The recurrence rate after ten years was 30%, and a higher final HVA resulted in higher pain levels. The limitations imposed by nonvalidated outcome measures precluded conclusions about the influence of HVA on function or quality of life.
Nitric oxide synthase (NOS) isoforms I and III were localized in the guinea pig cochlea by indirect immunohistochemistry using frozen sections and paraffin sections. NOS I staining was observed in the cytoplasm of outer hair cells, in nerve cell somata and fibers of the spiral ganglion, and in axonal profiles of the spiral lamina next to the base of inner hair cells. In addition, lining cells of the inner sulcus and limbus, and cells of the spiral ligament stained for NOS I but vascular walls remained unstained. NOS III reactivity was seen in the cytoplasm of outer and inner hair cell, in lining cells of the limbus, and on the endolymphatic surface of marginal cells. Staining for NOS III of spiral ganglion perikarya showed varying intensity. Endothelial cells of cochlear glomeruli reacted for NOS III. NOS III in vascular endothelial cells implies regulatory effects of nitric oxide (NO) on vascular wall tonus and cochlear blood supply. NOS I in cochlear neurons indicates these cells as possible sources for NO during neuronal activity. Activated neurons may provide NO that adjusts cochlear perfusion to neuronal activity. Finally, NO that is liberated from hair cells or afferent synaptic terminals may act as an inhibitor on N-methyl-D-aspartate (NMDA) receptors (negative feed-back inhibition).
Eleven patients with limited joint mobility and neuropathy were enrolled in a physical therapy program of passive joint mobilization at a rate of two sessions per week. Treatment resulted in a significant improvement in joint mobility after 10 sessions. Further improvement after 20 sessions did not reach the level of statistical significance, although near-normal joint mobility was attained. After completion of therapy, there was a progressive deterioration in joint mobility. No serious adverse effects were noted during treatment. This study provides some evidence that use of physical therapy may result in significant, although temporary, improvement in the mobility of the ankle and foot joints in diabetic patients with limited joint mobility and neuropathy. As limited joint mobility has been associated with the development of abnormally high pressures under the feet, which in turn may contribute to plantar ulceration in the susceptible neuropathic foot, the results indicate that physical therapy may be useful in the prevention of plantar ulceration in diabetic patients with limited joint mobility and neuropathy, although this must be verified by additional research.
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