ライフサイエンスコーパス: detrusor

1 remodeling of urinary bladder smooth muscle (detrusor).

2 uscles, and phasic contractions occur in the detrusor.

3 ion, capacity, compliance, and inappropriate detrusor activity during filling; (3) urethral pressure

4 tion consists of an inhibitory effect on the detrusor and presumably the lower rectum resulting from

5 l voiding with an uncoordination between the detrusor and urinary sphincter, and enuresis.

6 ssion in nerve fibers in the urinary bladder detrusor and urothelium was decreased or eliminated afte

7 activation of smooth muscle of the bladder (detrusor) and striated muscle of the external urethral s

8 tween layers of the bladder wall (mucosa vs. detrusor) and the presence and functional contribution o

9 taining was found in both the smooth muscle (detrusor) and urothelium layers of the urinary bladder.

10 cts of overactive sphincter afferents on the detrusor, and determination of the central nervous syste

11 Knockout of Ogg1 in detrusor cells resulted in accumulation of reactive oxyg

12 ic knock-out of Ogg1 in as few as 10% of the detrusor cells tripled the proliferation of the remainin

13 ulation has an indirect modulatory effect on detrusor contractility rather than a direct effect on th

14 ractivity and a smaller number have impaired detrusor contractility, sensory urgency, sphincteric inc

15 Mechanisms responsible for regulating detrusor contraction during filling are poorly understoo

16 How magnetic stimulation suppresses detrusor contraction is not known.

17 ceptor stimulation produces the main part of detrusor contraction.

18 and in forming the input limb to involuntary detrusor contractions in neurogenic and probably also no

19 evaluation at 8 weeks after SCI showed that detrusor contractions of the bladder recovered similarly

20 ) can result from an interaction of unstable detrusor contractions, delayed arousal from sleep, and n

21 ization of PDGFRalpha(+) cells and decreased detrusor contractions.

22 has a role beyond its known contribution to detrusor contractions.

23 ited currents activated by GSK and increased detrusor contractions.

24 results show that the extent of recovery of detrusor-EUS coordination depends on injury severity and

25 verely injured rats, the chronic recovery of detrusor-EUS coordination was very incomplete and correl

26 at the injury site and complete recovery of detrusor-EUS coordination.

27 residual supraspinal connections on chronic detrusor-EUS coordination.

28 ere we describe a novel pathway to stabilize detrusor excitability involving platelet-derived growth

29 amin-sensitive stabilizing factor regulating detrusor excitability is likely to be due to the express

30 4 channels during bladder filling stabilizes detrusor excitability.

31 ese cells might participate in regulation of detrusor excitability.

32 Bladder smooth muscle (detrusor) exhibits spontaneous rhythmic activity (tone)

33 phosphamide-induced bladder inflammation and detrusor expansion.

34 Although detrusor expresses the S1P receptors S1P1 and S1P2, only

35 Detrusor-external sphincter dyssynergia (DSD) is a commo

36 ies have demonstrated age-related changes in detrusor function and urothelial transmitter release but

37 le out baseline retention suggestive of poor detrusor function, and patients should be kept under car

38 rostatic surgery by providing information on detrusor function; and non-invasive urodynamic technique

39 nger intercontractile intervals (P<0.05) and detrusor hyperactivity (3-fold more prevoid contractions

40 formation of the NLRP3 complex resulting in detrusor hyperplasia.

41 d micturition pressure and fewer episodes of detrusor hyperreflexia.

42 Some bladders with detrusor hypertrophy function close to normal (compensat

43 of decompensated bladders to empty, despite detrusor hypertrophy, is associated with an overexpressi

44 trast, older animals with diabetes exhibited detrusor hypoactivity, findings consistent with clinical

45 rease in the number of CARTp-IR cells in rat detrusor in early postnatal development; 2) apoptotic ev

46 In children with NE and DVS, detrusor instability may play a major role in the causat

47 c, conservative therapies aimed at resolving detrusor instability or bladder outlet obstruction.

48 anical bladder outlet obstruction may induce detrusor instability with subsequent obstructed/overacti

49 ment for neuropathic bladder dysfunction and detrusor instability.

