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This paper presents the system analysis, design consideration, and implementation of a soft-switching zeta-flyback converter to achieve zero-voltage switching (ZVS). In the proposed converter, the zeta and flyback topologies are adopted in the output side to achieve the following features: to share the power components in the transformer primary side, to achieve the partial magnetizing flux reset, and to share the output power. The buck-boost type of active clamp is connected in parallel with the primary side of the isolation transformer to recycle the energy stored in the leakage inductor of isolated transformer and to limit the peak voltage stress of switching devices due to the transformer leakage inductor when the main switch is turned off. The active clamp circuit can make the switching devices to turn on at ZVS. Experimental results taken from a laboratory prototype rated at 240 W, input voltage of 150 V, output voltage of 12 V, and switching frequency of 150 kHz are presented to demonstrate the converter performance. Based on the experimental results, the circuit efficiency is about 90.5% at rated output power, and the output voltage variation is about 1%.

Expression of functionally active thrombomodulin (TM) on endothelial cells is critical for vascular thromboresistance. 3-Hydroxyl-3-methyl coenzyme A reductase inhibitors (statins) can protect the vasculature from inflammation and atherosclerosis caused by cholesterol-dependent and cholesterol-independent mechanisms. In the present study, the effects of atorvastatin on TM expression in the aorta of cholesterol-fed rabbits and in TNFalpha-treated human aortic endothelial cells (HAECs) were investigated. When rabbits were fed a 0.5% cholesterol diet with and without supplementation with atorvastatin for 9 weeks, the neointimal area in the thoracic aorta of the atorvastatin-treated group was significantly reduced and there was significant induction of TM protein expression. In HAECs, TNFalpha treatment decreased the expression of TM in a time- and dose-dependent manner and atorvastatin pretreatment upregulated the expression of TM mRNA and protein in HAECs with or without TNFalpha treatment. Atorvastatin also inhibited monocyte adhesion to control and TNFalpha-treated HAECs via TM expression. ERK1/2 phosphorylation was significantly reduced by 24 h pretreatment with atorvastatin, whereas TNFalpha increased the phosphorylation of the MAPKs, p38, JNK, and ERK1/2. Blocking the transcriptional activation of NF-kappaB and nuclear translocation of NF-kappaB p65 prevented the TNFalpha-induced downregulation of TM. Atorvastatin regulated TM expression in control and TNFalpha-treated HAECs by inhibiting the activation of ERK and NF-kappaB. The increase in endothelial TM activity in response to atorvastatin constitutes an important pleiotropic effect of this commonly used compound and may be of clinical significance in cardiovascular disorders in which deficient endothelial TM plays a pathophysiological role.

This paper presents the system analysis and design consideration of zero voltage switching (ZVS) converter with series-connected transformers. Based on the operation behavior each transformer in the adopted converter can be operated as an inductor or a transformer. Therefore no output filter inductor is needed in the adopted converter. To reduce the voltage stress of switching device in the conventional forward converter, active snubber based on a clamp switch and a clamp capacitor is used to recycle the energy stored in the transformer leakage. The center-tapped topology is used at the secondary side to achieve full-wave rectification. Finally experimental results for a 100 W (5 V/20 A) prototype circuit are provided to confirm the converter performance