The Parallel Persistent Memory Model

We consider a parallel computational model that consists of $P$ processors, each with a fast local ephemeral memory of limited size, and sharing a large persistent memory. The model allows for each processor to fault with bounded probability, and possibly restart. On faulting all processor state and local ephemeral memory are lost, but the persistent memory remains. This model is motivated by upcoming non-volatile memories that are as fast as existing random access memory, are accessible at the granularity of cache lines, and have the capability of surviving power outages. It is further motivated by the observation that in large parallel systems, failure of processors and their caches is not unusual. Within the model we develop a framework for developing locality efficient parallel algorithms that are resilient to failures. There are several challenges, including the need to recover from failures, the desire to do this in an asynchronous setting (i.e., not blocking other processors when one fails), and the need for synchronization primitives that are robust to failures. We describe approaches to solve these challenges based on breaking computations into what we call capsules, which have certain properties, and developing a work-stealing scheduler that functions properly within the context of failures. The scheduler guarantees a time bound of $O(W/P_A + D(P/P_A) \lceil\log_{1/f} W\rceil)$ in expectation, where $W$ and $D$ are the work and depth of the computation (in the absence of failures), $P_A$ is the average number of processors available during the computation, and $f \le 1/2$ is the probability that a capsule fails. Within the model and using the proposed methods, we develop efficient algorithms for parallel sorting and other primitives.Comment: This paper is the full version of a paper at SPAA 2018 with the same nam

Dissociable learning processes, associative theory, and testimonial reviews: A comment on Smith and Church (2018

Smith and Church (Psychonomic Bulletin & Review, 25, 1565–1584 2018) present a “testimonial” review of dissociable learning processes in comparative and cognitive psychology, by which we mean they include only the portion of the available evidence that is consistent with their conclusions. For example, they conclude that learning the information-integration category-learning task with immediate feedback is implicit, but do not consider the evidence that people readily report explicit strategies in this task, nor that this task can be accommodated by accounts that make no distinction between implicit and explicit processes. They also consider some of the neuroscience relating to information-integration category learning, but do not report those aspects that are more consistent with an explicit than an implicit account. They further conclude that delay conditioning in humans is implicit, but do not report evidence that delay conditioning requires awareness; nor do they present the evidence that conditioned taste aversion, which should be explicit under their account, can be implicit. We agree with Smith and Church that it is helpful to have a clear definition of associative theory, but suggest that their definition may be unnecessarily restrictive. We propose an alternative definition of associative theory and briefly describe an experimental procedure that we think may better distinguish between associative and non-associative processes

The immunomodulator PSK induces in vitro cytotoxic activity in tumour cell lines via arrest of cell cycle and induction of apoptosis

Background Protein-bound polysaccharide (PSK) is derived from the CM-101 strain of the fungus Coriolus versicolor and has shown anticancer activity in vitro and in in vivo experimental models and human cancers. Several randomized clinical trials have demonstrated that PSK has great potential in adjuvant cancer therapy, with positive results in the adjuvant treatment of gastric, esophageal, colorectal, breast and lung cancers. These studies have suggested the efficacy of PSK as an immunomodulator of biological responses. The precise molecular mechanisms responsible for its biological activity have yet to be fully elucidated.Methods The in vitro cytotoxic anti-tumour activity of PSK has been evaluated in various tumour cell lines derived from leukaemias, melanomas, fibrosarcomas and cervix, lung, pancreas and gastric cancers. Tumour cell proliferation in vitro was measured by BrdU incorporation and viable cell count. Effect of PSK on human peripheral blood lymphocyte (PBL) proliferation in vitro was also analyzed. Studies of cell cycle and apoptosis were performed in PSK-treated cells.Results PSK showed in vitro inhibition of tumour cell proliferation as measured by BrdU incorporation and viable cell count. The inhibition ranged from 22 to 84%. Inhibition mechanisms were identified as cell cycle arrest, with cell accumulation in G0/G1 phase and increase in apoptosis and caspase-3 expression. These results indicate that PSK has a direct cytotoxic activity in vitro, inhibiting tumour cell proliferation. In contrast, PSK shows a synergistic effect with IL-2 that increases PBL proliferation.Conclusion These results indicate that PSK has cytotoxic activity in vitro on tumour cell lines. This new cytotoxic activity of PSK on tumour cells is independent of its previously described immunomodulatory activity on NK cells.AGL was supported by FIS Postdoctoral Research Contract CP03/00111. Studies were partially supported by a grant from Kureha Chemical Industry (Japan)

