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Abnormal proprioception of the knee joint has been documented after rupture of the anterior cruciate ligament (ACL) and may result in the loss of muscular reflexes. Excessive loading from the lack of muscular control may predispose the joint to osteoarthrosis. To investigate this problem, 10 patients were studied at an average of 31.6 months after ACL reconstruction. Three tests of joint proprioception and measurements of the vertical component of heel strike force during normal gait were used. A normal control group also was studied. For two of the proprioception tests (reproduction of passive motion and relative reproduction), there were no statistical differences among the uninjured (control) limbs, the normal contralateral limb of patients with a reconstructed ACL, and the extremity with a reconstructed ACL. In the third test (threshold of detection of motion), which previously has been shown to be adversely affected by ACL injury, the measurements for both extremities of patients with a reconstructed ACL were more accurate than those for the control group. The reconstructed extremity performed less accurately than the contralateral extremity (p < 0.05). The heel strike transient (vertical component of ground reaction force at heel strike) for uninjured and ACL-reconstructed limbs was not significantly different. In fact, the extremity with the reconstructed ACL had a lower transient than the uninjured extremity. Heel strike transients in patients with a reconstructed ACL were higher than those in the controls, but the differences were significant only when corrected for velocity of gait. These results indicate that a well done ACL reconstruction with appropriate rehabilitation can result in proprioception that is essentially equal to that of the contralateral limb. 相似文献
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Insulin regulation of Na/K pump activity in rat hepatoma cells 总被引:3,自引:0,他引:3
Insulin rapidly increases Na/K pump activity in HTC rat hepatoma cells in tissue culture, as measured by the ouabain-sensitive influx of the potassium analogue 86Rb+. Increased influx is observed within minutes and is maximal (70% above control) within 1-2 h. The effect appears to be mediated by the insulin receptors, as: the concentration dependence on insulin is identical to that for insulin induction of tyrosine aminotransferase and stimulation of 2-aminoisobutyric acid transport, proinsulin is 6% as potent as insulin, and the effect is blocked by anti-receptor antibodies. The early stimulation of potassium influx is not blocked by cycloheximide and is not associated with an increased number of pump sites as measured by 3H-ouabain binding. The insulin effect is blocked by amiloride, which blocks sodium influx, and is mimicked by the sodium ionophore monensin, which increases sodium influx and intracellular accumulation. Insulin also rapidly increases the initial rate of 22Na+ influx, suggesting that insulin may enhance Na/K pump activity, in part, by increasing intracellular sodium concentration. Incubation of HTC cells with insulin for 24 h causes complete unresponsiveness to the insulin induction of transaminase and stimulation of amino acid transport, a phenomenon mediated by postbinding mechanisms. In contrast, similar incubation with insulin does not cause unresponsiveness to the insulin stimulation of Na/K pump activity. Therefore, the site of regulation of responsiveness to insulin must be distal to, or separate from, those events causing stimulation of ion fluxes. 相似文献