HALLS: An Energy-Efficient Highly Adaptable Last Level STT-RAM Cache for Multicore Systems

Spin-Transfer Torque RAM (STT-RAM) is widely considered a promising alternative to SRAM in the memory hierarchy due to STT-RAM's non-volatility, low leakage power, high density, and fast read speed. The STT-RAM's small feature size is particularly desirable for the last-level cache (LLC), which typically consumes a large area of silicon die. However, long write latency and high write energy still remain challenges of implementing STT-RAMs in the CPU cache. An increasingly popular method for addressing this challenge involves trading off the non-volatility for reduced write speed and write energy by relaxing the STT-RAM's data retention time. However, in order to maximize energy saving potential, the cache configurations, including STT-RAM's retention time, must be dynamically adapted to executing applications' variable memory needs. In this paper, we propose a highly adaptable last level STT-RAM cache (HALLS) that allows the LLC configurations and retention time to be adapted to applications' runtime execution requirements. We also propose low-overhead runtime tuning algorithms to dynamically determine the best (lowest energy) cache configurations and retention times for executing applications. Compared to prior work, HALLS reduced the average energy consumption by 60.57% in a quad-core system, while introducing marginal latency overhead.Comment: To Appear on IEEE Transactions on Computers (TC

MirrorCache: An Energy-Efficient Relaxed Retention L1 STTRAM Cache

Spin-Transfer Torque RAM (STTRAM) is a promising alternative to SRAMs in on-chip caches, due to several advantages, including non-volatility, low leakage, high integration density, and CMOS compatibility. However, STTRAMs' wide adoption in resource-constrained systems is impeded, in part, by high write energy and latency. A popular approach to mitigating these overheads involves relaxing the STTRAM's retention time, in order to reduce the write latency and energy. However, this approach usually requires a dynamic refresh scheme to maintain cache blocks' data integrity beyond the retention time, and typically requires an external refresh buffer. In this paper, we propose mirrorCache-an energy-efficient, buffer-free refresh scheme. MirrorCache leverages the STTRAM cell's compact feature size, and uses an auxiliary segment with the same size as the logical cache size to handle the refresh operations without the overheads of an external refresh buffer. Our experiments show that, compared to prior work, mirrorCache can reduce the average cache energy by at least 39.7% for a variety of systems.This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Predicting Bleeding and Thrombosis Complications in Patients with Continuous Flow Left Ventricular Assist Devices

Background: Left ventricular assist device (LVAD) therapy has been proven to relieve heart failure symptoms and improve survival, but is not devoid of bleeding and/or thrombotic complications. Risk stratification tools have been utilized in other cardiovascular disease populations to estimate the risk of bleeding and thrombosis with and without anticoagulation, including the HAS-BLED, HEMORR2HAGES, CHADS2 and CHA2DS2-VASc models. The study objective was to evaluate the predictive value of available risk models for bleeding and thrombotic complications in patients with an LVAD within one year of implantation. Methods: This was a retrospective, single-center analysis of patients implanted with the HeartMate II continuous-flow LVAD from July 2011 to June 2016. All patients who received an LVAD within the study period were eligible for inclusion. The primary endpoint was the first occurrence of bleeding or thrombosis within one year from implantation. Baseline risk model scores were calculated at the time of LVAD implantation. Chi-square and student’s t-test were used to measure baseline differences and compare mean risk model scores between patients who had an event. A receiver operator characteristic (ROC) curve analysis was performed to evaluate the accuracy of the risk models to predict an event. Results: A total of 129 patients underwent LVAD implantation within the study time period. Mean CHADS2, CHA2DS2-VASc, and HAS-BLED scores were not significantly different in patients with and without an event. The mean HEMORR2HAGES score was 3.09 and 2.51 in those with and without a bleeding event, respectively (p = 0.008). The ROC curve area for the HEMORR2HAGES model was the highest at 0.620. Conclusion: The HAS-BLED, HEMORR2HAGES, CHADS2and CHA2DS2-VASc risk stratification models did not accurately predict bleeding or thrombosis events in our population. The mean HEMORR2HAGES model score was higher in patients who experienced a bleeding event. However, this model did not have strong positive predictive value. Better risk models are needed to predict bleeding and thrombotic events in this patient population

Learning about time within the spinal cord: evidence that spinal neurons can abstract and store an index of regularity