Aging-Aware Request Scheduling for Non-Volatile Main Memory

Modern computing systems are embracing non-volatile memory (NVM) to implement high-capacity and low-cost main memory. Elevated operating voltages of NVM accelerate the aging of CMOS transistors in the peripheral circuitry of each memory bank. Aggressive device scaling increases power density and temperature, which further accelerates aging, challenging the reliable operation of NVM-based main memory. We propose HEBE, an architectural technique to mitigate the circuit aging-related problems of NVM-based main memory. HEBE is built on three contributions. First, we propose a new analytical model that can dynamically track the aging in the peripheral circuitry of each memory bank based on the bank's utilization. Second, we develop an intelligent memory request scheduler that exploits this aging model at run time to de-stress the peripheral circuitry of a memory bank only when its aging exceeds a critical threshold. Third, we introduce an isolation transistor to decouple parts of a peripheral circuit operating at different voltages, allowing the decoupled logic blocks to undergo long-latency de-stress operations independently and off the critical path of memory read and write accesses, improving performance. We evaluate HEBE with workloads from the SPEC CPU2017 Benchmark suite. Our results show that HEBE significantly improves both performance and lifetime of NVM-based main memory.Comment: To appear in ASP-DAC 202

CdSe Quantum Dot (QD)-Induced Morphological and Functional Impairments to Liver in Mice

Quantum dots (QDs), as unique nanoparticle probes, have been used in in vivo fluorescence imaging such as cancers. Due to the novel characteristics in fluorescence, QDs represent a family of promising substances to be used in experimental and clinical imaging. Thus far, the toxicity and harmful health effects from exposure (including environmental exposure) to QDs are not recognized, but are largely concerned by the public. To assess the biological effects of QDs, we established a mouse model of acute and chronic exposure to QDs. Results from the present study suggested that QD particles could readily spread into various organs, and liver was the major organ for QD accumulation in mice from both the acute and chronic exposure. QDs caused significant impairments to livers from mice with both acute and chronic QD exposure as reflected by morphological alternation to the hepatic lobules and increased oxidative stress. Moreover, QDs remarkably induced the production of intracellular reactive oxygen species (ROS) along with cytotoxicity, as characterized by a significant increase of the malondialdehyde (MDA) level within hepatocytes. However, the increase of the MDA level in response to QD treatment could be partially blunted by the pre-treatment of cells with beta-mercaptoethanol (β-ME). These data suggested ROS played a crucial role in causing oxidative stress-associated cellular damage from QD exposure; nevertheless other unidentified mediators might also be involved in QD-mediated cellular impairments. Importantly, we demonstrated that the hepatoxicity caused by QDs in vivo and in vitro was much greater than that induced by cadmium ions at a similar or even a higher dose. Taken together, the mechanism underlying QD-mediated biological influences might derive from the toxicity of QD particles themselves, and from free cadmium ions liberated from QDs as well

Distractors associated with reward break through the focus of attention

In the present study, we investigated the conditions in which rewarded distractors have the ability to capture attention, even when attention is directed toward the target location. Experiment 1 showed that when the probability of obtaining reward was high, all salient distractors captured attention, even when they were not associated with reward. This effect may have been caused by participants suboptimally using the 100%-valid endogenous location cue. Experiment 2 confirmed this result by showing that salient distractors did not capture attention in a block in which no reward was expected. In Experiment 3, the probability of the presence of a distractor was high, but it only signaled reward availability on a low number of trials. The results showed that those very infrequent distractors that signaled reward captured attention, whereas the distractors (both frequent and infrequent ones) not associated with reward were simply ignored. The latter experiment indicates that even when attention is directed to a location in space, stimuli associated with reward break through the focus of attention, but equally salient stimuli not associated with reward do not

Thermal Tolerance of the Coffee Berry Borer Hypothenemus hampei: Predictions of Climate Change Impact on a Tropical Insect Pest

Coffee is predicted to be severely affected by climate change. We determined the thermal tolerance of the coffee berry borer , Hypothenemus hampei, the most devastating pest of coffee worldwide, and make inferences on the possible effects of climate change using climatic data from Colombia, Kenya, Tanzania, and Ethiopia. For this, the effect of eight temperature regimes (15, 20, 23, 25, 27, 30, 33 and 35°C) on the bionomics of H. hampei was studied. Successful egg to adult development occurred between 20–30°C. Using linear regression and a modified Logan model, the lower and upper thresholds for development were estimated at 14.9 and 32°C, respectively. In Kenya and Colombia, the number of pest generations per year was considerably and positively correlated with the warming tolerance. Analysing 32 years of climatic data from Jimma (Ethiopia) revealed that before 1984 it was too cold for H. hampei to complete even one generation per year, but thereafter, because of rising temperatures in the area, 1–2 generations per year/coffee season could be completed. Calculated data on warming tolerance and thermal safety margins of H. hampei for the three East African locations showed considerably high variability compared to the Colombian site. The model indicates that for every 1°C rise in thermal optimum (Topt.), the maximum intrinsic rate of increase (rmax) will increase by an average of 8.5%. The effects of climate change on the further range of H. hampei distribution and possible adaption strategies are discussed. Abstracts in Spanish and French are provided as supplementary material Abstract S1 and Abstract S2