The Reaction between KCO and Ethylene Glycol in Deep Eutectic Solvents.

Understanding intermolecular interactions is important for the design of deep eutectic solvents. Herein, potassium carbonate (KCO) and ethylene glycol (EG) are used to form deep eutectic solvents. The interactions between KCO and EG are studied using nuclear magnetic resonance (NMR) and Fourier transform infrared (FTIR) spectra.

CO capture by imidazolium-based deep eutectic solvents: the effect of steric hindrance of N-heterocyclic carbenes.

CO capture by deep eutectic solvents (DESs) formed between 1,3-bis(isopropyl)imidazolium 1,2,4-triazolide ([IiPim][Triz]) and ethylene glycol (EG) is investigated in this study. [IiPim][Triz]-EG DESs exhibit a capacity of ∼1.0 mol CO per mol DES at 1.

Porcupine inhibitor CGX1321 alleviates heart failure with preserved ejection fraction in mice by blocking WNT signaling.

Heart failure with preserved ejection fraction (HFpEF) is highly prevalent, and lacks effective treatment. The aberration of WNT pathway underlies many pathological processes including cardiac fibrosis and hypertrophy, while porcupine is an acyltransferase essential for the secretion of WNT ligands. In this study we investigated the role of WNT signaling pathway in HFpEF as well as whether blocking WNT signaling by a novel porcupine inhibitor CGX1321 alleviated HFpEF.

Association of Nonalcoholic Fatty Liver Disease with Ventricular Tachycardia and Sinus Arrest in Patients with Non-ST-Segment Elevation Myocardial Infarction.

Nonalcoholic fatty liver disease (NAFLD) is an emerging driver of cardiac arrhythmias. However, the relationship between NAFLD and malignant arrhythmia in non-ST-segment elevation myocardial infarction (NSTEMI) patients is still unclear.In this study, 358 NSTEMI inpatients were enrolled.

SO capture by 2-pyridineethanol through the formation of a zwitterionic liquid.

In this work, we report the SO capture by 2-pyridineethanol (2-PyEtOH). 2-PyEtOH exhibits a high SO capacity, up to 1.16 g SO per g solvent at 1.

CO Absorption Mechanism by the Deep Eutectic Solvents Formed by Monoethanolamine-Based Protic Ionic Liquid and Ethylene Glycol.

Deep eutectic solvents (DESs) have been widely used to capture CO in recent years. Understanding CO mechanisms by DESs is crucial to the design of efficient DESs for carbon capture. In this work, we studied the CO absorption mechanism by DESs based on ethylene glycol (EG) and protic ionic liquid ([MEAH][Im]), formed by monoethanolamine (MEA) with imidazole (Im).

Deep eutectic solvents composed of bio-phenol-derived superbase ionic liquids and ethylene glycol for CO capture.

Deep eutectic solvents (DESs) formed by bio-phenol-derived superbase ionic liquids (ILs) and ethylene glycol (EG) exhibit a high CO capacity, up to 1.0 mol CO/mol DESs, which is much better than those of the parent ILs. Surprisingly, mechanism results indicate that CO reacts with EG, but doesn't react with phenolic anions in the solvent, which is different from other DESs formed by superbase ILs and EG.

The Influence of Hydrogen Bond Donors on the CO Absorption Mechanism by the Bio-Phenol-Based Deep Eutectic Solvents.

Recently, deep eutectic solvents (DESs), a new type of solvent, have been studied widely for CO capture. In this work, the anion-functionalized deep eutectic solvents composed of phenol-based ionic liquids (ILs) and hydrogen bond donors (HBDs) ethylene glycol (EG) or 4-methylimidazole (4CH-Im) were synthesized for CO capture. The phenol-based ILs used in this study were prepared from bio-derived phenols carvacrol (Car) and thymol (Thy).

The Protective Role of Yin-Yang 1 in Cardiac Injury and Remodeling After Myocardial Infarction.

Background Exploring potential therapeutic target is of great significance for myocardial infarction (MI) and post-MI heart failure. Transcription factor Yin-Yang 1 (YY1) is an essential regulator of apoptosis and angiogenesis, but its role in MI is unclear. Methods and Results The expression of YY1 was assessed in the C57BL/6J mouse heart following MI.

Gastrin mediates cardioprotection through angiogenesis after myocardial infarction by activating the HIF-1α/VEGF signalling pathway.

Acute myocardial infarction (MI) is one of the leading causes of death in humans. Our previous studies showed that gastrin alleviated acute myocardial ischaemia-reperfusion injury. We hypothesize that gastrin might protect against heart injury after MI by promoting angiogenesis.

CO Absorption Mechanism by the Nonaqueous Solvent Consisting of Hindered Amine 2-[(1,1-dimethylethyl)amino]ethanol and Ethylene Glycol.

In this work, we studied the CO absorption mechanism by nonaqueous solvent comprising hindered amine 2-[(1,1-dimethylethyl)amino]ethanol (TBAE) and ethylene glycol (EG). The NMR and FTIR results indicated that CO reacted with an -OH group of EG rather than the -OH of TBAE by producing hydroxyethyl carbonate species. A possible reaction pathway was suggested, which involves two steps.

