SHARPE: Variation-Aware Formal Statistical Timing Analysis in RTL

Variations in timing can occur due to multiple sources on a chip. Many circuit level statistical techniques are used to analyze timing in the presence of these sources of variation. At the system (higher) level of design, however, timing estimation/verification is not performed. The design at the Register Transfer Level (RTL) is unaware of the underlying statistics and timing variations. It is desirable to have ``variation awareness'' at the higher level, and estimate block level delay distributions early in the design cycle, to evaluate design choices quickly and minimize post-synthesis simulation costs. In this paper, we introduce SHARPE, a rigorous, systematic timing analysis/verification methodology and tool flow to find statistical delay invariants in RTL. We treat the RTL source code as a program and use static program analysis techniques to compute probabilities. We model the probabilistic RTL modules as Discrete Time Markov Chains (DTMCs) that are then checked formally for probabilistic invariants using PRISM, a probabilistic model checker. Our technique is illustrated on the RTL description of the datapath of OR1200, an open source embedded processor.Ope

Statistical Guarantees of Performance for MIMO Designs

Coordinated Science Laboratory was formerly known as Control Systems LaboratoryUILU-ENG-09-221

Myeloid and plasmacytoid dendritic cells transfer HIV-1 preferentially to antigen-specific CD4+ T cells

Dendritic cells (DCs) are essential antigen-presenting cells for the induction of T cell immunity against pathogens such as human immunodeficiency virus (HIV)-1. At the same time, HIV-1 replication is strongly enhanced in DC–T cell clusters, potentially undermining this process. We found that immature CD123+ plasmacytoid DCs (PDCs) and CD11c+ myeloid DCs (MDCs) were susceptible to both a CCR5- and a CXCR4-using HIV-1 isolate in vitro and were able to efficiently transfer that infection to autologous CD4+ T cells. Soon after HIV-1 exposure, both PDCs and MDCs were able to transfer the virus to T cells in the absence of a productive infection. However, once a productive infection was established in the DCs, newly synthesized virus was predominantly spread to T cells. HIV-1 exposure of the MDCs and PDCs did not inhibit their ability to present cytomegalovirus (CMV) antigens and activate CMV-specific memory T cells. As a result, both PDCs and MDCs preferentially transmitted HIV-1 to the responding CMV antigen–specific CD4+ T cells rather than to nonresponding T cells. This suggests that the induction of antigen-specific T cell responses by DCs, a process crucial to immune defense, can lead to preferential HIV-1 infection and the deletion of responding CD4+ T cells

Differential Susceptibility to Human Immunodeficiency Virus Type 1 Infection of Myeloid and Plasmacytoid Dendritic Cells

Human immunodeficiency virus type 1 (HIV-1) infection of dendritic cells (DCs) plays an important role in HIV-1 transmission and pathogenesis. Here, we studied the susceptibility of ex vivo-isolated CD11c(+) myeloid DCs (MDCs) and CD123(+) plasmacytoid DCs (PDCs) to HIV-1 infection and the function of these cells early after infection. Both DC subsets were susceptible to CCR5- and CXCR4-using HIV-1 isolates (BaL and IIIB, respectively). However, MDCs were more susceptible to HIV-1(BaL) infection than donor-matched PDCs. In addition, HIV-1(BaL) infected MDCs more efficiently than HIV-1(IIIB), whereas PDCs were equally susceptible to both isolates. While exposure to HIV-1 alone resulted in only weak maturation of DCs, Toll-like receptor 7/8 ligation induced full maturation in both infected and uninfected DCs. Maturation did not increase HIV-1 replication in infected DCs, and infected DCs retained their ability to produce tumor necrosis factor alpha after stimulation. Both HIV-1 isolates induced alpha interferon production exclusively in PDCs, irrespective of productive infection. In conclusion, PDCs and MDCs were susceptible to HIV-1 infection, but neither displayed functional defects as a consequence of infection. The difference in susceptibility of PDCs and MDCs to HIV-1 may have implications for HIV-1 transmission and DC-mediated transfer of HIV-1 to T cells