Reducing muscle effort in walking through powered exoskeletons.

This paper presents a novel assistive control for lower limb exoskeletons. The controller provides the user with a scaled version of the Winter's nominal torque profile, which is adapted online to the specific gait features of the user. The proposed assistive controller is implemented on the ALEX II exoskeleton and tested on two healthy subjects. Experimental results show that when assisted by the exoskeleton users can reduce the muscle effort compared to free walking.

Dysbaric osteonecrosis: a consequence of intravascular bubble formation, endothelial damage, and platelet thrombosis.

Survival and turnover of platelets, fibrinogen, and plasminogen were measured in association with hyperbaric exposure in man. In addition, kinetic and vascular studies were carried out in a hyperbaric swine model to assess the role of vascular injury and thrombosis in the pathogenesis of dysbaric osteonecrosis. In man, significant increases in platelet and fibrinogen consumption were directly associated with dive depth and with repetitive exposure at lesser depths. The increased destruction of platelets and fibrinogen was not accompanied by reduced blood levels because of compensatory shifts in production rats and distribution between circulating and storage compartments. Platelet consumption was substantially greater than fibrinogen destruction with respect to both severity and duration. Platelet function inhibitors decreased platelet consumption. Increased fibrinogen consumption was sometimes associated with reduced plasminogen survival, but levels of fibrinogen/fibrin degradation products were never measurably altered from normal values. The relationships among platelet and fibrinogen consumption, vascular changes, and dysbaric osteonecrosis were studied in hyperbaric swine. Consumption of hemostatic factors was most severe with rapid, uncontrolled decompression, low oxygen concentrations, and deeper or repetitive dives. Platelet consumption induced by hyperbaric exposure resolved spontaneously with time, suggesting a repair process after the simulated diving conditions were discontinued. Interruption of increased platelet and fibrinogen consumption in the swine model required either moderation of the dive profile or a combination of drugs that inhibit platelet function (dipyridamole or sudoxicam) together with an anticoagulant (warfarin or heparin). Repeated hyperbaric exposure under conditions that uniformly produced femoral osteonecrosis and consumption of platelets and fibrinogen was associated with detectable endothelial injury and arterial intimal lesion formation. Since the diving characteristics of increasing depth and inadequate decompression were associated with both the most severe consumption and the highest frequency of intravascular bubble formation, we postulate that intravascular bubbles, formed during hyperbaria, produce osteonecrosis, perhaps through the following sequence: (1) bubble-related endothelial cell damage; (2) platelet thrombus formation with secondary fibrin deposition; (3) microvascular occlusion; and (4) platelet-dependent arterial narrowing through intimal lesion formation. The role of antithrombotic therapy in the prevention of dysbaric osteonecrosis remains to be determined.

Chronic pain states: their relationship to impairment and disability.

Chronic pain patients (101) were assigned ratings of impairment and disability and were assessed for organic pathology and pain behavior through comprehensive testing procedures. As predicted, higher ratings of impairment and disability were significantly associated with higher levels of both physical pathology and pain behaviors. These results indicate that conditioning and pathologic processes significantly influence impairment and disability ratings. Many patients showed higher disability than impairment ratings, which suggests the possibility of gainful employment in less demanding jobs. However, the current disability system rewards sickness and dysfunction and discourages patients from resuming work.

Bone collagen in dysbaric osteonecrosis.

Experimental dysbaric osteonecrosis associated with inadequate decompression has been induced in mature female swine. The bone collagen from the radiologically defined lesion in the femur has been analyzed. The total collagen contents were the same for the epiphyseal (F-1), the metaphyseal (F-2), and the diaphyseal (F-3) regions. Soluble bone collagen content obtained by sequential extraction of the samples with acetic acid urea, guanidine, lithium chloride and potassium thiocyanate, decreased by approximately 20% in going from the F-1 to the F-2 to the F-3 regions for both experimental and control samples. The amino acid compositions and acrylamide gel electrophoresis patterns were the same for control and experimental samples. Spectral changes with the MBTH reaction were different for control and experimental collagen samples from all bone regions. The spectral shift and pattern changes which occurred from pH 4 to pH 1 suggested a higher average content of unsaturation in the collagen associated aldehyde groups in the experimental than in the control samples. These findings suggest an enhanced ability to remodel collagen which would be consistent with the histological observation of increased derangement of collagen fibers in the experimental bone samples.