ライフサイエンスコーパス: hypoalgesia

1 MDL28170 prevented capsaicin-induced thermal hypoalgesia.

2 ectations and experience can lead to placebo hypoalgesia.

3 e known to influence the strength of placebo hypoalgesia.

4 pioid-mediated, but not non-opioid-mediated, hypoalgesia.

5 luid) ingestion does not, by itself, produce hypoalgesia.

6 a and attenuates mu-opioid-receptor-mediated hypoalgesia.

7 V1 phosphorylation, resulting in significant hypoalgesia.

8 llodynia with a simultaneous unilateral heat hypoalgesia.

9 specificity of the PAG's role in conditional hypoalgesia.

10 diabetic nerves and NGF deprivation produces hypoalgesia.

11 ffects in reinforcement learning and placebo hypoalgesia.

12 s to noxious stimuli and produces behavioral hypoalgesia.

13 However, placebo hypoalgesia, although mediated by associative learning,

14 at 8 mo of age exhibited loss of sensation, hypoalgesia (an increase in mechanical threshold), and d

15 es delta- and kappa-opioid-receptor-mediated hypoalgesia and attenuates mu-opioid-receptor-mediated h

16 hypoxia marker (IGFBP-1) was associated with hypoalgesia and increased potency to opioid analgesia; o

17 mal MNCV and SNCV and alleviation of thermal hypoalgesia and intraepidermal nerve fiber loss but not

18 AMP resulted in a similar pattern, with heat hypoalgesia and mechanical allodynia occurring simultane

19 B2 activation contributed to the mechanical hypoalgesia and MNCV deficits in both diabetic genotypes

20 rspective reviews recent findings in placebo hypoalgesia and provides a conceptual account of how exp

21 allodynia and essentially corrected thermal hypoalgesia and sensory nerve conduction deficit without

22 crease in nerve conduction velocity, thermal hypoalgesia, and a reduction in intraepidermal nerve fib

23 crease in nerve conduction velocity, thermal hypoalgesia, and intraepidermal nerve fiber profiles.

24 epletion of sensory nerve terminals, thermal hypoalgesia, and nerve conduction slowing in diverse rod

25 te and the high-intensity tail flick assays (hypoalgesia), but there was no difference in the low-int

26 These results suggest that conditional hypoalgesia (CHA) is subserved by mu but not kappa opioi

27 longer-lasting mechanical allodynia and heat hypoalgesia compared with injection of capsaicin into sk

28 Our results indicate that in placebo hypoalgesia contextual treatment information engages pre

29 tion velocity (MNCV), mechanical and thermal hypoalgesia, Erb B2 phosphorylation (pErb B2), and epide

30 uring milk letdown, cause varying degrees of hypoalgesia in 10-day-old rats.

31 otor activity, increased ring catalepsy, and hypoalgesia in hotplate and formalin tests.

32 s applied to the PAG block the expression of hypoalgesia in rats exposed to a Pavlovian signal for sh

33 onduction slowing and thermal and mechanical hypoalgesia in the absence of any reduction of hyperglyc

34 ent to decrease MNCV and induce a mechanical hypoalgesia in the absence of diabetes.

35 ion deficits, tactile allodynia, and thermal hypoalgesia in the absence of intraepidermal nerve fiber

36 ction velocity, prevented the development of hypoalgesia in the hind paw, and reduced superoxide and

37 hedgehog-IgG fusion protein, as was thermal hypoalgesia in the paw.

38 sible for the expression of several forms of hypoalgesia in the rat.

39 in a secondary mechanical allodynia and heat hypoalgesia lasting approximately 3 hr.

40 titers showed significant (P < 0.05) thermal hypoalgesia measured using the hot plate test (52 degree

41 est that selective visceral hyperalgesia and hypoalgesia of peripheral or central origin may be prese

42 rning has been central in explaining placebo hypoalgesia, placebo hypoalgesic effects show little ext

43 These results support the idea that hypoalgesia produced by aversive auditory stimuli uses a

44 This form of stress-induced hypoalgesia represents a response to unconditional fear

45 ies, resulting in less extinction of placebo hypoalgesia.SIGNIFICANCE STATEMENT In aversive and appet

46 conduction velocity (SNCV) deficits, thermal hypoalgesia, tactile allodynia, and a remarkable ( appro

47 ented or alleviated diabetes-induced thermal hypoalgesia, tactile allodynia, motor and sensory nerve

48 Hyperextension-induced hypoalgesia terminated immediately with stretch cessatio

49 Heat hypoalgesia that occurs after injection into deep tissue

50 a stimulus-bound, partially opioid-mediated hypoalgesia that previous research has shown to be poten

51 n modulation through treatment cues (placebo hypoalgesia, treatment context) with pain modulation thr

52 High doses of chemotherapy produced hypoalgesia whereas lower doses produced hyperalgesia.

53 activation after a bout of VCS that produced hypoalgesia, with and without co-administration of AF.