Tomas Olsson

Extending an industrial robot controller: implementation and applications of a fast open sensor interface

This paper describes the design and implementation of a platform for fast external sensor integration in an industrial robot control system. As an application and motivating example, the implementation of force controlled grinding and deburring within the AUTOFETT-project (EU Growth Programme) is reported.

Brain damage in a mouse model of global cerebral ischemia. Effect of NMDA receptor blockade

The importance of particular genes in neuronal death following global cerebral ischemia can readily be studied in genetically modified mice provided a reliable model of ischemia is available. For that purpose, we developed a mouse model of global cerebral ischemia that induces consistent damage to different regions of the brain and with a low mortality rate. Twelve minutes of ischemia was induced in C57BL/6 mice by bilateral common carotid artery occlusion under halothane anesthesia and artificial ventilation. Body and brain temperature were monitored and cortical cerebral blood flow in each hemisphere was measured by laser Doppler flowmeter before, during, and for 5 min after ischemia. Extensive damage was found in the striatum and marked cell damage was observed in the CA1 and CA2 regions of hippocampus and in thalamus. Mild damage was seen in the CA3 region, dentate gyrus and cortex. Hippocampal damage in the CA1 region is delayed and developed over 48 h. Intraischemic hypothermia of 33 degrees C provided a robust neuroprotection. The non-competitive N-methyl-D-aspartate receptor blocker, MK-801, did not provide protection in the hippocampus, cortex, striatum or thalamus when administered 30 min prior to ischemia or 2 h after the end of ischemia, but selectively mitigated damage in the hippocampus, when administered immediately following ischemia. This model of global cerebral ischemia may be useful in pharmacological and genomic studies of ischemic brain damage.

Overexpression of UCP2 Protects Thalamic Neurons following Global Ischemia in the Mouse

Uncoupling protein 2 (UCP2) is upregulated in the brain after sublethal ischemia, and overexpression of UCP2 is neuroprotective in several models of neurodegenerative disease. We investigated if increased levels of UCP2 diminished neuronal damage after global brain ischemia by subjecting mice overexpressing UCP2 (UCP2/3tg) and wild-type littermates (wt) to a 12-min global ischemia. The histopathological outcome in the cortex, hippocampus, striatum, and thalamus was evaluated at 4 days of recovery, allowing maturation of the selective neuronal death. Global ischemia led to extensive cell death in the striatum, thalamus, and in the CA1 and CA2, and less-pronounced cell death in the CA3 and dentate gyrus (DG) hippocampal subfields. Histologic damage was significantly lower in the ventral posterolateral VPL and medial VPM thalamic nuclei in UCP2/3tg animals compared with wt. These thalamic regions showed a larger increase in UCP2 expression in UCP2/3tg compared with wt animals relative to the nonprotected DG. In the other regions studied, the histologic damage was lower or equal in UCP2/3tg animals compared with wt. Consequently, neuroprotection in the thalamus correlated with a high expression of UCP2, which is neuroprotective in a number of models of neurodegenerative diseases.

Deletion of the adenosine A1 receptor gene does not alter neuronal damage following ischaemia in vivo or in vitro

Extracellular adenosine is dramatically increased during cerebral ischaemia and is considered to be neuroprotective due to its inhibitory effect on synaptic transmission mediated by the adenosine A1 receptor (A1R). We investigated the importance of the A1R in a mouse model of global ischaemia and in a murine hippocampal slice culture model of in vitro ischaemia, using mice with the A1R gene deleted. In brains from mice lacking the A1R, damage induced by global ischaemia was similar to that in wild‐type animals. In contrast, treatment with a selective A1R antagonist [8‐cyclo‐pentyl theophylline (8‐CPT)], administered before the ischaemic insult in naive wild‐type mice, exacerbated the neuronal damage following global ischaemia. Although the inhibitory action of adenosine on excitatory neurotransmission in hippocampal slices was lost in A1R knockout mice, there was no difference in damage between slices from wild‐type and knockout mice after in vitro ischaemia. The results suggest that some effects of the A1R are compensated for in knockout animals.

Gene deletion of cystatin C aggravates brain damage following focal ischemia but mitigates the neuronal injury after global ischemia in the mouse.

