ライフサイエンスコーパス: visceral pain

1 iding a suitable target for the treatment of visceral pain.

2 lamus and the DC play major roles in chronic visceral pain.

3 onal hyperexcitability in a model of chronic visceral pain.

4 , and may be a potential target for treating visceral pain.

5 odels of acute pain, postoperative pain, and visceral pain.

6 or mediator of acute, acute inflammatory, or visceral pain.

7 tinal motility and modulation of somatic and visceral pain.

8 mechanisms by which the ECS links stress and visceral pain.

9 able probiotics have the potential to modify visceral pain.

10 ut motility, and increases the perception of visceral pain.

11 eptive effects in assays of inflammatory and visceral pain.

12 revented chronic stress-induced increases in visceral pain.

13 the involvement of TLR4 in the modulation of visceral pain.

14 (including opioid-induced constipation), and visceral pain.

15 hysiologic response, and brain processing of visceral pain.

16 reducing amygdala engagement during expected visceral pain.

17 ly to contribute to the emergence of chronic visceral pain.

18 of negative affect on central processing of visceral pain.

19 era may be insufficient in targeting chronic visceral pain.

20 sumatriptan was investigated in 2 models of visceral pain.

21 bs of the functional responses associated to visceral pain.

22 ify the receptor involved in facilitation of visceral pain.

23 redict efficacy of medications developed for visceral pain.

24 e sensation and pattern of referral of their visceral pain.

25 stions closely related to clinically treated visceral pain.

26 d interpretation of brain-imaging studies of visceral pain.

27 g butyrate enemas to induce non-inflammatory visceral pain, acute morphine administration produced do

28 ception, motility, and central processing of visceral pain; although further research is required in

29 rious acute stimuli such as ischemic insult, visceral pain and electroconvulsive shock.

30 fferents during mesenteric ischaemia induces visceral pain and evokes excitatory cardiovascular respo

31 le of neurokinin (NK) B and NK3 receptors in visceral pain and gastrointestinal disorders has not bee

32 ite stable activation of networks processing visceral pain and its anticipation.

33 Genetic mechanisms associated with visceral pain and motor functions in health and function

34 y motor cortex) for the treatment of chronic visceral pain and new parameters of stimulation, such as

35 The TLR4 deficiency reduced visceral pain and prevented the development of chronic p

36 fferents during mesenteric ischaemia induces visceral pain and reflexly excites the cardiovascular sy

37 network involved in aversive conditioning of visceral pain and, thus, anticipation.

38 a mouse p-phenylquinone (PPQ) model of acute visceral pain, and a rat spinal nerve ligation (SNL) mod

39 complex CNS disorders including depression, visceral pain, and cocaine addiction.

40 to NTS2, may be potentially useful to treat visceral pain, and psychosis without concomitant side ef

41 hase included areas commonly associated with visceral pain (anterior cingulate cortex, insula, and pr

42 on sensory neurons and their contribution to visceral pain are unknown.

43 These results show that visceral pain arising from the proximal colon activates

44 1 antagonist SB-366791 markedly reduced both visceral pain behavior and referred somatic hyperalgesia

45 Visceral pain behaviors were assessed as degree of hunch

46 one-methiodide did not induce an increase in visceral pain behaviors.

47 te to our understanding of the processing of visceral pain, but also have clinical implications for t

48 mote gastrointestinal motility and attenuate visceral pain, but concerns about adverse reactions have

49 tential site of action for the modulation of visceral pain by triptans.

50 tate of "latent sensitization" to subsequent visceral pain characterized by extended duration of hype

51 nt of strategies that may improve therapy of visceral pain conditions using already available medicat

52 ld induce a state of latent sensitization to visceral pain conditions.

53 that central sensitisation may contribute to visceral pain disorders.

54 2Y-dependent mechanisms in the generation of visceral pain during gastrointestinal disease.

55 We have shown that actual and anticipated visceral pain elicit similar cortical responses.

56 n of the MCC and related areas involved with visceral pain encoding are associated with poor clinical

57 Developments in the scientific visceral pain field are encouraging.

58 Visceral pain following infection or inflammation is a m

59 and spinal plasticity in the maintenance of visceral pain from pancreatitis.

60 could be useful to treat transient and acute visceral pain from the uterine cervix.

61 owever, their efficacy in treatment of acute visceral pain has not been explored.

62 Migraine and visceral pain have also been associated with voltage-gat

63 fer in the central nervous system, underlies visceral pain hypersensitivity and non-cardiac chest pai

64 The prolonged visceral pain hypersensitivity in patients with non-card

65 via the EP-1 receptor, contributes to human visceral pain hypersensitivity.

66 Detection of visceral pain in chronic pancreatitis predicts pain reli

67 are able to counteract inflammation-induced visceral pain in mice.

