The relationship between p38 mitogen-activated protein kinase and AMP-activated protein kinase during myocardial ischemia

Although AMPK and p38 MAPK are both activated during myocardial ischemia, the activation of p38 MAPK occurs independently of AMPK

The relative stabilities of the copper hydroxyl sulphates

The literature contains considerable disagreements on the relative stabilities of the members of the copper hydroxyl sulphate family. Titration of copper sulphate with sodium hydroxide is claimed by some to produce only brochantite, while other reports indicate that antlerite and a dihydrate of antlerite are produced in the titration. Most stability field diagrams show that antlerite is the more stable stoichiomer at pH 4 and sulphate activity of 0.05-1. We have reexamined this stoichiometric family by titration of aqueous copper sulphate with sodium hydroxide and sodium carbonate, reverse titration of sodium hydroxide with copper sulphate and simultaneous addition of copper sulphate and sodium hydroxide at a variety of mole ratios, concentrations, temperatures and reaction times. We have also explored the reaction of copper hydroxide with copper sulphate and the reaction of weak bases, such as sodium acetate, sodium carbonate and urea, with copper sulphate. Our work indicates that: (1) antlerite is not formed in reactions of 0.05 to 1.2 m CuSO4 with 0.05-1.0 m NaOH or Na2 CO3 at room temperature; (2) antlerite is formed in the addition of small concentrations of base (≤0.01 M) to 1 M CuSO4 at 80°C, but not at room temperature or with 0.01 M CuSO4 at 80°C; (3) the formation of Cu5 (SO4)2 (OH)6.4 H2O occurs at large Cu2+ to base mole ratios; (4) the compound described in the literature as antlerite dihydrate is actually Cu5 (SO4)2 (OH)6.4 H2O; (5) at mole ratios of Cu2+, to OH- ranging from 2:1 to 1:2 the predominant product is brochantite; and (6) brochantite and Cu5 (SO4)2 (OH)6.4 H2O are converted to antlerite in the presence of 1 M CuSO4 (the latter requires temperatures of 80°C or greater). The Ksp (ion activity product) values of antlerite and brochantite were determined to be 2.53 (0.01) × 10-48 and 1.01 (0.01) × 10-69, respectively, using atomic absorption spectroscopy and Visual MINTEQ after equilibration in solutions of varying ionic strength and pH for six days. These values are in good agreement with those from the literature. However, after 6 months, antlerite in contact with solution is partially converted to brochantite and hence is metastable with a relatively low conversion rate. The Ksp value for antlerite must therefore be considered approximate. The relative stabilities of the copper hydroxyl sulphates are rationalized using appropriate equations and Gibbs energy calculations. A Gibbs free energy of formation for Cu5 (SO4) 2(OH)6.4 H2O of -3442. kJ/mol was obtained from the simple salt approximation. The very restricied conditions required for the formation, of antlerite are rationalized with a stability field diagram at 80°C. © 2007 The Mineralogical Society

The relative stabilities of the copper hydroxyl sulphates

The literature contains considerable disagreements on the relative stabilities of the members of the copper hydroxyl sulphate family. Titration of copper sulphate with sodium hydroxide is claimed by some to produce only brochantite, while other reports indicate that antlerite and a dihydrate of antlerite are produced in the titration. Most stability field diagrams show that antlerite is the more stable stoichiomer at pH 4 and sulphate activity of 0.05-1. We have reexamined this stoichiometric family by titration of aqueous copper sulphate with sodium hydroxide and sodium carbonate, reverse titration of sodium hydroxide with copper sulphate and simultaneous addition of copper sulphate and sodium hydroxide at a variety of mole ratios, concentrations, temperatures and reaction times. We have also explored the reaction of copper hydroxide with copper sulphate and the reaction of weak bases, such as sodium acetate, sodium carbonate and urea, with copper sulphate. Our work indicates that: (1) antlerite is not formed in reactions of 0.05 to 1.2 m CuSO4 with 0.05-1.0 m NaOH or Na2 CO3 at room temperature; (2) antlerite is formed in the addition of small concentrations of base (≤0.01 M) to 1 M CuSO4 at 80°C, but not at room temperature or with 0.01 M CuSO4 at 80°C; (3) the formation of Cu5 (SO4)2 (OH)6.4 H2O occurs at large Cu2+ to base mole ratios; (4) the compound described in the literature as antlerite dihydrate is actually Cu5 (SO4)2 (OH)6.4 H2O; (5) at mole ratios of Cu2+, to OH- ranging from 2:1 to 1:2 the predominant product is brochantite; and (6) brochantite and Cu5 (SO4)2 (OH)6.4 H2O are converted to antlerite in the presence of 1 M CuSO4 (the latter requires temperatures of 80°C or greater). The Ksp (ion activity product) values of antlerite and brochantite were determined to be 2.53 (0.01) × 10-48 and 1.01 (0.01) × 10-69, respectively, using atomic absorption spectroscopy and Visual MINTEQ after equilibration in solutions of varying ionic strength and pH for six days. These values are in good agreement with those from the literature. However, after 6 months, antlerite in contact with solution is partially converted to brochantite and hence is metastable with a relatively low conversion rate. The Ksp value for antlerite must therefore be considered approximate. The relative stabilities of the copper hydroxyl sulphates are rationalized using appropriate equations and Gibbs energy calculations. A Gibbs free energy of formation for Cu5 (SO4) 2(OH)6.4 H2O of -3442. kJ/mol was obtained from the simple salt approximation. The very restricied conditions required for the formation, of antlerite are rationalized with a stability field diagram at 80°C. © 2007 The Mineralogical Society

