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.

Recent progress in forward error correction and its interplay with transmission impairments

Abstract: Recent progress in forward error correction (FEC) for optical communications is reviewed. The various types of FEC are classified as belonging to one of three generations. A third-generation FEC, based on a block turbo code, has been fully integrated in very large scale integration, and thanks to the use of 3-bit soft decision, a net coding gain of 10.1 dB was demonstrated experimentally. That has brought a number of positive impacts to existing systems. The Shannon limit is discussed for hard and soft decision decoding. The interplay between FEC and error bursts is discussed. Fast polarization scrambling with FEC has been effective in mitigating polarization mode dispersion (PMD). The error count function has proved useful for the adaptive equalization of both chromatic dispersion and PMD

Packaged semiconductor chip

Abstract: A semiconductor device includes a substrate having a recess; a semiconductor chip disposed in the recess; a plurality of external electrodes disposed on the substrate; a lid covering the recess; and a heat radiator disposed between the semiconductor chip and the substrate for transmitting heat generated by the semiconductor chip to the substrate for radiation.

Rescue of thymocytes and T cell hybridomas from glucocorticoid‐induced apoptosis by stimulation via the T cell receptor/CD3 complex: a possible in vitro model for positive selection of the T cell repertoire

Abstract: Positive and negative selection events are involved in determining useful T cell clones to mature in the thymus. Accumulating evidence suggests that immature self-reactive thymocytes undergo apoptotic death (negative selection) upon stimulation via the T cell receptors (TcR). A similar phenomenon of activation-induced death has been reported in T cell hybridomas. On the other hand, little is known about the mechanism of the positive selection. Apoptosis in rodent thymocytes or T cell hybridomas is also known to be induced by glucocorticoids in vitro at concentrations within the physiologic range. We report here that the TcR/CD3-mediated stimulation and glucocorticoids mutually inhibit the apoptosis in T cell hybridomas. The production of interleukin 2 by the rescued cells indicated that the TcR/CD3-mediated signal was transduced into the cells. Thymocytes were also rescued from glucocorticoid-induced apoptosis by the stimulation with antibodies to TcR/CD3 molecules. The rescue of thymocytes, however, was observed only at a narrow concentration range of each of the antibodies, suggesting that the proper stimulation via the TcR/CD3 is required for the rescue. If thymocytes in situ are differentially stimulated according to the affinity of the TcR towards self, only the thymocytes whose TcR have proper affinity towards self may be rescued from glucocorticoid-induced apoptosis. Therefore, we propose a hypothesis that the positive selection of the T cell repertoire is based on the inhibition of glucocorticoid-induced apoptosis in immature thymocytes bearing TcR with proper affinity for self by the TcR-mediated signals in situ. Furthermore, the selection may be influenced by the peak level of glucocorticoid concentration, since the proper concentration range of the anti-TcR/CD3 antibody for the rescue was variable depending on the glucocorticoid concentration.