ACTH therapy in infantile spasms: relationship between dose of ACTH and initial effect or long-term prognosis

The relationship between the dose of ACTH and the initial effect was investigated in 41 children with infantile spasms. More than 0.015 mg (0.6 IU)/kg/day of ACTH was needed for a good initial response of seizures and electroencephalographic abnormalities. The relationship between the dose of ACTH and long-term prognosis was investigated in 29 patients. There was no relationship between the daily or total ACTH dosage, provided the dose was greater than 0.015 mg (0.6 IU)/kg/day, and the outcome of seizures and electroencephalographic abnormalities; however, ACTH 0.04-0.06 mg (1.6-2.4 IU)/kg/day and a total ACTH dose of 1.1-1.5 mg (44-60 IU)/kg resulted in better mental development than smaller doses of ACTH. Side effects of ACTH increased with dosage. Too small or too large a dose of ACTH does not lead to better mental development. The proper dose of ACTH should be used with careful attention to potential side effects.     

Direct evidence for the up‐regulation of Vps34 regulated by PKCγ during short‐term treatment with morphine

In this study, we investigated whether PKCγ could be associated with functional changes of vacuolar protein sorting 34 (Vps34) during morphine treatment using primary cultures of cerebral cortical neurons from mice. The immunoprecipitation analysis showed that p‐PKCγ and Vps34 are present together in molecular complexes. The treatment with morphine increases PKCγ and Vps34 levels. Phosphorylation of PKCγ increased Vps34 level. The inhibition of morphine‐induced increase in PKCγ phosphorylation reduced Vps34 level. These results indicates that opioid receptor activation increases PKCγ phosphorylation in the neurons and, in turn, upregulates Vps34 during short‐term treatment with neurons. Synapse 63:365–368, 2009. © 2009 Wiley‐Liss, Inc.     

Association of NMDA receptor sites and seizures of El mice.

To investigate the possible role of N-methyl-D-aspartate (NMDA) receptors in the seizures of El mice, a genetic animal model of epilepsy, we measured [3H]3-[(+)-2-(carboxypiperazin-4-yl)][1,2-3H]- propyl-1-phosphonic acid (CPP) binding in several brain regions of El and ddY mice. At 22-24 weeks of age, the maximum number of binding sites (Bmax) of [3H]CPP was lower only in the cerebral cortex of both stimulated and unstimulated El mice (El(+) and El(-), respectively) than in that of ddY mice. A reduction in Bmax values of cortical [3H]CPP binding of El mice was detected after the age of 12 weeks. Cortical [3H]CPP binding in El(+) mice decreased further transiently after evoked seizures. No significant change was observed in El(-) mice after postural stimulation. These results suggest that El(+) and El(-) mice share seizure propensity and that activation of NMDA receptors is involved in the seizures of El mice.     

A case of neoplastic angioendotheliosis--possible mechanism of JC virus infection for the selective growth of tumor cells in the blood vessel]

A case of 55-year-old man pathologically proven as neoplastic angioendotheliosis was reported. He initially developed sensory disturbance and motor weakness in the lower extremities. After admission, he showed progressive deterioration of higher brain functions with moderate fever. Routine laboratory examinations revealed elevated serum LDH level and erythrocyte sedimentation rate without leukocytosis or increased serum globulin level. Immunological tests were normal, except positive RA. Immunocytochemical investigation of tumor cells in the blood vessel gave the results that these cells appeared to be derived from B cells. Southern blot analyses of the brain samples revealed clear positive bands corresponding to JC virus DNA in the blot. JC virus has been known to infect the endothelial cells of the blood vessel as well as urethral epithelial cells. We discussed the possible mechanism of the selective growth of tumor cells in the blood vessel in terms of possible JC virus infection to the endothelial cells of the blood vessel and abnormal recognition between tumor cells and endothelial cells.