Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
We describe here the defects that arise in the central nervous system (CNS) of quail embryos when they develop in the absence of vitamin A. It has been assumed that because of the effects of excess vitamin A and its metabolites, particularly retinoic acid (RA), on the CNS they are involved in various aspects of CNS development. We show that this is indeed the case, because these deficient quail embryos have three defects in their CNS. First, the posterior hindbrain fails to develop because the cells fated to form this part of the CNS in the very early embryo die by apoptosis. Second, the neural tube fails to extend neurites into the periphery both in vivo and in vitro. Third, the neural crest cells throughout the embryo die by apoptosis. These results demonstrate a crucial requirement for vitamin A in CNS development.
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Source |
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http://dx.doi.org/10.1093/jn/128.2.471S | DOI Listing |
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