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
Objective: The aim: To evaluate the levels of plasminogen activator type 1 inhibitor, asymmetric dimethylarginine and endothelial nitric oxide synthase on day 10-14 in patients, depending on the presence or absence of concomitant type 2 diabetes and the type of reperfusion therapy.
Patients And Methods: Materials and methods: The study involved 130 patients with acute myocardial infarction, divided into 2 groups: Group 1 consisted of patients with acute myocardial infarction with type 2 diabetes mellitus (n = 73), Group 2 comprised patients with acute type 2 diabetes mellitus (n = 57). The quantitative content of IAP-1 was determined by enzymelinked immunosorbent assay using a commercial test system manufactured by Technoclone PAI-1 ELISA Kit (Austria), NOS - Enzyme-Linked Immunosorbent Assay (ELISA) Kit for Nitric Oxide Synthase Endothelial (NOS) ADMA ELISA Kit (Austria).
Results: Results and conclusions: Percutaneous coronary intervention contributes to a significant reduction in the content of ADMA, which is a marker of endothelial dysfunction and increase NOS on the 10-14th day of acute myocardial infarction compared with standard therapy. During PCI, the level of IAP-1 did not significantly change in the time course of treatment due to post-inflammatory and post-traumatic activation of platelets in the vascular wall.
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