An EMO Joint Pruning with Multiple Sub-networks: Fast and Effect

The network pruning algorithm based on evolutionary multi-objective (EMO) can balance the pruning rate and performance of the network. However, its population-based nature often suffers from the complex pruning optimization space and the highly resource-consuming pruning structure verification process, which limits its application. To this end, this paper proposes an EMO joint pruning with multiple sub-networks (EMO-PMS) to reduce space complexity and resource consumption. First, a divide-and-conquer EMO network pruning framework is proposed, which decomposes the complex EMO pruning task on the whole network into easier sub-tasks on multiple sub-networks. On the one hand, this decomposition reduces the pruning optimization space and decreases the optimization difficulty; on the other hand, the smaller network structure converges faster, so the computational resource consumption of the proposed algorithm is lower. Secondly, a sub-network training method based on cross-network constraints is designed so that the sub-network can process the features generated by the previous one through feature constraints. This method allows sub-networks optimized independently to collaborate better and improves the overall performance of the pruned network. Finally, a multiple sub-networks joint pruning method based on EMO is proposed. For one thing, it can accurately measure the feature processing capability of the sub-networks with the pre-trained feature selector. For another, it can combine multi-objective pruning results on multiple sub-networks through global performance impairment ranking to design a joint pruning scheme. The proposed algorithm is validated on three datasets with different challenging. Compared with fifteen advanced pruning algorithms, the experiment results exhibit the effectiveness and efficiency of the proposed algorithm

Numerical Study on the Influence of Different Waving Bottom Form on the Fluid Surface Wave

Abstract: In the present study, the effect of waving bottom on the surface wave is studied. Basing on the fundamental equations of potential flow theory and boundary conditions, using the multiple scales perturbation method to derive the first-order and the second-order approximate equation which the fluid surface waves satisfied in the presence of waving bottom. Under the second-order approximation, the fluid surface waveform in first-order approximate equation is numerically simulated with MATLAB in the presence of different waving bottom form. The results show that: the fluid surface waveform is composed of a harmonic wave which has the same frequency with waving bottom and a pair of KdV solitary waves that spread to both the right and the left side when the waving bottom wave is a harmonic wave; and when the waving bottom is a solitary wave packet, it consists of a solitary wave which is closely related to the specific form of waving bottom and a couple of KdV solitary waves. With the development of time, three waves in fluid surface do not affect each other and they propagate independently. Thus it can be seen the waving bottom is effective for maintaining surface wave energy balance income and expenditure in the spreading process

Study on the significance and mechanism of ASGR1 in hepatocellular carcinoma

Objective·To explore the significance and mechanism of asialoglycoprotein receptor 1 (ASGR1) in hepatocellular carcinoma.Methods·The expression of ASGR1 in patients with liver cancer in The Cancer Genome Atlas (TCGA) database was analyzed by R language and the related survival curves were drawn. The Human Protein Atlas (HPA) database was used to obtain the immunohistochemistry (IHC) data of normal human liver tissue and liver cancer tissue to analyze the protein expression of ASGR1. By using the hydrodynamic tail vein injection (HTVI) delivery method, Asgr1 was knocked out in the liver of fully immune mice to explore its tumorigenic function in vivo. Gene knockout efficiency was verified by Western blotting (WB). The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and correlation analysis were performed by using R language. The GSEA hallmark correlation pathway analysis was performed by using Gene Set Enrichment Analysis (GSEA) software. The expression level of key genes of glycolysis in mouse liver cancer tissue was verified by quantitative real-time PCR (qPCR).Results·ASGR1 was significantly low-expressed in liver cancer tissue, and the low expression of ASGR1 in liver cancer patients was associated with poorer overall survival (OS), disease-free interval (DFI), progression-free interval (PFI), and disease-specific survival (DSS). The higher the degree of tumor grade, the lower the expression level of ASGR1 in patients with liver cancer. Immunohistochemistry showed that the protein expression of ASGR1 in normal human liver tissue was significantly higher than that in liver cancer tissue. In an immunocompetent mouse model of hepatocellular carcinoma, knockout of endogenous Asgr1 in mice increased the size and number of tumor nodules in liver tissue. In the TCGA database, patients with liver cancer in the ASGR1 low-expression group were enriched in multiple cancer and metabolic pathways. The expression of ASGR1 was negatively correlated with some key genes of glycolysis. The level of glycolysis in liver cancer tissues of mice in the Asgr1 knockout group was higher than that in the control group. It was suggested that the low expression of ASGR1 be likely to promote the growth and development of liver cancer and strengthen metabolic reprogramming to promote the anabolic development of tumors.Conclusion·The expression of ASGR1 is significantly reduced in patients with liver cancer, which is positively correlated with the prognosis of patients. Knocking out Asgr1 in mice can promote the occurrence and development of hepatocellular carcinoma. ASGR1 can be used as a potential biomarker for poor prognosis of liver cancer and a new target for potential treatment

