Community stop-smoking contests in the COMMIT trial: relationship of participation to costs. Community Intervention trials.

BACKGROUND: This study quantifies resources used to conduct 26 community-wide quit-smoking contests, the percentage of smokers that participated in these contests, and the statistical associations between resource inputs and participation percentages. METHODS: Data collected from the 11 COMMIT intervention communities (adult population range 47,490-185,913) included number of contest participants, contest procedures, and resource inputs. Stepwise regression was used to find the most meaningful association(s) of independent variables with contest participation percentage. RESULTS: Contest participation percentages ranged from 0.27 to 3.11% of smokers (mean = 1.26%). Total cost (COMMIT and community-contributed resources and dollar expenditures) to conduct a contest averaged $24,857 (range $5,751-$74,556), or $78.57 per contest participant. Expenditures in various specific resource categories varied greatly. Total expenditures per smoker in the community (excluding expenditures for prizes) was the independent variable most highly correlated with contest participation percentage, accounting for 63% of the total variability in participation percentages. CONCLUSIONS: The percentage of smoker participation in community-wide stop-smoking contests appears primarily to be a function of total resource expenditures, regardless of the specific types of resources funded. Stop-smoking contests are judged to be quite cost effective. Study strengths and weaknesses are discussed.

Glial cytokines as neuropathogenic factors in HIV infection: pathogenic similarities to Alzheimer's disease.

The mechanisms by which human immunodeficiency virus (HIV) infection provokes progressive neurodegeneration and dementia in acquired immunodeficiency syndrome (AIDS) remain obscure. In HIV-infected (HIV+) individuals, we found that the brain cells preferentially infected by HIV, viz. the microglia, were abundant, activated, and intensely immunopositive for interleukin-1 alpha (IL-1 alpha), an immune response-generated cytokine that increases the synthesis and processing of beta-amyloid precursor proteins (beta-APP) and promotes proliferation and activation of astroglia. We also found an increase in the number of activated astroglia expressing elevated levels of S100 beta, a cytokine that increases intraneuronal calcium levels and promotes excessive growth of neuronal processes (neurites). These glial changes were accompanied by increased expression of beta-APP immunoreaction product in neurons and overgrown (dystrophic) neurites. In addition, some neurons contained monoclonal antibody Tau-2 immunopositive, neurofibrillary tangle-like structures. Our findings provide evidence that glial activation with increased expression of IL-1 alpha and S100 beta may be important in the neuropathogenesis of AIDS dementia. We propose that HIV infection promotes excessive microglial IL-1 alpha expression with consequent astrogliosis and increased expression of S100 beta. Overexpression of these two cytokines may then be involved in AIDS neuropathogenesis by inducing gliosis, growth of dystrophic neurites, and calcium-mediated neuronal cell loss in AIDS.

Increased S100 beta neurotrophic activity in Alzheimer's disease temporal lobe.

The confirming diagnosis of Alzheimer's disease includes an assessment of the concentration of neuritic plaques in the temporal lobe of the brain. The presence of abnormal levels of neurotrophic factors in Alzheimer's disease is one possible explanation for the increased concentration of aggregates of overgrown neurites in the neuritic plaques of Alzheimer's disease. The protein S100 beta, a neurotrophic factor produced by astroglia in the brain, induces neurite outgrowth in cerebral cortical neurons. The generation of specific S100 beta antibodies, the cloning of a full-length cDNA encoding the S100 beta mRNA, and the development of a neurite extension assay system for S100 beta allowed testing of the hypothesis that Alzheimer's disease S100 beta expression is elevated in brain temporal lobe where neuritic plaques are concentrated. The levels of S100 beta protein, mRNA, and specific neurotrophic activity were elevated 10-20-fold in extracts of temporal lobe from autopsy samples of Alzheimer's disease patients compared to those of aged control patients. The cells containing the increased S100 beta were reactive astrocytes; the neuritic plaques were surrounded by S100 beta-containing astrocytes. The elevated levels of S100 beta provides a link between the prominent reactive gliosis and neuritic plaque formation in this common disease of the elderly and raises the possibility that S100 beta contributes to Alzheimer's disease neuropathology.

Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease.

Interleukin 1, an immune response-generated cytokine that stimulates astrocyte proliferation and reactivity (astrogliosis), was present in up to 30 times as many glial cells in tissue sections of brain from patients with Down syndrome and Alzheimer disease compared with age-matched control subjects. Most interleukin 1-immunoreactive glia in Down syndrome and Alzheimer disease were classified as microglia. The number of interleukin 1 immunoreactive neurons did not appear to differ in Down syndrome and Alzheimer disease compared with control brain. Numerous temporal lobe astrocytes in Alzheimer disease and postnatal Down syndrome were intensely interleukin 1-, S-100-, and glial fibrillary acidic protein-immunoreactive and had reactive structure. Interleukin 1 levels in Alzheimer disease temporal lobe homogenates were elevated, as were the levels of S-100 and glial fibrillary acidic protein, two proteins reportedly elevated in reactive astrocytes. These data suggest that increased expression of S-100 in Down syndrome, resulting from duplication of the gene on chromosome 21 that encodes the beta subunit of S-100, may be augmented by elevation of interleukin 1. As a corollary, the astrogliosis in Alzheimer disease may be promoted by elevation of interleukin 1.

Topographic organization and collateralization of the projections of the anterior and laterodorsal thalamic nuclei to cingulate areas 24 and 29 in the rat.

Fast blue and Rhodamine microspheres were used to analyze the topography and collateralization of the limbic nuclei of the thalamus to 4 defined areas of the cingulate gyrus (anterior 24, posterior 24, anterior 29, and posterior 29). The anterodorsal nucleus and the anteroventral nucleus project to posterior area 24 and all of area 29. The anteromedial nucleus projects generally to both areas 24 and 29, but principally to anterior area 24. The laterodorsal nucleus projects only to area 29. The anterior and posterior portions of the thalamic nuclei topographically project to the anterior and posterior regions of the cingulate gyrus, respectively. Neurons in the medial region of the anterior nuclei project to the anterior area of the cingulate gyrus while neurons located in the lateral region project to posterior areas. Collaterals (9-13%) from the anteromedial nucleus project diffusely to areas 24 and 29, while collaterals from other nuclei project primarily to areas adjacent to each other. Modulation of limbic system functions probably occurs via these projection fibers. Furthermore, the idea appears to be reinforced that at least a dual and coupled function exists for these direct thalamocingulate connections.

Innervation of the superficial pineal of the rat using retrograde tracing methods.

Fast blue (FB), rhodamine microspheres (RH), horseradish peroxidase (HRP), and wheat germ agglutinin-horseradish peroxidase conjugate (WGA-HRP) were used as retrograde tracers to study the innervation of the rat superficial pineal gland (SP). One of the tracers was injected into the gland of each animal. All four retrograde tracers injected into the gland always labeled neurons in the superior cervical ganglia (SCG). No retrograde labeling was ever seen in the suprachiasmatic nuclei, paraventricular hypothalamic nuclei, lateral hypothalamus, habenular nuclei, amygdalar nuclei, or superior salivatory nuclei. Retrograde labeling was seen in the anterior hypothalamic nuclei, anterior thalamic nuclei, lateral geniculate bodies, and midbrain tectal structures when a tracer spread from the injection site to the overlying cortex, tectum, or commissures. Control studies included injection of tracer into the subarachnoid space around the SP or into structures adjacent to the SP. Only the injection of FB or WGA-HRP into the subarachnoid space labeled neurons in the SCG. This labeling was probably due to the spread of tracer to the choroid plexus. These results agree with recent work confirming the existence of a direct projection of the SCG into the interstitium around pinealocytes. The evidence does not substantiate an innervation originating in the habenular nuclei; the superior salivatory nuclei; or any other diencephalic, midbrain, pontine, or medullary structure.