Mitsubishi

About: Mitsubishi is a company organization based out in Tokyo, Japan. It is known for research contribution in the topics: Layer (electronics) & Signal. The organization has 53115 authors who have published 54821 publications receiving 870150 citations. The organization is also known as: Mitsubishi Group of Companies & Mitsubishi Companies.

Apparatus for controlling electric motor

Abstract: A control apparatus for controlling the main circuit for driving an AC electric motor consisting of a diode converter and a pulse width modulation (PWM) power converting device, in which it is arranged that the DC current as the output of the diode converter is detected by a current detector, the AC component of this DC current is filtered through a high-pass filter, and a pulse-width-modulation control is exercised by a control circuit in response to the output of the high-pass filter so that the DC current as the output of the diode converter may be smoothed out in the main circuit by the PWM power converting device. By such arrangement, this control apparatus of an electric motor is made smaller in size and simplified in structure and enabled to control the power factor of the power source of the diode converter to close to 1.0.

Computer vision for interactive computer graphics

Abstract: Vision can be a powerful interface device for computers because of its potential for sensing body position, head orientation, direction of gaze, pointing commands, and gestures. Such unencumbered interaction can make computers easier to use. We describe vision algorithms for interactive graphics and present vision-controlled graphics applications using these algorithms. Some applications employ an artificial retina chip for image detection or preprocessing.

FTY720, sphingosine 1-phosphate receptor modulator, ameliorates experimental autoimmune encephalomyelitis by inhibition of T cell infiltration.

Abstract: FTY720, a sphingosine 1-phosphate receptor modulator, induces a marked decrease in the number of peripheral blood lymphocytes and exerts immunomodulating activity in various experimental allograft and autoimmune disease models. In this study, we evaluated the effect of FTY720 and its active metabolite, (S)-enantiomer of FTY720-phosphate [(S)-FTY720-P] on experimental autoimmune encephalomyelitis (EAE) in rats and mice. Prophylactic administration of FTY720 at 0.1 to 1 mg/kg almost completely prevented the development of EAE, and therapeutic treatment with FTY720 significantly inhibited the progression of EAE and EAE-associated histological change in the spinal cords of LEW rats induced by immunization with myelin basic protein. Consistent with rat EAE, the development of proteolipid protein-induced EAE in SJL/J mice was almost completely prevented and infiltration of CD4(+) T cells into spinal cord was decreased by prophylactic treatment with FTY720 and (S)-FTY720-P. When FTY720 or (S)-FTY720-P was given after establishment of EAE in SJL/J mice, the relapse of EAE was markedly inhibited as compared with interferon-beta, and the area of demyelination and the infiltration of CD4(+) T cells were decreased in spinal cords of EAE mice. Similar therapeutic effect by FTY720 was obtained in myelin oligodendrocyte glycoprotein-induced EAE in C57BL/6 mice. These results indicate that FTY720 exhibits not only a prophylactic but also a therapeutic effect on EAE in rats and mice, and that the effect of FTY720 on EAE appears to be due to a reduction of the infiltration of myelin antigen-specific CD4(+) T cells into the inflammation site.

The paternal methylation imprint of the mouse H19 locus is acquired in the gonocyte stage during foetal testis development.

Abstract: Background Germline-specific differential DNA methylation that persists through fertilization and embryonic development is thought to be the ‘imprint’ distinguishing the parental alleles of imprinted genes. If such methylation is to work as the imprinting mechanism, however, it has to be reprogrammed following each passage through the germline. Previous studies on maternally methylated genes have shown that their methylation imprints are first erased in primordial germ cells (PGCs) and then re-established during oocyte growth. Results We have examined the timing of the reprogramming of the paternal methylation imprint of the mouse H19 gene during germ cell development. In both male and female PGCs, the paternal allele is partially methylated whereas the maternal allele is unmethylated. This partial methylation is completely erased in the female germline by entry into meiosis, establishing the oocyte methylation pattern. In the male germline, both alleles become methylated, mainly during the gonocyte stage, establishing the sperm methylation pattern. Conclusion The paternal methylation imprint of H19 is established in the male germline and erased in the female germline at specific developmental stages. The identification of the timings of the methylation and demethylation should help to identify and characterize the biochemical basis of the reprogramming of imprinting.