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
A hypothesis is proposed admitting the participation of apometallothioneines (AMT) as a common link in the etiopathogenesis of hypertonic disease (HD) and some diseases with polygene heredity. The preconditions of the hypothesis are discussed (role of genetic disposition, external factors as salt, stress, tobacco smoking, alcohol, microelements--V and Cd and glucocorticoids in the origination of arterial hypertension). AMT homeostasis is discussed as well as the possible connection with the metabolism of Zn and Cu and Cu in organism. The chelating capacity of AMT makes it a potential regulatory protein, associated with the activity of Zn- and Cu-dependent enzymes and metalloenzymes. The mosaicism of pathology is explained with the genetic polymorphism of those enzymes (D beta H, MAO, etc), regardless of the common etiopathogenetic link. Some schemes are presented illustrating the hypothesis. The tendencies of the future studies are outlined in searching of direct proofs of the hypothesis.
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