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This paper proposes a new neutral point potential control technique for the neutral-point-clamped three-level inverter. Utilizing the phase current polarity information, this technique distributes the redundant voltage vectors in a manner to obtain stable neutral point voltage under all operating conditions including the zero-power-factor condition. Detailed analysis and computer simulations show the superiority of the proposed method. The feasibility of the proposed method has been proven via laboratory experiments. Index Terms--Current polarity, inverter, neutral point potential, space vector, stabilization.

Abstract: Objective: This study tested the hypothesis that 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitor affects T cell-mediated autoimmunity through inhibition of nuclear factor-κB (NFκB) and reduces the severity of experimental autoimmune myocarditis (EAM). Methods: EAM was induced in Lewis rats by immunization with myosin. High-dose or low-dose fluvastatin or vehicle was administered orally for 3 weeks to rats with EAM. Results: Fluvastatin reduced the pathophysiological severity of myocarditis. Fluvastatin inhibited expression of NFκB in the nuclei of myocardium in EAM. Fluvastatin reduced production of Th1-type cytokines, including interferon (IFN)-γ and interleukin (IL)-2, and inhibited expression of inflammatory cytokine mRNAs in the myocardium. Infiltration of CD4-positive T cells into the myocardium and T cell proliferative responses were suppressed by fluvastatin. Plasma lipid levels did not differ between the groups. Conclusions: Fluvastatin ameliorates EAM by inhibiting T cell responses and suppressing Th1-type and inflammatory cytokines via inactivation of nuclear factor-κB, and this activity is independent of cholesterol reduction. [Copyright &y& Elsevier]

Acute cardiac allograft rejection is still a major complication after heart transplantation. Acute rejection usually responds to conventional immunosuppressants, however, the nonspecific nature of the immunosuppression and the toxicities of the drugs can be life threatening and may compromise the recipient's quality of life. In addition, cardiac allograft arteriosclerosis or chronic rejection limits the long-term survival of recipients. Such conditions cannot be prevented with conventional therapies. To overcome acute and chronic rejection of cardiac allograft as well as ischemia/reperfusion injury associated with organ preservation many novel approaches have been proposed. Gene transfection of the donor organ during organ preservation is an attractive method, because the transfected genes would not affect recipients and treatment could be delivered specifically to the site of inflammation. This method could be useful to prevent graft failure without systemic adverse effects. Here we shall review current advances in gene therapies to prevent and treat organ failure of transplanted allografts.