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A Novel Boost-Input Full-Bridge Converter
Takahiro Sonoda,Tamotsu Ninomiya,Satoshi Tomioka,Kei Sato,Hiroto Terashi 전력전자학회 2005 JOURNAL OF POWER ELECTRONICS Vol.5 No.3
In order to correct the power boost topology has been used for easy control. But conventional boost topology has the following drawbacks: switching voltage surge, cross conduction current and right-half-plane zero of its control transfer function. Furthermore, in this topology the output voltage is always higher than the input voltage. As a result, a first-stage boost PFC converter needs to be connected with a second-stage DC-DC converter. A new topology which can be used as single stage PFC converter is proposed in this paper.
A Novel Boost-Input Full-Bridge Converter
Sonoda Takahiro,Ninomiya Tamotsu,Tomioka Satoshi,Sato Kei,Terashi Hiroto The Korean Institute of Power Electronics 2005 JOURNAL OF POWER ELECTRONICS Vol.5 No.3
In order to correct the power boost topology has been used for easy control. But conventional boost topology has the following drawbacks: switching voltage surge, cross conduction current and right-half-plane zero of its control transfer function. Furthermore, in this topology the output voltage is always higher than the input voltage. As a result, a first-stage boost PFC converter needs to be connected with a second-stage DC-DC converter. A new topology which can be used as single stage PFC converter is proposed in this paper.
Original Article : Role of UCP2 Expression after Hepatic Warm Ischemia-Reperfusion in the Rat
( Mizuki Ninomiya ),( Ken Shirabe ),( Mitsuo Shimada ),( Takahiro Terashi ),( Yoshihiko Maehara ) 대한간학회 2011 Gut and Liver Vol.5 No.4
Background/Aims: The role of uncoupling protein-2 (UCP2) in the liver is currently unclear. Emerging evidence suggests a relationship between UCP2 and oxidative stress. In the present study, we tested the hypothesis that UCP2 expression in the liver might change during warm ischemia-reperfusion (I/R) according to oxidative stress. Methods: Wistar rats were subjected to 40 (short ischemia) or 90 (long ischemia) minutes of partial lobar ischemia followed by 4 hours of reperfusion. UCP2 expression in the ischemic and nonischemic lobes was assessed using reverse transcription-polymerase chain reaction and immunohistochemistry. Malondialdehyde concentrations in the liver tissue were also compared. Results: Malondialdehyde concentrations in the ischemic lobes were significantly higher in the long ischemia group. In the ischemic lobes of the short ischemia group, UCP2 protein expression was induced in hepatocytes, which did not express the protein prior to treatment, and the expression levels were higher than in the long ischemia group. The intralobular distribution of UCP2 seemed to correlate inversely with that of the necrotic area. UCP2 expression was observed, even in nonischemic lobes with similar intralobular heterogeneity. Conclusions: UCP2 was induced in hepatocytes after warm I/R. Although the primitive role of UCP2 expression may be cytoprotective in nature, its actual protective effect in hepatic I/R may be minimal. (Gut Liver 2011;5:486-492)