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
In the present study, we examined the role of fractalkine (Fkn), a member of the chemokine family, in the pathogenesis of sickle cell disease (SCD). Eighty-seven children with sickle cell disease and 55 healthy children were enrolled in the study. Complete blood counts, serum levels of C-reactive protein, tumor necrosis factor-α, interferon-γ and fractalkine, and gene expression levels of Fkn were investigated. Serum Fkn levels and Fkn gene expression values were significantly higher in the SCD group compared to control group (P < 0.05). The findings of elevated serum Fkn and Fkn gene expression in both vaso-occlusive crisis and stable forms of SCD suggest that this chemokine may be involved in the pathogenesis of inflammation observed in SCD. This study is the first to our knowledge to describe the relationship of Fkn and inflammation in SCD.
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Source |
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http://dx.doi.org/10.1007/s12185-014-1718-4 | DOI Listing |
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