In this paper, we present a comprehensive performance comparison of MPI implementations over InfiniBand, Myrinet and Quadrics. Our performance evaluation consists of two major parts. The first part consists of a set of MPI level micro-benchmarks that characterize different aspects of MPI implementations. The second part of the performance evaluation consists of application level benchmarks. We have used the NAS Parallel Benchmarks and the sweep3D benchmark. We not only present the overall performance results, but also relate application communication characteristics to the information we acquired from the micro-benchmarks. Our results show that the three MPI implementations all have their advantages and disadvantages. For our 8-node cluster, InfiniBand can offer significant performance improvements for a number of applications compared with Myrinet and Quadrics when using the PCI-X bus. Even with just the PCI bus, InfiniBand can still perform better if the applications are bandwidth-bound.
E2F-mediated control of gene expression is believed to have an essential role in the control of cellular proliferation. Using a conditional gene-targeting approach, we show that the targeted disruption of the entire E2F activator subclass composed of E2f1, E2f2, and E2f3 in mouse embryonic fibroblasts leads to the activation of p53 and the induction of p53 target genes, including p21 CIP1 . Consequently, cyclin-dependent kinase activity and retinoblastoma (Rb) phosphorylation are dramatically inhibited, leading to Rb/E2F-mediated repression of E2F target gene expression and a severe block in cellular proliferation. Inactivation of p53 in E2f1-, E2f2-, and E2f3-deficient cells, either by spontaneous mutation or by conditional gene ablation, prevented the induction of p21 CIP1 and many other p53 target genes. As a result, cyclin-dependent kinase activity, Rb phosphorylation, and E2F target gene expression were restored to nearly normal levels, rendering cells responsive to normal growth signals. These findings suggest that a critical function of the E2F1, E2F2, and E2F3 activators is in the control of a p53-dependent axis that indirectly regulates E2F-mediated transcriptional repression and cellular proliferation.
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