ライフサイエンスコーパス: pain response

1 unding keratinocytes and thereby inhibit the pain response.

2 1 with pain flare-up; 3 patients reported a pain response.

3 8 (53%; 95% CI 42-64) had at least a partial pain response.

4 , namely increased pain threshold and higher pain response.

5 esting (QST) is a method that quantifies the pain response.

6 extent of metastatic disease did not impact pain response.

7 dden) was the significant factor influencing pain response.

8 e and female rodents without altering normal pain response.

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

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

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

12 ividually and collectively is related to the pain response.

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

14 red affective-motivational modulation of the pain response.

15 bility and may contribute to the neuropathic pain response.

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

17 sory neurons to increase CGRP expression and pain responses.

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

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

20 In addition, STING agonists alone can elicit pain responses.

21 nsing kinases to mediate cell biological and pain responses.

22 nscriptional repressor, is known to modulate pain responses.

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

24 changes potentially account for the altered pain responses.

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

26 tissue incision induced resolving immune and pain responses.

27 mal baseline pain, but impaired inflammatory pain responses.

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

29 ntified patterns within 335 parent described pain responses.

30 it dramatically reduced formaldehyde-induced pain responses.

31 bone metastases experienced similar overall pain response after SBRT compared with cEBRT.

32 neuropathic injury, and preserved protective pain responses, all without affecting motor or cardiovas

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

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

35 approach to explore individual variations in pain response and identify ventral tegmental area glutam

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

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

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

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

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

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

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

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

44 ions, we show that AH inhibits TRPV1-related pain responses and currents by interacting with a region

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

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

47 ht stimuli presentation were correlated with pain responses and examined post- vs pre-anesthesia.

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

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

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

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

52 nges in behavior are not due to nonselective pain responses and that the ventral nerve cords and cros

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

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

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

56 g SELP-415K significantly reduced behavioral pain responses, and reduced animal mass loss compared to

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

58 Pain responses are often misunderstood, given that the c

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

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

61 The primary endpoint was abdominal pain response, as defined by the US Food and Drug Admini

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

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

64 , SBRT was associated with a higher complete pain response at 1 (RR, 1.43; 95% CI, 1.02-2.01), 3 (RR,

65 Overall and complete pain response at 1, 3, and 6 months after radiotherapy,

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

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

68 The primary end point of pain response at 3 months favored cEBRT (41.3% for SRS v

69 or the primary end point of patient-reported pain response at 3 months was not found, and there were

70 Pain response at midterm outcome was strongly related to

71 The primary endpoint was complete or partial pain response based on a reduction of the BPI-SF average

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

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

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

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

76 PBN-SL(Tacr1) neurons alone did not trigger pain responses but instead served to dramatically height

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

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

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

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

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

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

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

84 The primary end point was patient-reported pain response defined as at least a 3-point improvement

85 OVA-induced increases in pain responses depended on mast cells, IgE, and signal t

86 Abdominal pain response did not differ significantly between the p

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

88 han 1, 59% (128) had a clinically meaningful pain response during treatment.

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

90 Studies assessing cold pressor test (CPT) pain responses during treatment seeking, pharmacological

91 177Lu-EDTMP has pain response efficacy similar to that of 153Sm-EDTMP an

92 xtensive neurogenic inflammatory, flare, and pain responses following application of the TRPA1 channe

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

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

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

96 primary endpoint was a clinically meaningful pain response (>=2-point improvement from baseline for t

97 The primary outcome was pain response (>=30% decrease in Brief Pain Inventory to

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

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

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

101 The authors studied neural and subjective pain response in a randomized active-control trial of mi

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

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

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

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

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

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

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

109 r calcitonin gene-related peptide in driving pain responses in elevated ICP.

110 33 demonstrated effectiveness by decreasing pain responses in formalin-induced tonic pain, in capsai

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

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

113 ed that an orexin antagonist could normalize pain responses in male animals.

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

115 onal modulation of pain ratings and enhanced pain responses in pregenual anterior cingulate cortex an

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

117 own that prolactin promotes female-selective pain responses in rodents.

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

119 EAS in mice of both sexes reduced late phase pain responses in the formalin paw test.

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

121 by noxious stimuli and silencing them blocks pain responses in two different models of pain.

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

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

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

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

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

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

128 There were no genotype differences in pain responses, morphine analgesia and tolerance, heroin

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

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

131 and females with neuropathic or inflammatory pain, responses of PBN neurons remain amplified for at l

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

133 vious research has been limited in assessing pain responses only during low-force contractions.

134 no statistically significant differences in pain response or analgesic usage at any time between the

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

136 stically significant reductions in abdominal pain response or overall symptom relief, when using US F

137 bo, there were no significant differences in pain response or pain medication usage at any time betwe

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

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

140 s-induced sensitization of fear learning and pain responses preferentially in female mice, indicating

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

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

143 he ITT meta-analyses showed that the overall pain response rates did not differ between cEBRT and SBR

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

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

146 f MiR34/449 miRNAs perturb thermally induced pain response thresholds and compromised delicate motor

147 ike herpes simplex virus 1 (HSV-1), triggers pain responses through STING expression in nociceptors.

148 Since cabazitaxel improved pain response, time to pain progression, time to symptom

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

150 sal horn (DH; another key structure for CIPN pain response) tissues from vehicle and paclitaxel treat

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

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

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

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

155 date our model by reproducing the wind-up of pain response to repeated stimulation.

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

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

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

159 The pain response to saline was not significantly altered af

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

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

162 ownregulation of prolactin receptor long and pain responses to a normally innocuous TRPA1 stimulus.

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

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

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

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

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

168 Behavioral pain responses to noxious mechanical stimulation were in

169 Most patients showed low pain responses to probing.

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

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

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

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

174 Pain responses varied with severity.

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

176 A pain response was achieved in 58/350 patients in the IPT

177 Pain response was achieved in a higher proportion of pat

178 Pain response was also assessed in a straight leg raisin

179 Pain response was analysed in the intention-to-treat pop

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

181 Pain response was assessed with International Bone Metas

182 In 7 RCTs, overall pain response was defined according to the International

183 Pain response was measured via self-reported intensity a

184 Pain response was observed in 51 (46%) of 111 patients w

185 The complete pain response was reported in 6 RCTs, all defined accord

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

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

188 Seven distinct categories of pain responses were identified.

189 PSNL-initiated pain responses were reduced following cre-mediated Lpar1

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

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

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

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

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

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