GraphR: Accelerating Graph Processing Using ReRAM

This paper presents GRAPHR, the first ReRAM-based graph processing accelerator. GRAPHR follows the principle of near-data processing and explores the opportunity of performing massive parallel analog operations with low hardware and energy cost. The analog computation is suit- able for graph processing because: 1) The algorithms are iterative and could inherently tolerate the imprecision; 2) Both probability calculation (e.g., PageRank and Collaborative Filtering) and typical graph algorithms involving integers (e.g., BFS/SSSP) are resilient to errors. The key insight of GRAPHR is that if a vertex program of a graph algorithm can be expressed in sparse matrix vector multiplication (SpMV), it can be efficiently performed by ReRAM crossbar. We show that this assumption is generally true for a large set of graph algorithms. GRAPHR is a novel accelerator architecture consisting of two components: memory ReRAM and graph engine (GE). The core graph computations are performed in sparse matrix format in GEs (ReRAM crossbars). The vector/matrix-based graph computation is not new, but ReRAM offers the unique opportunity to realize the massive parallelism with unprecedented energy efficiency and low hardware cost. With small subgraphs processed by GEs, the gain of performing parallel operations overshadows the wastes due to sparsity. The experiment results show that GRAPHR achieves a 16.01x (up to 132.67x) speedup and a 33.82x energy saving on geometric mean compared to a CPU baseline system. Com- pared to GPU, GRAPHR achieves 1.69x to 2.19x speedup and consumes 4.77x to 8.91x less energy. GRAPHR gains a speedup of 1.16x to 4.12x, and is 3.67x to 10.96x more energy efficiency compared to PIM-based architecture.Comment: Accepted to HPCA 201

DNA Methylation and Non-small Cell Lung Cancer

Genomic DNA methylation is a major form of epigenetic modification. Hypermethylation could affect the binding of transcription factors to DNA and change the structure of chromatin resulting in silence of tumor suppressor genes, which plays an important role in cancer initiation and progression. In recent years, the study of DNA methylation in lung cancer, mostly in non-small cell lung cancer, has made great progress and become a new target for early detection, risk assessment, prognosis and cancer therapy

SoK: MEV Countermeasures: Theory and Practice

Blockchains offer strong security guarantees, but they cannot protect the ordering of transactions. Powerful players, such as miners, sequencers, and sophisticated bots, can reap significant profits by selectively including, excluding, or re-ordering user transactions. Such profits are called Miner/Maximal Extractable Value or MEV. MEV bears profound implications for blockchain security and decentralization. While numerous countermeasures have been proposed, there is no agreement on the best solution. Moreover, solutions developed in academic literature differ quite drastically from what is widely adopted by practitioners. For these reasons, this paper systematizes the knowledge of the theory and practice of MEV countermeasures. The contribution is twofold. First, we present a comprehensive taxonomy of 28 proposed MEV countermeasures, covering four different technical directions. Secondly, we empirically studied the most popular MEV- auction-based solution with rich blockchain and mempool data. In addition to gaining insights into MEV auction platforms' real-world operations, our study shed light on the prevalent censorship by MEV auction platforms as a result of the recent OFAC sanction, and its implication on blockchain properties

HyPar: Towards Hybrid Parallelism for Deep Learning Accelerator Array

With the rise of artificial intelligence in recent years, Deep Neural Networks (DNNs) have been widely used in many domains. To achieve high performance and energy efficiency, hardware acceleration (especially inference) of DNNs is intensively studied both in academia and industry. However, we still face two challenges: large DNN models and datasets, which incur frequent off-chip memory accesses; and the training of DNNs, which is not well-explored in recent accelerator designs. To truly provide high throughput and energy efficient acceleration for the training of deep and large models, we inevitably need to use multiple accelerators to explore the coarse-grain parallelism, compared to the fine-grain parallelism inside a layer considered in most of the existing architectures. It poses the key research question to seek the best organization of computation and dataflow among accelerators. In this paper, we propose a solution HyPar to determine layer-wise parallelism for deep neural network training with an array of DNN accelerators. HyPar partitions the feature map tensors (input and output), the kernel tensors, the gradient tensors, and the error tensors for the DNN accelerators. A partition constitutes the choice of parallelism for weighted layers. The optimization target is to search a partition that minimizes the total communication during training a complete DNN. To solve this problem, we propose a communication model to explain the source and amount of communications. Then, we use a hierarchical layer-wise dynamic programming method to search for the partition for each layer.Comment: To appear in the 2019 25th International Symposium on High-Performance Computer Architecture (HPCA 2019

PLOD1 contributes to proliferation and glycolysis in hepatocellular carcinoma by regulating E2F1

Purpose: To evaluate the effect of procollagen-lysine 1,2-oxoglutarate 5-dioxygenase 1 (PLOD1) in hepatocellular carcinoma (HCC). Methods: HCC cells were subjected to loss of function assays via transfection with siRNA targeting PLOD1. Colony formation and cell counting kit 8 (CCK8) were used to determine cell proliferation. Cell cycle was evaluated by flow cytometry while extracellular acidification rate (ECAR) levels, glucose consumption, and lactate production were determined to investigate aerobic glycolysis. Results: PLOD1 was significantly up-regulated in HCC tissues and cells compared to normal tissues and cells (p < 0.001). Silencing of PLOD1 significantly repressed cell proliferation (p < 0.001) and induced cell cycle arrest in HCC at the G1 phase. ECAR levels, glucose consumption, and lactate production in HCC were reduced by knockdown of PLOD1. Loss of PLOD1 down-regulated the expression of E2F1, while over-expression of E2F1 attenuated PLOD1 knockdown-induced decreases in cell viability, glucose consumption, and lactate production in HCC. Conclusion: Knockdown of PLOD1 inhibits cell proliferation and aerobic glycolysis in HCC via down-regulation of E2F1. Thus, PLOD1 may help in developing an effective strategy for the management of liver cancer

Maximizing spin-orbit torque efficiency of Ta(O)/Py via modulating oxygen-induced interface orbital hybridization

Spin-orbit torques due to interfacial Rashba and spin Hall effects have been widely considered as a potentially more efficient approach than the conventional spin-transfer torque to control the magnetization of ferromagnets. We report a comprehensive study of spin-orbit torque efficiency in Ta(O)/Ni81Fe19 bilayers by tuning low-oxidation of \b{eta}-phase tantalum, and find that the spin Hall angle {\theta}DL increases from ~ -0.18 of the pure Ta/Py to the maximum value ~ -0.30 of Ta(O)/Py with 7.8% oxidation. Furthermore, we distinguish the efficiency of the spin-orbit torque generated by the bulk spin Hall effect and by interfacial Rashba effect, respectively, via a series of Py/Cu(0-2 nm)/Ta(O) control experiments. The latter has more than twofold enhancement, and even more significant than that of the former at the optimum oxidation level. Our results indicate that 65% enhancement of the efficiency should be related to the modulation of the interfacial Rashba-like spin-orbit torque due to oxygen-induced orbital hybridization cross the interface. Our results suggest that the modulation of interfacial coupling via oxygen-induced orbital hybridization can be an alternative method to boost the change-spin conversion rate.Comment: 15 pages, 4 figure