50 s, increase bladder compliance, and decrease detrusor instability.

51 Overactivity in the detrusor is a common clinical problem.

52 ctivity for c-kit was detected in mucosa and detrusor layers of pig bladder.

53 ICs, was investigated in the mucosa and the detrusor layers of the pig bladder.

54 uption of SHH signaling, a known mediator of detrusor morphogenesis.

55 -labeling, was up-regulated in fetal bladder detrusor muscle and lamina propria cells and that this w

56 Three types existed in the detrusor muscle and one major type in the sub-urothelium

57 ammation, increased mast cell numbers in the detrusor muscle have been reported in a subset of IC pat

58 eflexively increases activity of the bladder detrusor muscle in anesthetized rats.

59 The strong expression of PARs in the detrusor muscle indicates the need for studies on the ro

60 ccount of this evidence, we propose that the detrusor muscle is arranged into modules, which are circ

61 ooth muscle cells (SMCs) in vitro and in the detrusor muscle of a mechanically overloaded bladder in

62 c component of neurotransmission in isolated detrusor muscle of guinea pig urinary bladder.

63 s assumption by studying E-C coupling in the detrusor muscle of wild type and Homer1(-/-) mice and by

64 al recording from smooth muscle cells of the detrusor muscle revealed spontaneous depolarizations, di

65 omplished by suppressing contractions of the detrusor muscle that lines the bladder wall.

66 ls subjacent to the epithelium and a thinner detrusor muscle that was not attributable to disruption

67 as associated with higher sensitivity of the detrusor muscle to muscarinic stimulation and membrane d

68 S1P-induced contraction of detrusor muscle was dependent on stretch and intracellul

69 Most nerve endings were located in detrusor muscle where the three types could be identifie

70 he hypogastric (presumably inhibitory to the detrusor muscle).

71 e pelvic nerve (presumably excitatory to the detrusor muscle); and a pathway involving the pelvic ner

72 ereas PAR-1 and PAR-2 are predominant in the detrusor muscle, and PAR-4 is expressed in peripheral ne

73 an explanation for purinergic relaxation in detrusor muscles and show that there are no discrete inh

74 eported a new class of interstitial cells in detrusor muscles and showed that these cells could be id

75 mooth muscle cells (SMCs) were isolated from detrusor muscles of PDGFRalpha(+)/eGFP and smMHC/Cre/eGF

76 ient contraction and prolonged relaxation of detrusor muscles.

77 Experiments used isolated guinea-pig detrusor myocytes and store Ca(2+) content was estimated

78 fold increase in the cross-sectional area of detrusor myocytes following PBOO in male New Zealand Whi

79 iological studies using isolated rat bladder detrusor myocytes have demonstrated that compound 79 pro

80 re performed in wholemounts of urothelium or detrusor or cryostat sections of the bladder.

81 Neurogenic detrusor overactivity (NDO) is a well known consequence

82 Neurogenic detrusor overactivity (NDO) is among the most challengin

83 multiple sclerosis often develop neurogenic detrusor overactivity (NDO), which currently lacks a uni

84 Approximately half have detrusor overactivity and a smaller number have impaired

85 established in the management of refractory detrusor overactivity and overactive bladder.

86 urrent therapeutic alternatives for managing detrusor overactivity and possible future developments a

87 wn to increase cystometric capacity, inhibit detrusor overactivity and resolve overactive bladder sym

88 treatment, both in patients with neurogenic detrusor overactivity and those with idiopathic detrusor

89 nary incontinence, overflow incontinence and detrusor overactivity are the major categories of urinar

90 Bladders of DKO animals exhibited detrusor overactivity at an early stage: increased frequ

91 Detrusor overactivity is a relatively common yet embarra

92 Detrusor overactivity is a relatively common yet embarra

93 in our understanding of the pathogenesis of detrusor overactivity is slow but steady.

