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1  in pigmented mice that die postnatally from megacolon.
2 erized by pigmentation defects, deafness and megacolon.
3 alectomy due to previous adrenal surgery and megacolon.
4  the bowel, leading to bowel obstruction and megacolon.
5 t completely white and die as juveniles from megacolon.
6 rung syndrome and its murine model, Dominant megacolon.
7 redominantly white and die as juveniles from megacolon.
8 iarrhea, pseudomembranous colitis, and toxic megacolon.
9 tion, bleeding, vasculitis, cancer and toxic megacolon.
10  of peristalsis and the development of toxic megacolon.
11 I-related complication, including 2 cases of megacolon, 1 colectomy, and 22 intensive care unit (ICU)
12  lethal spotting mutation that develop fetal megacolon after aganglionosis of the terminal colon) wer
13 n penetrance and expressivity of aganglionic megacolon analogous to the variation observed in patient
14 syndromes from mild diarrhea to severe toxic megacolon and death.
15             Nup35 mutants developed a severe megacolon and exhibited a reduced lifespan.
16 ype B (EDNRB) produce congenital aganglionic megacolon and pigment abnormalities in mice and humans.
17 vary in severity from mild diarrhea to toxic megacolon and/or death.
18  in which myenteric neuronal hyperplasia and megacolon are seen.
19  lethal (sl) rats, which exhibit aganglionic megacolon associated with white coat color.
20 of the following: colonic perforation, toxic megacolon, colectomy, admission to an intensive care uni
21                       Congenital aganglionic megacolon, commonly known as Hirschsprung disease (HSCR)
22                                     Dominant megacolon (Dom) is a mutation in an uncharacterized muri
23  of neural crest development in the Dominant megacolon (Dom) mice is associated with a Sox10 mutation
24 se subclinical peripheral disease, including megacolon, enlarged stomach and urinary bladder, soft ti
25 el approaches to the treatment of congenital megacolon (Hirschsprung's disease) based on the colonisa
26 t CDI comprising any of the following: toxic megacolon, ileus, perforation, or colectomy.
27 schsprung's disease in humans or aganglionic megacolon in animals.
28 rmline mutations in c-ret lead to congenital megacolon in humans, while a loss-of-function allele (re
29 atment related; one death (due to sepsis and megacolon) in the placebo group was deemed to be treatme
30 ng disease (HSCR), or congenital aganglionic megacolon, is the most common cause of congenital bowel
31 ng disease (HSCR), or congenital aganglionic megacolon, is the most frequent cause of congenital bowe
32 nfluenced by rectal biopsy, transit studies, megacolon/megarectum, degree of soiling/incontinence, an
33 -Hirschsprung syndrome patients nor Dominant megacolon mice have dysmyelinating features, suggesting
34 hal spotted and piebald lethal, the Dominant megacolon mutation directly or indirectly affects microe
35 train type with severe disease (ileus, toxic megacolon, or pseudomembranous colitis within 5 days; or
36 re episodes of septic shock (P = .07), toxic megacolon (P = .04), and recurrences (P = .04).
37 ulting in asplenogenesis and hyperganglionic megacolon, respectively.
38 infection with hypotension, shock, ileus, or megacolon) should be treated with oral vancomycin and IV
39 nts with MEN 2B have intestinal neuromas and megacolon that can cause significant gastrointestinal pr
40 nsgenic mice thus represent a novel model of megacolon that results from increased smooth muscle cell
41 uate in severe colitis, complicated by toxic megacolon with impending intestinal perforation.
42                   Enx-deficient mice develop megacolon with massive distension of the proximal colon.