Search

This paper proposes a new current control strategy that is based on the internal model principle for a current balancer in single-phase three-wire distribution systems. The proposed current control strategy includes a sinusoidal reference input model to achieve the zero steady-state error tracking. The appropriate control gains of this control strategy can be systematically determined by using a state-feedback controller design method via linear matrix inequalities. The basic principle of the proposed control strategy is discussed in detail, and then confirmed by digital computer simulation using the PSIM software. A prototype experimental model is constructed and tested. Experimental results demonstrate that zero steady-state error tracking is achieved by the proposed control strategy. Also, balanced source currents are obtained on the secondary side of a pole-mounted distribution transformer while the load conditions are unbalanced. © 2013 Institute of Electrical Engineers of Japan. Published by John Wiley & Sons, Inc.

Baicalein, a flavonoid derived from Scutellaria baicalensis Georgi, is known to protect neural tissue from damage. Several studies have found that baicalein reduces brain infarction following focal brain ischaemia. However, there are few reports on the protective effects of baicalein following global brain ischaemia. Therefore, the current study was designed to address the effects of baicalein on neuronal damage and matrix metalloproteinase (MMP; gelatinase) activity in the hippocampus after transient global ischaemia. C57BL/6 mice were subjected to transient global brain ischaemia for 20 min and sacrificed 72 h after ischaemic insult. Baicalein (200 mg/kg, once daily, as a suspension in 0.5% carboxymethylcellulose) or an equal volume of vehicle was orally administered to the mice from 7 days prior to the ischaemic insult until sacrifice. After global ischaemia neuronal damage was significant in CA1 and CA2 pyramidal cell layers. In baicalein-treated mice, neuronal damage from the ischaemic insult was significantly less than that in vehicle-treated mice. Baicalein administration also inhibited MMP-9 activity in the hippocampus. These data demonstrate that baicalein reduces hippocampal neuronal damage after transient global ischaemia. Besides its possible protective mechanisms, the protective role of baicalein against global ischaemia may operate, at least in part, through the inhibition of MMP-9 activity. Copyright © 2012 John Wiley & Sons, Ltd.

Previous studies have demonstrated that (–)-epigallocatechin gallate (EGCG), a green tea polyphenol, protects against ischemia and reperfusion-induced injury in many organ systems. Here, we test the hypothesis that part of EGCG's neuroprotective effects may involve a modulation of matrix metalloproteinases (MMPs) after cerebral ischemia. C57BL/6 mice were subjected to 20 min of transient global cerebral ischemia. EGCG (50 mg/kg) or vehicle (saline) was administered i.p. immediately after ischemia. Brains were examined 3 days after ischemia. The effects of EGCG on MMP (gelatinase) activity and neuronal damage in the hippocampus were assessed. Gelatin gel zymography showed induction of active forms of MMP-9 protein after transient global cerebral ischemia. In situ zymography showed that ischemic gelatinase activity occurred primarily in pyramidal neuronal areas after brain ischemia. Mice treated with EGCG showed significantly reduced gelatinase levels. Neuronal damage was evident in CA1 and CA2 pyramidal sectors, corresponding to TUNEL-positive signals. In EGCG-treated mice, delayed neuronal damage was significantly reduced compared with vehicle-treated mice. These results demonstrate that the green tea polyphenol EGCG suppresses MMP-9 activation and reduces the development of delayed neuronal death after transient global cerebral ischemia in mouse brain. © 2008 Wiley-Liss, Inc.

Previous studies have demonstrated that pioglitazone, a peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, inhibits ischemia-induced injury in various tissues including neural tissue. Pioglitazone has also been shown to reduce matrix metalloproteinase (MMP) activity. Because MMP is known to play a major role in the pathophysiology of brain ischemia, the present study was undertaken to test whether pioglitazone attenuates ischemic neuronal damage through MMP inhibition. C57BL/6 mice were subjected to global brain ischemia for 20 min. Animals were killed 72 h after ischemia. Oral pioglitazone (40 mg/kg/day, as a suspension in 0.5% carboxymethylcellulose) was administered to mice twice daily for 3 days before ischemia and twice daily after ischemia until the animals were killed. We investigated gelatinase activity by zymography and laminin immunohistochemistry. Histological analysis was also performed to test the protective effect of pioglitazone on neuronal damage. Mice treated with pioglitazone had attenuated gelatinase activity. Gelatin gel and in situ zymography showed up-regulation of gelatinase activity after ischemia. Pioglitazone significantly inhibited ischemia-induced elevation of the active form of MMP-9. Pioglitazone also reduced up-regulation of in situ gelatinase activity and laminin breakdown induced by ischemia in the hippocampus. There was marked neuronal damage in the CA1 and CA2 areas after ischemia. Neuronal damage in mice was significantly decreased by pioglitazone treatment, compared with vehicle-treated mice. Pioglitazone also inhibited TdT-mediated dUTP nick end labeling staining in CA1 and CA2 areas. Pioglitazone, a PPARgamma agonist, reduces delayed neuronal damage induced by global ischemia through inhibition of MMP-9 activity.

