A three-leg model producing tetrapod and tripod coordination patterns of ipsilateral legs in the stick insect

Insect locomotion requires the precise coordination of the movement of all six legs. Detailed investigations have revealed that the movement of the legs is controlled by local dedicated neuronal networks, which interact to produce walking of the animal. The stick insect is well suited to experimental investigations aimed at understanding the mechanisms of insect locomotion. Beside the experimental approach, models have also been constructed to elucidate those mechanisms. Here, we describe a model that replicates both the tetrapod and tripod coordination pattern of three ipsilateral legs. The model is based on an earlier insect leg model, which includes the three main leg joints, three antagonistic muscle pairs, and their local neuronal control networks. These networks are coupled via angular signals to establish intraleg coordination of the three neuromuscular systems during locomotion. In the present three-leg model, we coupled three such leg models, representing front, middle, and hind leg, in this way. The coupling was between the levator-depressor local control networks of the three legs. The model could successfully simulate tetrapod and tripod coordination patterns, as well as the transition between them. The simulations showed that for the interleg coordination during tripod, the position signals of the levator-depressor neuromuscular systems sent between the legs were sufficient, while in tetrapod, additional information on the angular velocities in the same system was necessary, and together with the position information also sufficient. We therefore suggest that, during stepping, the connections between the levator-depressor neuromuscular systems of the different legs are of primary importance

Modeling and Hemofiltration Treatment of Acute Inflammation

The body responds to endotoxins by triggering the acute inflammatory response system to eliminate the threat posed by gram-negative bacteria (endotoxin) and restore health. However, an uncontrolled inflammatory response can lead to tissue damage, organ failure, and ultimately death; this is clinically known as sepsis. Mathematical models of acute inflammatory disease have the potential to guide treatment decisions in critically ill patients. In this work, an 8-state (8-D) differential equation model of the acute inflammatory response system to endotoxin challenge was developed. Endotoxin challenges at 3 and 12 mg/kg were administered to rats, and dynamic cytokine data for interleukin (IL)-6, tumor necrosis factor (TNF), and IL-10 were obtained and used to calibrate the model. Evaluation of competing model structures was performed by analyzing model predictions at 3, 6, and 12 mg/kg endotoxin challenges with respect to experimental data from rats. Subsequently, a model predictive control (MPC) algorithm was synthesized to control a hemoadsorption (HA) device, a blood purification treatment for acute inflammation. A particle filter (PF) algorithm was implemented to estimate the full state vector of the endotoxemic rat based on time series cytokine measurements. Treatment simulations show that: (i) the apparent primary mechanism of HA efficacy is white blood cell (WBC) capture, with cytokine capture a secondary benefit; and (ii) differential filtering of cytokines and WBC does not provide substantial improvement in treatment outcomes vs. existing HA devices