Utilizing MOFs Melt-Foaming to Design Functionalized Carbon Foams for 100% Deep-Discharge and Ultrahigh Capacity Sodium Metal Anodes.

Meltable metal-organic frameworks (MOFs) offer significant accessibility to chemistry and moldability for developing carbon-based materials. However, the scarcity of low melting point MOFs poses challenges for related design. Here, we propose a MOFs melt-foaming strategy toward Ni single atoms/quantum dots-functionalized carbon foams (NiSA/QD@CFs).

MELATONIN ATTENUATES RENAL ISCHEMIA-REPERFUSION INJURY BY REGULATING MITOCHONDRIAL DYNAMICS AND AUTOPHAGY THROUGH AMPK/DRP1.

Ischemia-reperfusion injury (IRI) often stems from an imbalance between mitochondrial dynamics and autophagy. Melatonin mitigates IRI by regulating mitochondrial dynamics. However, the precise molecular mechanism underlying the role of melatonin in reducing IRI through modulating mitochondrial dynamics remains elusive.

Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axis.

Introduction: Naringenin exerts a protective effect on myocardial ischemia and reperfusion. It has been reported that miR-223-3p is a potential target for the treatment of myocardial infarction (MI). In view of the unreported correlation between Naringenin and miR-223-3p, this study was designed to confirm that the ameliorative effects of Naringenin on MI is directly related to the regulation of miR-223-3p.

Prognostic value of the SYNTAX score on myocardial injury and salvage in STEMI patients after primary percutaneous coronary intervention: a single-center retrospective observational study.

Background: SYNTAX score (SS) was shown to positively correlate with postprocedural myocardial injury in patients after elective coronary artery intervention, but evidence about the association of SS with myocardial salvage in ST-segment elevation myocardial infarction (STEMI) patients is still needed. This study aimed to evaluate the prognostic value of SS for myocardial injury and salvage assessed by cardiac magnetic resonance (CMR) after primary percutaneous coronary intervention (PCI) in STEMI patients.

Methods: This single-center retrospective study consecutively enrolled STEMI patients who had undergone primary PCI within 12 h from symptom onset.

Different Changing Patterns of Three NOS-NO System Activities after Ischemia-Reperfusion in Rabbit with AMI.

NOS-NO system activity is closely correlated with ischemia-reperfusion injury (IRI) and NOS subtypes were suggested to play different roles in IRI. In this work, the activity of serum NOS, NO levels, and ischemic necrosis after reperfusion in rabbit with AMI at different time was studied. We also explored the NOS-NO system activity changes and its correlation with myocardial ischemia and necrosis.

Homocysteine induces mitochondrial dysfunction and oxidative stress in myocardial ischemia/reperfusion injury through stimulating ROS production and the ERK1/2 signaling pathway.

Acute oxidative stress and mitochondrial dysfunction are crucial for acute myocardial ischemia-reperfusion (AMI/R) injury, which may induce cell or mitochondrial membrane rupture and myocardial infarction. Plasma homocysteine (Hcy) expression levels are positively associated with risk of cardiovascular disease, and ERK1/2 exert anti-apoptotic and cardioprotective effects on AMI/R injury. However, the precise molecular mechanism of action underlying the effects of Hcy and the ERK1/2 signaling pathway on mitochondrial dysfunction and oxidative stress in AMI/R injury remains unclear.

Impact of Compound Hypertonic Saline Solution on Decompensated Heart Failure.

The aim of the present study was to evaluate the effects of hypertonic saline solution (C-HSS) with high dose furosemide on hospitalization time, readmission, and mortality in patients with New York Heart Association (NYHA) class III heart failure.Decompensated heart failure patients (NYHA III) with chronic ischemic or nonischemic cardiomyopathy and ejection fraction < 40% were divided into 2 groups in an open-label random manner: the first group received a 1-hour intravenous infusion of furosemide (100 mg) plus compound C-HSS (100 mL) twice daily and underwent serious water restriction (500 mL/day); the second group received furosemide intravenous bolus (100 mg) twice a day and water restriction (500 mL/day), without C-HSS. Both groups had normal sodium (120 mmol sodium) intake.

Effects of Rosuvastatin and MiR-126 on Myocardial Injury Induced by Acute Myocardial Infarction in Rats: Role of Vascular Endothelial Growth Factor A (VEGF-A).

BACKGROUND The present study investigated the effects of VEGF-A targeted by miR-126 on myocardial injury after acute myocardial infarction (AMI) in rats, along with the contributions of rosuvastatin to the synergic effect. MATERIAL AND METHODS SD rats were obtained to construct AMI models by ligating their left anterior descending coronary arteries (LAD). We conducted echocardiography to check the 6 involved indexes: left ventricular ejection fractions (LVEF), fractional shortening (FS), left ventricular end-systolic volume (LVV), left ventricular end-diastolic volume (LVVd), cardiac output (CO), and heart rate (HR).