68 associated with the onset or exacerbation of visceral pain in patients with irritable bowel syndrome

69 sed by sensory neurons, mediates somatic and visceral pain in response to direct activation or noxiou

70 rategies are considered for the treatment of visceral pain in such conditions as renal colic, interst

71 c mechanisms regulate chronic stress-induced visceral pain in the peripheral nervous systems of rats.

72 gic mechanosensory transduction can initiate visceral pain in urinary bladder, ureter, gut and uterus

73 determine if ACC neuron activation enhances visceral pain in viscerally hypersensitive rats and to i

74 tment reduces excitability and G-CSF-induced visceral pain in vivo.

75 ainst P2X3 may have therapeutic potential in visceral pain indications.

76 This condition likely reflects enhanced visceral "pain" intensity as a consequence of persistent

77 translation of efficacy in animal models of visceral pain into the clinic.

78 The perception of visceral pain is a complex process involving the spinal

79 Visceral pain is a prevalent clinical problem and one of

80 An important step in understanding visceral pain is the development of comprehensive phenot

81 in mice and humans but its significance for visceral pain is unknown.

82 he formalin, complete Freund's adjuvant, and visceral pain models.

83 lockade of referred hypersensitivity in both visceral pain models.

84 a lot of effort into the development of new visceral pain models.

85 esses either inflammatory or noninflammatory visceral pain, most likely through peripheral 5HT1(B)/(D

86 overlap of gastroduodenal symptoms, such as visceral pain or hypersensitivity, is often observed in

87 Visceral pain originates from visceral organs in respons

88 en made towards improving the translation of visceral pain, particularly with regard to the activatio

89 ng evidence in support of the existence of a visceral pain pathway that ascends in the dorsal column

90 ative behavioural models evoking somatic and visceral pain pathways, we identify the requirement for

91 enal and rectal barostat studies to evaluate visceral pain perception measured with a visual analog s

92 rain-imaging studies to date have confounded visceral pain perception with anticipation.

93 In mice, it attenuates visceral pain perception, indicating an antinociceptive

94 s suggest sex differences in somatic but not visceral pain perception, motility, and central processi

95 can prevent the establishment of persistent visceral pain postcolitis.

96 Here we examine the role of NaV 1.7 in visceral pain processing and the development of referred

97 Current models of visceral pain processing derived from metabolic brain im

98 entral nervous system (CNS) abnormalities in visceral pain processing in IBS.

99 c noxious heat pain, but is not required for visceral pain processing, and advocate that pharmacologi

100 ng aetiology, physiology and pharmacology of visceral pain proves the clinical importance of this pai

101 have shown a significant tonic modulation of visceral pain, raising the question of whether endogenou

102 of these models addresses specific types of visceral pain, related to the urogenital tract (n=3), to

103 displayed spontaneous, morphine-reversible, visceral pain-related behaviors such as hunching and voc

104 tage pancreatic cancer displayed significant visceral pain-related behaviors, whereas systemic admini

105 ficantly, OEA administration in mice induced visceral pain-related behaviours that were inhibited by

106 uroticism, of which little is known about in visceral pain research.

107 ed that this caused a robust increase in the visceral pain response.

108 f/f/p) mutant mice showed normal thermal and visceral pain responses but were less sensitive to mecha

109 e in the modulation of ACC sensitization and visceral pain responses in VH rats.

110 C) neurons has a critical role in modulating visceral pain responses in viscerally hypersensitive (VH

111 C plays a critical role in the modulation of visceral pain responses in viscerally hypersensitive rat

112 LR4 specific antagonist, TAK-242, attenuated visceral pain sensation in animals with functional TLR4

113 d histone acetylation of genes that regulate visceral pain sensation in the peripheral nervous system

114 However, the central contribution of TLR4 in visceral pain sensation remains elusive.

115 he gut microbiota is required for the normal visceral pain sensation.

116 tic (noxious heat pain threshold) but not in visceral pain signalling.

117 ce or correct microbial dysbiosis may impact visceral pain.SIGNIFICANCE STATEMENT Commercially availa

118 siology of irritable bowel syndrome (IBS), a visceral pain syndrome occurring more commonly in women.

119 volved in sensory and cognitive appraisal of visceral pain; the right prefrontal cortex seems to be i

120 hosocial impairment, high life stress, a low visceral pain threshold, and activation of the midcingul

121 heral NMDA receptors are important in normal visceral pain transmission, and may provide a novel mech

122 t potent antinociception in a mouse model of visceral pain upon systemic administration.

123 s, and Cat-S activates nociceptors to induce visceral pain via protease-activated receptor-2.

124 Visceral pain was evaluated with colorectal distension.

125 Visceral pain was measured in response to colorectal dis

126 la (RVM), a site of descending modulation of visceral pain, was determined by (1) testing the effects

127 ht be used to promote motility and alleviate visceral pain, while restricting systemic bioavailabilit