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
Vascular adventitial lesion as a new etiological factor of atherosclerosis (AS) has been confirmed by the results of several different animal models, and some evidence supports adventitial inflammation as the main cause, but the exact mechanism is still elusive. The data from some studies confirm that some link exists between the adventitial inflammation (which also might happen in the periadventitial fat) and atherosclerotic lesions. Aquaporin7 (AQP7) as an aquaglyceroporin, which regulates the permeation of glycerol through the cell membrane and located in the adipose tissue, shows some relationship with obesity. The result of the studies about AQP7-knockout mice and different expression of AQP7 in the cutaneous abdominal adipose tissue among people with different body types proved this phenomenon. Meanwhile, some degree of dysfunction of AQP7 has been proved in the obese. Until now, no study has shown us the data on the correlation of the expression of AQP7 in the periadventitial fat with the severity of atherosclerotic lesions. It is proposed that dysfunction of AQP7 in the periadventitial fat may trigger the adventitial inflammation. Attempts to confirm this hypothesis may lead to new directions in the study of the pathogenesis of AS and the development of a novel agent for this disorder.
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Source |
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http://dx.doi.org/10.1016/j.mehy.2007.04.022 | DOI Listing |
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