Cystatin C is distributed in all human tissues and fluids with a particular abundance in the cerebrospinal fluid. Cystatin C is a strong endogenous inhibitor of lysosomal cysteine proteases, such as cathepsin B, L, H and S, that are involved in various biological processes such as degradation of cellular proteins and regulation of enzymes, as well as in pathological processes. Pharmacological inhibition of cathepsins has been shown to reduce neuronal damage after brain ischemia, suggesting that cystatin C is an endogenous neuroprotectant. Cystatin C has also amyloidogenic properties and is co-localized with beta-amyloid in degenerated neurons in Alzheimers disease, suggesting a role in neuronal degeneration. To test the hypothesis that endogenous cystatin C is neuroprotective during brain ischemia, global and focal brain ischemia was induced in mice with the cystatin C gene knocked out. Following focal ischemia, larger brain infarcts were found in cystatin C knockout mice, probably due to a reduced inhibition of the cathepsins during ischemia. In contrast, brain damage after global ischemia was diminished in cystatin C knockout mice, suggesting that cystatin C has an aggravating effect on selective neuronal damage after global ischemia.

Force control and visual servoing using planar surface identification

When designing flexible multi-sensor based robot systems, one important problem is how to combine the measurements from disparate sensors such as cameras and force sensors. In this paper, we present a method for combining direct force control and visual servoing in the presence of unknown planar surfaces. The control algorithm involves a force feedback control loop and a vision based reference trajectory as a feed-forward signal. The vision system is based on a constrained image-based visual servoing algorithm designed for surface following, where the location and orientation of the planar constraint surface is estimated online using position-, force- and visual data. We show how data from a simple and efficient camera calibration method can be used in combination with force and position data to improve the estimation and reference trajectories. The method is validated through experiments involving force controlled drawing on an unknown surface. The robot will grasp a pen and use it to draw lines between a number of markers drawn on a white-board, while the contact force is kept constant. Despite its simplicity, the performance of the method is satisfactory.

Sensor Integration in Task-level Programming and Industrial Robotic Task Execution Control

Presents an approach to improved performance and flexibility in industrial robotics by means of sensor integration and feedback control in task‐level programming and task execution. Also presents feasibility studies in support of the ideas. Discusses some solutions to the problem using six degrees of freedom force control together with the ABB S4CPlus system as an illustrative example. Consider various problems in the design of an open sensor interface for industrial robotics and discusses possible solutions. Finally, presents experimental results from industrial force controlled grinding.

Implementation of Industrial Robot Force Control Case Study: High Power Stub Grinding and Deburring

In this paper, the results from a joint industry-academia project in industrial robotic force control are presented. The extension and implementation of an external sensor system for an industrial robot system, which can be used for high-bandwidth force control, are described. Results from two industrial applications using the system are presented, a stub grinding application using a new compliant grinding end-effector integrated with the robot control system, and a deburring application with a stiff tool requiring high-bandwidth force control in six degrees of freedom. Using the system an easily reconfigurable control structure was achieved, which was able to control contact forces with a sampling bandwidth of an order of magnitude higher than for conventional robot controllers

Flexible force-vision control for surface following using multiple cameras

A flexible method for six-degree-of-freedom combined vision/force control for interaction with a stiff uncalibrated environment is presented. An edge-based rigid-body tracker is used in an observer-based controller, and combined with a six-degree-of-freedom force- or impedance controller. The effect of error sources such as image space measurement noise and calibration errors are considered. Finally, the method is validated in simulations and a surface following experiment using an industrial robot.

Posterior accumulation of tau and concordant hypometabolism in an early-onset Alzheimer's disease patient with presenilin-1 mutation

It is unclear whether the distribution of tau pathology differs between cases with early-onset familial Alzheimers disease (AD) and sporadic AD. We present positron emission tomography (PET) data from a young patient with a presenilin-1 mutation (Thr116Asn). 18F-flutemetamol PET showed a distribution of amyloid-β fibrils similar to sporadic AD. However, the pattern of tau pathology, revealed using 18F-AV1451 PET, showed higher uptake in posterior cingulate, precuneus, parietal and occipital cortices compared to late-onset sporadic AD. Further, the tau pathology, but not amyloid pathology, exhibited a very clear inverse relationship with 18F-fluorodeoxyglucose-metabolism, indicating neuronal hypometabolism in regions affected by tau aggregates.