Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 144
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 144
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 212
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3106
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
The intracellular signaling mechanisms that mediate the regulation of parathyroid hormone (PTH) secretion by parathyroid glands are becoming increasingly more understood. Extracellular calcium modulates parathyroid function by acting on a G protein-coupled calcium-sensing receptor, which activates the hydrolysis of membrane phospholipids by phospholipases C, D, and A2 to generate intracellular signals. Arachidonic acid (AA) produced by phospholiphase A2 (PLA2) appears to play a crucial role throughout the generation of downstream-oxygenated products. Recent studies demonstrate the activation of the PLA2 via an intracellular calcium increase, and that the elevation of cytosolic calcium also overcomes the repressive effect of high extracellular phosphate on AA production. Furthermore, a role of the mitogen-activated protein (MAP) kinase cascade has also been documented in PLA2 activation.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1046/j.1523-1755.63.s85.4.x | DOI Listing |
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