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
For many years, mitochondrial respiration was thought to follow an "all or nothing" paradigm supporting the notion that in the normal O2 concentration range, respiration is mainly controlled by tissue demands. However, nitric oxide produced by cytosol or mitochondrial nitric oxide synthases adapts respiration to different physiologic conditions and increases the mitochondrial production of O2 active species that contributes to NO clearance. Because mitochondrial NO utilization is sensitive to environmental or hormonal modulation, and because diffusible active species, like H2O2, are able to regulate genes related to proliferation, quiescence, and death, we surmised that the two mechanisms converge to elicit the different responses in cell physiology.
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Source |
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http://dx.doi.org/10.1016/S0076-6879(05)96034-5 | DOI Listing |
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