A SIMD architecture for hard real-time systems

Emerging safety-critical systems require high-performance data-parallel architectures and, problematically, ones that can guarantee tight and safe worst-case execution times. Given the complexity of existing architectures like GPUs, it is unlikely that sufficiently accurate models and algorithms for timing analysis will emerge in the foreseeable future. This motivates a clean-slate approach to designing a real-time data-parallel architecture. In this work I present Sim-D: a wide-SIMD architecture for hard real-time systems. Similar to GPUs, Sim-D performs hardware strip-mining to schedule the work for a compute kernel in entities called work-groups. Sim-D schedules the work for each work-group as a sequence of uninterruptible access- and execute program phases, interleaving the phases of two work-groups. By providing performance isolation between the memory- and compute resources, the execution time of each phase can be tightly bound through static analysis. I present a predictable closed-page DRAM controller that processes requests for large 1D- and 2D blocks of data, as well as indirect indexed transfers. These large transfers coalesce the data requests of a whole work-group. For a linear 4KiB transfer over a 64-bit data bus, the utilisation provably exceeds 78% for DDR4-3200AA DRAM. For 2D blocks, a well-chosen tiling configuration can achieve near-similar efficiency. I show that bounds on the execution time of indexed transfers are pessimistic by nature, but propose a novel snoopy indexed transfer mechanism that permits more reasonable bounds when the buffer size is limited. Finally, I present a worst-case execution time calculation algorithm for Sim-D. This algorithm is paired with two hardware work-group scheduling policies that deterministically reduce run-time variance. The worst-case execution time analysis algorithm combines static control flow analysis with a simulation-based cost model for execution and DRAM transfers. Its key novelty is the addition of a stage that considers work-group scheduling effects. I show that the work-group scheduling policies degrade performance on average by 8.9%, but permit the calculation of worst-case execution time bounds that are tight within 14.3% on average for benchmarks that avoid inefficient indexed transfers

Cellular distribution of vascular endothelial growth factor A (VEGFA) and B (VEGFB) and VEGF receptors 1 and 2 in focal cortical dysplasia type IIB

Members of the vascular endothelial growth factor (VEGF) family are key signaling proteins in the induction and regulation of angiogenesis, both during development and in pathological conditions. However, signaling mediated through VEGF family proteins and their receptors has recently been shown to have direct effects on neurons and glial cells. In the present study, we immunocytochemically investigated the expression and cellular distribution of VEGFA, VEGFB, and their associated receptors (VEGFR-1 and VEGFR-2) in focal cortical dysplasia (FCD) type IIB from patients with medically intractable epilepsy. Histologically normal temporal cortex and perilesional regions displayed neuronal immunoreactivity (IR) for VEGFA, VEGFB, and VEGF receptors (VEGFR-1 and VEGFR-2), mainly in pyramidal neurons. Weak IR was observed in blood vessels and there was no notable glial IR within the grey and white matter. In all FCD specimens, VEGFA, VEGFB, and both VEGF receptors were highly expressed in dysplastic neurons. IR in astroglial and balloon cells was observed for VEGFA and its receptors. VEGFR-1 displayed strong endothelial staining in FCD. Double-labeling also showed expression of VEGFA, VEGFB and VEGFR-1 in cells of the microglia/macrophage lineage. The neuronal expression of both VEGFA and VEGFB, together with their specific receptors in FCD, suggests autocrine/paracrine effects on dysplastic neurons. These autocrine/paracrine effects could play a role in the development of FCD, preventing the death of abnormal neuronal cells. In addition, the expression of VEGFA and its receptors in glial cells within the dysplastic cortex indicates that VEGF-mediated signaling could contribute to astroglial activation and associated inflammatory reactions