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
Sepsis refers to the deleterious and non-resolving systemic inflammatory response of the host to microbial infection and is the leading cause of death in intensive care units. The pathogenesis of sepsis is highly complex. It is principally attributable to dysregulation of the innate immune system. Damage-associated molecular patterns (DAMPs) are actively secreted by innate immune cells and/or released passively by injured or damaged cells in response to infection or injury. In the present review, we highlight emerging evidence that supports the notion that extracellular DAMPs act as crucial proinflammatory danger signals. Furthermore, we discuss the potential of a wide array of DAMPs as therapeutic targets in sepsis.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.arr.2015.03.003 | DOI Listing |
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