Platelet Acetyl-CoA Carboxylase Phosphorylation A Risk Stratification Marker That Reveals Platelet-Lipid Interplay in Coronary Artery Disease Patients

Adenosine monophosphate-activated protein kinase (AMPK) acetyl-CoA carboxylase (ACC) signaling is activated in platelets by atherogenic lipids, particularly by oxidized low-density lipoproteins, through a CD36-dependent pathway. More interestingly, increased platelet AMPK-induced ACC phosphorylation is associated with the severity of coronary artery calcification as well as acute coronary events in coronary artery disease patients. Therefore, AMPK-induced ACC phosphorylation is a potential marker for risk stratification in suspected coronary artery disease patients. The inhibition of ACC resulting from its phosphorylation impacts platelet lipid content by down-regulating triglycerides, which in turn may affect platelet function. (C) 2019 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.Host-parasite interactio

Fibroblast growth factor 23: a biomarker of fibrosis and prognosis in heart failure with preserved ejection fraction : Fibroblast growth factor 23

Aims Besides regulating calcium‐phosphate metabolism, fibroblast growth factor 23 (FGF‐23) has been associated with incident heart failure (HF) and left ventricular hypertrophy. However, data about FGF‐23 in HF and preserved ejection fraction (HFpEF) remain limited. The aim of this study was to assess the association between FGF‐23 levels, clinical and imaging characteristics, particularly diffuse myocardial fibrosis, and prognosis in HFpEF patients. Methods and results We prospectively included 143 consecutive HFpEF patients (78 ± 8 years, 61% female patients) and 31 controls of similar age and gender (75 ± 6 years, 61% female patients). All subjects underwent a complete two‐dimensional echocardiography and cardiac magnetic resonance with extracellular volume (ECV) assessment by T1 mapping. FGF‐23 was measured at baseline. Among the patients, differences in clinical and imaging characteristics across tertiles of FGF‐23 levels were analysed with a trend test across the ordered groups. Patients were followed over time for a primary endpoint of all‐cause mortality and first HF hospitalization and a secondary endpoint of all‐cause mortality. Median FGF‐23 was significantly higher in HFpEF patients compared with controls of similar age and gender (247 [115; 548] RU/mL vs. 61 [51; 68] RU/mL, P < 0.001). Among HFpEF patients, higher FGF‐23 levels were associated with female sex, higher incidence of atrial fibrillation, lower haemoglobin, worse renal function, and higher N terminal pro brain natriuretic peptide levels (P for trend < 0.05 for all). Regarding imaging characteristics, patients with higher FGF‐23 levels had greater left atrial volumes, worse right ventricular systolic function, and more fibrosis estimated by ECV (P for trend < 0.05 for all). FGF‐23 was moderately correlated with ECV (r = 0.46, P < 0.001). Over a mean follow‐up of 30 ± 8 months, 43 patients (31%) died and 69 patients (49%) were hospitalized for HF. A total of 87 patients (62%) reached the primary composite endpoint of all‐cause mortality and/or first HF hospitalization. In multivariate Cox regression analysis for the primary endpoint, FGF‐23 (HR: 3.44 [2.01; 5.90], P < 0.001) and E wave velocities (HR: 1.01 [1.00; 1.02], P = 0.034) were independent predictors of the primary composite endpoint. In multivariate Cox regression analysis for the secondary endpoint, ferritin (HR: 1.02 [1.01; 1.03], P < 0.001), FGF‐23 (HR: 2.85 [1.26; 6.44], P = 0.012), and ECV (HR: 1.26 [1.03; 1.23], P = 0.008) were independent predictors of all‐cause mortality. Conclusions Fibroblast growth factor 23 (FGF‐23) levels were significantly higher in HFpEF patients compared with controls of similar age and gender. FGF‐23 was correlated with fibrosis evaluated by ECV. High levels of FGF‐23 were significantly associated with signs of disease severity such as worse renal function, larger left atrial volumes, and right ventricular dysfunction. Moreover, FGF‐23 was a strong predictor of poor outcome (mortality and first HF hospitalization)