[Diabetic neuropathy].
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Biomedical subjects
Publications and source records attributed to E Matikainen.
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21 diabetic patients were examined neurologically and neurophysiologically and were divided into two groups: one with neuropathy (10 patients) and the other without neuropathy (11 patients). Ultrastructural dimensions and density of capillaries in the gastrocnemius muscle were examined in 11 patients. Capillary basement membranes were significantly thicker in patients with neuropathy (p less than 0.05), whereas there was no difference in endothelial, luminal or pericytial fractions of the total capillary area. No difference was found in capillary densities of capillary/fiber (C/F) ratios. Muscle blood flow was estimated using the 133Xe clearance method in all the patients, and was found to be reduced in the 4 patients with the most severe neuropathy (p less than 0.01) even though there was no difference on the whole between the groups with or without neuropathy. The results suggest that the development of diabetic neuropathy is associated with basement membrane thickening. The causes of the basement membrane thickening are discussed.
Sixty patients with varying degrees of noise-induced hearing loss (NIHL) after long-term exposure to intense impulse noise from firearms, but without manifest clinical symptoms of vestibular pathology, were tested for body sway using a stable platform. The results were compared with those from 115 healthy referents examined in the same way. Subjects with NIHL showed significantly more body sway, estimated as movement of the centre of gravity in the horizontal plane, than did the referents. Subjects with more severe NIHL showed more sway than subjects with milder acoustic trauma. The results show that body sway is increased in patients with NIHL from exposure to impulse noise of high intensity in a way suggesting an exposure-effect relationship. This suggests subclinical disturbances of the vestibular system in these patients. The underlying mechanism may be simultaneous mechanical damage to both the cochlear and vestibular partitions by intense impulse noise.
C57BL/6J/BOM mice were given 15% (w/v) ethanol solution as their sole drinking fluid. Nerve conduction velocities (NCV) and motor coordination (ataxia) of the unanesthetized animals were examined after a single IP injection of 3.0 g ethanol/kg body weight at 6, and 9 months after the start of drinking and after 3 months of abstinence. During chronic consumption of ethanol, tolerance for relative conduction time (RCT) change developed in six months. This tolerance was not observed after 9 months of ethanol treatment. The tolerance for ataxia persisted throughout the period of ethanol treatment. After a three month's abstinence, no differences between the controls and the animals previously on ethanol were observed regarding responses to acute ethanol administration. These observations suggest that different mechanisms underlie the development of tolerance for the effect of ethanol on peripheral nerve conductance and for the ataxia from ethanol in the central nervous system.