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
To examine the influence that nicotine exposure has on early embryo development, the present study has applied real-time RT-PCR to investigate changes in Oct-4 and Rex-1 expression in mouse embryonic stem (ES) cells exposed to nicotine alone or in the presence of tubocurarine. Oct-4 is regarded as a candidate master regulator gene for the initiation, maintenance, and differentiation of pluripotent cells. Zfp42/Rex-1, another specific gene of pluripotent cells, also plays a critical role in maintaining stem cell character and pluripotency. Results indicated that nicotine (10-1000 nM) enhanced Oct-4 and Rex-1 expression without altering beta-actin expression. This up-regulation with nicotine (100-1000 nM) was prevented with tubocurarine (10 microM), a nicotinic acetylcholine receptor (nAChRs) antagonist. We conclude that nicotine may influence Oct-4 and Rex-1 expression in ES cells through a mechanism involving the nAChRs.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.reprotox.2004.10.008 | DOI Listing |
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