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
Some parameters of hemostasis and cytokine production during the fatal and nonfatal course of experimental human versus murine infection caused by Dengue virus (DV) were studied. Its lethal dose administration induced a rapid development of anemia, thrombocytopenia and a change in packed cell volume. These changes were not so profound in the nonfatal group of infected mice. There was an excess production of both proinflammatory (TNF-alpha, IL-1beta) and anti-inflammatory (IL-6, IL-10) cytokines in the fatal group. In mice of this group, the early rise of IFN-gamma and IL-12 corresponded to the parameters observed in patients with severe forms of DV infection. The findings provide evidence that the proposed model may be used for the experimental study of the immunopathogenesis of the disease.
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