ライフサイエンスコーパス: dysmotility

1 and often confirms the clinical suspicion of dysmotility.

2 ith esophageal atresia and severe esophageal dysmotility.

3 expressing cells to prevent pathological gut dysmotility.

4 evelopmental anomalies, including intestinal dysmotility.

5 d supporting glia that results in intestinal dysmotility.

6 a fibrosis, strictures, or esophageal muscle dysmotility.

7 ogy stands to transform our ability to treat dysmotility.

8 y induce TLR4-mediated neurodegeneration and dysmotility.

9 ntial as a cell therapy for gastrointestinal dysmotility.

10 be targetable in conditions characterized by dysmotility.

11 ct to driving enteric neuropathy and colonic dysmotility.

12 t exhibit WD-induced myenteric cell loss and dysmotility.

13 mice did not exhibit myenteric cell loss or dysmotility.

14 g disease characterized by severe intestinal dysmotility.

15 ) analogs may develop enteric neuropathy and dysmotility.

16 etry and/or a barostat, can identify colonic dysmotility.

17 infertility, resulting from cilia and sperm dysmotility.

18 om defecation disorders and advanced colonic dysmotility.

19 to the brush border due to small intestinal dysmotility.

20 ecrease the inflammation that contributes to dysmotility.

21 phages within the muscularis associated with dysmotility.

22 scle groups associated with gastrointestinal dysmotility.

23 ticipates in mediating early TLR4-transduced dysmotility.

24 ession/signaling in causing gastrointestinal dysmotility.

25 translated well into human gastrointestinal dysmotility.

26 ferent forms of experimental antigen-induced dysmotility.

27 d induced mast cell degranulation in mid-gut dysmotility.

28 ce of urinary retention and gastrointestinal dysmotility.

29 or, could lead to new therapies for pain and dysmotility.

30 ese cells may contribute to gastrointestinal dysmotilities.

31 arditis (0.52%), and self-limited esophageal dysmotility (0.04%).

32 h potential impact on global health included dysmotility (59%), hypertension (37%), osteoporosis (22%

33 re more likely to have underlying esophageal dysmotility (95.6% vs. 70.7% respectively; p < 0.001), p

34 ecture and neurochemical profile, intestinal dysmotility, abnormal mucosal secretion, reduced levels

35 ish, planaria, and mice also display ciliary dysmotility accompanied by ODA loss.

36 use model had time-dependent gastro-duodenal dysmotility after LPS-injection that paralleled zonulin

37 r mechanisms, which contribute to intestinal dysmotility after selective intestinal I/R injury.

38 Autoimmune gastrointestinal dysmotility (AGID) is a limited form of autoimmune auton

39 m of clinical features (including severe gut dysmotility and a movement disorder) and electrographic

40 al-Mylk-knockout mouse model with severe gut dysmotility and abnormal function of the bladder support

41 ities of gastric motility (corpus and fundus dysmotility and antral hypomotility), pyloric resistance

42 Gastrointestinal (GI) dysmotility and associated conditions affect over 20% of

43 y effects of LPS leading to gastrointestinal dysmotility and enhanced immune activation.

44 ribute to the secondary GI events, including dysmotility and increased mucosal permeability.

45 s might contribute to NEC through intestinal dysmotility and increased TLR4 activation, suggesting en

46 ortant pathogenetic role in gastrointestinal dysmotility and may destroy enteric neurons.

47 nd consistent clinical signs were severe gut dysmotility and neurological abnormalities, including le

48 ies, who showed the common occurrence of gut dysmotility and neurological manifestations reminiscent

49 mutations in CCDC114 are a cause of ciliary dysmotility and PCD and further demonstrate the utility

50 assembly and that its variants cause ciliary dysmotility and PCD with laterality defects.

51 anding the role of eosinophils in intestinal dysmotility and protein loss.

52 nitis (EAEG) manifests with gastrointestinal dysmotility and rapidly progresses to lethal ileus.

53 stinal surgery protects against postsurgical dysmotility and reduces the severity of postoperative il

54 14 years, IQR (12.25, 18)] developed gastric dysmotility and were HP2 isoform-producing.

55 nutrient malabsorption, bowel dilatation and dysmotility, and changes in bacterial flora influence th

56 nes interleukin-4 and -13 in antigen-induced dysmotility, and interleukin-5 in the pathogenesis of mu

57 pmental disorders including gastrointestinal dysmotility, and investigate the underlying molecular ba

58 ctive phenotype that prevents neuronal loss, dysmotility, and maintains energy balance during subsequ

59 verse effects, including anxiety, anhedonia, dysmotility, and, in children exposed in utero, an incre

60 son, WNV-triggered ENS injury and intestinal dysmotility appeared to not require infiltrating monocyt

61 es in the regulation of gut hormones and gut dysmotility are believed to play a role.

