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
Autologous adipose tissue transplantation is widely used for cosmetic and reconstruction of various areas in the body, often to repair soft tissue volume loss or contoured deformation. However, the application of fat transplantation is limited by unstable and unpredictable volume retention rates. At present, promoting adipose tissue survival and inhibiting its death is the key to improve the effect of autologous fat transplantation. In this paper, we propose a hypothesis that ferroptosis exists in fat transplantation. The bases of this hypothesis include the following: (1) the association between ferroptosis and other programmed cell death; (2) the association between ferroptosis and ischemia-reperfusion injury; and (3) the use of ferroptosis inhibitors in the field of fat transplantation.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1097/SCS.0000000000009508 | DOI Listing |
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