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Article: Abnormalities of neuropeptides and neural markers in the esophagus of fetal rats with adriamycin induced esophageal atresia

TitleAbnormalities of neuropeptides and neural markers in the esophagus of fetal rats with adriamycin induced esophageal atresia
Authors
Issue Date1997
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/jpedsurg
Citation
Journal of Pediatric Surgery, 1997, v. 32 n. 10, p. 1420-1423 How to Cite?
AbstractBackground/Purpose: To investigate the distribution of neural markers and neuropeptides in esophageal atresia (EA). Methods: A fetal rat model with Adriamycin-induced EA was used. The animals were divided into four groups: (1) control group, (2) saline-injected group, (3) Adriamycin administered but without the development of EA, and (4) Adriamycin-induced EA group. Specimens of the distal esophagus from each group were immunostained using antibodies to S100, protein gene product 9.5 (PGP), somatostatin, vasoactive intestine peptide (VIP), bombesin, galanin, substance P, neuropeptide Y (NPY), calcitonin gene-related product (CGRP), met-encephalin, nitric oxide synthase, and tyrosine hydroxylase. Results: The total cross-sectional area of the distal atretic esophagus was significantly smaller than controls (P = .01), the submucosa being the component most affected (0.0465 v 0.0234 mm). Immunoreactivity for S100 and galanin were significantly elevated in the atresia group (0.0288 v 0.0079 and .001 v 0.000). In addition, there was also an increase in CGRP and Substance P in the atretic group. Conclusion: The elevated levels of S100 and galanin could explain the disordered motility observed in patients who had esophageal atresia.
Persistent Identifierhttp://hdl.handle.net/10722/225235
ISSN
2015 Impact Factor: 1.733
2015 SCImago Journal Rankings: 0.802

 

DC FieldValueLanguage
dc.contributor.authorCheng, W-
dc.contributor.authorBishop, AE-
dc.contributor.authorSpitz, L-
dc.contributor.authorPolak, JM-
dc.date.accessioned2016-04-29T01:54:29Z-
dc.date.available2016-04-29T01:54:29Z-
dc.date.issued1997-
dc.identifier.citationJournal of Pediatric Surgery, 1997, v. 32 n. 10, p. 1420-1423-
dc.identifier.issn0022-3468-
dc.identifier.urihttp://hdl.handle.net/10722/225235-
dc.description.abstractBackground/Purpose: To investigate the distribution of neural markers and neuropeptides in esophageal atresia (EA). Methods: A fetal rat model with Adriamycin-induced EA was used. The animals were divided into four groups: (1) control group, (2) saline-injected group, (3) Adriamycin administered but without the development of EA, and (4) Adriamycin-induced EA group. Specimens of the distal esophagus from each group were immunostained using antibodies to S100, protein gene product 9.5 (PGP), somatostatin, vasoactive intestine peptide (VIP), bombesin, galanin, substance P, neuropeptide Y (NPY), calcitonin gene-related product (CGRP), met-encephalin, nitric oxide synthase, and tyrosine hydroxylase. Results: The total cross-sectional area of the distal atretic esophagus was significantly smaller than controls (P = .01), the submucosa being the component most affected (0.0465 v 0.0234 mm). Immunoreactivity for S100 and galanin were significantly elevated in the atresia group (0.0288 v 0.0079 and .001 v 0.000). In addition, there was also an increase in CGRP and Substance P in the atretic group. Conclusion: The elevated levels of S100 and galanin could explain the disordered motility observed in patients who had esophageal atresia.-
dc.languageeng-
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/jpedsurg-
dc.relation.ispartofJournal of Pediatric Surgery-
dc.subject.meshAntibiotics, Antineoplastic-
dc.subject.meshBiomarkers - analysis-
dc.subject.meshEsophageal Atresia - chemically induced - embryology - metabolism - surgery-
dc.subject.meshEsophagus - chemistry - embryology - metabolism-
dc.subject.meshNeuropeptides - analysis - biosynthesis-
dc.titleAbnormalities of neuropeptides and neural markers in the esophagus of fetal rats with adriamycin induced esophageal atresia-
dc.typeArticle-
dc.identifier.emailCheng, W: weicheng@hkucc.hku.hk-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0022-3468(97)90552-2-
dc.identifier.pmid9349759-
dc.identifier.scopuseid_2-s2.0-0030762132-
dc.identifier.hkuros24419-
dc.identifier.volume32-
dc.identifier.issue10-
dc.identifier.spage1420-
dc.identifier.epage1423-
dc.publisher.placeUnited States-

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