Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3165
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
98%
921
2 minutes
20
Malignant arrhythmias related to hypokalemia are a key risk factor for cardiac arrest, but the specific mechanism remains unclear. In this study, using electrophysiological mapping and transcriptomics techniques, the effects of hypokalemia and paclitaxel (SAL) on isolated rat hearts were investigated. Hypokalemia (3.5-2.0 mmol/L) dose-dependently triggered abnormal arrhythmias and increased the incidence of arrhythmias, while SAL (5 ug/ml) improved this situation. Transcriptomics revealed that hypokalemia upregulated Mt-nd6 and disrupted the inflammatory/immune pathways, while SAL reversed these changes and activated PPAR-related genes. SAL improves the electrophysiological abnormalities caused by hypokalemia by regulating inflammation, immunity and energy metabolism, and has the potential to treat related arrhythmias.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12378503 | PMC |
http://dx.doi.org/10.3389/fcvm.2025.1628940 | DOI Listing |