S-model speed planning of NURBS curve based on uniaxial performance limitation

As more complex curves are used in current productions, curve speed planning has become a key technique to overcome the bottleneck of high-speed and high-precision computerized numerical control (CNC) systems. This paper first establishes the model of particle velocity, acceleration and jerk in Cartesian coordinate system, and then improves the uniaxial performance limit algorithm.We set up a real-time speed planning process of spline curves, design a S-model look-ahead algorithm, simplify the S-model speed planning algorithm, and achieve real-time non-uniform rational B-splines (NUBRS) curve S-model speed planning based on uniaxial performance limitation. Simulation results show that all the actual interpolation velocity, acceleration and jerk under the proposed method meet the preset single-axis limit. Experimental results show that the tracking performance under the proposed method has been significantly improved compared with that under the small line segments method. Compared with the NUBRS curve trapezoidal model speed planning, the vibration spikes during machining can be eliminated

Abstract 1289: Role of deregulation of Pol III-dependent transcription in phenotypic alteration.

Abstract The products of RNA polymerase III (Pol III)-dependent genes, such as tRNAs and 5S rRNA, are elevated in both transformed and tumor cells suggesting that they play a crucial role in tumorigenesis. An increase in Brf1 (TFIIIB-related factor 1), a subunit of TFIIIB in Pol III transcription machinery, augments Pol III gene transcription and is sufficient for cell transformation and tumor formation (1). We have demonstrated, for the first time, that enhancement of Brf1 expression and Pol III gene transcription are correlated to liver tumor formation in mice (2). This implies that Brf1 may be a key molecule during liver tumor development. Our early study demonstrated that MSK1 (mitogen- and stress-activated protein kinase 1) mediates H3S28ph (3), Our recent study have indicated that reduction of H3S28ph (histone H3 phosphorylation at serine 28) results in repression of Brf1 and Pol III gene transcription (4). Blocking MSK1 inhibits cell transformation (5) and tumor formation (6). To further determine the role of Brf1 and the signaling and epigenetic regulating events in phenotypic alteration induced by DEN (diethylnitrosamine) which is a chemical carcinogen and is used to induce liver tumor (7), we utilized DEN (200μg/ml) to treat AML-12 cells, an immortalized mouse hepatocyte line to extract cell lysates and total RNA. Our results indicate that DEN treatment increased Brf1 expression and Pol III gene, tRNALeu and 5S rRNA, transcription. DEN strongly induced phosphorylation of MSK1 at serine 376 and Threonine 581. DEN also induces H3phs at both H3S10ph and H3S28ph in AML-12 cells. Interestingly, DEN-induced H3ph in tumor stem cells of mouse liver is significantly stronger than in non-tumor AML-12 cells. MSK1 chemical inhibitor, H89 decreased the induction of Pol III genes. DEN increased the rate of AML-12 cell proliferation. Furthermore, DEN induced colony formation of AML-12 cells in soft agar. Repression of Brf1 by its siRNA reduced Pol III gene transcription and inhibited the cell transformation by DEN. Taken together, these results demonstrate that DEN activates MSK1 and induces H3ph, which in turn mediate Brf1 expression to upregulate RNA Pol III transcription, resulting in increasing in cell proliferation and cell transformation. These studies will allow us to further uncover a novel molecular mechanism of hepatocellular carcinoma by using MSK KO mice and conditional Brf1 KO mice. [This project was supported by NIH grant AA017288 and AA021114 to Shuping Zhong.] Citation Format: Shuping Zhong, Qingsong Zhang, Ganggang Shi. Role of deregulation of Pol III-dependent transcription in phenotypic alteration. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1289. doi:10.1158/1538-7445.AM2013-1289</jats:p