Durvalumab Plus Carboplatin/Paclitaxel Followed by Maintenance Durvalumab With or Without Olaparib as First-Line Treatment for Advanced Endometrial Cancer: The Phase III DUO-E Trial

PURPOSE Immunotherapy and chemotherapy combinations have shown activity in endometrial cancer, with greater benefit in mismatch repair (MMR)-deficient (dMMR) than MMR-proficient (pMMR) disease. Adding a poly(ADP-ribose) polymerase inhibitor may improve outcomes, especially in pMMR disease. METHODS This phase III, global, double-blind, placebo-controlled trial randomly assigned eligible patients with newly diagnosed advanced or recurrent endometrial cancer 1:1:1 to: carboplatin/paclitaxel plus durvalumab placebo followed by placebo maintenance (control arm); carboplatin/paclitaxel plus durvalumab followed by maintenance durvalumab plus olaparib placebo (durvalumab arm); or carboplatin/paclitaxel plus durvalumab followed by maintenance durvalumab plus olaparib (durvalumab + olaparib arm). The primary end points were progression-free survival (PFS) in the durvalumab arm versus control and the durvalumab + olaparib arm versus control. RESULTS Seven hundred eighteen patients were randomly assigned. In the intention-to-treat population, statistically significant PFS benefit was observed in the durvalumab (hazard ratio [HR], 0.71 [95% CI, 0.57 to 0.89]; P = .003) and durvalumab + olaparib arms (HR, 0.55 [95% CI, 0.43 to 0.69]; P < .0001) versus control. Prespecified, exploratory subgroup analyses showed PFS benefit in dMMR (HR [durvalumab v control], 0.42 [95% CI, 0.22 to 0.80]; HR [durvalumab + olaparib v control], 0.41 [95% CI, 0.21 to 0.75]) and pMMR subgroups (HR [durvalumab v control], 0.77 [95% CI, 0.60 to 0.97]; HR [durvalumab + olaparib v control] 0.57; [95% CI, 0.44 to 0.73]); and in PD-L1-positive subgroups (HR [durvalumab v control], 0.63 [95% CI, 0.48 to 0.83]; HR [durvalumab + olaparib v control], 0.42 [95% CI, 0.31 to 0.57]). Interim overall survival results (maturity approximately 28%) were supportive of the primary outcomes (durvalumab v control: HR, 0.77 [95% CI, 0.56 to 1.07]; P = .120; durvalumab + olaparib v control: HR, 0.59 [95% CI, 0.42 to 0.83]; P = .003). The safety profiles of the experimental arms were generally consistent with individual agents. CONCLUSION Carboplatin/paclitaxel plus durvalumab followed by maintenance durvalumab with or without olaparib demonstrated a statistically significant and clinically meaningful PFS benefit in patients with advanced or recurrent endometrial cancer

Study on the Surface Morphology of Micro-Particles and the Oxide Layer on Silicon Carbide Crystal Using Nanosecond Green Laser Cleaning Assisted with Airflow

With a focus on the particle pollutants on the surface of silicon carbide crystal materials, this paper establishes a laser cleaning model for the fine particles found in silicon carbide crystal materials and proposes a new nanosecond green laser cleaning method assisted by airflow, which can effectively remove microparticles and the oxide layer on the substrate surface. Abaqus software and ANSYS Fluent software were used to simulate changes in the cleaning temperature field and the distribution of particles and dust during cleaning simulation, respectively. Based on the experimental research, and by using a nanosecond green laser to produce a wavelength of 532 nm, the direct irradiation of a nanosecond green laser on the surface of the element, and the particle contaminants on the surface of the silicon carbide material, optimized the process parameters to achieve a better cleaning efficiency. A green laser was used as a light source to conduct experiments to control the wind force of the gas chamber. The influence of the laser energy, scanning speed, and other parameters on the final cleaning efficiency was studied. The parameters of the silicon carbide before and after cleaning were characterized. The research shows that laser cleaning assisted with airflow is an efficient cleaning method that can be used to clean microparticles without damaging silicon carbide crystal substrate and to reduce the surface roughness of silicon carbide material from 1.63 to 0.34 μm, with an airflow of 0.2 Mpa

Study on the Surface Morphology of Micro-Particles and the Oxide Layer on Silicon Carbide Crystal Using Nanosecond Green Laser Cleaning Assisted with Airflow

