1999
DOI: 10.1016/s0022-3468(99)90258-0
|View full text |Cite
|
Sign up to set email alerts
|

Esophageal atresia with tracheoesophageal fistula: Suggested mechanism in faulty organogenesis

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

2
38
0
1

Year Published

2000
2000
2019
2019

Publication Types

Select...
7
1

Relationship

0
8

Authors

Journals

citations
Cited by 59 publications
(41 citation statements)
references
References 8 publications
2
38
0
1
Order By: Relevance
“…In our study, histological assessments of the EA and TEF and control specimens essentially confirmed previously reported observations in an adriamycin rat model [2,3,15]. In addition, Cheng et al [14] found neuropeptide abnormality in the lower esophagus morphological abnormality of the distal esophagus.…”
Section: Discussionsupporting
confidence: 91%
See 2 more Smart Citations
“…In our study, histological assessments of the EA and TEF and control specimens essentially confirmed previously reported observations in an adriamycin rat model [2,3,15]. In addition, Cheng et al [14] found neuropeptide abnormality in the lower esophagus morphological abnormality of the distal esophagus.…”
Section: Discussionsupporting
confidence: 91%
“…The adriamycin rat model produces EA and TEF similar to the most common human anatomic variant allows better understanding pathophysiology of EA and associated anomalies [1,2,15]. In this experimental study we have found several histological and morphological changes in distal esophagus, tracheobronchial tree, and lung parenchyma.…”
Section: Discussionmentioning
confidence: 62%
See 1 more Smart Citation
“…25 The study was prompted by observations that such human congenital pulmonary malformations as lung hypoplasia, tracheoesophageal fistula, and esophageal atresia may be attributed to defective SHH signaling. [26][27][28][29] Taken together, these studies illustrate how molecular technology may be used to identify the timing of PNEC fate restriction and lineage relationships during morphogenesis. 17 In the immature, developing lung markers of NE differentiation are co-expressed with the epithelial markers before they are restricted to specific PNECs, suggesting a common cellular origin for airway cells.…”
mentioning
confidence: 89%
“…None of the patients had well-developed lower esophagus. Lack of stimulus from swallowing or different organogenesis of lower esophagus as suggested previously, might be the causative factors [13]. However, none of our patients had anastomotic leak in postoperative period.…”
Section: Discussionmentioning
confidence: 49%