Planar tool radius compensation for CNC systems based on NURBS interpolation

This paper introduces the realization of a tool radius compensation algorithm for NURBS trajectory. First, a single-segment NURBS trajectory tool radius compensation algorithm is developed. Different from the straight line and arc trajectory, the self-intersection phenomenon is prone to happen when calculating a single NURBS tool center trajectory, and the self-intersection will cause the overcut of workpiece. To avoid this situation, the algorithm introduced in this paper can detect whether the NURBS tool center track has caused overcut, and deal with the self-processing. Second, the tool radius compensation algorithm with multi-segment NURBS trajectory is implemented. The focus of this part is the tool radius compensation of the trajectory transfer, and the trajectory transfer is divided into two types: the extension type and the shortened type. For the shortened type transfer, cross-processing is needed to avoid the overcut of workpiece at the transfer. When calculating the tool radius compensation of the shortened type, we not only need to find the intersection of the tool center trajectory of two adjacent NURBS curves, but also need to select the intersection we need when a number of intersections exist. For the extension type transfer, in order to ensure the continuity of the tool center trajectory, we need to extend the tool center trajectory or add arc-segment at the transfer. The proposed algorithm can automatically decide where to extend the tool center trajectory or add arc-segment to achieve the best efficiency. Finally, the algorithm can output the calculated NURBS tool center trajectory in the form of linear segment interpolation G code or NURBS interpolation G code according to the processing needs. Simulations on VERICUT and experiments on three-axis CNC machine tool shows the effectiveness and validation of the tool path compensation algorithm.</jats:p

Abstract 2446: Signaling event of alcohol-induced deregulation of Pol III genes in breast cancer cells

Abstract Alcohol intake is consistently associated with an increased risk of breast cancer. Alcohol consumption is more pronounced in ER+ breast cancer cases than in ER- cases. However, its mechanism remains to be determined. We reported that alcohol induces Pol III gene (RNA polymerase III-dependent genes) transcription in vivo and in vitro. We continue to define novel and unexpected targets, MSK1 (mitogen- stress-activated protein kinase 1) and Brf1 (TFIIIB-related factor 1), in the alcohol-induced response. Our aim is to delineate the mechanisms regulating the processes of deregulation of Pol III genes, cell transformation and tumorgenesis through this alcohol-induced response. Brf1 specifically regulates Pol III gene transcription. Changes in Pol III gene and Brf1 expression tightly link to cell transformation and tumor formation. Alcohol-induced deregulation of Pol III genes may be fundamental to the development of breast cancer. We have reported that a) enhancement of Brf1 and Pol III gene expression is correlated with tumor formation in alcohol-fed mice; b) alcohol increases ERα activity to elevate Brf1 and Pol III gene expression; c) alcohol activates JNK1 to increase ERα and Brf1 expression; d) ethanol induces H3ph (histone H3 phosphorylation), e) H3ph elevates Brf1 expression. However, nothing is known about the role of MSK1 in transcription of Brf1 and Pol III genes. Analysis of signal event has revealed that ethanol markedly stimulates phosphorylation of MSK1 at serine 376 and threonine 581 in MCF-7 cells. Blocking MSK1 singling decreases cellular level of Brf1 expression and Pol III gene transcription. Further analysis indicates that MSK1 mediates ERα expression. Inhibition of MSK signaling decreases alcohol-induced ERE-Luc reporter activity. Repression of ERα expression by its siRNA reduces alcohol-induced anchorage-independent growth of MCF-7 cells. Our results have demonstrated that repression of MSK1 by its siRNA decreases colony formation of MCF-7 cells. Further analysis of ChIP assay indicates that ethanol treatment increases occupancy of ERα to Brf1 promoter. These results support the idea that alcohol activates MSK1 and enhances ERα and Brf1 expression resulting greater phenotypic changes. Together, our studies indicate that ethanol-induced MSK1 activation may play a critical role in alcohol-induced cell transformation and alcohol-associated ER+ breast cancer. *: The project is supported by NIH grants AA017288 and AA021114 to Shuping Zhong Citation Format: Shuping Zhong, Qingsong Zhang, Ganggang Shi. Signaling event of alcohol-induced deregulation of Pol III genes in breast cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2446. doi:10.1158/1538-7445.AM2014-2446</jats:p

