Resource Sharing in Custom Instruction Set Extensions

Customised processor performance generally increases as additional custom instructions are added. However, performance is not the only metric that modern systems must take into account; die area and energy efficiency are equally important. Resource sharing during synthesis of instruction set extensions (ISEs) can reduce significantly the die area and energy consumption of a customized processor. This may increase the number of custom instructions that can be synthesized with a given area budget. Resource sharing involves combining the graph representations of two or more ISEs which contain a similar sub-graph. This coupling of multiple sub-graphs, if performed naively, can increase the latency of the extension instructions considerably. And yet, as we show in this paper, an appropriate level of resource sharing provides a significantly simpler design with only modest increases in average latency for extension instructions. Based on existing resource-sharing techniques, this study presents a new heuristic that controls the degree of resource sharing between a given set of custom instructions. Our main contributions are the introduction of a parametric method for exploring the trade-offs that can be achieved between instruction latency and implementation complexity, and the coupling of design-space exploration with fast area-delay models for the operators comprising each ISE. We present experimental evidence that our heuristic exposes a broad range of design points, allowing advantageous trade-offs between die area and latency to be found and exploited

The design and performance of a conflict-avoiding cache

High performance architectures depend heavily on efficient multi-level memory hierarchies to minimize the cost of accessing data. This dependence will increase with the expected increases in relative distance to main memory. There have been a number of published proposals for cache conflict-avoidance schemes. We investigate the design and performance of conflict-avoiding cache architectures based on polynomial modulus functions, which earlier research has shown to be highly effective at reducing conflict miss ratios. We examine a number of practical implementation issues and present experimental evidence to support the claim that pseudo-randomly indexed caches are both effective in performance terms and practical from an implementation viewpoint.Peer Reviewe

Distributed modulo scheduling

Wide-issue ILP machines can be built using the VLIW approach as many of the hardware complexities found in superscalar processors can be transferred to the compiler. However, the scalability of VLIW architectures is still constrained by the size and number of ports of the register file required by a large number of functional units. Organizations composed by clusters of a few functional units and small private register files have been proposed to deal with this problem, an approach highly dependent on scheduling and partitioning strategies. This paper presents DMS, an algorithm that integrates modulo scheduling and code partitioning in a single procedure. Experimental results have shown the algorithm is effective for configurations up to 8 clusters, or even more when targeting vectorizable loops. 1 Keywords: ILP, VLIW, Clustering, Software Pipelining 1. Introduction Current microprocessor technology relies on two basic approaches to improve performance. One is to increase clock rates..

Anti-inflammatory treatment improves high-density lipoprotein function in rheumatoid arthritis

OBJECTIVE: Patients with rheumatoid arthritis (RA) are at increased cardiovascular risk. Recent studies suggest that high-density lipoprotein (HDL) may lose its protective vascular phenotype in inflammatory conditions. However, the effects of common anti-inflammatory treatments on HDL function are not yet known. METHODS: We compared the function of HDL in 18 patients with RA and 18 matched healthy controls. Subsequently, patients were randomised to (methotrexate+infliximab (M+I) (5 mg/kg)) or methotrexate+placebo (M+P) infusions for 54 weeks. At week 54 and thereafter, all patients received infliximab therapy until completion of the trial (110 weeks), enabling assessment of the impact of 1 year of infliximab therapy in all patients. HDL functional properties were assessed at baseline, 54 weeks and 110 weeks by measuring the impact on endothelial nitric oxide (NO) bioavailability and superoxide production (SO), paraoxonase activity (PON-1) and cholesterol efflux. RESULTS: All HDL vascular assays were impaired in patients compared with controls. After 54 weeks, NO in response to HDL was significantly greater in patients who received M+I compared with those who received M+P. Endothelial SO in response to HDL was reduced in both groups, but PON-1 and cholesterol efflux remained unchanged. All vascular measures improved compared with baseline after ≥1 infliximab therapy in the analysis at 110 weeks. No significant trend was noted for cholesterol efflux. CONCLUSIONS: HDL function can be improved with anti-inflammatory treatment in patients with RA. The M+I combination was superior to the M+P alone, suggesting that the tumour necrosis factor-α pathway may have a role in HDL vascular properties

SOCS3 Is Essential in the Regulation of Fetal Liver Erythropoiesis

AbstractSOCS3 (CIS3/JAB2) is an SH2-containing protein that binds to the activation loop of Janus kinases, inhibiting kinase activity, and thereby suppressing cytokine signaling. During embryonic development, SOCS3 is highly expressed in erythroid lineage cells and is Epo independent. Transgene-mediated expression blocks fetal erythropoiesis, resulting in embryonic lethality. SOCS3 deletion results in an embryonic lethality at 12–16 days associated with marked erythrocytosis. Moreover, the in vitro proliferative capacity of progenitors is greatly increased. SOCS3-deficient fetal liver stem cells can reconstitute hematopoiesis in lethally irradiated adults, indicating that its absence does not disturb bone marrow erythropoiesis. Reconstitution of lymphoid lineages in JAK3-deficient mice also occurs normally. The results demonstrate that SOCS3 is critical in negatively regulating fetal liver hematopoiesis