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
The clinical and radiological variability seen in different forms of osteopetrosis, all due to impaired osteoclastic bone resorption, reflect many causal genes. Both defective differentiation of osteoclasts from hematopoietic stem cells as well as disturbed functioning of osteoclasts can be the underlying pathogenic mechanism. Pathogenic variants in PLEKHM1 and SNX10 can be classified among the latter as they impair vesicular transport within the osteoclast and therefore result in the absence of a ruffled border. Some of the typical radiological hallmarks of osteopetrosis can be seen, and most cases present as a relatively mild form segregating in an autosomal recessive mode of inheritance.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.bone.2022.116520 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!