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1  of long bones), and enteric nervous system (aganglionosis).
2  form of Hirschsprung disease (total colonic aganglionosis).
3  of formation of enteric ganglia (intestinal aganglionosis).
4 n age 15, range 4-32 years; 86% rectosigmoid aganglionosis).
5 using recombinant protein, led to intestinal aganglionosis.
6 t whose dys-regulation is a cause of enteric aganglionosis.
7 layed precursor migration, and induced bowel aganglionosis.
8  mycophenolate-induced migration defects and aganglionosis.
9  able to sensitize Pax3(+/-) mice to colonic aganglionosis.
10  in Hirschsprung's disease (HSCR) or colonic aganglionosis.
11 changes in the colon, is sufficient to cause aganglionosis.
12 ltured avian intestine also leads to hindgut aganglionosis.
13 stinct effects on penetrance and severity of aganglionosis.
14 s to the variation observed in patients with aganglionosis.
15 rk producing variation between patients with aganglionosis.
16 progeny exhibiting significantly more severe aganglionosis.
17  cochlear neurosensory deafness, and enteric aganglionosis.
18 glionic small intestine of mice with colonic aganglionosis.
19 der-dependent, and varies with the extent of aganglionosis.
20 er birth due to congenital distal intestinal aganglionosis.
21 stem as well as hypopigmentation and enteric aganglionosis.
22 oat color spotting and congenital intestinal aganglionosis.
23 sion, rather than a secondary consequence of aganglionosis.
24  otherwise lesser cellular defects result in aganglionosis.
25 c nervous system (ENS) in a model of colonic aganglionosis.
26 tion, Meis3-depleted embryos exhibit colonic aganglionosis, a disorder in which the hindgut is devoid
27 use line (Hry) that displays partial enteric aganglionosis, a loss of melanocytes, and decreased Sox1
28 usion of the ribs, short limbs, distal colon aganglionosis, abnormal migration and axonal projections
29  Mutations in either component cause colonic aganglionosis, also called Hirschsprung disease.
30 ncy differences by gender, segment length of aganglionosis and familiality.
31  functional deficits associated with colonic aganglionosis and gastroparesis, indicating their therap
32     Sox10(Dom)/+ mice exhibit variability of aganglionosis and hypopigmentation influenced by genetic
33 the concurrent development of distal colonic aganglionosis and intestinal ganglioneuromas.
34 utations are associated with both intestinal aganglionosis and MEN-associated tumors.
35 HSCR cases and Sox10 alleles in mice exhibit aganglionosis and pigmentary anomalies typical of a subs
36 ome (WS4), which is characterized by enteric aganglionosis and pigmentation defects.
37 chyme, based on the phenotypes of intestinal aganglionosis and renal agenesis observed in homozygous
38 tor (GDNF), both exhibit complete intestinal aganglionosis and renal defects.
39 tor (GDNF), exhibit both complete intestinal aganglionosis and renal defects.
40   Mutations in Ret and GDNF cause intestinal aganglionosis and renal dysplasia.
41 ereas mice lacking Ret(M) exhibit intestinal aganglionosis and the absence of kidneys with other geni
42 ine gene which is associated with intestinal aganglionosis and the focal absence of melanocytes in he
43  and intestinal infarction, total intestinal aganglionosis, and nonrecoverable congenital secretory d
44         The thought that ganglia proximal to aganglionosis are normal has guided surgical procedures
45 anglia deficits in Sox10Dom mice and defined aganglionosis as a quantitative trait in Sox10Dom interc
46  however, is not sufficient to cause colonic aganglionosis as alterations in the balance of NCC proli
47 deficiency, for example, leads to intestinal aganglionosis (Hirschsprung disease), whereas overactive
48 l medullary thyroid carcinoma and intestinal aganglionosis (Hirschsprung disease).
