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1 chemistry, and in vitro culture of EGCs from aganglionic and ganglionated segments of Ednrb-null mice
2 typically managed by surgical removal of the aganglionic bowel and reconstruction of the intestinal t
3  Application of GDNF to cultured explants of aganglionic bowel from children with HSCR induced prolif
4 efficiently both wild-type and RET-deficient aganglionic bowel in organ culture.
5 NF application to cultured explants of human aganglionic bowel induced proliferation of Schwann cells
6 It is based on the principle to open spastic aganglionic bowel segments by performing a myotomy throu
7 , nine identified genes had higher levels in aganglionic bowel than in WT animals suggesting that int
8       HSCR is treated by surgical removal of aganglionic bowel, but many children continue to have se
9 two-fold higher expression in wild type than aganglionic bowel.
10 sease (HSCR), in which infants are born with aganglionic bowel.
11  surgical intervention with resection of the aganglionic bowel.
12            Exogenous luminal GDNF penetrated aganglionic colon epithelium of Hol(Tg/Tg) mice, inducin
13                                        Human aganglionic colon explants from children with HSCR were
14 ent of enteric neurons and accumulate in the aganglionic colon of ls/ls mice.
15  features typical of Hirschsprung's disease (aganglionic colon).
16 bsence of GFAP+ intraganglionic (IG) glia in aganglionic colon, while CAMK2b+ extraganglionic (EG) gl
17 f donor ENCCs to invade a recipient piece of aganglionic colon.
18 s of the extrinsic nerve fibers found in the aganglionic colon.
19 sprung disease, which is characterized by an aganglionic distal bowel.
20                Intracellular recordings from aganglionic gastrointestinal muscles showed normal slow
21 ere also capable of colonising wild-type and aganglionic gut in organ culture and had the potential t
22  mouse bowel into wild-type or RET-deficient aganglionic gut in organ culture, results in extensive r
23 's disease) based on the colonisation of the aganglionic gut with progenitors derived from normogangl
24 ural tube adjacent to somites 3-6 to produce aganglionic gut.
25 us system precursor cells and thus create an aganglionic hindgut model in vivo.
26                                           In aganglionic hindguts, TNC expression is strong throughou
27 s and glia in distal bowel tissues that were aganglionic in control mice, had a significant increase
28                        The terminal colon is aganglionic in mice lacking endothelin-3 or its receptor
29  laminin alpha 1 was examined in the totally aganglionic intestine of E15 and newborn c-ret -/- mice,
30  variation in penetrance and expressivity of aganglionic megacolon analogous to the variation observe
31 n receptor type B (EDNRB) produce congenital aganglionic megacolon and pigment abnormalities in mice
32  in spotting lethal (sl) rats, which exhibit aganglionic megacolon associated with white coat color.
33 ndgut of Hirschsprung's disease in humans or aganglionic megacolon in animals.
34                                   Congenital aganglionic megacolon, commonly known as Hirschsprung di
35   Hirschsprung disease (HSCR), or congenital aganglionic megacolon, is the most common cause of conge
36   Hirschsprung disease (HSCR), or congenital aganglionic megacolon, is the most frequent cause of con
37 ins, and neurogenic potential of EGCs in the aganglionic mouse and human colon.
38 ion to compare gene expression in E14 and P0 aganglionic or wild type mouse intestine.
39 pe and RET-deficient gut and showed that the aganglionic phenotype observed in vivo is consistently r
40 gut by advancing on extrinsic fibers and, in aganglionic preparations, they form a small number of ne
41  fail to colonize the terminal hindgut, this aganglionic region becomes non-functional and results in
42 nsplanting wild-type NCSCs directly into the aganglionic region of the Ednrb(sl/sl) gut, where they e
43                                  EGCs in the aganglionic segment (comprising EGs and SLCs) exhibited
44           The accurate identification of the aganglionic segment depends on the histologic evaluation
45 th lentiviral-GFP, and transplanted into the aganglionic segment in vivo.
46 network complexity of EGCs isolated from the aganglionic segment, acting through a non-canonical NCAM
47 ncomplete penetrance, variation in length of aganglionic segment, and sex bias observed in human HSCR
48                       Despite removal of the aganglionic segment, gastrointestinal (GI) problems pers
49 s well as those diagnosed with short or long aganglionic segment.
50 R, ganglionic segments mirrored controls and aganglionic segments featured only Schwann-like enteric
51   Crucially, these glial subtypes persist in aganglionic segments of patients with HSCR, offering a n
52             Slow waves developed normally in aganglionic segments of small bowel placed into organ cu