213 resultados para Joint Compensation Scheme
Resumo:
There is an increasing attention of exploiting compliant materials for the purpose of legged locomotion, because they provide significant advantages in locomotion performance with respect to energy efficiency and stability. Toward establishing a fundamental basis for this line of research, a minimalistic locomotion model of a single legged system is explored in this paper. By analyzing the dynamic behavior of the system in simulation and a physical robotic platform, it is shown that a stable locomotion process can be achieved without the necessity of sensory feedback. In addition, further analysis characterizes the relation between motor control and the natural body dynamics determined by morphological properties such as body mass and spring constant. © 2006 The authors.
Resumo:
This paper studies the random-coding exponent of joint source-channel coding for a scheme where source messages are assigned to disjoint subsets (referred to as classes), and codewords are independently generated according to a distribution that depends on the class index of the source message. For discrete memoryless systems, two optimally chosen classes and product distributions are found to be sufficient to attain the sphere-packing exponent in those cases where it is tight. © 2014 IEEE.
Resumo:
How do neurons develop, control, and maintain their electrical signaling properties in spite of ongoing protein turnover and perturbations to activity? From generic assumptions about the molecular biology underlying channel expression, we derive a simple model and show how it encodes an "activity set point" in single neurons. The model generates diverse self-regulating cell types and relates correlations in conductance expression observed in vivo to underlying channel expression rates. Synaptic as well as intrinsic conductances can be regulated to make a self-assembling central pattern generator network; thus, network-level homeostasis can emerge from cell-autonomous regulation rules. Finally, we demonstrate that the outcome of homeostatic regulation depends on the complement of ion channels expressed in cells: in some cases, loss of specific ion channels can be compensated; in others, the homeostatic mechanism itself causes pathological loss of function.