CODAG: Characterizing and Optimizing Decompression Algorithms for GPUs

Data compression and decompression have become vital components of big-data applications to manage the exponential growth in the amount of data collected and stored. Furthermore, big-data applications have increasingly adopted GPUs due to their high compute throughput and memory bandwidth. Prior works presume that decompression is memory-bound and have dedicated most of the GPU's threads to data movement and adopted complex software techniques to hide memory latency for reading compressed data and writing uncompressed data. This paper shows that these techniques lead to poor GPU resource utilization as most threads end up waiting for the few decoding threads, exposing compute and synchronization latencies. Based on this observation, we propose CODAG, a novel and simple kernel architecture for high throughput decompression on GPUs. CODAG eliminates the use of specialized groups of threads, frees up compute resources to increase the number of parallel decompression streams, and leverages the ample compute activities and the GPU's hardware scheduler to tolerate synchronization, compute, and memory latencies. Furthermore, CODAG provides a framework for users to easily incorporate new decompression algorithms without being burdened with implementing complex optimizations to hide memory latency. We validate our proposed architecture with three different encoding techniques, RLE v1, RLE v2, and Deflate, and a wide range of large datasets from different domains. We show that CODAG provides 13.46x, 5.69x, and 1.18x speed up for RLE v1, RLE v2, and Deflate, respectively, when compared to the state-of-the-art decompressors from NVIDIA RAPIDS

On the Application of Joint-Domain Dictionary Mapping for Multiple Power Disturbance Assessment

This paper proposes a joint-domain dictionary mapping method to obtain high assessment accuracy of multiple power disturbances. Firstly, in order to achieve resolutions in both the time and frequency domains, a joint-domain dictionary is proposed which consists of a discrete Hartley base and an identity matrix. Due to the low correlation between the discrete Hartley base and the identity matrix, the joint-domain dictionary mapping can separately capture the approximations of the sinusoidal components and transients. Since the mapping coefficients contain the physical quantities, the eigenvalues of each component can be effectively estimated. A quantified eigenvalue classifier was designed for identifying power disturbances using the estimated eigenvalues. The proposed method was compared with several advanced methods through simulated power disturbances under different noise conditions, and actual data from the Institute of Electrical and Electronics Engineers Power and Energy Society database. The results reveal that the joint-domain dictionary mapping technique shows good performance on parameter estimation and recognition precision, even dealing with complicated multiple power disturbances

Active power decoupling and controlling for single-phase FACTS device

Single-phase FACTS device has a bulky and short-life electrolytic capacitor to absorb the ripple pulsating at twice of the line frequency in DC side, resulting in lower power density. This paper introduced a structure of three-phase bridge which added an additional leg connected to an AC capacitor based on single-phase H-bridge. The 2-ripple energy of the electrolytic capacitor in single-phase H-bridge could be transformed to the film capacitor of the AC side in three-phase H bridge. The size of single-phase FACTS is reduced by ten times compared to the single-phase H-bridge. A simple control strategy had been studied, through two kinds of controllers: the digital quais-PR controller had been used to control gird current and AC capacitor voltage and current; the two cosine controller had been used to eliminate the rest of two-ripple harmonic in the DC side, there was no controller to maintain DC voltage. The experiments verified the feasibility of the control strategy

KAP1 Positively Modulates Influenza A Virus Replication by Interacting with PB2 and NS1 Proteins in Human Lung Epithelial Cells

Influenza virus only encodes a dozen of viral proteins, which need to use host machinery to complete the viral life cycle. Previously, KAP1 was identified as one host protein that potentially interacts with influenza viral proteins in HEK 293 cells. However, the role of KAP1 in influenza virus replication in human lung alveolar epithelial cells and the underlying mechanism remains unclear. In this study, we first generated KAP1 KO A549 cells by CRISPR/Cas9 gene editing. KAP1 deletion had no significant effect on the cell viability and lack of KAP1 expression significantly reduced the influenza A virus replication. Moreover, we demonstrated that KAP1 is involved in the influenza virus entry, transcription/replication of viral genome, and viral protein synthesis in human lung epithelial cells and confirmed that KAP1 interacted with PB2 and NS1 viral proteins during the virus infection. Further study showed that KAP1 inhibited the production of type I IFN and overexpression of KAP1 significantly reduced the IFN-β production. In addition, influenza virus infection induces the deSUMOylation and enhanced phosphorylation of KAP1. Our results suggested that KAP1 is required for the replication of influenza A virus and mediates the replication of influenza A virus by facilitating viral infectivity and synthesis of viral proteins, enhancing viral polymerase activity, and inhibiting the type I IFN production

Characterization of Six Diamide Insecticides on Ryanodine Receptor: Resistance and Species Selectivity

