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1 itivity of peripheral nerves to light touch (tactile allodynia).
2 s tactile stimulation elicits pain behavior (tactile allodynia).
3 ontribute to peripheral inflammation-induced tactile allodynia.
4 5-LOX (Zileuton) dose-dependently attenuated tactile allodynia.
5 carrageenan-induced thermal hyperalgesia and tactile allodynia.
6 ateral spinal dorsal horn of rats displaying tactile allodynia.
7 ulation do not display a learning deficit or tactile allodynia.
8 these afferents contributes to the resulting tactile allodynia.
9  and intraepidermal nerve fiber loss but not tactile allodynia.
10 2delta-1 subunit and reversed injury-induced tactile allodynia.
11 hermore, to the behavioural manifestation of tactile allodynia.
12 2delta-1 subunit upregulation and diminished tactile allodynia.
13 rog/day) for 5 days significantly attenuated tactile allodynia.
14 onset and diminished in rats recovering from tactile allodynia.
15 rn, has been implicated in the expression of tactile allodynia.
16  nerve-ligated rats and its correlation with tactile allodynia, a neuropathic pain state defined as r
17 normal chow after 16 weeks on HFD alleviated tactile allodynia and essentially corrected thermal hypo
18 ion of activin A protein alone caused robust tactile allodynia and increased CGRP in the DRG.
19                                              Tactile allodynia and mechanical hyperalgesia were asses
20 ation of dynorphin A(1-17) antiserum blocked tactile allodynia and reversed thermal hyperalgesia to a
21 ed rats, i.th. morphine was inactive against tactile allodynia and showed diminished in potency again
22 s delivering morphine displayed time-related tactile allodynia and thermal hyperalgesia (i.e., opioid
23 k-out mice developed significantly increased tactile allodynia and thermal hyperalgesia in both the e
24 sed with DAMGO, but not saline, demonstrated tactile allodynia and thermal hyperalgesia of the hindpa
25          Correlating with the development of tactile allodynia and thermal hyperalgesia, spinal CaMKI
26       SCI animals also exhibited symptoms of tactile allodynia and thermal hyperalgesia.
27 locity (SNCV) deficits, thermal hypoalgesia, tactile allodynia, and a remarkable ( approximately 78%)
28 motor and sensory nerve conduction deficits, tactile allodynia, and thermal hypoalgesia in the absenc
29 .th.) morphine is ineffective in suppressing tactile allodynia at fully antinociceptive doses in thes
30 d and dorsal root ganglia (DRG) of rats with tactile allodynia because of either tight ligation of th
31 XA(3), or HXB(3) evoked profound, persistent tactile allodynia, but 12(S)-HpETE and HXA(3) produced r
32         Selective reversal of injury-induced tactile allodynia by NPY receptor antagonists would have
33 siRNA normalized mechanical hyperalgesia and tactile allodynia caused by SNL but had no significant e
34                                     Profound tactile allodynia developed in all the resiniferotoxin-t
35                               Also, profound tactile allodynia developed in all the RTX-treated rats
36 hic pain model in which gabapentin-sensitive tactile allodynia develops after tight ligation of the l
37                                    Moreover, tactile allodynia did not develop as an unwanted side ef
38   Systemic A-134974 dose-dependently reduced tactile allodynia (ED(50)=5 micromol/kg, i.p.) for up to
39 es were lateralized and in proportion to the tactile allodynia exhibited by SNI animals.
40 stration of the TAT-4BB reversed M3G-induced tactile allodynia in a dose-dependent manner but did not
41 t tool molecule 20 (AM-1488), which reversed tactile allodynia in a mouse spared-nerve injury (SNI) m
42 n a hyperalgesia at the site of injury and a tactile allodynia in areas adjacent to the injury site.
43      Finally, we analyzed the development of tactile allodynia in diabetic mice lacking expression of
44                  Importantly, the absence of tactile allodynia in diabetic NF-kappaB p50(-/-) mice su
45 lazine completely blocked the development of tactile allodynia in diabetic rats, whereas relatively m
46                   The complete inhibition of tactile allodynia in experimental diabetes by sulfasalaz
47 algesic tolerance, thermal hyperalgesia, and tactile allodynia in response to chronic intrathecal mor
48 hese compounds, 23 dose dependently reversed tactile allodynia in the Chung model of neuropathic pain
49 f formalin-induced flinching, and attenuated tactile allodynia in the spinal nerve ligation model of
50 mically and spinally can effectively relieve tactile allodynia in this animal model of postherpetic n
51 .8 muM, respectively) and carrageenan-evoked tactile allodynia in vivo.
52 ct of systemic and intrathecal gabapentin on tactile allodynia induced by resiniferotoxin in rats.
53                                  The delayed tactile allodynia induced by RTX is likely attributable
54  nerve crush resulted in a patchy but marked tactile allodynia manifesting first at 3 weeks and persi
55 viated diabetes-induced thermal hypoalgesia, tactile allodynia, motor and sensory nerve conduction ve
56 cation of icilin (0.1nM to 1microM) affected tactile allodynia or thermal hyperalgesia after SNL, but
57  syndrome) or by mechanical hyperalgesia and tactile allodynia (pain in response to nonpainful stimul
58                       Behavioral testing for tactile allodynia, performed one week prior to STZ injec
59                                              Tactile allodynia produced by placing a plastic cuff aro
60  such as the loss of tactile sensitivity and tactile allodynia seen in patients who have diabetes, in
61 as more potent (ED(50)=10 nmol) in relieving tactile allodynia than delivering the compound by intrac
62 ited time-dependent and reversible cutaneous tactile allodynia that was maintained throughout and tra
63 novel AK inhibitor A-134974 potently reduces tactile allodynia through interactions with spinal sites
64 ats with streptozotocin-induced diabetes and tactile allodynia, using in situ hybridization and immun
65 elopment of diabetes-induced retinopathy and tactile allodynia was investigated.
66                                              Tactile allodynia was present in both injured and adjace
67                     Moreover, injury-induced tactile allodynia was reversed by inhibiting and exacerb
68 ssess the role of NO in nerve injury-induced tactile allodynia, we examined neuronal NO synthase (nNO
69 orn neurons may result in the development of tactile allodynia, where non-painful stimuli gain the ca

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