Model and experiments to optimize co-adaptation in a simplified myoelectric control system.

OBJECTIVE: To compensate for a limb lost in an amputation, myoelectric prostheses use surface electromyography (EMG) from the remaining muscles to control the prosthesis. Despite considerable progress, myoelectric controls remain markedly different from the way we normally control movements, and require intense user adaptation. To overcome this, our goal is to explore concurrent machine co-adaptation techniques that are developed in the field of brain-machine interface, and that are beginning to be used in myoelectric controls. APPROACH: We combined a simplified myoelectric control with a perturbation for which human adaptation is well characterized and modeled, in order to explore co-adaptation settings in a principled manner. RESULTS: First, we reproduced results obtained in a classical visuomotor rotation paradigm in our simplified myoelectric context, where we rotate the muscle pulling vectors used to reconstruct wrist force from EMG. Then, a model of human adaptation in response to directional error was used to simulate various co-adaptation settings, where perturbations and machine co-adaptation are both applied on muscle pulling vectors. These simulations established that a relatively low gain of machine co-adaptation that minimizes final errors generates slow and incomplete adaptation, while higher gains increase adaptation rate but also errors by amplifying noise. After experimental verification on real subjects, we tested a variable gain that cumulates the advantages of both, and implemented it with directionally tuned neurons similar to those used to model human adaptation. This enables machine co-adaptation to locally improve myoelectric control, and to absorb more challenging perturbations. SIGNIFICANCE: The simplified context used here enabled to explore co-adaptation settings in both simulations and experiments, and to raise important considerations such as the need for a variable gain encoded locally. The benefits and limits of extending this approach to more complex and functional myoelectric contexts are discussed.

Membrane and intracellular platelet-activating factor receptor expression in leukemic blasts of patients with acute myeloid and lymphoid leukemia.

Platelet-activating factor (PAF), a phospholipid mediator with a wide range of actions on mature leukocytes, acts through PAF-receptors (PAF-Rs) on the membranes of responsive cells. No results are available concerning the putative presence of PAF-Rs on leukemic blasts. Using multiparameter flow cytometry, we assessed intracellular and membrane PAF-Rs on blast cells of acute myeloid leukemic (AML) and acute lymphoid leukemic (ALL) patients. Membrane PAF-Rs were documented in 7/15 cases of ALL and 0/28 cases of AML. Putative intracellular PAF-Rs were found in blasts of 8/8 ALL and 13/13 AML patients. Vitamin D(3) and dimethyl sulfoxide that induced the expression of PAF-Rs on the membrane of the human promyelocytic leukemia cell line, HL60, failed to induce their expression on the membranes of CD34(+) AML blasts. The lack of membrane PAF-Rs on the membranes of AML blasts confirms that these receptors represent a marker of mature cells and that their membrane induction is a consequence of cell maturation and differentiation.