c nerve developed significant mechanical and thermal hyperalgesia as tested by the withdrawal respons
78 (2)(*-) (1 microM) led to the development of thermal hyperalgesia associated with a profound localize
79 fibre nociceptors and is responsible for the thermal hyperalgesia associated with inflammatory pain.
81 While DM alone was effective in reducing thermal hyperalgesia at three tested doses (15, 30 or 60
82 but not spinally, reduced carrageenan-evoked thermal hyperalgesia but had no effect by any route with
83 MAPK signaling pathway in the production of thermal hyperalgesia, but not inflammation, in the mouse
85 also plays a critical role in development of thermal hyperalgesia, but the underlying mechanism remai
87 suggest that complement fragment C5a induces thermal hyperalgesia by triggering macrophage-dependent
89 vivo, 52 fully reversed carrageenan-induced thermal hyperalgesia (CITH) in rats and dose-dependently
92 opment of permanent mechanical allodynia and thermal hyperalgesia due to interruption and subsequent
95 c indwelling intrathecal catheters the acute thermal hyperalgesia evoked by the spinal delivery of su
97 displayed time-related tactile allodynia and thermal hyperalgesia (i.e., opioid-induced "pain"); plac
100 ption, and reversed mechanical allodynia and thermal hyperalgesia in a model of neuropathic pain.
101 as effective at reversing both allodynia and thermal hyperalgesia in a standard Chung (spinal nerve l
102 inhibitors blocked mechanical allodynia and thermal hyperalgesia in all three pain models although t
104 Wild-type mice exhibited mechanical but not thermal hyperalgesia in both paws 1 d after acid injecti
105 ignificantly increased tactile allodynia and thermal hyperalgesia in both the early (first week) and
108 ype V1) plays a key role in the induction of thermal hyperalgesia in inflammatory pain models, we eva
110 ts BD-1063 and S1RA abolished mechanical and thermal hyperalgesia in mice with carrageenan-induced ac
114 Cdk5 activity is associated with attenuated thermal hyperalgesia in TGF-beta1 receptor conditional k
117 the TRPV1 antagonist decreased inflammatory thermal hyperalgesia in transgenic but not wild-type ani
118 intra-CeA infusion of tetrodotoxin produced thermal hyperalgesia in unstressed rats and blocked the
119 eral inflammation, mechanical allodynia, and thermal hyperalgesia in vector control animals that pers
120 cation of cis-45, which was shown to reverse thermal hyperalgesia in vivo in the spinal nerve ligatio
121 hecal administration of bradykinin induces a thermal hyperalgesia in vivo, which is reduced by inhibi
123 hermore, activin administration caused acute thermal hyperalgesia in wild-type mice, but not in TRPV1
124 NGF negated both neutrophil accumulation and thermal hyperalgesia, indicating the dependence of NGF o
125 s displayed enhanced scratching behavior and thermal hyperalgesia indicative of peripheral neuroinfla
126 sevanol (1-10 mg/kg) significantly reversed thermal hyperalgesia induced by complete Freund's adjuva
127 s; however, it was ineffective at preventing thermal hyperalgesia induced by complete Freund's adjuva
128 in rats) and was also effective at reducing thermal hyperalgesia induced by complete Freund's adjuva
129 sensitization of capsaicin receptors and the thermal hyperalgesia induced by PGE2, and suggest that p
130 nce P (SP; 20 nmol) or NMDA (2 nmol) and the thermal hyperalgesia induced by the injection of carrage
132 of hairy hind foot skin in rats, a transient thermal hyperalgesia lasting <2 h, and longlasting prima
134 We find that UV-treated larvae develop both thermal hyperalgesia, manifested as an exaggerated respo
135 lantation (TCI) produces bone cancer-related thermal hyperalgesia, mechanical allodynia, spontaneous
137 These findings suggest that inflammatory thermal hyperalgesia mediated by TRPV1 may be further ag
139 t saline, demonstrated tactile allodynia and thermal hyperalgesia of the hindpaws (during the DAMGO i
140 of melatonin alone was effective in reducing thermal hyperalgesia only at the highest dose (120 mg/kg
141 ith the development of tactile allodynia and thermal hyperalgesia, spinal CaMKIIalpha activity was si
142 us opioid enkephalin (ENK) in the RVM during thermal hyperalgesia, suggesting potential in situ inter
143 ministration of A-784168 blocked CFA-induced thermal hyperalgesia, suggesting that both peripheral an
145 are involved in the mechanical allodynia and thermal hyperalgesia that develop following cold injury
146 (intrathecal, IT) application of SP produces thermal hyperalgesia that is mediated by activation of t
147 inducing but not maintaining mechanical and thermal hyperalgesia that is mediated by CaMKIIalpha sig
148 emin, neurturin, GDNF, or NGF produced acute thermal hyperalgesia that lasted up to 4 h; combined inj
149 on of spinal neurons, and the mechanical and thermal hyperalgesia that normally occurs after peripher
151 into mouse hindpaw led to the development of thermal hyperalgesia that was attenuated by administrati
152 ceramide (10 mug) led to the development of thermal hyperalgesia that was dependent on induction of
153 njection of a PAR2 agonist caused persistent thermal hyperalgesia that was prevented by antagonism or
156 e ligation reversed mechanical allodynia and thermal hyperalgesia; the antiallodynic effect lasted 6
157 ng the initiation of mechanical allodynia or thermal hyperalgesia, these cells may not be as importan
158 als from developing mechanical allodynia and thermal hyperalgesia throughout the 96 h after CFA.
159 serum blocked tactile allodynia and reversed thermal hyperalgesia to above baseline levels (i.e., ant
160 F-kappaB expression and nerve injury-induced thermal hyperalgesia using a rat model of constriction s
161 lthough local administration of NGF mediates thermal hyperalgesia via mechanisms involving concomitan
170 By focusing on the mechanisms of C5a-induced thermal hyperalgesia, we show that this process requires
171 sponses assessed by mechanical allodynia and thermal hyperalgesia were almost identical in the two mo
173 of TRPA1 in vitro but did not cause pain or thermal hyperalgesia when injected into the hind paw of
174 nical hyperalgesia, mechanical allodynia and thermal hyperalgesia, which are blocked following co-inj
175 pression and the behavioral manifestation of thermal hyperalgesia, which is likely to be mediated thr
176 an induced a time-dependent inflammation and thermal hyperalgesia, which was maximal 4 h post adminis
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