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
Unidirectional fluxes of calcium were studied in the absence of electrochemical gradients across rat descending colon segments in vitro. Dietary calcium restriction and 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]enhanced absorption by increasing the mucosal-to-serosal fluxes, whereas secretory (serosal-to-mucosal) fluxes were unchanged. Low-calcium diet also stimulated calcium uptake by everted gut sac segments of ascending as well as descending colon, whereas transverse colon was unresponsive. These results show that the colon is a target organ for 1,25-(OH)2D3 and demonstrate the participation of colon in the intestinal adaptation to calcium deprivation.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1152/ajpgi.1980.238.2.G75 | DOI Listing |
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