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Aims: In recent years, we have developed the concept of 'clinical pathway based on integrated traditional Chinese and western medicine for the management of Chronic heart failure (CHF)'. The purpose of this study was to assess the implementation effects of multifaceted optimization management of chronic heart failure. Methods: A total of nine physicians in optimization group from nine research sites received multifaceted intervention (a 1‐day training session on how to implement the optimization programme, a written optimization programme for CHF management, supervision from daily quality coordinator, and 1‐monthly monitoring and feedback of performance measure) with respect to the management of CHF, comparing to nine physicians in control group who did not receive the aforementioned multifaceted intervention and diagnosed and treated CHF patients with conventional programme (usual care). After that, a total of 256 patients with CHF were enrolled and randomly assigned to receive optimization programme [integration of usual care and traditional Chinese medicine (TCM) treatment] or conventional programme (usual care) for the treatment of CHF. The primary outcome was the change in New York Heart Association (NYHA) functional classification during 24 weeks of treatment. Results: When compared with usual care, multifaceted optimization management resulted in superior improvements in NYHA functional classification at the 12‐week visit (P = 0.023), the 16‐week, 20‐week, and 24‐week visits (P < 0.001). It also demonstrated superior performance in comparison with the conventional programme with respect to readmission rate for major adverse cardiovascular events (MACEs), readmission rate for worsening heart failure, plasma N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) level, left ventricular ejection fraction (LVEF), patient TCM syndrome scores, quality of life, and patients with heart failure with reduced ejection fraction (HFrEF) in optimization group more likely received beta‐blockers and ACE inhibitors or ARBs than those in control group (P = 0.038 and P = 0.013, respectively). Conclusions: It is likely that the multifaceted optimization programme used in this study is feasible would benefit patients with CHF in NYHA functional classification, readmission for worsening heart failure, plasma NT‐proBNP level, LVEF, patient TCM syndrome scores, and quality of life. Additionally, it would improve hospital personnel adherence to evidence‐based performance measures for HFrEF. [ABSTRACT FROM AUTHOR]

Background: Aldehyde dehydrogenase-2 (ALDH2) has a protective effect on ischemic heart disease. Here, we examined the protective effects of ALDH2 on cardiac fibrosis through modulation of the Wnt/β-catenin signaling pathway in a rat model of myocardial infarction (MI).Methods: Wistar rats were divided into the sham (control), MI (model), and ALDH2 activator (Alda-1) groups. After 10 days of treatment, the left ventricular (LV) remodeling parameters of each animal were evaluated by echocardiography. Myocardial fibrosis was evaluated by Masson's trichrome staining and Sirius Red staining. Expression levels of collagen types I and III and α-smooth muscle actin (α-SMA) were examined. Finally, the expression and activity of ALDH2 and the levels of several Wnt-related proteins and genes, such as phosphoglycogen synthase kinase (GSK)-3β, GSK-3β, β-catenin, Wnt-1, WNT1-inducible signaling-pathway protein 1, and tumor necrosis factor (TNF)-α, were also analyzed.Results: After MI, the heart weight/body weight ratio, LV dimension at end diastole, and LV dimension at end systole were decreased, while the LV ejection fraction and LV fractional shortening were increased in the Alda-1 group. Myocardial fibrosis was also reduced in the Alda-1 group, accompanied by decreased expression collagen types I and III and α-SMA. β-Catenin, phosphorylated GSK-3β, and Wnt-1 levels were significantly increased in the model group. Interestingly, this alteration was partly reversed by Alda-1 treatment. Immunohistochemical staining showed that numerous WNT1-inducible signaling-pathway protein 1 (WISP-1)- and TNF-α-positive cells were found in the model group. However, few WISP-1- and TNF-α-positive cells were detected in the Alda-1 group.Conclusion: The reduction of cardiac fibrosis and the down-regulation of β-catenin, phosphorylated GSK-3β, Wnt-1, and WISP-1 may be mediated by increased ALDH2 activity, leading to reduction of MI-related cardiac fibrosis. [ABSTRACT FROM AUTHOR]

Background: Aldehyde dehydrogenase-2 (ALDH2) has a protective effect on ischemic heart disease. Here, we examined the protective effects of ALDH2 on cardiac fibrosis through modulation of the Wnt/β-catenin signaling pathway in a rat model of myocardial infarction (MI)., Methods: Wistar rats were divided into the sham (control), MI (model), and ALDH2 activator (Alda-1) groups. After 10 days of treatment, the left ventricular (LV) remodeling parameters of each animal were evaluated by echocardiography. Myocardial fibrosis was evaluated by Masson's trichrome staining and Sirius Red staining. Expression levels of collagen types I and III and α-smooth muscle actin (α-SMA) were examined. Finally, the expression and activity of ALDH2 and the levels of several Wnt-related proteins and genes, such as phosphoglycogen synthase kinase (GSK)-3β, GSK-3β, β-catenin, Wnt-1, WNT1-inducible signaling-pathway protein 1, and tumor necrosis factor (TNF)-α, were also analyzed., Results: After MI, the heart weight/body weight ratio, LV dimension at end diastole, and LV dimension at end systole were decreased, while the LV ejection fraction and LV fractional shortening were increased in the Alda-1 group. Myocardial fibrosis was also reduced in the Alda-1 group, accompanied by decreased expression collagen types I and III and α-SMA. β-Catenin, phosphorylated GSK-3β, and Wnt-1 levels were significantly increased in the model group. Interestingly, this alteration was partly reversed by Alda-1 treatment. Immunohistochemical staining showed that numerous WNT1-inducible signaling-pathway protein 1 (WISP-1)- and TNF-α-positive cells were found in the model group. However, few WISP-1- and TNF-α-positive cells were detected in the Alda-1 group., Conclusion: The reduction of cardiac fibrosis and the down-regulation of β-catenin, phosphorylated GSK-3β, Wnt-1, and WISP-1 may be mediated by increased ALDH2 activity, leading to reduction of MI-related cardiac fibrosis.

A solid-phase extraction (SPE) -reversed-phase high performance liquid chromatographic (RP-HPLC) method for the determination of phoxim and diazinon in oranges has been developed. The analytical procedure involved in the ultrasonic extraction with methanol, the purification using a C18 SPE column, and the separation on a liquid chromatography column by the isocratic elution with acetonitrile-water (85 : 15, v/v) at the flow rate of 0.7 mL/min and the ultraviolet wavelength of 254 nm. The results demonstrated that the linear ranges of phoxim and diazinon were 0.1 - 10.0 mg/L and 0.4 - 10.0 mg/L, and the detection limits of 4.1 and 6.7 microg/L, respectively. The average recoveries ranged from 87.3% to 102.7% with the relative standard deviations of 0.9% - 4.9% at the spiking levels of 0.10 and 0.5 mg/kg in orange samples. The analytical results obtained by SPE were compared with those of the matrix solid-phase dispersion (MSPD) cleanup method. The recovery of diazinon using the SPE cleanup method was better, but the MSPD cleanup method was much suitable for phoxim. The lower background can be obtained via each cleanup method.