To improve the accuracy of predicting non-invasive blood glucose concentration in the near-infrared spectrum, we utilized the Particle Swarm Optimization (PSO) algorithm to optimize hyperparameters for the Multi-Kerne...To improve the accuracy of predicting non-invasive blood glucose concentration in the near-infrared spectrum, we utilized the Particle Swarm Optimization (PSO) algorithm to optimize hyperparameters for the Multi-Kernel Learning Support Vector Machine (MKL-SVR). With these optimized hyperparameters, we established a non-invasive blood glucose regression model, referred to as the PSO-MKL-SVR model. Subsequently, we conducted a comparative analysis between the PSO-MKL-SVR model and the PSO-SVR model. In a dataset comprising ten volunteers, the PSO-MKL-SVR model exhibited significant precision improvements, including a 16.03% reduction in Mean Square Error and a 0.29% increase in the Squared Correlation Coefficient. Moreover, there was a 0.14% higher probability of the Clark’s Error Grid Analysis falling within Zone A. Additionally, the PSO-MKL-SVR model demonstrated a faster operational speed compared to the PSO-SVR model.展开更多
将OpenMP并行运算库和Intel Math Kernel Library10.2科学计算库运用到高阶地球重力场反演,显著提高了计算效率。模拟结果表明:1)在以单历元为解算单元形成子法方程系数矩阵时,OpenMP可下三角压缩存储,其内存销耗和时间销耗均比较小;2)...将OpenMP并行运算库和Intel Math Kernel Library10.2科学计算库运用到高阶地球重力场反演,显著提高了计算效率。模拟结果表明:1)在以单历元为解算单元形成子法方程系数矩阵时,OpenMP可下三角压缩存储,其内存销耗和时间销耗均比较小;2)当利用多个历元组成高维系数矩阵,然后再形成法方程时,MKL算法才能体现出高效性能;3)MKL求逆算法效率远高于OpenMP算法;4)综合利用OpenMP和MKL算法的优势,可显著提高高阶地球重力场反演的效率。展开更多
Tumor necrosis factor alpha(TNF-a) is a cytokine that can potently stimulate the synthesis of a range of proinflammatory mediators in macrophages. The underlying epigenetic mechanism, however, is underexplored. Here w...Tumor necrosis factor alpha(TNF-a) is a cytokine that can potently stimulate the synthesis of a range of proinflammatory mediators in macrophages. The underlying epigenetic mechanism, however, is underexplored. Here we report that the transcriptional modulator megakaryocytic leukemia 1(MKL1) is associated with a histone H3 K4 methyltransferase activity. Re-ChIP assay suggests that MKL1 interacts with and recruits WDR5, a component of the COMPASS complex responsible for H3 K4 methylation, to the promoter regions of pro-inflammatory genes in macrophages treated with TNF-α. WDR5 enhances the ability of MKL1 to stimulate the promoter activities of proinflammatory genes. In contrast, silencing of WDR5 attenuates TNF-a induced production of pro-inflammatory mediators and erases the H3 K4 methylation from the gene promoters. Of interest, the chromatin remodeling protein BRG1 also plays an essential role in maintaining H3 K4 methylation on MKL1 target promoters by interacting with WDR5. MKL1 knockdown disrupts the interaction between BRG1 and WDR5. Together, our data illustrate a role for MKL1 in moderating the crosstalk between BRG1 and WDR5 to activate TNF-a induced pro-inflammatory transcription in macrophages.展开更多
文摘To improve the accuracy of predicting non-invasive blood glucose concentration in the near-infrared spectrum, we utilized the Particle Swarm Optimization (PSO) algorithm to optimize hyperparameters for the Multi-Kernel Learning Support Vector Machine (MKL-SVR). With these optimized hyperparameters, we established a non-invasive blood glucose regression model, referred to as the PSO-MKL-SVR model. Subsequently, we conducted a comparative analysis between the PSO-MKL-SVR model and the PSO-SVR model. In a dataset comprising ten volunteers, the PSO-MKL-SVR model exhibited significant precision improvements, including a 16.03% reduction in Mean Square Error and a 0.29% increase in the Squared Correlation Coefficient. Moreover, there was a 0.14% higher probability of the Clark’s Error Grid Analysis falling within Zone A. Additionally, the PSO-MKL-SVR model demonstrated a faster operational speed compared to the PSO-SVR model.
文摘将OpenMP并行运算库和Intel Math Kernel Library10.2科学计算库运用到高阶地球重力场反演,显著提高了计算效率。模拟结果表明:1)在以单历元为解算单元形成子法方程系数矩阵时,OpenMP可下三角压缩存储,其内存销耗和时间销耗均比较小;2)当利用多个历元组成高维系数矩阵,然后再形成法方程时,MKL算法才能体现出高效性能;3)MKL求逆算法效率远高于OpenMP算法;4)综合利用OpenMP和MKL算法的优势,可显著提高高阶地球重力场反演的效率。
基金the National Natural Science Foundation of China (81570420) supported by the Qinglan Project of the Education Commission of Jiangsu Province
文摘Tumor necrosis factor alpha(TNF-a) is a cytokine that can potently stimulate the synthesis of a range of proinflammatory mediators in macrophages. The underlying epigenetic mechanism, however, is underexplored. Here we report that the transcriptional modulator megakaryocytic leukemia 1(MKL1) is associated with a histone H3 K4 methyltransferase activity. Re-ChIP assay suggests that MKL1 interacts with and recruits WDR5, a component of the COMPASS complex responsible for H3 K4 methylation, to the promoter regions of pro-inflammatory genes in macrophages treated with TNF-α. WDR5 enhances the ability of MKL1 to stimulate the promoter activities of proinflammatory genes. In contrast, silencing of WDR5 attenuates TNF-a induced production of pro-inflammatory mediators and erases the H3 K4 methylation from the gene promoters. Of interest, the chromatin remodeling protein BRG1 also plays an essential role in maintaining H3 K4 methylation on MKL1 target promoters by interacting with WDR5. MKL1 knockdown disrupts the interaction between BRG1 and WDR5. Together, our data illustrate a role for MKL1 in moderating the crosstalk between BRG1 and WDR5 to activate TNF-a induced pro-inflammatory transcription in macrophages.