94 Detrusor overactivity is the occurrence of abnormal incr

95 onventional treatments like drug therapy for detrusor overactivity or sling procedures for female str

96 Detrusor overactivity poses a major challenge to physici

97 tract dysfunction, especially for those with detrusor overactivity refractory to anticholinergics, is

98 We propose that detrusor overactivity results from exaggerated symptomat

99 ts acting on alternative pathways underlying detrusor overactivity with the intention of improving st

100 ive in reducing incontinence associated with detrusor overactivity, and repeated treatments appear sa

101 with pressure-flow urodynamics demonstrating detrusor overactivity, in the setting of a clinically re

102 r hypersensitivity as well as non-neurogenic detrusor overactivity, there is up-regulation of unmyeli

103 by targeting alternative pathways affecting detrusor overactivity.

104 ave transformed the management of neurogenic detrusor overactivity.

105 act symptoms/overactive bladder syndrome/and detrusor overactivity.

106 rusor overactivity and those with idiopathic detrusor overactivity.

107 gaining importance in the pathophysiology of detrusor overactivity.

108 neurogenic and probably also non-neurogenic detrusor overactivity.

109 es, which diagnose obstruction by evaluating detrusor pressure and flow rate during voiding.

110 IL-1beta-induced detrusor proliferation and hypertrophy could be reversed

111 rheumatoid arthritis therapeutic, prevented detrusor proliferation in conditioned media experiments

112 be a useful marker to estimate the degree of detrusor remodeling and contractile dysfunction in PBOO.

113 orded potent KCOs that possessed the desired detrusor selectivity when administered orally.

114 Inhibition of TREK-1 channels in the human detrusor significantly delayed relaxation of the stretch

115 hesis that NDO is associated with changes in detrusor smooth muscle (DSM) large conductance Ca(2+)-ac

116 While Hpse2 is largely dispensable for detrusor smooth muscle and urothelial cell fate determin

117 ied higher levels of expression of TREK-1 in detrusor smooth muscle cells in comparison to bladder mu

118 he transient rise of intracellular Ca(2+) in detrusor smooth muscle cells is due to the release of Ca

119 We speculate that enhanced apoptosis in detrusor smooth muscle cells is part of a remodeling res

120 stimulation were examined on preparations of detrusor smooth muscle from guinea-pig urinary bladder u

121 lso a feature of differentiated vascular and detrusor smooth muscle in the bladder.

122 thral walls contract at the same time as the detrusor smooth muscle in the body of the bladder.

123 on-induced expression of TNC and CTGF in the detrusor smooth muscle of bladders from wild-type mice w

124 ession was also detected in the vascular and detrusor smooth muscle of the human bladder.

125 sine-1-phosphate (S1P), in regulating rabbit detrusor smooth muscle tone and contraction.

126 ur results demonstrate that S1P may regulate detrusor smooth muscle tone and suggest that dysregulati

127 natal day [P]1, P3), CARTp-IR cell bodies in detrusor smooth muscle were observed in large clusters (

128 ut the bladder, including the urothelium and detrusor smooth muscle.

129 ile 1 in the relaxation of precontracted rat detrusor strips can also be obtained with cyanobenzylami

130 adders demonstrated basal PCs whilst denuded-detrusor strips did not.

131 Detrusor strips from 5-HT3Avs/vs mice failed to contract

132 ic contractions (PCs) in mucosal and denuded-detrusor strips from juvenile and adult pigs were assess

133 duced PCs of both juvenile and adult denuded-detrusor strips, although strips from juvenile bladders

134 tion was studied in vitro using isolated rat detrusor strips.

135 th muscle between the urothelium and bladder detrusor, termed the muscularis mucosa.

136 Detrusor tissue from these mice was used to identify two

137 rect evidence that the response of the human detrusor to mechanical stretch is regulated by activatio

138 UAB) can be used as a general term, covering detrusor underactivity as the urodynamic diagnosis, and

139 rwent a urodynamic study, which demonstrated detrusor underactivity of the bladder in 7 patients.

140 obstruction, and urinary retention owing to detrusor underactivity.

141 found that GFRalpha3-IR axons innervated the detrusor, vasculature, and urothelium, but only part of

142 ethral angle, intraprostatic protrusion, and detrusor wall thickness are used to find a noninvasive w

143 IR, but the noradrenergic innervation of the detrusor was GFRalpha3-negative.

144 channels in ICCs-DM were responsible for the detrusor weak contractility of Diabetic cystopathy (DCP)