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
Endometriosis is a common gynecological disease defined by extrauterine growth of endometrial glands and stroma. A variety of theories have been proposed to account for the pathogenesis of this disease, including retrograde transplantation theory, metaplasia of coelomic epithelium, hematogenic and lymphogenic spread, and remnants of the Mŭllerian duct. However, the etiopathology of endometriosis is still obscure. In this article, we aim to summarize recent researches concerning the growth mechanisms of endometriotic cells in implanted sites systematically, including the adhesion, invasion, angiogenesis, proliferation, apoptosis of endometriotic cells, variations of the immune molecules and endometriotic cells themselves, which may provide clues for future researches in the pathogenesis of endometriosis.
Download full-text PDF |
Source |
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http://dx.doi.org/10.3109/09513590.2011.650662 | DOI Listing |
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