49              Thorough gut histology revealed aganglionosis, hypoganglionosis, and intestinal smooth m
50 the enteric nervous system (ENS) can lead to aganglionosis in a variable portion of the distal gastro
51  pathway (EdnrB, Edn3, Ece1) and severity of aganglionosis in an extended pedigree of B6C3FeLe.Sox10D
52                     Patients presenting with aganglionosis in association with hypopigmentation are c
53 iciency of Tcof1 and Pax3 results in colonic aganglionosis in mice and may contribute to the pathogen
54 f-function allele (ret.k-) causes intestinal aganglionosis in mice.
55 ected individuals and non-complementation of aganglionosis in mouse intercrosses between Ret null and
56       At one end of the spectrum is complete aganglionosis in patients with end-stage or fulminant di
57 tations of this gene cause distal intestinal aganglionosis in rodents, but its mechanism of action is
58 that vitamin A depletion causes distal bowel aganglionosis in serum retinol-binding-protein-deficient
59 ed with increased penetrance and more severe aganglionosis in Sox10Dom mutants.
60           We have developed a novel model of aganglionosis in which enteric neural crest-derived cell
61 utation-associated HSCR), and Ret(9/-) (with aganglionosis induced by mycophenolate).
62 s the incidence and severity of distal bowel aganglionosis induced by vitamin A deficiency in Rbp4(-/
63 mulative evidence suggests that variation of aganglionosis is due to gene interactions that modulate
64 nt1::Cre;R26iDTR mice in which focal colonic aganglionosis is simultaneously created by diphtheria to
65        Hirschsprung's disease, or congenital aganglionosis, is a developmental disorder of the enteri
66 ung disease (HSCR), or congenital intestinal aganglionosis, is a relatively common disorder of neural
67 ility, allowing improved survival over other aganglionosis models.
68 on of enteric neural crest cells, leading to aganglionosis most commonly in the rectosigmoid colon.
69 ecretion may arise when ENS defects short of aganglionosis occur during development.
70 owledgment of random events that may lead to aganglionosis of the distal bowel.
71 ic neurocristopathy clinically recognized by aganglionosis of the distal gastrointestinal tract.
72 thelin receptor B (EDNRB) signaling leads to aganglionosis of the distal gut (Hirschsprung's disease)
73 schsprung disease (HSCR), which is marked by aganglionosis of the gastrointestinal (GI) tract.
74 stoma (NB) with Hirschsprung disease (HSCR) (aganglionosis of the terminal bowel) and congenital cent
75  to Hirschsprung's disease (HSCR; congenital aganglionosis of the terminal bowel), which is still imp
76  mutation that develop fetal megacolon after aganglionosis of the terminal colon) were prepared to re
77          Using a non-lethal model of colonic aganglionosis, our results demonstrate the potential of
78  = 0.13) and significantly so with length of aganglionosis (p = 7.6 x 10(-5)) and familiality (p = 6.
79  proteins including Shc, caused distal colon aganglionosis reminiscent of Hirschsprung disease (HSCR)
80  by 1 month of age and had distal intestinal aganglionosis reminiscent of Hirschsprung disease (HSCR)
81 uses Hirschsprung disease with total colonic aganglionosis, restored ENCC function.
82      Importantly, our studies establish that aganglionosis results only with severely reduced gene ex
83 stine, ENCC migration is arrested and distal aganglionosis results, suggesting that ENCCs require the
84 glionosis that are analogous to the variable aganglionosis seen in human HSCR families.
85 is required to rescue a mouse model of total aganglionosis, suggesting opportunities in the treatment
86         Removal of the ceca leads to hindgut aganglionosis, suggesting that they are required for ENS
87 and 11 do not coincide with previously known aganglionosis susceptibility genes or modifier loci and
88 on in penetrance and expressivity of enteric aganglionosis that are analogous to the variable agangli
89  mutants ranges over a continuum from severe aganglionosis to no detectable phenotype in the gut.
90          To study the development of colonic aganglionosis we have utilized a novel knockout mouse (E
91 identify genes that modulate Sox10-dependent aganglionosis, we performed a single nucleotide polymorp
92 PSC) lines from 1 patient with total colonic aganglionosis (with the G731del mutation in RET) and fro