Muninis a distributed shared memory (DSM) system
Muninis a distributed shared memory (DSM) system
Distributed shared memory (DSM) is an abstraction of shared memory on a distributed-memory machine. Hardware DSM systems support this abstraction at the architecture level; software DSM systems support the abstraction within the runtime system. One of the key problems in building an efficient software DSM system is to reduce the amount of communication needed to keep the distributed memories consistent. In this article we present four techniques for doing so: software release consistency; multiple consistency protocols; write-shared protocols; and an update-with-timeout mechanism. These techniques have been implemented in the Munin DSM system. We compare the performance of seven Munin application programs: first to their performance when implemented using message passing, and then to their performance when running on a conventional software DSM system that does not embody the preceding techniques. On a 16-processor cluster of workstations, Munin's performance is within 5% of message passing for four out of the seven applications. For the other three, performance is within 29 to 33%. Detailed analysis of two of these three applications indicates that the addition of a function-shipping capability would bring their performance to within 7% of the message-passing performance. Compared to a conventional DSM system, Munin achieves performance improvements ranging from a few to several hundred percent, depending on the application.
Microprocessor voltage levels include substantial margin to deal with process variation, system power supply variation, workload induced thermal and voltage variation, aging, random uncertainty, and test inaccuracy. This margin allows the microprocessor to operate correctly during worst-case conditions, but during typical conditions it is larger than necessary and wastes energy. We present a mechanism that reduces excess voltage margin by (1) introducing a critical path monitor (CPM) circuit that measures available timing margin in real-time, (2) coupling the CPM output to the clock generation circuit to adjust clock frequency within cycles in response to excess or inadequate timing margin, and (3) adjusting the processor voltage level periodically in firmware to achieve a specified average clock frequency target. We implemented this mechanism in a prototype IBM POWER7 server. During better-than-worst case conditions our guardband management mechanism reduces the average voltage setting 137-152 mV below nominal, resulting in average processor power reduction of 24% with no performance loss while running industry-standard benchmarks.
A large portion of the power consumption of data centers can be attributed to cooling. In dynamic thermal management mechanisms for data centers and servers, thermal setpoints are typically chosen statically and conservatively, which leaves significant room for improvement in the form of improved energy efficiency. In this paper, we propose two hierarchical thermal-aware power optimization techniques that are complementary to each other and achieve (i) lower overall system power with no performance penalty or (ii) higher performance within the same power budget.At the data center level, we trade off facility Heating, Ventilation and Air Conditioning (HVAC) power with server fan power by choosing between two thermal setpoints for the HVAC chiller based on the cooling zone utilization levels. This optimization can reduce total data center total power by as much as 12.4%-17%, with no performance penalty.At the server level, we trade off fan power and circuit leakage power by dynamically adjusting the server thermal setpoint, allowing the system to heat up when this saves more fan power than it costs in terms of leakage power. We evaluate this optimization on an IBM POWER 750 and find that it reduces total server power by up to 5.4% with no performance penalty for workloads that heavily exercise a server.
Antinuclear autoantibodies (ANA) displaying a dense fine speckled pattern (DFS, ICAP AC-2) on HEp-2 cells are frequently observed in clinical laboratory referrals, often associated with anti-DFS70 specificity. Anti-DFS70 positive patients rarely develop systemic autoimmune rheumatic disease (SARD), especially in the absence of clinical evidence or additional anti-extractable nuclear antigen (ENA) antibodies, prompting suggestions that an isolated DFS70-specific ENA may be an exclusionary finding for SARD. In this study, the frequency and diagnostic significance of anti-DFS70 autoantibodies was investigated in a community hospital cohort of patients undergoing routine ANA testing. ANA screening was performed by HEp-20-10-based indirect immunofluorescence, followed by ENA profiling using a multiparametric line immunoassay (LIA). Of 6,511 patient samples tested for ANA in 2016, the DFS pattern was identified in 1,758 (27.0%), 720 (41.0%) of which were anti-DFS70 positive by LIA. Of these, 526 (73.1%) revealed isolated anti-DFS70 reactivity, while 194 (26.9%) showed additional ENA specificities. Among 1,038 anti-DFS70 negative or borderline samples, 778 (75.0%) were ENA profile negative, while the remaining 260 (25.0%) showed a varied presence of other ENA specificities. Chart reviews of patients with an isolated anti-DFS70 ANA affirmed that ANA-related SARD is rare in the absence of clinical evidence or other ENA specificities, there being no case thus far identified. Rheumatoid arthritis patients occasionally had an isolated anti-DFS70 ANA and were positive for rheumatoid factor and anti-cyclic citrullinated peptide antibodies. In conclusion, the recognition of a DFS ANA pattern using a mitotic-rich HEp-2 substrate, followed by confirmation of anti-DFS70 specificity should be a routine ANA testing service. Use of an expanded ENA profile and clinical correlation is necessary to affirm the “isolation” of anti-DFS70 as the cause of an ANA. Recognition of isolated anti-DFS70 ANA enables reassurance of patients that SARD is unlikely, thus avoiding referral for more extensive testing. The presence of significant elevations of other ENAs may reflect SARD and warrants close clinical correlation and follow-up.
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