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Life-threatening sepsis with high mortality and morbidity is an important cause of acute kidney injury and myocardial dysfunction. In this study, we investigated the protective effect of Micromeria congesta (MC) against kidney and heart damage caused by lipopolysaccharide (LPS) used as a sepsis model. Control, LPS, LPS + 25 mg/kg MC and LPS + 50 mg/kg MC groups were established from rats for the study.

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Objective: Proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors are a standard therapy for patients who respond poorly to or cannot tolerate statins. However, identifying responders to PCSK9 inhibitors remains unclear. This study investigates the characteristics of patients who achieve target LDL-C reduction (< 70 mg/dl) after PCSK9 inhibitor therapy.

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Background: Chronic low-grade inflammation is a well-known risk factor for coronary heart disease (CHD) and future cardiovascular events. Anti-inflammatory therapy can reduce the risk of ischemic cardiovascular disease (CVD) events following myocardial infarction (MI). However, it remains unknown to what extent inflammation at the time of an acute event predicts long-term outcomes.

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Myocardial infarction (MI) compromises the cardiac microvascular endothelial barrier, increasing leakage and inflammation. HIF2α, predominantly expressed in cardiac endothelial cells during ischemia, has an unclear role in barrier function during MI. Here, we show that inducible, adult endothelial-specific deletion of Hif2α in mice leads to increased mortality, cardiac leakage, inflammation, reduced heart function, and adverse remodeling after MI.

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Induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) have emerged as a pivotal model for research. Specialized devices can generate Extracellular Field Potential (EFP) measurements from these cells, analogous to the ventricular complex of the electrocardiogram. However, electrophysiological analysis can be complex and requires specialized expertise, posing a barrier to broader adoption in non-specialized labs.

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