62 , because manometry helps in part to exclude dysmotility as a cause of symptoms.

63 sed woman developed chronic gastrointestinal dysmotility as a consequence of acute cytomegalovirus in

64 vous system, which may contribute to colonic dysmotility associated with diverticulitis.

65 he inflamed colon and this may contribute to dysmotility associated with inflammatory diseases.

66 ice were protected from the inflammation and dysmotility associated with POI.

67 stinal transplantation contributing to graft dysmotility, bacterial translocation, and possibly, acut

68 with NEC typically display gastrointestinal dysmotility before systemic disease is manifest, suggest

69 on is believed to underlie ageing-associated dysmotilities but the mechanisms have not been fully elu

70 ripheral neuropathy, severe gastrointestinal dysmotility, cachexia and leukoencephalopathy.

71 e external ophthalmoplegia; gastrointestinal dysmotility; cachexia; peripheral neuropathy; and leucoe

72 efined clinically by severe gastrointestinal dysmotility; cachexia; ptosis, ophthalmoparesis, or both

73 pecimens from patients with gastrointestinal dysmotility, CD8 T cell-mediated ganglionitis was detect

74 inherited disorder of ciliary and flagellar dysmotility characterized by chronic upper and lower res

75 riants in sixteen autism genes, highlighting dysmotility, consistent with potential enteric neuron dy

76 resentation and causes of chronic intestinal dysmotility continue to expand.

77 ystemic disease is manifest, suggesting that dysmotility could drive NEC development.

78 New onset esophageal dysmotility, delayed gastric emptying time, and abnormal

79 r isolated or syndromic ocular and/or facial dysmotility disorders, but who did not have the combined

80 ial disease characterized by predominant gut dysmotility, encephalopathy, and neuromuscular abnormali

81 oss in the premature intestine could lead to dysmotility, exaggerated TLR4 signaling, and NEC develop

82 l smooth muscle that are responsible for the dysmotility following small bowel transplantation (SBTX)

83 acological approach preventing postoperative dysmotility for clinical intestinal transplantation.

84 remaining 184 (80%) had at least 1 region of dysmotility, for a total of 336 regions of abnormal moti

85 visual pathway damage, and ptosis and ocular dysmotility from extraocular muscle involvement.

86 atches as well as the development of gastric dysmotility, gastromegaly and cachexia.

87 uld have indicated that treatment of gastric dysmotility had been postponed in any patient.

88 ce implicating mucosal allergic responses in dysmotility has been extended to include disorders consi

89 ich is mechanistically linked to gallbladder dysmotility in critical illness.

90 fects their daily life, the mechanisms of GI dysmotility in DM1 remain an understudied aspect of the

91 igate myogenic mechanisms contributing to GI dysmotility in DM1.

92 ochondrial fragmentation, depolarization and dysmotility in genetically diverse ALS patient reprogram

93 These effects could contribute to dysmotility in HSCR, which predominantly affects males,

94 ise mechanisms that lead to gastrointestinal dysmotility in inflammatory bowel diseases have not been

95 PYY receptor blockade rescued dysmotility in mice lacking epithelial RET.

96 study highlights the frequent occurrence of dysmotility in more than 1 region of the gastrointestina

97 ute CMV infection can cause gastrointestinal dysmotility in nonimmunocompromised individuals and that

98 be a reliable screening tool for esophageal dysmotility in patients with elevated average maximum IB

99 Mechanisms of intestinal dysmotility in patients with pseudoobstruction and colon

100 Zonulin correlated with gastric dysmotility in patients.

101 otential mechanism for the continued gastric dysmotility in postsurgical HSCR patients.

102 vity reduced cellular inflammation and bowel dysmotility in rat and mouse models of POI.

103 advanced the assessment of gastrointestinal dysmotility in SSc.

104 t concurrence of both upper- and lower-tract dysmotility in the same patients.

105 ological state, intestinal inflammation, and dysmotility in three cohorts of IBD patients.