Gastrodia elata (GE) Blume, a traditional herbal agent, has been used mainly in anticonvulsive treatment in Asia. Recently, extracts of GE were evaluated for their potential as neuroprotectives and antioxidants. This study was designed to examine the antioxidant effect of the ether fraction of the methanol extract (EFME) of GE along with its major constituents vanillin, vanillyl alcohol, hydroxybenzaldehyde and hydroxybenzyl alcohol. In experiment 1, gerbils were treated with EFME of GE at a dosage of 500 mg/kg/day for 2 weeks. Oxidative stress was induced with H(2)O(2) or ferrous ion, and lipid peroxidation was measured. In experiment 2, oxidative stress was induced with various concentrations of H(2)O(2) or ferrous ammonium sulfate, and lipid peroxidation was measured. To compare the antioxidant potency, the inhibitory concentration 50% (IC(50)) was determined. EFME of GE reduced auto-peroxidation and H(2)O(2)-induced lipid peroxidation. However, it did not significantly reduce ferrous ammonium sulfate-induced lipid peroxidation. The order of antioxidation potency was as follows: hydroxybenzyl alcohol > vanillyl alcohol > vanillin > hydroxybenzaldehyde. In the case of hydroxybenzaldehyde, its antioxidant effect was more potent than that of melatonin. The excellent antioxidant effects of GE and its main constituents may have potential in the treatment of lipid peroxidation-associated neurological disease.

Previous studies have demonstrated that a green tea polyphenol, (-)-epigallocatechine gallate (EGCG), has a potent free radical scavenging and antioxidant effect. Glutamate leads to excitotoxicity and oxidative stress, which are important pathophysiologic responses to cerebral ischemia resulting in brain edema and neuronal damage. We investigated the effect of EGCG on excitotoxic neuronal damage in a culture system and the effect on brain edema formation and lesion after unilateral cerebral ischemia in gerbils. In vitro, excitotoxicity was induced by 24-hr incubation with N-methyl-D-aspartate (NMDA; 10 microM), AMPA (10 microM), or kainate (20 microM). EGCG (5 microM) was added to the culture media alone or with excitotoxins. We examined malondialdehyde (MDA) level and neuronal viability to evaluate the effect of EGCG. In vivo, unilateral cerebral ischemia was induced by occlusion of the right common carotid artery for 30, 60, or 90 min and followed by reperfusion of 24 hr. Brain edema, MDA, and infarction were examined to evaluate the protective effect of EGCG. EGCG (25 or 50 mg/kg, intraperitoneally) was administered twice, at 30 min before and immediately after ischemia. EGCG reduced excitotoxin-induced MDA production and neuronal damage in the culture system. In the in vivo study, treatment of gerbils with the lower EGCG dose failed to show neuroprotective effects; however, the higher EGCG dose attenuated the increase in MDA level caused by cerebral ischemia. EGCG also reduced the formation of postischemic brain edema and infarct volume. These results demonstrate EGCG may have future possibilities as a neuroprotective agent against excitotoxicity-related neurologic disorders such as brain ischemia.

We fabricated a nematic liquid crystal(NLC) cell which has initially π-twist state stabilized by pixel-isolation walls without any chiral dopant. The pixel-isolation walls are formed by phase separation between liquid crystal molecules and fluorinated polymer material under the condition of a vertical electric field. In comparison with a conventional pi cell, the initially π-twisted NLC cell needs no nucleus for the transition from splay to bend state and exhibits reduced driving voltage. Also, the cell has fast response properties similar to the conventional pi cell.

In this paper we propose a configuration for a single-cell gap single-driving-circuit transflective LCD, which is composed of the optically compensated bend (OCB) mode in the transmissive region and the hybrid aligned nematic (HAN) mode in the reflective region. Optical compensation was made with positive A plates, negative C plates, and wide-band quarter-wave plates (WB QWPs). Both the reflective mode and the transmissive mode operate in the normally white mode and have the same gamma curve. WB QWPs provide wide viewing angle characteristics of the transmissive mode.