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The etiology and pathophysiology of Paget's disease of bone are not yet entirely defined. There is evidence suggesting the participation of the immune system in the pathophysiology of this disease. Hence, we examined T cell mitogenic proliferation, NK cell activity, T cell subsets, interleukin-1 (IL-1), and interleukin-6(IL-6) production by peripheral mononuclear cells and IL-6 levels in the peripheral blood sera of 17 Paget's patients aged (74.5 +/- 2.4 years) and of 17 elderly control subjects (74.7 +/- 2.2 years). Pagetic patients were found to have immunological parameters not significantly different from those of the elderly control group. Moreover, the results obtained from Paget's patients with the active form of the disease did not differ from those of patients with inactive disease. Therefore, at least on the basis of the parameters used in this study, it is possible to conclude that the cellular immunity of Paget's patients is not different from that of elderly control subjects and that the role of IL-1 and IL-6 in this disease should be reviewed.

RNA viruses with segmented genomes were the first model used for molecular analysis of viral neuropathogenesis, since they could be analysed genetically by reassortment. Four viruses with non-segmented genomes have been used as models of neurovirulence and demyelinating disease: JHM coronavirus, Theiler's virus, Sindbis virus and Semliki Forest virus (SFV). Virus gene expression in the central nervous system of infected animals has been measured by in situ hybridization and immunocytochemistry. Cell tropism has been analysed by neural cell culture. Infectious clones have been constructed for Theiler's virus, Sindbis virus and SFV, and these allow analysis of the sequences involved in the determination of neuropathogenesis, through the construction of chimeric viruses and site-specific mutagenesis. Measles and rubella viruses have been studied in animal systems because of their importance for human disease. The importance of two recently discovered mechanisms of neuropathogenesis, antibody-induced modulation of virus multiplication, and persistence of virus in the absence of multiplication, remains to be assessed.

Immunogold-silver staining of mixed rat cerebellar neuron/glial cell cultures, using Ranscht monoclonal antibody, resulted in labelling of neuronal processes and oligodendrocytes. This antibody was originally believed to react with galactocerebroside alone, and it was concluded that labelling by it resulted from the presence of myelin [2]. Electron microscopic examination of the cultures did not reveal myelination. Infection of such cultures with rubella virus resulted in a cytopathic effect. This effect was initially characterized as a disaggregation of neuronal processes, and the disruption of a layer of membranous material covering both cell bodies and processes. The virus causes disruption of cultures of pure glial cells, but there is no evidence of virus multiplication or cytopathic effect in pure neuron cultures. The cytopathic effect in mixed neuron/glial cell cultures is concluded to be glial cell mediated.

Fifty volunteers slept two nonconsecutive nights in a sleep laboratory under electropolygraphic control. They were awakened for one report per night. Awakenings were made, in counterbalanced order, from slow wave sleep (SWS--stage 3-4 and stage 4) and rapid eye movement (REM) sleep. Following dream reporting, subjects were asked to identify memory sources of their dream imagery. Two independent judges reliably rated mentation reports for temporal units and for several content and structural dimensions. The same judges also categorized memory sources as autobiographical episodes, abstract self-references, or semantic knowledge. We found that REM reports were significantly longer than SWS reports. Minor content SWS-REM differences were also detected. Moreover, semantic knowledge was more frequently mentioned as a dream source for REM than for SWS dream reports. These findings are interpreted as supporting the hypothesis that dreaming is a continuous process that is not unique to REM sleep. Different levels of engagement of the cognitive system are responsible for the few SWS-REM differences that have been detected.