This paper deals with the simulation of eight bus system having fixed capacitor and thyristor controlled reactor. The system is modeled and simulated using MATLAB. The simulation results are presented. The power and control circuits are simulated. The current drawn by the (TCR) varies with the variation in the firing angle. The simulation results are compared with the theoretical results.

Chimeric antigen RECEPTOR- (CAR-) based immunotherapies (CARs), as one of the newest methods for immunotherapy, have heralded a new era of treating cancer. When the CAR is derived from an antibody, the resultant cell should combine the desirable targeting features of an antibody (e.g. lack of requirement for major histocompatibility complex recognition, ability to recognize self antigens). These potential benefits result in the identification of tumor-sprcific antigens which in turneliminates tumor cells by summoning cytokines and co-stimulatory molecules that kill other tumor cells.This review briefly describes basic CAR structure and function, how their antigenic targets are selected, and the development and advancements of this technology to improve their function intumor micro-environment. Afterwards, several examples of successful treatments with the help of this technology are presented and finally, we take a glance at the side effects of this method.

One of the important issues in electric arc furnace (EAF) of the steel industries is the effective compensation of the EAF. In this paper, firstly an optimal design model for the EAF is presented. Then, a thyristor controlled reactor ((TCR)) is installed in parallel with the (TCR). The parameters of the (TCR) are designed optimally to compensate the reactive power of the EAF. In the proposed method, a hyperbolic-exponential model is considered for the EAF and also a sinusoidal voltage flicker with the frequency in the range human vision (between 4-14 Hz) is included. In addition, the presence of the harmonic filters with the (TCR) is discussed. The results of the simulation show that the (TCR) can compensate the effects sinusoidal voltage flicker. Moreover, the results indicate that compared to the other methods, the average time response is about the half period of a cycle.

New Page 1 Transforming growth factor beta (TGF-b) is a mediator released by nearly all cell types. It has suppression activity on the immune system, but exactly how this effect is carried out is not clear. Previous experiments showed that IgG interacts with or carriers active TGF-b, that could suppresses cytotoxic T-CELL responses to an immunogenic tumor in mice. Since T cell RECEPTOR ((TCR)) has structural similarities with IgG, we asked the question whether a specific (TCR) could interfere with and enhance the suppressive effect of TGF-b on T-CELL proliferation. T-CELL lines were established by limiting dilution and specific (TCR) were extracted and purified. Mixed lymphocyte reaction (MLR) was carried out using DA (RT1a) vs. LEW (RT11) lymph node cells and DA vs. PVG (RT1u) lymph node cells. DA cells were used as responder cells and PVG/LEW as stimulator cells. Proliferation of DA cells was examined with different concentration of TGF-b by adding 1mci 3H-thymidine 24 hours prior to harvesting the cells.  The results showed that the presence of a specific (TCR) does not have any effect on the percentage of suppression when already fully suppressed by TGF-b.  However, it does have an effect on TGF-b stimulated suppression under certain conditions. When (TCR) was added at the same concentration as TGF-b (1-2 ng/ml), inhibited TGF-b stimulated suppression of proliferation, but when added at higher concentration than TGF-b, this effect disappeared, and the proliferation was suppressed in the same way, as (TCR) was absent. Thus, (TCR) interaction with TGF-b could play an important role in the homeostasis of immunity by augmenting the proliferation of activated dominant lymphocyte clones. This would promote suppression of activation/proliferation of new specific antigen-reactive clones that may arise during ongoing immunity, and also suppressing some autoimmune diseases