Mitsubishi

About: Mitsubishi is a company organization based out in Tokyo, Japan. It is known for research contribution in the topics: Signal & Layer (electronics). 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.

Invariant V(alpha)19i T cells regulate autoimmune inflammation.

Abstract: T cells expressing an invariant V(alpha)19-J(alpha)33 T cell receptor alpha-chain (V(alpha)19i TCR) are restricted by the nonpolymorphic major histocompatibility complex class Ib molecule MR1. Whether V(alpha)19i T cells are involved in autoimmunity is not understood. Here we demonstrate that T cells expressing the V(alpha)19i TCR transgene inhibited the induction and progression of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Similarly, EAE was exacerbated in MR1-deficient mice, which lack V(alpha)19i T cells. EAE suppression was accompanied by reduced production of inflammatory mediators and increased secretion of interleukin 10. Interleukin 10 production occurred at least in part through interactions between B cells and V(alpha)19i T cells mediated by the ICOS costimulatory molecule. These results suggest an immunoregulatory function for V(alpha)19i T cells.

Backlight for liquid crystal display device

Abstract: A backlight provides uniform emanating light for a liquid crystal display. In the backlight, light emitted from a light source is incident on a receiving end surface of a light guide plate and emanates through a top surface toward a liquid crystal panel. A bottom surface includes a reflecting hollow wedge extending along the receiving end surface and varying in depth, as measured from the bottom surface, in correspondence with distance from the end surface. A dividing flat portion orthogonal to the reflecting hollow wedge divides the reflecting hollowed portion, and an output surface includes a prism having parallel ridges extending in a direction orthogonal to the receiving end surface.

Poly(L-proline)-binding proteins from chick embryos are a profilin and a profilactin.

Abstract: Two poly(L-proline)-binding proteins (PBP-1 and PBP-2) were purified from chick embryos by using a poly(L-proline)-agarose column. PBP-1 was composed of two different polypeptides (molecular masses of 42 kDa and 15 kDa). The molar ratio of the two proteins in the complex was 1:1. The other poly(L-proline)-binding protein, PBP-2, was the 15-kDa protein itself. The 42-kDa protein was confirmed to be an actin from the amino acid composition, by immunochemical evidence and by its ability to self-polymerize. In addition, the 42 + 15-kDa protein complex (PBP-1) inhibited DNase I, just as a monomeric actin did. The amino acid composition of the 15-kDa protein was similar to that of mammalian profilin and it inhibited the salt-induced polymerization of rabbit skeletal muscle actin. Therefore, we conclude that the two poly(L-proline)-binding proteins from the chick embryo are a profilactin and a profilin in chick embryo. The ability of profilactin to bind poly(L-proline) must be due to profilin itself, because the profilin has a greater affinity for poly(L-proline) than does profilactin. Additionally, both the monomeric and filamentous actin from rabbit skeletal muscle have no affinity for poly(L-proline).

Numerical control apparatus

Abstract: A numerical control apparatus comprising a display device capable of displaying not only the configuration of a workpiece to be machined and the machining paths of machining tools relative to the workpiece but also the movement of the workpiece as a machining path of relative movement of the machining tool with respect to a stationary workpiece. The machining path of the relative movement of the machining tool is obtained based on data representing the movement of the workpiece per se.

Neuronal death in vitro: parallelism between survivability of hippocampal neurones and sustained elevation of cytosolic Ca2+ after exposure to glutamate receptor agonist.

Abstract: Hippocampal neurones isolated from rat embryos were maintained on glial monolayers in a medium containing no L-glutamate (Glu). The administration of Glu for a limited period induced a massive death (loss) of neurones. The degree of neuronal loss increased with time after exposure to Glu. The extent of neuronal loss assessed 24 h after exposure to Glu was dependent upon the concentration Glu and on the duration of the exposure. An increase in concentration of external Ca2+ during the exposure to Glu enhanced the extent of loss. By contrast, an increment in concentration of environmental Mg2+ reduced the loss. The inhibitor of spike firing, tetrodotoxin (TTX) and the suppressor of Ca2+ entry, nitrendipine, both decreased the extent of loss, when delivered prior to Glu. The toxicity of Glu became progressively more apparent with further days of culture. The cytosolic concentration of Ca2+ ([Ca2+]i) in single hippocampal neurones was monitored by microscopic fluorometry under conditions equivalent to those in the death assay. The time required for the recovery of [Ca2+]i from the level elevated by exposure to Glu to pre-stimulus levels closely paralleled the degree of neuronal loss; i.e. high doses of Glu, long periods of exposure, high concentrations of external Ca2+, low concentrations of external Mg2+, and extended days of culture all retarded [Ca2+]i recovery, while TTX and nitrendipine accelerated it. These findings show that neuronal death resulting from an extraneous excitation (excitotoxicity) can be analyzed in vitro. Furthermore, substantial support has been provided to the hypothesis that excitotoxicity has as an underlying mechanism, an excess loading of Ca2+ in neuronal cytoplasm.