The role of G protein-coupled receptor kinase 4 in cardiomyocyte injury after myocardial infarction.

Aims: G protein-coupled receptor kinase 4 (GRK4) has been reported to play an important role in hypertension, but little is known about its role in cardiomyocytes and myocardial infarction (MI). The goal of present study is to explore the role of GRK4 in the pathogenesis and progression of MI.

Methods And Results: We studied the expression and distribution pattern of GRK4 in mouse heart after MI.

Integrin-Linked Kinase Activation Prevents Ventricular Arrhythmias Induced by Ischemia/Reperfusion Via Inhibition of Connexin 43 Remodeling.

Ischemia reperfusion (I/R)-induced arrhythmia is a serious complication in patients with cardiac infarction. Remodeling of connexin (Cx) 43, manifested as phosphorylation, contributes significantly to arrhythmogenesis. Integrin-linked kinase (ILK) attenuated ventricular remodeling and improved cardiac function in rats after myocardial infarction.

Efficient non-aqueous solvent formed by 2-piperidineethanol and ethylene glycol for CO absorption.

The non-aqueous solvent formed by 2-piperidineethanol (2-PE) and ethylene glycol (EG) exhibited a high CO2 capacity of up to 0.97 mol CO2 per mol amine at 25 °C and 1.0 atm and a low regeneration temperature of 50 °C, indicating the low energy consumption in the regeneration process.

Efficient CO absorption by azolide-based deep eutectic solvents.

Deep eutectic solvents formed by solid azolide ionic liquids and ethylene glycol (EG) can efficiently capture CO2. Surprisingly, NMR and FTIR results indicated that CO2 reacted with the -OH group of EG to form a carbonate species rather than reacting with azolide anions to form a carbamate species during the absorption process.

A novel porcupine inhibitor blocks WNT pathways and attenuates cardiac hypertrophy.

WNT pathways are critically involved in the cardiac hypertrophy growth. Porcupine, an acyltransferase that specifically enables secretion of all WNT ligands, became a highly druggable target for inhibiting WNT pathways. Here we test if a novel small-molecule porcupine inhibitor CGX1321, which has entered human clinical trials as an anti-cancer agent, exerts an anti-hypertrophic effect.

SO absorption in EmimCl-TEG deep eutectic solvents.

Deep eutectic solvents (DESs) based on 1-ethyl-3-methylimidazolium chloride (EmimCl) and triethylene glycol (TEG) with different molar ratios (from 6 : 1 to 1 : 1) were prepared. FTIR and theoretical calculation indicated that the C2-H on the imidazolium ring form hydrogen bonds with the hydroxyl group rather than the ether O atom of the TEG. The EmimCl-TEG DESs can efficiently capture SO2; in particular, EmimCl-TEG (6 : 1) can capture 0.

Therapeutic effect of a novel Wnt pathway inhibitor on cardiac regeneration after myocardial infarction.

After myocardial infarction (MI), the heart is difficult to repair because of great loss of cardiomyoctyes and lack of cardiac regeneration. Novel drug candidates that aim at reducing pathological remodeling and stimulating cardiac regeneration are highly desirable. In the present study, we identified if and how a novel porcupine inhibitor CGX1321 influenced MI and cardiac regeneration.

Dedifferentiation, Proliferation, and Redifferentiation of Adult Mammalian Cardiomyocytes After Ischemic Injury.

Background: Adult mammalian hearts have a limited ability to generate new cardiomyocytes. Proliferation of existing adult cardiomyocytes (ACMs) is a potential source of new cardiomyocytes. Understanding the fundamental biology of ACM proliferation could be of great clinical significance for treating myocardial infarction (MI).

Mesenchymal stem cells-derived extracellular vesicles, via miR-210, improve infarcted cardiac function by promotion of angiogenesis.

Mesenchymal stem cells (MSCs) exert therapeutic effect on treating acute myocardial infarction. Recent evidence showed that paracrine function rather than direct differentiation predominately contributes to the beneficial effects of MSCs, but how the paracrine factors function are not fully elucidated. In the present study, we tested if extracellular vesicles (EVs) secreted by MSC promotes angiogenesis in infracted heart via microRNAs.

Metformin promotes the survival of transplanted cardiosphere-derived cells thereby enhancing their therapeutic effect against myocardial infarction.

Background: Transplantation of cardiosphere-derived cells (CDCs) has been shown to exert a therapeutic effect in patients with myocardial infarction (MI). However, poor survival of transplanted CDCs limits their beneficial effect. Metformin (MET) activates AMP-activated protein kinase (AMPK) which is associated with cell survival.

Mitochondrial DNA oxidative damage contributes to cardiomyocyte ischemia/reperfusion-injury in rats: cardioprotective role of lycopene.

Mitochondrial (mt) dysfunction and oxidative stress are involved in the pathogenesis of ischemia/reperfusion (I/R)-injury. Lycopene, a lipophilic antioxidant found mainly in tomatoes and in other vegetables and fruits, can protect mtDNA against oxidative damage. However, the role of mtDNA in myocardial I/R-injury is unclear.