Planar tool radius compensation for CNC systems based on NURBS interpolation

This paper introduces the realization of a tool radius compensation algorithm for NURBS trajectory. First, a single-segment NURBS trajectory tool radius compensation algorithm is developed. Different from the straight line and arc trajectory, the self-intersection phenomenon is prone to happen when calculating a single NURBS tool center trajectory, and the self-intersection will cause the overcut of workpiece. To avoid this situation, the algorithm introduced in this paper can detect whether the NURBS tool center track has caused overcut, and deal with the self-processing. Second, the tool radius compensation algorithm with multi-segment NURBS trajectory is implemented. The focus of this part is the tool radius compensation of the trajectory transfer, and the trajectory transfer is divided into two types: the extension type and the shortened type. For the shortened type transfer, cross-processing is needed to avoid the overcut of workpiece at the transfer. When calculating the tool radius compensation of the shortened type, we not only need to find the intersection of the tool center trajectory of two adjacent NURBS curves, but also need to select the intersection we need when a number of intersections exist. For the extension type transfer, in order to ensure the continuity of the tool center trajectory, we need to extend the tool center trajectory or add arc-segment at the transfer. The proposed algorithm can automatically decide where to extend the tool center trajectory or add arc-segment to achieve the best efficiency. Finally, the algorithm can output the calculated NURBS tool center trajectory in the form of linear segment interpolation G code or NURBS interpolation G code according to the processing needs. Simulations on VERICUT and experiments on three-axis CNC machine tool shows the effectiveness and validation of the tool path compensation algorithm

Reference modification for trajectory tracking using hybrid offline and online neural networks learning

In this paper, we propose a hybrid offline/online neural networks learning method, which combines complementary advantages of two types of neural networks (NNs): deep NN (DNN) and single-layer radial basis function NN (RBFNN). Firstly, after analyzing the mechatronic system’s model, we select reasonable features as the input of the DNN to learn the inverse dynamic characteristics of the closed-loop system offline, so as to establish the mapping between the desired trajectory and the reference trajectory of the system. The trained DNN is used to generate a new reference trajectory and compensate for the tracking error in advance, which can speed up the convergence of online learning control based on RBFNN. This reference trajectory is further modified iteratively when the tracking task is repeated. For this purpose, a single-layer RBFNN model is established, and an online learning algorithm is developed to update the RBFNN parameters. The proposed hybrid offline/online NN method can improve the tracking performance of mechatronic systems by modifying the reference trajectory on top of the baseline controller without affecting the system stability. To verify the effectiveness of this method, we conduct experiments on a piezoelectric drive platform

Reference modification for trajectory tracking using hybrid offline and online neural networks learning

AbstractIn this paper, we propose a hybrid offline/online neural networks learning method, which combines complementary advantages of two types of neural networks (NNs): deep NN (DNN) and single-layer radial basis function NN (RBFNN). Firstly, after analyzing the mechatronic system’s model, we select reasonable features as the input of the DNN to learn the inverse dynamic characteristics of the closed-loop system offline, so as to establish the mapping between the desired trajectory and the reference trajectory of the system. The trained DNN is used to generate a new reference trajectory and compensate for the tracking error in advance, which can speed up the convergence of online learning control based on RBFNN. This reference trajectory is further modified iteratively when the tracking task is repeated. For this purpose, a single-layer RBFNN model is established, and an online learning algorithm is developed to update the RBFNN parameters. The proposed hybrid offline/online NN method can improve the tracking performance of mechatronic systems by modifying the reference trajectory on top of the baseline controller without affecting the system stability. To verify the effectiveness of this method, we conduct experiments on a piezoelectric drive platform.</jats:p