Bionic Path Planning Fusing Episodic Memory Based on RatSLAM.

Inspired by rodents' ability to navigate freely in a given space, bionavigation systems provide alternatives to traditional probabilistic solutions. This paper proposed a bionic path planning method based on RatSLAM to provide a novel viewpoint for robots to make a more flexible and intelligent navigation scheme. A neural network fusing historic episodic memory was proposed to improve the connectivity of the episodic cognitive map.

Correlated Skin Surface and Tumor Motion Modeling for Treatment Planning in Robotic Radiosurgery.

In robotic radiosurgery, motion tracking is crucial for accurate treatment planning of tumor inside the thoracic or abdominal cavity. Currently, motion characterization for respiration tracking mainly focuses on markers that are placed on the surface of human chest. Nevertheless, limited markers are not capable of expressing the comprehensive motion feature of the human chest and abdomen.

Robustness Improvement of Visual Templates Matching Based on Frequency-Tuned Model in RatSLAM.

This paper describes an improved brain-inspired simultaneous localization and mapping (RatSLAM) that extracts visual features from saliency maps using a frequency-tuned (FT) model. In the traditional RatSLAM algorithm, the visual template feature is organized as a one-dimensional vector whose values only depend on pixel intensity; therefore, this feature is susceptible to changes in illumination intensity. In contrast to this approach, which directly generates visual templates from raw RGB images, we propose an FT model that converts RGB images into saliency maps to obtain visual templates.

Intelligent Control for Human-Robot Cooperation in Orthopedics Surgery.

Cooperation between surgeon and robot is one of the key technologies that limit the robot to be widely used in orthopedic clinics. In this study, the evolution of human-robot cooperation methods and the control strategies for typical human-robot cooperation in robot-assisted orthopedics surgery were reviewed at first. Then an intelligent admittance control method, which combines the fuzzy model reference learning control with the virtual constraint control, is proposed to solve the requirements of intuitive human-robot interaction during orthopedics surgery.

[Vegetation change of Yamzho Yumco Basin in southern Tibet based on SPOT-VGT NDVI].

The area we studied is Lake Yamzho Yumco Basin (28 degrees 27'-29 degrees 12'N, 90 degrees 08'-91 degrees 45'E), the largest inland lake basin in southern Tibetan Plateau, China. Using the SPOT-VGT NDVI vegetation index from 1998 to 2007 in the basin, the temporal and spatial variation characteristics of NDVI and its correlation with the major climatic factors (air temperature, precipitation) were analyzed. The results show that the average NDVI of the lake basin ranges from 0.

Mixed lineage kinase-3 stabilizes and functionally cooperates with TRIBBLES-3 to compromise mitochondrial integrity in cytokine-induced death of pancreatic beta cells.

Mixed lineage kinases (MLKs) have been implicated in cytokine signaling as well as in cell death pathways. Our studies show that MLK3 is activated in leukocyte-infiltrated islets of non-obese diabetic mice and that MLK3 activation compromises mitochondrial integrity and induces apoptosis of beta cells. Using an ex vivo model of islet-splenocyte co-culture, we show that MLK3 mediates its effects via the pseudokinase TRB3, a mammalian homolog of Drosophila Tribbles.

Glucose regulates steady-state levels of PDX1 via the reciprocal actions of GSK3 and AKT kinases.

The pancreatic beta cell is sensitive to even small changes in PDX1 protein levels; consequently, Pdx1 haploinsufficiency can inhibit beta cell growth and decrease insulin biosynthesis and gene expression, leading to compromised glucose-stimulated insulin secretion. Using metabolic labeling of primary islets and a cultured beta cell line, we show that glucose levels modulate PDX1 protein phosphorylation at a novel C-terminal GSK3 consensus that maps to serines 268 and 272. A decrease in glucose levels triggers increased turnover of the PDX1 protein in a GSK3-dependent manner, such that PDX1 phosphomutants are refractory to the destabilizing effect of low glucose.