106 DYRK1A reveals that perturbation causes gut dysmotility in vivo, which can be ameliorated by treatme

107 Colonic dysmotility, in particular, remains poorly managed by co

108 mechanisms that appear to be involved in the dysmotility, including defects in neurons, smooth muscle

109 with varying degrees of success for several dysmotility, inflammatory, hormonal, and neurologic diso

110 Intestinal dysmotility is a component of many neurodegenerative dis

111 After intestinal transplant, immune-mediated dysmotility is common.

112 Small-bowel dysmotility is recognized in a number of diseases, but i

113 Gastrointestinal dysmotility is the most prominent manifestation, with re

114 e external ophthalmoplegia, gastrointestinal dysmotility, leukoencephalopathy, thin body habitus, and

115 +/- 15 years old, 75% were female, 70% with dysmotility-like FD, and 30% with ulcer-like FD) were ra

116 Gastrointestinal dysmotility may be involved in the development of bacter

117 indings need confirmation, they suggest that dysmotility may result subsequent to these infections.

118 requiring dilatation, persistent esophageal dysmotility (mid esophageal hematoma), and vocal cord pa

119 as the presence of a DeMeester score >14 or dysmotility more severe than "mild nonspecific disorder"

120 y might be involved in the prodromal gastric dysmotility observed in patients with early-stage Parkin

121 re, but is underrecognized as a cause for GI dysmotilities of varying anatomic extent, severity, and

122 eterogeneous inherited disorder arising from dysmotility of motile cilia and sperm.

123 joint contractures, dysmorphic features and dysmotility of the gut.

124 Dysmotility of transplanted small bowel results from rep

125 J (B6) background and very low penetrance of dysmotility on a 129SvJ (129) background.

126 n elevated AM-IBP correlates with esophageal dysmotility on HRM and/or delayed esophageal emptying on

127 r barium tablet arrest on TBE and esophageal dysmotility on HRM.

128 nt lymphoproliferative disorder (n=1), graft dysmotility or dysfunction (n=3), ACR with severe infect

129 stinal mucosal inflammation (associated with dysmotility or short bowel) were significantly shorter t

130 cardia syndrome, idiopathic gastrointestinal dysmotility, or diabetic autonomic neuropathy (9 percent

131 in a swine model of oesophageal and stomach dysmotility (p < 0.05, student's t-test).

132 s and contribute to intestinal inflammation, dysmotility, pain, neuroplasticity, and tumorigenesis.

133 five family members with distinctive ocular dysmotility patterns that co-segregated with a novel hyp

134 HP2 correlated with gastric dysmotility (r = - 0.51, CI - 0.81 to 0.003, p = 0.048).

135 gmus, gastroesophageal reflux, constipation, dysmotility, recurrent infections, seizures, and structu

136 abnormalities, poor growth, gastrointestinal dysmotility, renal tubular acidosis, seizures, and episo

137 tes gut motility, thereby contributing to GI dysmotilities reported in HIV patients.

138 ffuse SSc, calcinosis, Raynaud's, esophageal dysmotility, sclerodactyly, and telangiectasias syndrome

139 inosis cutis, Raynaud's syndrome, esophageal dysmotility, sclerodactyly, and telangiectasias) syndrom

140 (calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia) syndrome.

141 erance, secretomotor, upper gastrointestinal dysmotility, sleep dysfunction, urinary, and autonomic d

142 l diseases frequently cause gastrointestinal dysmotility, suggesting that they may also affect the en

143 sinophil infiltration in proximal and distal dysmotility syndromes (oesophageal, gastric and colorect

144 Intestinal dysmotility syndromes have been epidemiologically associ

145 were intestinal gastroschisis and intestinal dysmotility syndromes in children, and mesenteric thromb

146 (CIPO) is characterized by severe intestinal dysmotility that mimics a mechanical subocclusion with n

147 stem (ENS) and glia, which led to intestinal dysmotility; these T cells used multiple and redundant e

148 ient mice develop transient gastrointestinal dysmotility, urinary retention, dilated pupils, reduced

149 teric neurons, acetylcholine deficiency, and dysmotility via TGF-beta2.

150 Gallbladder dysmotility was associated with the impaired FGF19 respo

151 Gastrointestinal dysmotility was confirmed by delayed emptying on gastric

152 Gastric dysmotility was reduced similarly in Ztm and WT mice in

153 A single region of dysmotility was seen in 92 patients (50%), 2 regions in

154 urgery causes postoperative gastrointestinal dysmotility which can progress to paralytic ileus.

155 NF-RET signaling in patients with intestinal dysmotility which is associated with reduction in neural

156 a (PCD), a disorder characterized by ciliary dysmotility; yet, radial spoke functions remain unclear.