Diabetes is known to be one of the risk factors for dementia; however, neuropathic changes in the brain of patients with the disease have not been completely revealed. So in the present study, we investigated the brain function of rats with diabetes induced by streptozotocin (STZ), one of the most commonly used animal models for diabetes. In the diabetic rats, immediately working memory performance was impaired in the Y-maze task and neuronal cytoskeleton proteins such as calbindin, synaptophysin, and syntaxin were reduced. Furthermore, morphological observation by Golgi staining showed a decrease in the number of basal dendrites and abnormality of spine structure. Next, we measured the content of brain-derived neurotrophic factor (BDNF) in the diabetic brain, because BDNF is one of the essential proteins for the maintenance of neuronal functions including synapse function and neuronal transmissions. In the diabetic brains, both protein and mRNA levels of BDNF were severely reduced. These results suggest that, in diabetes, synapse dysfunction is, at least in part, caused by a failure of BDNF synthesis in the brain.

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PubMedDate not supplied

Factor V deficiency in a patient with rheumatoid arthritis.

Factor V deficiency associated with rheumatoid arthritis was found in a 54-year-old woman. Hereditary factor V deficiency is very rare; only about 150 cases have been reported since its discovery in 1943. This appears to be the first case report of factor V deficiency associated with rheumatoid arthritis in the literature.

Arthritis, Rheumatoid↗

PubMedDate not supplied

Canine distemper myoclonus and sleep: observation of a case.

Evolution of myoclonus was analysed electromyographically throughout quiet wakefulness, NREM sleep and REM sleep in a dog with canine distemper myoclonus. Compared with quiet wakefulness, the frequency of myoclonus was decreased and the intensity of discharges in individual myoclonic bursts was also lowered during NREM sleep. When NREM sleep shifted to REM sleep, neither of these parameters was noticeably altered. However, as REM sleep continued, the former was increased markedly and the latter was further attenuated. In general, violent motor activity was concurrent in the limbs, trunk and/or head. Thus, the increase in the frequency of myoclonus seemed to be similar in nature to the phasic event during REM sleep. This indicated that lower motoneurons producing myoclonic discharges responded well to supraspinal influences. In successive myoclonic bursts, a significant and consistent positive correlation existed between the silent period and the subsequent discharge period throughout the three different levels of consciousness, that is, the longer the silent period, the longer the subsequent episode of myoclonus. Therefore, this feature may be intrinsic to myoclonic firing of lower motoneurons in canine distemper myoclonus. These findings may support the idea that hyperexcitability of the lower motoneurons is primarily responsible for the genesis of canine distemper myoclonus.

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