With a focus on the particle pollutants on the surface of silicon carbide crystal materials, this paper establishes a laser cleaning model for the fine particles found in silicon carbide crystal materials and proposes a new nanosecond green laser cleaning method assisted by airflow, which can effectively remove microparticles and the oxide layer on the substrate surface. Abaqus software and ANSYS Fluent software were used to simulate changes in the cleaning temperature field and the distribution of particles and dust during cleaning simulation, respectively. Based on the experimental research, and by using a nanosecond green laser to produce a wavelength of 532 nm, the direct irradiation of a nanosecond green laser on the surface of the element, and the particle contaminants on the surface of the silicon carbide material, optimized the process parameters to achieve a better cleaning efficiency. A green laser was used as a light source to conduct experiments to control the wind force of the gas chamber. The influence of the laser energy, scanning speed, and other parameters on the final cleaning efficiency was studied. The parameters of the silicon carbide before and after cleaning were characterized. The research shows that laser cleaning assisted with airflow is an efficient cleaning method that can be used to clean microparticles without damaging silicon carbide crystal substrate and to reduce the surface roughness of silicon carbide material from 1.63 to 0.34 &mu;m, with an airflow of 0.2 Mpa

WolfPath : accelerating iterative traversing-based graph processing algorithms on GPU

There is the significant interest nowadays in developing the frameworks of parallelizing the processing for the large graphs such as social networks, Web graphs, etc. Most parallel graph processing frameworks employ iterative processing model. However, by benchmarking the state-of-art GPU-based graph processing frameworks, we observed that the performance of iterative traversing-based graph algorithms (such as Bread First Search, Single Source Shortest Path and so on) on GPU is limited by the frequent data exchange between host and GPU. In order to tackle the problem, we develop a GPU-based graph framework called WolfPath to accelerate the processing of iterative traversing-based graph processing algorithms. In WolfPath, the iterative process is guided by the graph diameter to eliminate the frequent data exchange between host and GPU. To accomplish this goal, WolfPath proposes a data structure called Layered Edge list to represent the graph, from which the graph diameter is known before the start of graph processing. In order to enhance the applicability of our WolfPath framework, a graph preprocessing algorithm is also developed in this work to convert any graph into the format of the Layered Edge list. We conducted extensive experiments to verify the effectiveness of WolfPath. The experimental results show that WolfPath achieves significant speedup over the state-of-art GPU-based in-memory and out-of-memory graph processing frameworks

MTHFR C677T polymorphism and risk of congenital heart defects: evidence from 29 case-control and TDT studies.

BACKGROUND: Methylenetetrahydrofolate reductase (MTHFR) is an important enzyme for folate metabolism in humans; it is encoded by the MTHFR gene. Several studies have assessed the association between MTHFR C677T polymorphism and the risk of congenital heart defects (CHDs), while the results were inconsistent. METHODS AND FINDINGS: Multiple electronic databases were searched to identify relevant studies published up to July 22, 2012. Data from case-control and TDT studies were integrated in an allelic model using the Catmap and Metafor software. Twenty-nine publications were included in this meta-analysis. The overall meta-analysis showed significant association between MTHFR C677T polymorphism and CHDs risk in children with heterogeneity (P heterogeneity = 0.000) and publication bias (P egger = 0.039), but it turned into null after the trim-and-fill method was implemented (OR = 1.12, 95% CI = 0.95-1.31). Nevertheless, positive results were obtained after stratified by ethnicity and sample size in all subgroups except the mixed population. For mothers, there was significant association between the variant and CHDs without heterogeneity (P heterogeneity = 0.150, OR = 1.16, 95% CI = 1.05-1.29) and publication bias (P egger = 0.981). However, the results varied across each subgroup in the stratified analysis of ethnicity and sample size. CONCLUSIONS: Both infant and maternal MTHFR C677T polymorphisms may contribute to the risk of CHDs

A crucial role for GRK2 in regulation of endothelial cell nitric oxide synthase function in portal hypertension

Nitric oxide (NO) production by endothelial cell nitric oxide synthase (eNOS) in sinusoidal endothelial cells is reduced in the injured liver and leads to intrahepatic portal hypertension. We sought to understand the mechanism underlying defective eNOS function. Phosphorylation of the serine-threonine kinase Akt, which activates eNOS, was substantially reduced in sinusoidal endothelial cells from injured livers. Overexpression of Akt in vivo restored phosphorylation of Akt and production of NO and reduced portal pressure in portal hypertensive rats. We found that Akt physically interacts with G-protein-coupled receptor kinase-2 (GRK2), and that this interaction inhibits Akt activity. Furthermore, GRK2 expression increased in sinusoidal endothelial cells from portal hypertensive rats and knockdown of GRK2 restored Akt phosphorylation and NO production, and normalized portal pressure. Finally, after liver injury, GRK2-deficient mice developed less severe portal hypertension than control mice. Thus, an important mechanism underlying impaired activity of eNOS in injured sinusoidal endothelial cells is defective phosphorylation of Akt caused by overexpression of GRK2 after injury