ライフサイエンスコーパス: gastric motility

1 ric-NST or -DMN neuron responsiveness, or on gastric motility.

2 nsulin or central 2-DG causes an increase in gastric motility.

3 f the vago-vagal reflex circuitry regulating gastric motility.

4 omach of a patient with significantly slowed gastric motility.

5 r (mu, delta, and kappa) stimulation affects gastric motility.

6 reduced chylous lymph-induced inhibition of gastric motility.

7 more potent than control lymph in inhibiting gastric motility.

8 ay be responsible for oesophageal control of gastric motility.

9 gastrin release, gastric acid secretion, and gastric motility.

10 ich may be prostaglandin dependent, inhibits gastric motility.

11 t correlation was found between symptoms and gastric motility.

12 n and inhibition of NTS SST neurons enhanced gastric motility.

13 constipation, nausea, dysphagia, and reduced gastric motility.

14 al pre-motor neurons in the DMV that control gastric motility.

15 lity of assisting in the evaluation of human gastric motility.

16 aptic pathway modulates the vagal control of gastric motility.

17 jects, including satiety or satiation (21%), gastric motility (14%), psychological factors (13%), and

18 Antidepressants and newer gastric motility agents show promise.

19 ) the pathway mediating reflex inhibition of gastric motility and (2) activation of duodenal vagal af

20 (60 nl)(-1)) in mNTS produced inhibition of gastric motility and an increase in intragastric pressur

21 nteric-sympathetic-spinal pathway to inhibit gastric motility and appetite.

22 of vagal efferent motoneurons that regulate gastric motility and emptying and consequently influence

23 glia neurons contributes to the reduction in gastric motility and emptying associated with opioid use

24 ration has previously been shown to increase gastric motility and emptying.

25 Gastric motility and haptoglobin (HP) 2 isoform quantifi

26 scles of the stomach is important for normal gastric motility and is impaired in motility disorders.

27 eceptors in the brainstem appear to modulate gastric motility and pancreatic exocrine secretion.

28 ts that alpha-1 agonists have in suppressing gastric motility and producing anorexia.

29 od flow, and nutrient uptake and suppressing gastric motility and secretion.

30 and DMV neuronal excitability, dysregulated gastric motility and tone and emptying, and prevented th

31 ngs of DMV neurons and in vivo recordings of gastric motility and tone demonstrated that, following p

32 18 mmHg) provoked a significant reduction in gastric motility and tone recorded with strain gauges.

33 em slice preparations, in vivo recordings of gastric motility and tone, measurement of gastric emptyi

34 est that glucoprivation-induced increases in gastric motility are dependent on intact hindbrain astro

35 ogastrography (EGG) non-invasively evaluates gastric motility but is viewed as lacking clinical utili

36 detector for the purpose of evaluating human gastric motility by detecting the presence of gastric pe

37 It affects gastric motility by stimulating interdigestive antrum an

38 induced by erythromycin, and retardation of gastric motility caused by morphine.

39 erstand the network dynamics associated with gastric motility control in the DVC, we focused on anoth

40 of gastroparesis comprises abnormalities of gastric motility (corpus and fundus dysmotility and antr

41 Gastroparesis is a complex gastric motility disorder characterized by nausea, vomit

42 een suggested as a therapy for patients with gastric motility disorders or morbid obesity.

43 s may provide a novel treatment for diabetic gastric motility disorders.

44 omodulation device treatments for addressing gastric motility disorders.

45 nal bloating and loss of appetite typical of gastric motility disorders.

46 dies investigating ghrelin mimetics to treat gastric motility disorders.

47 This study evaluated gastric motility in children with AM.

48 xamined the relationship between zonulin and gastric motility in critical care patients and a transla

49 aracterization of patterns of development of gastric motility in early infancy.

50 pathophysiologic roles of 5-HT deficiency in gastric motility in mice and humans.

51 ed in electroacupuncture (EA) stimulation of gastric motility in mice.

52 l for each site) of CRF in the DVC decreased gastric motility in rats pretreated with the muscarinic

53 iew focuses on progress made in the field of gastric motility in the past year, emphasizing advances

54 findings suggest a possible role of abnormal gastric motility in the pathogenesis of AM.

55 erstanding Helicobacter pylori infection and gastric motility in the pediatric population.

56 relationship between utilizable nutrient and gastric motility is well recognized, the explanation of

57 nds and activates enteric neurons to promote gastric motility, likely to stimulate digestion and incr

58 mputational framework constituted of a novel gastric motility network (GMN) model we address the hypo

59 asing digestive discomfort and alteration of gastric motility not only in healthy subjects but also i

60 tion of CRF(2) receptors and the decrease in gastric motility observed following microinjection of CR

61 contractility; electrical activity; regional gastric motility of the fundus, antrum, and pylorus; and

62 tion in critically ill adults; however, poor gastric motility often prevents nutritional targets bein

63 on pacemaker activity, mechanical responses, gastric motility patterns, gastric emptying and GI trans

64 e dorsal vagal complex (DVC) is essential to gastric motility regulation.

65 roles of EC cell-derived 5-HT in regulating gastric motility remain a major point of conjecture.

66 e receptors on regulating nitrergic-mediated gastric motility remains inconclusive.

67 However, the effect of these neurons on gastric motility remains unknown.

68 n of NTS NPY neurons increased and decreased gastric motility, respectively, whereas both activation

69 tiology is likely multifactorial, related to gastric motility, respiratory secretions, and medication

70 ed by thyrotrophin-releasing hormone and the gastric motility response to DMV microinjections of TRH

71 tion of gastroparesis and other disorders of gastric motility; Society of Nuclear Medicine and Molecu

72 of inhibitory effects of central opioids on gastric motility still remains unclear.

73 duced gastric retention in an acute model of gastric motility that traces the passage of a food bolus

74 ring GES can yield additional information on gastric motility to help explain patients' symptoms.

75 wnstream NST neurons that, in turn, suppress gastric motility via action on neurons in the dorsal mot

76 Gastric motility was characterized in spontaneously diab

77 Inhibition of gastric motility was measured manometrically in urethane