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- Publisher Website: 10.1016/0016-5085(86)90259-3
- Scopus: eid_2-s2.0-0022461866
- PMID: 3516786
- WOS: WOS:A1986C312700011
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Article: Development Profile Of Neuron-Specific Enolase In Human Gut And Its Implications In Hirschsprung's Disease
Title | Development Profile Of Neuron-Specific Enolase In Human Gut And Its Implications In Hirschsprung's Disease |
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Authors | |
Issue Date | 1986 |
Publisher | WB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro |
Citation | Gastroenterology, 1986, v. 90 n. 6, p. 1901-1906 How to Cite? |
Abstract | The Most Widely Held View On The Pathogenesis Of Hirschsprung's Disease As An Arrest Of Neuroblast Migration In The Gut Was Based On The Hypothesis Of A Single Craniocaudal Gradient Of Development Of Enteric Neurons. Recent Experimental Studies In Animals, However, Have Revived A Contradictory Hypothesis Of A Dual Gradient Of Neuronal Development; Such Data Are Not Available In Humans. To Test These Hypotheses In Humans, We Studied The Pylorus, Ileum, And Colon Of 28 Fetuses With Gestational Ages Of 9-21 Wk, Using Immunohistochemical Localization Of Neuron-Specific Enolase, A Specific Neuronal Marker Indicative Of Differentiation. Development Of The Enteric Nervous System Was Shown To Be Most Advanced In The Pylorus, Less So In The Colon, And Least So In The Ileum. The Findings Support The Hypothesis Of A Dual Gradient Of Neuronal Development Proceeding From Both Ends Of The Middle Of The Gut In Midtrimester Human Fetuses And Suggest That The Pathogenesis Of Hirschsprung's Disease Needs To Be Reconsidered. |
Persistent Identifier | http://hdl.handle.net/10722/220834 |
ISSN | 2023 Impact Factor: 25.7 2023 SCImago Journal Rankings: 7.362 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Tam, PKH | en_US |
dc.contributor.author | Lister, J | en_US |
dc.date.accessioned | 2015-10-19T07:22:00Z | - |
dc.date.available | 2015-10-19T07:22:00Z | - |
dc.date.issued | 1986 | - |
dc.identifier.citation | Gastroenterology, 1986, v. 90 n. 6, p. 1901-1906 | en_US |
dc.identifier.issn | 0016-5085 | - |
dc.identifier.uri | http://hdl.handle.net/10722/220834 | - |
dc.description.abstract | The Most Widely Held View On The Pathogenesis Of Hirschsprung's Disease As An Arrest Of Neuroblast Migration In The Gut Was Based On The Hypothesis Of A Single Craniocaudal Gradient Of Development Of Enteric Neurons. Recent Experimental Studies In Animals, However, Have Revived A Contradictory Hypothesis Of A Dual Gradient Of Neuronal Development; Such Data Are Not Available In Humans. To Test These Hypotheses In Humans, We Studied The Pylorus, Ileum, And Colon Of 28 Fetuses With Gestational Ages Of 9-21 Wk, Using Immunohistochemical Localization Of Neuron-Specific Enolase, A Specific Neuronal Marker Indicative Of Differentiation. Development Of The Enteric Nervous System Was Shown To Be Most Advanced In The Pylorus, Less So In The Colon, And Least So In The Ileum. The Findings Support The Hypothesis Of A Dual Gradient Of Neuronal Development Proceeding From Both Ends Of The Middle Of The Gut In Midtrimester Human Fetuses And Suggest That The Pathogenesis Of Hirschsprung's Disease Needs To Be Reconsidered. | en_US |
dc.language | eng | en_US |
dc.publisher | WB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro | en_US |
dc.relation.ispartof | Gastroenterology | en_US |
dc.title | Development Profile Of Neuron-Specific Enolase In Human Gut And Its Implications In Hirschsprung's Disease | en_US |
dc.type | Article | en_US |
dc.identifier.email | Tam, PKH:paultam@hkucc.hku.hk | - |
dc.identifier.authority | Tam, PKH=rp00060 | - |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1016/0016-5085(86)90259-3 | - |
dc.identifier.pmid | 3516786 | - |
dc.identifier.scopus | eid_2-s2.0-0022461866 | - |
dc.identifier.volume | 90 | - |
dc.identifier.issue | 6 | - |
dc.identifier.spage | 1901 | - |
dc.identifier.epage | 1906 | - |
dc.identifier.isi | WOS:A1986C312700011 | - |
dc.identifier.issnl | 0016-5085 | - |