ライフサイエンスコーパス: pain response

1 unding keratinocytes and thereby inhibit the pain response.

2 ptor TRPA1 in sensory neurons and evoked the pain response.

3 omy group, 16 patients reported a successful pain response.

4 his caused a robust increase in the visceral pain response.

5 ividually and collectively is related to the pain response.

6 ors, which do not account for the effects on pain response.

7 red affective-motivational modulation of the pain response.

8 bility and may contribute to the neuropathic pain response.

9 omposite measure as complete, partial, or no pain response.

10 but not Slo2.1, results in enhanced itch and pain responses.

11 tissue incision induced resolving immune and pain responses.

12 mal baseline pain, but impaired inflammatory pain responses.

13 ce that parents can articulate their child's pain responses.

14 nscriptional repressor, is known to modulate pain responses.

15 ntified patterns within 335 parent described pain responses.

16 ct of background levels of stress upon their pain responses.

17 it dramatically reduced formaldehyde-induced pain responses.

18 changes potentially account for the altered pain responses.

19 sory neurons to increase CGRP expression and pain responses.

20 ism of CB(2) receptor-mediated inhibition of pain responses.

21 e amygdala to decrease anxiety, fear, and/or pain responses.

22 Evolution to reduce general pain responses, although valuable for preying on venomou

23 re significant relationships between type of pain response and (1) pain severity; (2) causes of intel

24 s; (2) examine relationships between type of pain response and independent variables; (3) compare pai

25 s treated with formalin showed a spontaneous pain response and mechanical allodynia that persisted fo

26 per vertebra) were related to postprocedural pain response and midterm outcome after vertebroplasty.

27 s ethnic group is an important factor in the pain response and requires further study in an effort to

28 sed to examine relationships between type of pain response and selected demographic factors.

29 study provides evidence of: (1) extremes of pain responses and (2) a significant relationship betwee

30 ction in pain threshold, an amplification of pain responses and a spread of pain sensitivity to non-i

31 Thus, P2X3 is critical for peripheral pain responses and afferent pathways controlling urinary

32 male DRD5KO mice also show reduced formalin pain responses and decreased heat pain.

33 dala plays a key role in emotional-affective pain responses and depends on group I metabotropic gluta

34 between development of OA with accompanying pain responses and gradual alterations in cellular and s

35 Genetic silencing of CGRP neurons blocks pain responses and memory formation, whereas their optog

36 These mice show normal locomotor and pain responses and no difference in depressive-like beha

37 They also showed a loss of enhanced pain responses and spontaneous pain behavior upon treatm

38 such as suppression of food intake, enhanced pain response, and excessive grooming induced by intrace

39 startle magnitude, balance beam performance, pain response, and nerve myelination in both species.

40 de deficits in rotorod performance, aberrant pain responses, and abnormal myelin sheath folding.

41 a broad range of phenotypes, including ASUD, pain responses, and the development of tolerance to morp

42 Pain responses are often misunderstood, given that the c

43 examined various degrees of PSA decline and pain response as surrogates for the survival benefit obs

44 cally, the aims were to: (1) identify common pain responses as reported by parents; (2) examine relat

45 However, in behavioral assays for pain responses, ASIC3 null mutant mice displayed a reduc

46 hypersensitivity and contribute to abnormal pain responses associated with inflammatory injuries.

47 se of prostate-specific antigen [PSA50], and pain response at 12 weeks) were to undergo statistical t

48 The primary endpoint was overall pain response at 2 months, which was defined as the sum

49 Pain response at midterm outcome was strongly related to

50 ogical sources underlying the variability in pain responses between sexes have not been adequately ex

51 lation of sleep debt and also to exaggerated pain responses, both of which are rescued after restorat

52 phase 2 of the intraplantar formalin-evoked pain response but only a modest (20-30%) and nonsignific

53 nhibits acute, inflammatory, and neuropathic pain responses but does not cause central nervous system

54 e inhibitor, D-JNKI-1, did not affect normal pain responses but potently prevented and reversed SNL-i

55 tant mice showed normal thermal and visceral pain responses but were less sensitive to mechanical sti

56 In humans, however, pain responses can be modulated by spinal ACh, as eviden

57 y the patients; and 3) whether the patients' pain responses could be predicted by factors such as the

58 and debridement and to determine whether the pain responses could be predicted by the patient's age,

59 s disclosed that significant portions of the pain responses could be predicted by the patients' answe

60 greater understanding of genetic factors and pain responses could lead to potential treatments.

61 comotor activity, anxiety-like behaviors and pain responses did not differ across genotypes, indicati

62 ated with zymosan exhibited mild spontaneous pain responses during the first hour and mechanical allo

63 177Lu-EDTMP has pain response efficacy similar to that of 153Sm-EDTMP an

64 roduce these peptides display no significant pain responses following formalin injection and have an

65 Lower median pain responses following probing with the 0.63 mm probe

66 erse events were unexpected higher transient pain response (grade 3) localised to the treatment site

67 compared with nonresponders, patients with a pain response had a greater reduction in pain (mean redu

68 However, the role of the ACC in pain response has not been clearly defined.

69 ole and importance of these neuropeptides in pain responses has been debated.

