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
The normal cornea, the transparent "windscreen" of the eye, is devoid of both blood and lymphatic vessels. Nevertheless, both hem- and lymphangiogenesis can occur in response to severe corneal inflammation and can lead to blindness. Judah Folkman and co-workers exceedingly used the normally avascular cornea as the in vivo model system to study the mechanisms of angiogenesis and to test activators and inhibitors of angiogenesis in the last 3 decades. Recently, the cornea also became a successful model to study especially inflammatory lymphangiogenesis. As the last step in the circle from bedside to bench and back, we now are seeing the first (usually off-label) use of specific novel angiogenesis inhibitors in the diseased and pathologically vascularized human cornea to treat sight-threatening corneal angiogenesis and to promote graft survival after corneal transplantation by inhibiting lymphangiogenesis.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1089/lrb.2008.6348 | DOI Listing |
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