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: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
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
Establishment of various models for hypertensive diseases such as spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) clarified the importance of genetic factors in the pathogenesis of these diseases and further accelerated studies on their genetic mechanisms. Although various biochemical abnormalities have been detected and can be used as biochemical markers in these models, they have not been always closely related to blood pressure in F2 generation obtained by cross breeding between SHR and normotensive Wistar-Kyoto rats. Recent studies indicate that biomembrane abnormalities detected in erythrocytes and other membranes of SHR and SHRSP may not only be biochemical markers but also related to the pathogenesis of hypertensive diseases.
Download full-text PDF |
Source |
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http://dx.doi.org/10.3109/10641968109033696 | DOI Listing |
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