The interplay between the physical and mental health of patients recovering from myocardial infarction (MI) is crucial. Erectile dysfunction (ED) is a common sexual issue, particularly among patients who have had a myocardial infarction and arterial diseases, and it significantly affects self-esteem and overall psychological well-being. Despite significant advances in cardiac rehabilitation, the psychosocial aspects, especially those related to sexual health, remain underexplored.
View Article and Find Full Text PDFMetabolic syndrome (MetS) is a cluster of metabolic abnormalities affecting ~25% of adults and is linked to chronic diseases such as cardiovascular disease, cancer, and neurodegenerative diseases. Oxidative stress and inflammation are key drivers of MetS. Hesperidin, a citrus bioflavonoid, has demonstrated antioxidant and anti-inflammatory properties; however, its effects on MetS are not fully established.
View Article and Find Full Text PDFIntroduction: Marginal zone and follicular B cells are known to contribute to the development of angiotensin II-induced hypertension in mice, but the effector function(s) mediating this effect (e.g., antigen presentation, antibody secretion and/or cytokine production) are unknown.
View Article and Find Full Text PDFThe association between constipation and cardiovascular risk is unclear. This population-level matched cohort study compared the association of constipation with hypertension and incident cardiovascular events in 541,172 hospitalized patients aged ≥ 60 years. For each constipation admission, one exact age-matched non-constipated admission was randomly selected from all hospitalizations within 2 weeks to form the comparison cohort.
View Article and Find Full Text PDFIntroduction: Depletion of mature B cells affords protection against experimental hypertension. However, whether B cell-mediated hypertension is dependent on differentiation into antibody-secreting cells (ASCs) remains unclear. Using the proteasome inhibitor, bortezomib, the present study tested the effect of ASC reduction on angiotensin II-induced hypertension.
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