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Echinacea purpurea has been reported as a source of bioactive compounds and essential elements. Cichoric acid is a caffeic acid derivative known as appropriate marker for the quality of E. purpurea containing products. We have developed an efficient method of ultrasound-assisted extraction (UAE) of cichoric acid from roots of E. purpurea and optimized the process parameters. Comparison of the UAE and maceration techniques for the extraction of cichoric acid from of E. purpurea root was carried out. The concentration of cichoric acid in extracts was analyzed by high-performance liquid chromatography (HPLC). The optimum extraction parameters are 50% (v/v) ethanol – water mixture as solvent, sonication time of 10 min, solute to solvent ratio of 1/10, and extraction temperature of 30°C. The advantageous effect of ultrasonic waves on extraction of cichoric acid in comparison to maceration technique is established.

Background Most patients undergoing Transcatheter aortic valve implantation (TAVR) are elderly with significant co-morbidities and there is limited information available regarding factors that influence length of stay (LOS) post-procedure. The aim of this study was to identify the patient, and procedural factors that affect post-TAVR LOS using a contemporary multinational registry. Methods We conducted a retrospective cohort study, with patients recruited from three high volume tertiary institutions. The primary outcome was the LOS post-TAVR procedure. We examined patient and procedural factors in a cause-specific Cox multivariable regression model to elucidate their effect on LOS, accounting for the competing risk of post-procedural death. Hazard ratios (HR) greater than 1 indicate a shorter LOS, while HRs less than 1 indicate a longer LOS. Results The cohort consisted of 809 patients. Patient factors associated with longer LOS were older age, prior atrial fibrillation, and greater patient urgency. Patient factors associated with shorter LOS were lower NYHA class, higher ejection fraction and higher mean aortic valve gradients. Procedural characteristics associated with shorter LOS were conscious sedation (HR = 1.19, 95% CI 1.06–1.35, p = 0.004). Transapical access was associated with prolonged LOS (HR = 0.49, 95% CI 0.41–0.58, p

Post-TAVR complications and select echo measurements of study cohort. (DOC 65 kb)

OBJECTIVES The role of atrial myocytes and extracellular matrix (ECM) changes in atrial chamber remodeling was studied in a canine model of heart failure (HF). BACKGROUND Cardiac remodeling is a key process mediating the progression of HF. Studies of the structural mechanisms of cardiac remodeling have been limited to the left ventricle. The structural alterations associated with atrial chamber remodeling in evolving HF have not been studied. METHODS Age- and weight-matched dogs were subjected to right ventricular pacing (240 beats/min) for one and three weeks to produce early and severe HF, respectively. Atrial tissues were assessed for myocyte and ECM changes. RESULTS Right atrial and left atrial (LA) pressures were significantly increased in early and severe HF. The LA wall tension index was significantly increased at both HF stages by 116% and 443%, respectively. Atrial collagen synthesis and degradation were significantly increased in severe HF. Gelatinase activity was significantly increased at both early and severe stages of HF. Gelatin zymography showed increased matrix metalloproteinases (MMP)-9 with early HF and increased MMP-2 with severe HF. The LA wall tension index was significantly correlated with gelatinase activity and collagen synthesis. Although total atrial collagen content was not changed, disarray of collagen fibers was observed. Atrial myocyte hypertrophy without evidence of apoptosis was also present in severe HF. CONCLUSIONS There is marked atrial chamber remodeling in canine pacing-induced HF, which is characterized by myocyte hypertrophy and dynamic collagen turnover. Atrial remodeling may contribute to the development of atrial arrhythmias and pulmonary hypertension and could offer a novel therapeutic target.

Stimulation of HEL megakaryocytic cells by Fc gammaRIIA crosslinking is associated with tyrosine phosphorylation of syk and phospholipase C gamma2 (PLCgamma2) and is accompanied by formation of inositol phosphates and release of intracellular Ca2+. These responses are inhibited by the kinase inhibitors, staurosporine and ST271. In contrast, the G-protein receptor agonist, thrombin induces formation of inositol phosphates and release of intracellular calcium without an increase in tyrosine phosphorylation. The plant lectin wheat germ agglutinin (WGA) stimulates tyrosine phosphorylation of syk and PLCgamma2 but surprisingly does not stimulate formation of inositol phosphates and induce release of intracellular Ca2+. WGA also inhibited formation of inositol phosphates and release of intracellular Ca2+ by Fc gammaRIIA crosslinking and thrombin-stimulation. A similar inhibitory effect of WGA was observed against elevation of Ca2+ by the same two stimuli in MEG-01 megakaryotic cells. The results demonstrate a novel pathway of inhibition of PLC on crosslinking of cell surface proteins that is not present in platelets.

The role of the angiopoietin-1 (Ang1)–Tie2 pathway in the pathogenesis of pulmonary arterial hypertension (PAH) is controversial. Although Ang1 is well known to prevent endothelial activation and injury in systemic vascular beds, this pathway has been suggested to mediate pulmonary vascular remodeling in PAH. Therefore, we used transgenic models to determine the effect of increased or decreased Tie2 activity on the development of PAH. We now report modest spontaneous elevation in right ventricular systolic pressure in Tie2-deficient mice (Tie2+/−) compared with wild-type (WT) littermate controls, which was exacerbated upon chronic exposure to the clinically relevant PAH triggers, serotonin (5-HT) or interleukin-6 (IL-6). Moreover, overexpression of Ang1 in transgenic mice had no deleterious effect on pulmonary hemodynamics and, if anything, blunted the response to 5-HT. Exposure to 5-HT or IL-6 also decreased lung Ang1 expression, further reducing Tie2 activity and inducing pulmonary apoptosis in the Tie2+/− group only. Similarly, cultured pulmonary artery endothelial cells subjected to Tie2 silencing demonstrated increased susceptibility to apoptosis after 5-HT treatment. Finally, treatment of Tie2-deficient mice with Z-VAD, a pan-caspase inhibitor, prevented the pulmonary hypertensive response to 5-HT. Thus, these findings firmly establish that endothelial survival signaling via the Ang1–Tie2 pathway is protective in PAH.