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In order to reduce the energy consumption of the welding robot and ensure the cooperative movement of the robot joints, a trajectory planning method with optimal energy consumption based on improved sparrow search algorithm is proposed. Firstly, the trajectory planning model with optimal energy consumption is established based on the joint torque and angular velocity of the robot. To make the velocity, acceleration and jerk of each joint of the robot be bounded and continuous, the joint space trajectory is constructed with seventh degree B-spline curve. The total energy consumption of the robot is calculated by combining kinematic and dynamic parameters. On the basis of improved sparrow search algorithm, the time series corresponding to the optimal energy consumption is solved by using elite reverse learning, non-dominated sorting and Gaussian-Cauchy variation strategy, and then the optimal continuous motion trajectory of energy consumption is planned. The simulation results show that the proposed method can not only achieve continuous smooth control objective, but also effectively reduce energy consumption.

In this paper, we propose a new optimal trajectory planning method for the manipulator to optimize its operating efficiency and ensure the smoothness of the motion process. The position sequences in joint space corresponding to a specified trajectory in task space are obtained by using the inverse kinematic algorithm, and the seventh-degree B-spline curve interpolation method is used to construct the joint trajectory with controllable start–stop kinematic parameters, and continuous velocity, acceleration and jerk. The kinematic constraints of the manipulator are transformed into the control point constraints of the B-spline curve, the sequential quadratic programming method is used to solve the optimal motion time node, and then the time-optimal continuous jerk trajectory satisfying the nonlinear kinematic constraints is planned. Simulation results show that the proposed trajectory planning method provides the ideal trajectory for the joint controller, ensuring the manipulator can smoothly track any specified trajectory in the task space in the shortest time.

Abstract Aims/Introduction Glutamine is the most abundant amino acid in the circulation. In this study, we investigated cell signaling in the amplification of insulin secretion by glutamine. Materials and Methods Clonal pancreatic β‐cells MIN6‐K8, wild‐type B6 mouse islets, glutamate dehydrogenase (GDH) knockout clonal β‐cells (Glud1KOβCL), and glutamate‐oxaloacetate transaminase 1 (GOT1) knockout clonal β‐cells (Got1KOβCL) were studied. Insulin secretion from these cells and islets was examined under various conditions, and intracellular glutamine metabolism was assessed by metabolic flux analysis. Intracellular Ca2+ concentration ([Ca2+]i) was also measured. Results Glutamine dose‐dependently amplified insulin secretion in the presence of high glucose in both MIN6‐K8 cells and Glud1KOβCL. Inhibition of glutaminases, the enzymes that convert glutamine to glutamate, dramatically reduced the glutamine‐amplifying effect on insulin secretion. A substantial amount of glutamate was produced from glutamine through direct conversion by glutaminases. Glutamine also increased [Ca2+]i at high glucose, which was abolished by inhibition of glutaminases. Glutamic acid dimethylester (dm‐Glu), a membrane permeable glutamate precursor that is converted to glutamate in cells, increased [Ca2+]i as well as induced insulin secretion at high glucose. These effects of glutamine and dm‐Glu were dependent on calcium influx. Glutamine also induced insulin secretion in clonal β‐cells MIN6‐m14, which otherwise exhibit no insulin secretory response to glucose. Conclusions Glutamate converted from glutamine is an essential mediator that enhances calcium signaling in the glutamine‐amplifying effect on insulin secretion. Our data also suggest that glutamine exerts a permissive effect on glucose‐induced insulin secretion.