Prior studies have shown that intermittent noxious stimulation has divergent effects on spinal cord plasticity depending upon whether it occurs in a regular [fixed time (FT)] or irregular [variable time (VT)] manner: In spinally transected animals, VT stimulation to the tail or hind leg impaired spinal learning whereas an extended exposure to FT stimulation had a restorative/protective effect. These observations imply that lower level systems are sensitive to temporal relations. Using spinally transected rats, it is shown that the restorative effect of FT stimulation emerges after 540 shocks; fewer shocks generate a learning impairment. The transformative effect of FT stimulation is related to the number of shocks administered, not the duration of exposure. Administration of 360 FT shocks induces a learning deficit that lasts 24 hours. If a second bout of FT stimulation is given a day after the first, it restores the capacity to learn. This savings effect implies that the initial training episode had a lasting (memory-like) effect. Two bouts of shock had a transformative effect when applied at different locations or at difference frequencies, implying spinal systems abstract and store an index of regularity (rather than a specific interval). Implications of the results for step training and rehabilitation after injury are discussed

Impact of Behavioral Control on the Processing of Nociceptive Stimulation

How nociceptive signals are processed within the spinal cord, and whether these signals lead to behavioral signs of neuropathic pain, depends upon their relation to other events and behavior. Our work shows that these relations can have a lasting effect on spinal plasticity, inducing a form of learning that alters the effect of subsequent nociceptive stimuli. The capacity of lower spinal systems to adapt, in the absence of brain input, is examined in spinally transected rats that receive a nociceptive shock to the tibialis anterior muscle of one hind leg. If shock is delivered whenever the leg is extended (controllable stimulation), it induces an increase in flexion duration that minimizes net shock exposure. This learning is not observed in subjects that receive the same amount of shock independent of leg position (uncontrollable stimulation). These two forms of stimulation have a lasting, and divergent, effect on subsequent learning: controllable stimulation enables learning whereas uncontrollable stimulation disables it (learning deficit). Uncontrollable stimulation also enhances mechanical reactivity. We review evidence that training with controllable stimulation engages a brain-derived neurotrophic factor (BDNF)-dependent process that can both prevent and reverse the consequences of uncontrollable shock. We relate these effects to changes in BDNF protein and TrkB signaling. Controllable stimulation is also shown to counter the effects of peripheral inflammation (from intradermal capsaicin). A model is proposed that assumes nociceptive input is gated at an early sensory stage. This gate is sensitive to current environmental relations (between proprioceptive and nociceptive input), allowing stimulation to be classified as controllable or uncontrollable. We further propose that the status of this gate is affected by past experience and that a history of uncontrollable stimulation will promote the development of neuropathic pain

Maladaptive spinal plasticity opposes spinal learning and recovery in spinal cord injury

Synaptic plasticity within the spinal cord has great potential to facilitate recovery of function after spinal cord injury (SCI). Spinal plasticity can be induced in an activity-dependent manner even without input from the brain after complete SCI. A mechanistic basis for these effects is provided by research demonstrating that spinal synapses have many of the same plasticity mechanisms that are known to underlie learning and memory in the brain. In addition, the lumbar spinal cord can sustain several forms of learning and memory, including limb-position training. However, not all spinal plasticity promotes recovery of function. Central sensitization of nociceptive (pain) pathways in the spinal cord may emerge in response to various noxious inputs, demonstrating that plasticity within the spinal cord may contribute to maladaptive pain states. In this review we discuss interactions between adaptive and maladaptive forms of activity-dependent plasticity in the spinal cord below the level of SCI. The literature demonstrates that activity-dependent plasticity within the spinal cord must be carefully tuned to promote adaptive spinal training. Prior work from our group has shown that stimulation that is delivered in a limb position-dependent manner or on a fixed interval can induce adaptive plasticity that promotes future spinal cord learning and reduces nociceptive hyper-reactivity. On the other hand, stimulation that is delivered in an unsynchronized fashion, such as randomized electrical stimulation or peripheral skin injuries, can generate maladaptive spinal plasticity that undermines future spinal cord learning, reduces recovery of locomotor function, and promotes nociceptive hyper-reactivity after SCI. We review these basic phenomena, how these findings relate to the broader spinal plasticity literature, discuss the cellular and molecular mechanisms, and finally discuss implications of these and other findings for improved rehabilitative therapies after SCI