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Denson G. Fujikawa 2+ within the early Eighties it was once well-known that over the top Ca inflow, most likely via 2+ 2+ voltage-gated Ca channels, with a resultant bring up in intracellular Ca, used to be linked to neuronal loss of life from cerebral ischemia, hypoglycemia, and standing epilepticus (Siejo 1981). Calcium activation of phospholipases, with arachidonic acid accumulation and its oxidation, producing unfastened radicals, used to be considered a possible mechanism wherein neuronal harm happens. In cerebral ischemia and a pair of+ hypoglycemia, strength failure was once considered the cause of over the top Ca inflow, while in prestige epilepticus it was once suggestion that repetitive depolarizations have been in charge (Siejo 1981). in the meantime, John Olney chanced on that monosodium glutamate, the meals additive, while given to immature rats, was once linked to neuronal degeneration within the arcuate nucleus of the hypothalamus, which lacks a blood-brain barrier (Olney 1969). He up this statement with a sequence of observations within the Nineteen Seventies that management of kainic acid, which we now recognize prompts the GluR5-7 subtypes of glutamate receptor, and different glutamate analogues, triggered not just post-synaptic cytoplasmic swelling, but additionally dark-cell degeneration of neurons, while considered through electron microscopy (Olney 1971; Olney et al. 1974).

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There are several available approaches for the treatment of this condition. Vocal fold medialization is currently used by most otolaryngologists and is probably the standard of care for treating this condition. An alternative approach is laryngeal reinnervation, which has a number of potential advantages over medialization but which requires several months before a final result is achieved. e. to determine whether the theoretical advantages of reinnervation are actually achieved, and whether they outweigh the disadvantage of having to wait for them.

The strength and propulsion tests will be repeated for all subjects at the end of the 12 week period. The data will be analyzed to compare the shoulder joint forces, moments, patterns of muscle activity and reports of shoulder pain during WCP in the three seat positions and before and after the exercise program. Statistical significance of the findings will be determined by repeated measures MANOVA analyses with grouping factors for SCI level and exercise/control groups. ; Postdoctorate Fellow; University of Alberta Edmonton T6g 2E1, Canada Edmonton, Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant): The goal of this project is to evaluate the long-term efficacy of intraspinal microstimulation (ISMS) in restoring leg function after spinal cord injury (SCI).

These different functions are linked to differences in the length trajectory (sequence of length change) in relation to the motor activity of the muscles. Although we know that all three of these functions are performed by humans in walking and running, we know little of the conditions under which individual muscles operate while performing each function. Further we have no empirical data on the quantitative importance of each function to the cost of locomotion. The specific aims of this project are to: 1) Examine the in vivo contractile parameters (operational lengths, length trajectories, and amounts of series elasticity) for muscles that are active only while performing positive work in running and jumping; 2) Examine the prediction that during running and jumping actively lengthening muscles function to help stabilize the movement; 3) Quantify the relative energetic importance of the different mechanical functions served by muscles during running; 4) Measure the efficiency of fast and slow muscles under conditions of varying power output; 5) Quantify the influence of velocity dependent activation and deactivation on mechanical function of fast and slow muscles.

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