Incretins (GLP-1 and GIP) potentiate insulin secretion through cAMP signaling in pancreatic β-cells in a glucose-dependent manner. We recently proposed a mechanistic model of incretin-induced insulin secretion (IIIS) that requires two critical processes: 1) generation of cytosolic glutamate through the malate-aspartate (MA) shuttle in glucose metabolism and 2) glutamate transport into insulin granules by cAMP signaling to promote insulin granule exocytosis. To directly prove the model, we have established and characterized CRISPR/Cas9-engineered clonal mouse β-cell lines deficient for the genes critical in these two processes: aspartate aminotransferase 1 (AST1, gene symbol Got1), a key enzyme in the MA shuttle, which generates cytosolic glutamate, and the vesicular glutamate transporters (VGLUT1, VGLUT2, and VGLUT3, gene symbol Slc17a7, Slc17a6, and Slc17a8, respectively), which participate in glutamate transport into secretory vesicles. Got1 knockout (KO) β-cell lines were defective in cytosolic glutamate production from glucose and showed impaired IIIS. Unexpectedly, different from the previous finding that global Slc17a7 KO mice exhibited impaired IIIS from pancreatic islets, β-cell specific Slc17a7 KO mice showed no significant impairment in IIIS, as assessed by pancreas perfusion experiment. Single Slc17a7 KO β-cell lines also retained IIIS, probably due to compensatory upregulation of Slc17a6. Interestingly, triple KO of Slc17a7, Slc17a6, and Slc17a8 diminished IIIS, which was rescued by exogenously introduced wild-type Slc17a7 or Slc17a6 genes. The present study provides direct evidence for the essential roles of AST1 and VGLUTs in β-cell glutamate signaling for IIIS and also shows the usefulness of the CRISPR/Cas9 system for studying β-cells by simultaneous disruption of multiple genes.

In arsenic-endemic regions of the world, arsenic exposure correlates with diabetes mellitus. Multiple animal models of inorganic arsenic (iAs, as As3+) exposure have revealed that iAs-induced glucose intolerance manifests as a result of pancreatic β-cell dysfunction. To define the mechanisms responsible for this β-cell defect, the MIN6-K8 mouse β-cell line was exposed to environmentally relevant doses of iAs. Exposure to 0.1-1 µM iAs for 3 days significantly decreased glucose-induced insulin secretion (GIIS). Serotonin and its precursor, 5-hydroxytryptophan (5-HTP), were both decreased. Supplementation with 5-HTP, which loads the system with bioavailable 5-HTP and serotonin, rescued GIIS, suggesting that recovery of this pathway was sufficient to restore function. Exposure to iAs was accompanied by an increase in mRNA expression of UDP-glucuronosyltransferase 1 family, polypeptide a6a (Ugt1a6a), a phase-II detoxification enzyme that facilitates the disposal of cyclic amines, including serotonin, via glucuronidation. Elevated Ugt1a6a and UGT1A6 expression levels were observed in mouse and human islets, respectively, following 3 days of iAs exposure. Consistent with this finding, the enzymatic rate of serotonin glucuronidation was increased in iAs-exposed cells. Knockdown by siRNA of Ugt1a6a during iAs exposure restored GIIS in MIN6-K8 cells. This effect was prevented by blockade of serotonin biosynthesis, suggesting that the observed iAs-induced increase in Ugt1a6a affects GIIS by targeting serotonin or serotonin-related metabolites. Although it is not yet clear exactly which element(s) of the serotonin pathway is/are most responsible for iAs-induced GIIS dysfunction, this study provides evidence that UGT1A6A, acting on the serotonin pathway, regulates GIIS under both normal and pathological conditions. [ABSTRACT FROM AUTHOR]

The Northeast Cold Vortex (NECV) Is an Important weather system in the middle and high latitudes In East Asia. Its time scale is synoptic, yet the frequent activities of NECV have significant "climate effect" which influences not only the monthly temperature In the lower troposphere in Northeast China but also the Melyu rainfall in East Asia. On the basis of ERA-40 reanalysis data provided by ECMWF, the "climate effect" of NECV and Its relationship with Melyu in East Asia are studied. It Is shown that there Is significant correlation between NECV during the Melyu period and rainfall amount: strong NECV corresponds to more Melyu rainfall and weak NECV corresponds to less rainfall. In strong NECV years, the dry and cold air from the north is led to the south by NECV, converges with the lower-level warm and wet southwesterly on the north verge of Meiyu region, thus forms an unstable stratification of "upper dryness and lower wetness". Triggered by ascending motion, the Melyu rainfall amount Is more than usual. It Is on the contrary In weak NECV years. The anomalous SST in north Pacific in the previous year may be a factor that results In the anomalous NECV at Melyu period. The land-sea thermal contrast In summer facilitates NECV, while that in winter inhibits NECV. All of the above provide a meaningful result for the short-term climate prediction of NECV and Melyu. [ABSTRACT FROM AUTHOR]