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1 linked to incomplete ENS formation, such as Hirschsprung's disease.
2 tic approaches to neurocristopathies such as Hirschsprung's disease.
3 understanding newer therapeutic options for Hirschsprung's disease.
4 olons, and premature death, resembling human Hirschsprung's disease.
5 cristopathies, Waardenburg-Shah syndrome and Hirschsprung's disease.
6 ll migration have been shown to give rise to Hirschsprung's disease.
7 tive colitis, familial colonic polyposis, or Hirschsprung's disease.
8 lial medullary thyroid carcinoma (FMTC), and Hirschsprung's disease.
9 tunities in the treatment of severe forms of Hirschsprung's disease.
10 to human bowel motility disorders, including Hirschsprung's disease.
11 specific expression of genes associated with Hirschsprung's disease.
12 coding elements defined a widespread risk of Hirschsprung's disease (48.4% of patients and 17.1% of c
14 n colon samples from pediatric patients with Hirschsprung's disease and patients with chronic pseudo
17 ntrast, a RET mutant found in a patient with Hirschsprung's disease, as well as a RET/PTC1 mutant wit
19 es to the treatment of congenital megacolon (Hirschsprung's disease) based on the colonisation of the
20 ng leads to aganglionosis of the distal gut (Hirschsprung's disease), but it is unclear whether it is
21 stigate the cellular and molecular basis for Hirschsprung's disease caused by a mutation in the gene
25 addition, some patients with MEN 2A develop Hirschsprung's disease (HD), and all patients with MEN 2
29 rom variable lengths of the colon results in Hirschsprung's disease (HSCR) or colonic aganglionosis.
30 l and acquired enteric neuropathies, such as Hirschsprung's disease (HSCR), achalasia, intestinal neu
31 d to neurogastrointestinal disorders such as Hirschsprung's disease (HSCR), in which the ENS plays a
33 vous system (ENS) development is relevant to Hirschsprung's disease (HSCR; congenital aganglionosis o
34 e lack of ganglia in the terminal hindgut of Hirschsprung's disease in humans or aganglionic megacolo
38 s with defective migration of NCC that model Hirschsprung's disease, leading us to hypothesize that t
39 , anorectal malformations in 24 (47.1%), and Hirschsprung's disease, necrotising enterocolitis, and v
40 when they were significantly associated with Hirschsprung's disease or another neurodevelopmental dis
43 colons and 1 ileal specimen resected during Hirschsprung's disease pull-through surgery were cleared
44 r individual patients, the estimated risk of Hirschsprung's disease ranged from 5.33 cases per 100,00
45 ome-sequenced samples from 190 patients with Hirschsprung's disease to quantify the genetic burden in
47 usly shown to have a role in the etiology of Hirschsprung's disease, was misregulated within the gut
48 We report a 25-year-old woman with CCHS (no Hirschsprung's disease) who gave birth to a daughter who
49 s of a complex developmental anomaly such as Hirschsprung's disease will rely on unravelling its path
50 infectious diarrhea with zinc; achalasia and Hirschsprung's disease with botulinum toxin; weight loss
51 ced enteric nervous system characteristic of Hirschsprung's disease with reduced pigment cell number,