A replication study of Reducing the Risk, a theory-based sexuality curriculum for adolescents.

Reducing the Risk is a theory-based, sexuality education curriculum shown to influence the knowledge and behaviors of secondary students. This study determined whether the behavioral effects of the curriculum could be duplicated in a southern, rural state. In a quasiexperimental design, pretest and posttest inventories were administered to students in treatment and comparison groups to determine the influence of Reducing the Risk on sexual behaviors. Results of the 18-month study indicated students receiving the curriculum significantly delayed initiating sexual intercourse. Sexually active students in the treatment group were significantly more likely to protect themselves from STD/HIV and pregnancy than sexually active students in the comparison group. In addition, students receiving Reducing the Risk showed a significant increase in parent-child communication about sexual issues. These results reinforce previous research that found positive behavioral effects for students receiving the Reducing the Risk curriculum.

A quantitative histological study of early clinical and preclinical Alzheimer's disease.

Brains from 70 unselected general hospital necropsy cases aged 60-95 years were surveyed histologically for changes of Alzheimer's disease using Congo Red-Gallocyanin preparations. Counts were made of neurofibrillary tangles in two areas of the neocortex, the hippocampal formation and the substantia innominata. Neurons were counted in the subiculum of the hippocampus, the substantia innominata and the locus coeruleus. In addition, a retrospective enquiry was made concerning the mental health of the patients in the study; cognitive performance was graded on the Global Deterioration Scale (GDS 1-7). Four cases (5.7%) had clinical and pathological changes amounting to early Alzheimer's disease. Tangles were very numerous in all areas and there was a 30% deficit or more of neurons in at least two of the structures counted. Although the diagnosis of Alzheimer's disease was not recorded during life, all had shown signs of early cognitive decline (GDS grades 3-6). A further six cases (8.6%) showed excessive tangle accumulation which may represent preclinical Alzheimer's disease. Tangles were present in the temporal neocortex (Brodmann area 22), whereas they were absent in the remainder of the survey. Tangle density in the hippocampal formation (greater than 50 tangles in a 10 microns section) was also above the baseline level of the majority of cases. However, neuron loss was not widespread in these cases and none had shown evidence of cognitive impairment. The findings confirm that the early stages of Alzheimer's disease commonly occur amongst general hospital necropsies. The emergence of clinical signs of dementia appears to be related to the loss of a critical volume of neurons and not to tangle accumulation alone.

Age-related variations in the neuron content of the cerebral cortex in senile dementia of Alzheimer type.

The cell content of the cerebral cortex in senile dementia of Alzheimer type has been examined using a stereological method which combines gross cortical measurements and microscopical observations to give volumetric data on cells and neuropil. In the neocortex only the large (greater than 12 micron diameter) neuron fraction was found to be abnormal; the volume of these cells was reduced in most patients aged less than 80 years, but was not usually abnormal for age in older cases. Smaller neurons and glial cells showed no consistent change from normal values. Neuropil was diminished in both age groups, so that patients over 80 years of age tended to show cerebral atrophy without neocortical neuron loss. By contrast to the neocortex, the subiculum of the hippocampus consistently showed pathological neuron loss in both age groups.

The effect of advanced old age on the neurone content of the cerebral cortex. Observations with an automatic image analyser point counting method.

The effect of advanced old age on the nerve cell content of the cerebral cortex was examined in 19 non-demented persons aged 69-95 years, using a Quantimet 720 image analysing computer to make area proportion measurements. Neurone loss around 1.0% per annum was found both in the neocortex and in the medial hippocampus. There was also significant shrinkage of neurones in the hippocampus. Macroscopic measurements of the cerebral hemispheres by means of point-counting morphometry showed a corresponding reduction in the volume of white matter amounting to about 0.8% per annum, but only a minor change in the cortex volume. This finding is consistent with the occurrence of dendritic growth of surviving neocortical neurones. By contrast, there appears to be no compensatory dendritic proliferation in the medial hippocampus since tissue atrophy was commensurate with cell loss in this region.

Age, senile dementia and ventricular enlargement.

Necropsy measurements of cerebral ventricular volume and pericerebral space in senile dementia patients and age-matched controls indicate that ventricular enlargement is not an accurate diagnostic marker for cerebral atrophy. Furthermore, ventricles are of normal size for age in about 40% of all senile dementia patients including those with Alzheimer's disease.

A quantitative study of cerebral atrophy in old age and senile dementia.

Cerebral atrophy was measured by comparing brain volume and cranial capacity at necropsy on 20 severely demented patients aged 64--92 years and 18 non-demented controls of similar age. The volumes of cerebral cortex and white matter and of the lobes of the cerebral hemispheres were found by point-counting morphometry. Patients with Alzheimer type dementia aged less than 80 years mainly showed pathological cerebral atrophy with global loss of cerebral tissue (P less than 0.001) whereas over 80 years of age they generally showed selective atrophy of temporal cortex (P less than 0.005). The findings support the view that disease processes, not exaggerated age change, underlie primary neuronal dementia of Alzheimer type.

Quantitative changes in the cellularity of the rat subependymal plate after X-irradiation.

The brains of young adult rats were irradiated with a single dose of 8 Gy (800 rad) of 250 kVp X-rays. Within 2 weeks of treatment the cell population of the subependymal plate was reduced by 30%. During this period the cell cycle time remained unchanged but the labelling index was reduced. The cell population subsequently returned to normal after 39-52 weeks. Damage and subsequent recovery of the plate was due mainly to changes in the number of cells with small dark nuclei. Cells with small and large light nuclei were little affected. A model for the production and differentiation of cells in the subependymal region is proposed on the basis of age-related changes in the total number and proportions of the various cell types in the subependymal plate of normal rats. This is discussed both in terms of the radiation response of cells in the plate and the manifestation of delayed white matter necrosis after higher doses.

Changes in the neuroglial cell populations of the rat spinal cord after local X-irradiation.

A 16 mm length of cervical spinal cord of young adult female rats was irradiated with 4000 rad of 250 kV X rays. Counts of astrocyte and oligodendrocyte nuclei were made in the dorsal columns of both irradiated and control cervical cords during the latent period before the onset of radionecrosis. The numbers of both astrocyte and oligodendrocyte nuclei were reduced one month after exposure to radiation. Both cell populations showed an apparent recovery but this was subsequently followed by a rapid loss of cells prior to the development of white-matter necrosis. The oligodendrocyte population in unirradiated spinal cords increased with age, and mitotic figures were observed among the neuroglia of both irradiated and control cervical spinal cords. A slow, natural turnover of neuroglial cells in the cervical spinal cord is proposed and the relevance of this to the manifestation of delayed white matter necrosis is discussed.

The dose-latent period relationship in the irradiated cervical spinal cord of the rat.

The cervical spinal cords of young adult female rats were irradiated with various single and fractionated doses of 250 kV x rays. No relationship was evident between the dose and the latent period for myelopathy after irradiation of the rats' cervical cords, i.e., there was considerable variation in the mean latent periods between different groups of animals given a fixed single dose (4,000 rads). It was concluded that the latent period for myelopathy following irradiation of the cervical cord of the rat is not a reliable experimental end point for radiobiological investigations.