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
We report a case of primary biliary cirrhosis (PBC) that occurred in a 24-month-old male C57BL/6 mouse infected with Helicobacter pylori (H. pylori). Microscopically, the portal tract in the liver showed nonsuppurative destructive cholangitis with variable cytologic distortion of the epithelial cells and peribiliary lymphoplasmacytic infiltration. Immunohistochemistry using alpha-smooth muscle actin demonstrated fibrous bands associating with the wall of vasculature. The level of serum antivacuolating toxin IgG in this mouse showed the highest value (optical density=2.1470) of the H. pylori-infected group (n=13) (optical density=1.7168+/-0.1759, mean+/-SD). Spontaneously developed PBC-like lesions in C57BL/6 mice have been reported by several authors. However, this case strikingly resembles human PBC with its characterized histological features. Therefore, we propose that the increase in vacuolating toxin caused by H. pylori infection may be related to the development of PBC by molecular mimicry.
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Source |
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http://dx.doi.org/10.1097/MEG.0b013e3282f5e9db | DOI Listing |
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