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1 ilation of the urinary bladder and defective intestinal motility.
2 eurons, thereby enabling the coordination of intestinal motility.
3 cts in ascl1a-/- embryos also contributes to intestinal motility.
4 ition of PAK in edematous intestine improved intestinal motility.
5 e enteric nervous system (ENS), and abnormal intestinal motility.
6 oendocrine products in maintenance of normal intestinal motility.
7 te primarily to ischaemia-induced changes in intestinal motility.
8 reported in adult human gut, and OT affects intestinal motility.
9 ting novel and relevant information on small intestinal motility.
10 ting novel and relevant information on small intestinal motility.
11 et for modulating immune-mediated effects on intestinal motility.
12 esponsive eczema and a marked disturbance of intestinal motility.
13 hlights the importance of these compounds in intestinal motility.
14 nterstitial cells of Cajal in the control of intestinal motility.
15 in the regulation of smooth muscle tone and intestinal motility.
16 is associated with a subsequent decrease in intestinal motility.
17 sponses contributing to neural regulation of intestinal motility.
18 the walls of the intestinal tract, regulate intestinal motility, a well-characterized reflex control
21 t reduced intestine diameters, but increased intestinal motilities along with thickened muscle fibers
22 a subset IPANs and that these cells regulate intestinal motility and epithelial cell proliferation in
23 ups with exenatide, but suppression of small intestinal motility and flow was observed even in subjec
24 mportant molecular mechanism for controlling intestinal motility and secretion by regulating the exci
25 The mechanism is believed to be decreased intestinal motility and stool frequency resulting in mor
26 important gastrointestinal functions such as intestinal motility and transport, intestinal permeabili
27 ease of intestinal neuropeptides, control of intestinal motility, and/or modulation of intestinal flu
28 h intestinal barrier dysfunction and reduced intestinal motility as determined by in vivo intestinal
29 ew added to the basic understanding of small-intestinal motility as well as its alteration in disease
30 togen have the potential to influence gastro-intestinal motility; both are key components of hormone
31 s are also postulated to result from altered intestinal motility, but rotavirus infection had no effe
33 kely peptide candidate because inhibition of intestinal motility by fat in the distal gut correlated
34 ocus, which in humans is associated with the intestinal motility disorder known as Hirschsprung disea
35 y be relevant for understanding and treating intestinal motility disorders and also suggest that enha
37 n antibiotic treatment or chemically induced intestinal motility disturbance, and C. difficile exploi
39 ion between bacterial overgrowth and altered intestinal motility gathers support in a variety of cond
45 ng mainly at peripheral while increasing the intestinal motility in morphine-pelleted mice (ED(50) =
52 c smooth muscle cells, resulting in abnormal intestinal motility, severe abdominal pain, malnutrition
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