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
Heymann nephritis (HN) is an experimental autoimmune disease of rats characterized by immune-complex (IC) depositions on the epithelial side of the glomerular basement membrane (GBM) and by proteinuria. Several forms of HN have been produced by various investigators, but one thing has been common to all of them, namely their inducement by the development of pathogenic IgG autoantibodies (aabs). The aim of this review is to describe how pathogenic IgG aab production (which initiates and maintains the disease) in slowly progressive HN (SPHN) can be specifically terminated by injections of ICs made up of native rat renal tubular antigens and IgM antibodies directed against them.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.autrev.2005.04.002 | DOI Listing |
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