70 We show here that the absence of neuropathic pain response in infant male rats and mice following ner

71 ual disability use to describe their child's pain response in order to improve pain recognition and m

72 er H(2)O(2) or 15d-PGJ2 evoked a nocifensive/pain response in wild-type mice, but not in trpa1(-/-) m

73 eptor potential vanilloid subtype 1, mediate pain responses in a model of chronic pancreatitis.

74 inhibits acute, inflammatory and neuropathic pain responses in animal models.

75 oid receptor agonists significantly diminish pain responses in animal models; however, they exhibit o

76 esponses in these mutant mice, as opposed to pain responses in control littermates.

77 33 demonstrated effectiveness by decreasing pain responses in formalin-induced tonic pain, in capsai

78 -blind, randomized study examined behavioral pain responses in healthy human volunteers during mindfu

79 iabetic ob/ob mice without altering baseline pain responses in healthy mice.

80 tified allelic differences affecting chronic pain responses in mice and humans, which may enable a ne

81 pendent increases in pressor, heart rate and pain responses in rats, as well as an increase in latenc

82 n pain model (ip), (R)-10 (15 mg/kg) reduced pain responses in the acute and the chronic inflammatory

83 Here, we show that adult pain responses in the rat are 'primed' by tissue injury

84 modulation of ACC sensitization and visceral pain responses in VH rats.

85 s has a critical role in modulating visceral pain responses in viscerally hypersensitive (VH) rats.

86 critical role in the modulation of visceral pain responses in viscerally hypersensitive rats.

87 were related significantly to postprocedural pain response, including PMMA leakage.

88 duced freezing without affecting activity or pain responses; infusions into lateral ventricle or nucl

89 However, changes in cortical pain responses may be secondary to earlier amplification

90 ess correct neuropeptides, and mediate acute pain responses normally.

91 (median 9.3 v 10.0 months, respectively) or pain response (odds ratio, 0.84; 95% CI, 0.61 to 1.16; P

92 sychophysically verified large decrements in pain response ("offset-analgesia"; mean analgesia: 85%,

93 o significant differences postoperatively in pain response or need for analgesics between the study g

94 displayed a reduced latency to the onset of pain responses, or more pain-related behaviors, when sti

95 (PFS); tumor, prostate-specific antigen, and pain response; pharmacokinetics; and health-related qual

96 (median, 5.5 v 2.9 months, P < .001) but not pain response rate (12% v 9%; P = .128).

97 global benefit were nearly identical to the pain response rates and did not differ between the treat

98 al, mechanical, inflammatory and neuropathic pain responses relative to wild-type mice.

99 ormalin into the hind paw induces a biphasic pain response; the first phase is thought to result from

100 and palliation of metastatic disease such as pain response, time to progression and progression-free

101 observed in 5 subjects with a positive chest pain response to edrophonium and in none of the 5 subjec

102 eported that TRPA1 has a central role in the pain response to endogenous inflammatory mediators and t

103 the inflammatory process, and the patients' pain response to genitourinary insults.

104 nociceptive systems resulting in a decreased pain response to peripheral noxious stimuli.

105 x) correlated with initial pain severity and pain response to RT and can be used as a predictive fact

106 The pretreatment pain scores and pain response to RT were compared with FDG PET SUV(max)

107 ores were also significantly associated with pain response to RT.

108 The pain response to saline was not significantly altered af

109 f 263 patients, respectively, had an overall pain response to treatment (p=0.17; response difference

110 allocated to 20 Gy treatment had an overall pain response to treatment (p=0.21; response difference

111 Most patients showed low pain responses to both probing and instrumentation as ev

112 Most patients showed low pain responses to both probing and instrumentation.

113 identify their role in mediating behavioral pain responses to colonic distention in the normal gut.

114 se and catalase mimetic, EUK-134, diminished pain responses to formalin in wild-type mice, but EUK-13

115 f the mechanisms responsible for exaggerated pain responses to inflammatory injuries.

116 Behavioral pain responses to noxious mechanical stimulation were in

117 Most patients showed low pain responses to probing.

118 chanical hyperalgesia in mice and sensitized pain responses to the TRPV4 agonists 4alphaPDD and hypot

119 ponse and independent variables; (3) compare pain responses to those identified in the literature.

120 s defined as the sum of complete and partial pain responses to treatment, assessed using both Brief P

121 amined for post-treatment changes in PSA and pain response using Cox proportional hazards models to c

122 Pain responses varied with severity.

123 Four types of pain responses: vocalization, social behavior, muscle to

124 Pain response was achieved in a higher proportion of pat

125 Pain response was also assessed in a straight leg raisin

126 Pain response was assessed using the cold-pressor test (

127 Pain response was assessed with International Bone Metas

128 s indicated that this hypnotic modulation of pain responses was associated with differential recruitm

129 PSA or PSA kinetics, PSA normalization, and pain responses were highly prognostic but weaker surroga

130 Seven distinct categories of pain responses were identified.

131 The most commonly reported pain responses were within the categories of: vocalizati

132 pecific peptide agonist induced a behavioral pain response when infused into the pancreatic duct of a

133 cy and efficacy of this compound in blocking pain responses, where it showed an ED(50) of 42 mumol/kg

134 s in the acute stage of the inflammatory and pain response, whereas B1 receptors (B1R), through which

135 RGMa antibody also attenuated neuropathic pain responses, which was associated with fewer activate

136 odel, loss of these Grp(+) neurons increased pain responses while itch was decreased.