Bcl-2 is the best characterized inhibitor of apoptosis, although the molecular basis of this action is not fully understood. Using a protein interaction cloning procedure, we identi®ed a human gene designated as bis (mapped to chromosome 10q25) that encoded a novel Bcl-2-interacting protein. Bis protein showed no signi®cant homology with Bcl-2 family proteins and had no prominent functional motif. Co-immunoprecipitation analysis con®rmed that Bis interacted with Bcl-2 in vivo. DNA transfection experiments indicated that Bis itself exerted only weak anti-apoptotic activity, but was synergistic with Bcl-2 in preventing Bax-induced and Fas-mediated apoptosis. These results suggest that Bis is a novel modulator of cellular anti-apoptotic activity that functions through its interaction with Bcl-2.

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Abstract-In computational electromagnetics, the multilevel fast multipole algorithm (MLFMA) is used to reduce the computational complexity of the matrix vector product operations. In iteratively solving the dense linear systems arising from discretized hybrid integral equations, the sparse approximate inverse (SAI) preconditioning technique is employed to accelerate the convergence rate of the Krylov iterations. We show that a good quality SAI preconditioner can be constructed by using the near part matrix numerically generated in the MLFMA. The main purpose of this study is to show that this class of the SAI preconditioners are effective with the MLFMA and can reduce the number of Krylov iterations substantially. Our experimental results indicate that the SAI preconditioned MLFMA maintains the computational complexity of the MLFMA, but converges a lot faster, thus effectively reduces the overall simulation time.Index Terms-Electromagnetic scattering, Krylov methods, multilevel fast multipole algorithm (MLFMA), sparse approximate inverse (SAI) preconditioning.

Gangliosides abundant in the nervous system have been implicated in a broad range of biological functions, including the regulation of cell proliferation and death. Glutamate-induced cell death, which is accompanied by an accumulation of reactive oxygen species (ROS), is a major contributor to pathological cell death within the nervous system. However, the mechanism underlying this neuronal cell death has not been fully elucidated. In this study, we report that ganglioside GM3 is involved in neuronal cell death. GM3 was up-regulated in the mouse hippocampal cell line HT22 death caused by glutamate. Increment in GM3 levels by both the exogenous addition of GM3 and the overexpression of the GM3 synthase gene induced neuronal cell death. Overexpression of GM3 synthase by microinjecting mRNA into zebrafish embryos resulted in neuronal cell death in the central nervous system (CNS). Conversely, RNA interference-mediated silencing of GM3 synthase rescued glutamate-induced neuronal death, as evidenced by the inhibition of massive ROS production and intracellular calcium ion influx. 12-lipoxygenase (12-lipoxygenase) (12-LOX) was recruited to glycosphingolipid-enriched microdomains (GEM) in a GM3-dependent manner during oxidative glutamate toxicity. Our findings suggest that GM3 acts as not only a mediator of oxidative HT22 death by glutamate but also a modulator of in vivo neuronal cell death.