Chronic foot wounds are a leading cause of morbidity and hospitalization for patients with diabetes. Negative pressure wound therapy (NPWT) is known to promote healing of diabetic foot wounds, but the underlying molecular mechanisms remain elusive. We propose to gain molecular insights into the wound healing promoting signals underlying the effects of NPWT on diabetic foot wounds in humans.
View Article and Find Full Text PDFBackground: It has been shown that the β3-adrenergic receptor (β3-AR) gene Trp64Arg mutation was closely related to obesity and insulin resistance, and may be related to the prevalence of metabolic syndrome (MS). The aim of this study was to investigate the relationship between the β3-AR gene mutation and the prevalence of MS.
Methods: A seven-year follow-up study was initiated in 2000, with 496 samples of simplex obese subjects (body mass index ≥ 25 kg/m(2)) and 248 normal-weight subjects.
Objective: To investigate the relationship between Trp64Arg mutation in beta(3)-adrenergic receptor (beta(3)-AR) gene and the incidence of metabolic syndrome (MS).
Methods: A seven-year follow-up study was conducted in 386 simple obese subjects and 175 normal weight subjects in whom geno-typing of Trp64Arg mutation in beta(3)-AR gene was examined in 2000.
Results: There were no differences between a Trp64Trp homozygote group and a Trp64Arg heterozygote group of whether obese or normal weight subjects with respect to adiposity, blood pressure, lipid profile, fasting blood glucose and fasting insulin in the baseline.
A three-dimensional (3D) quantitative pharmacophore model was developed from a training set of structurally diverse substituted ureas against Raf-1 kinase, which was well validated to be highly predictive by two methods, namely, test set prediction and Cat-Scramble method. Then a virtual database searching was performed with the pharmacophore model as a 3D query, and the bioactivities of the retrieved hits were predicted by the pharmacophore. Subsequently, molecular docking was carried out on the selected hits whose estimated IC(50) was less than 1 microM.
View Article and Find Full Text PDFObjective: To study the ionic mechanism of reentrant arrhythmia.
Methods: Single myocytes were enzymatically isolated from the epicardium, midmyocardium and endocardium of the left ventricle free wall of rabbit, followed by whole-cell patch-clamp recording of the Na(+) current (I(Na)) of the 3 cellular subtypes (superfused with normal and then simulated ischemia solution). The currents in the 3 cellular subtypes before and after simulated ischemia lasting for 10, 20, and 30 min, respectively, were compared.