Ryanodine receptor (RyR) has been used as an insecticide target to control many destructive agricultural pests. The effectiveness of these insecticides has been limited by the spread of resistance mutations identified in pest RyRs, but the detailed molecular impacts of the individual mutations on the activity of different diamide compounds have not been fully explored. We created five HEK293 cell lines stably expressing wild type rabbit RyR1, wild type Spodoptera frugiperda RyR (Sf RyR), or Sf RyR carrying different resistance mutations, including G4891E, G4891E/I4734M, and Y4867F, respectively. R-CEPIA1er, a genetically encoded fluorescent protein, was also introduced in these cell lines to report the Ca2+ concentration in the endoplasmic reticulum. We systematically characterized the activities of six commercial diamide insecticides against different RyRs using the time-lapse fluorescence assay. Among them, cyantraniliprole (CYAN) displayed the highest activity against all three resistant Sf RyRs. The good performance of CYAN was confirmed by the toxicity assay using gene-edited Drosophila expressing the mutant RyRs, in which CYAN showed the lowest LD50 value for the double resistant mutant. In addition, we compared their acitivty between mammalian and insect RyRs and found that flubendiamide has the best insect-selectivity. The mechanism of the anti-resistance property and selectivity of the compounds was proposed based on the structural models generated by homology modeling and molecular docking. Our findings provide insights into the mechanism of insect resistance and guidance for developing effective RyR agonists that can selectively target resistant pests

Increased Urinary CD163 Levels in Systemic Vasculitis with Renal Involvement

Objectives. Systemic vasculitis includes a group of disorders characterized by inflammation of the vessel wall, involving multiple systems, and can cause malignant hypertension. CD163 is a specific marker of anti-inflammatory macrophages. This study is aimed at evaluating the CD163 levels in relation to systemic vasculitis and renal involvements. Methods. Urinary CD163 levels were retrospectively measured by enzyme-linked immunosorbent assay (ELISA) in 51 patients with systemic vasculitis, 42 essential hypertensions, and 36 healthy volunteers. The associations between urinary CD163 levels and clinical indicators were analyzed. Results. Urinary CD163 levels were significantly higher in patients with systemic vasculitis [68.20 (38.25~158.78) (pg/ml)] compared to essential hypertension [43.86 (23.30-60.71) (pg/ml)] (p=0.003) and the healthy volunteers [30.76 (9.30-54.16) (pg/ml)] (p<0.001). Furthermore, systemic vasculitis patients with renal involvement had significantly higher urinary CD163 levels relative to patients without renal involvement [86.95 (47.61 and 192.38) pg/ml] vs. [41.99 (17.70 and 71.95) pg/ml, p=0.005]. After control factors age, sex, and BMI, urinary CD163 levels in systemic vasculitis patients were positively correlated with serum creatinine, blood urea nitrogen, and β-2 microglobulin (r=0.45, 0.48, and 0.46; p=0.001, 0.001, and 0.002, respectively). In addition, we found the level of urinary CD163 in granulomatous vasculitis (including TA, GPA, and EGPA) was significantly higher than that in necrotizing vasculitis (including PAN) [86.95 (41.99 and 184.82) pg/ml] vs. [45.73 (21.43 and 74.43) pg/ml, p=0.016]. Conclusion. Urinary CD163 levels were significantly higher in patients with systemic vasculitis, especially in patients with renal involvement. Thus, urinary CD163 has the potential to be a biomarker for systemic vasculitis with renal involvement

KAP1 Positively Modulates Influenza A Virus Replication by Interacting with PB2 and NS1 Proteins in Human Lung Epithelial Cells

Influenza virus only encodes a dozen of viral proteins, which need to use host machinery to complete the viral life cycle. Previously, KAP1 was identified as one host protein that potentially interacts with influenza viral proteins in HEK 293 cells. However, the role of KAP1 in influenza virus replication in human lung alveolar epithelial cells and the underlying mechanism remains unclear. In this study, we first generated KAP1 KO A549 cells by CRISPR/Cas9 gene editing. KAP1 deletion had no significant effect on the cell viability and lack of KAP1 expression significantly reduced the influenza A virus replication. Moreover, we demonstrated that KAP1 is involved in the influenza virus entry, transcription/replication of viral genome, and viral protein synthesis in human lung epithelial cells and confirmed that KAP1 interacted with PB2 and NS1 viral proteins during the virus infection. Further study showed that KAP1 inhibited the production of type I IFN and overexpression of KAP1 significantly reduced the IFN-&beta; production. In addition, influenza virus infection induces the deSUMOylation and enhanced phosphorylation of KAP1. Our results suggested that KAP1 is required for the replication of influenza A virus and mediates the replication of influenza A virus by facilitating viral infectivity and synthesis of viral proteins, enhancing viral polymerase activity, and inhibiting the type I IFN production