A developmental-contextual approach to understanding sexuality education course content is used in this national study. Examining policy as a factor that may influence young people's environments and hence their development is an important role for developmental research. Using data from the CDC's School Health Policies and Programs Study (SHPPS) 2000 and the Alan Guttmacher Institute's State Policies in Brief Report (Alan Guttmacher Institute, 2001), three general topic areas are addressed. First, can school level be differentiated by the sexuality education topics taught at various school levels? Second, are there significant differences in state policies that regulate school-based sexuality education targeting different school levels? Third, how do state and classroom level variables contribute to variance in the likelihood of a given topic being taught as part of school health education? The two sources of data provide a nationally representative sample of 1,201 teachers and state level data from Department of Education administrators and policies from all 50 states. These data were analyzed using stepwise discriminant analysis and Hierarchical Linear Modeling (HLM). This study resulted in three primary findings. First, both state policies and classroom content were significantly different by school level. Second, state policy was not a good predictor of the course content being taught in the classroom. Third, teachers' desires for additional training significantly predicted the sexuality education course content taught in schools. Implications for both research and practice were discussed.

T cell development is regulated by signals generated in the interactions between developing thymocytes and the thymic stroma. Using fetal thymus organ culture (FTOC) as a model of T cell development, we investigated the ability of two potent signal modulators to influence this process. These studies show that both nicotine and tumor necrosis factor-alpha have the ability to influence T cell receptor (TCR) signaling and the maturational capacity of treated cultures. FTOC treated with low concentrations of nicotine produced more immature T cells and fewer mature T cells. These expanded populations of cells also expressed CD69, CD95 (FAS) and elevated levels of recombinase activating genes (RAG). This phenotype reflects the fact that these cells have received a positive selection signal, are for apoptosis and are likely attempting secondary TCR rearrangements. Nicotine effects were partially blocked by the nicotinic antagonist, d-tubocurarine. Furthermore, d-tubocurarine alone blocked the development of T cells entirely, suggesting the presence of an endogenous ligand that may engage nicotinic acetylcholine receptors and regulate normal thymopoeisis. These observations underscore the linkage between the nervous and the immune systems, not only in terms of shared resources, but also in terms of direct interactions between these two systems. In another study we used FTOC and an associated in vitro Type 1 diabetes mellitus model to reconcile the role of TNF-alpha in thymopoiesis with its role in diabetes. Our data indicate that thymocytes from NOD FTOC express lower levels of TNF receptors and produce more TNF-alpha compared to non-diabetic C57BL/6 (B6) FTOC. Neutralization of endogenous TNF-alpha in NOD FTOC with a soluble TNF receptor (sTNF R1) rescued insulin production in our in vitro diabetes model. NOD FTOC treated with TNF-alpha produced greater numbers of mature T cells and a higher percentage of cells expressing CD95L (Fas ligand). Treatment with sTNF R1 had the opposite effect. TNF-alpha's known ability to attenuate TCR signaling coupled with these observations suggest that its overproduction in these animals may be driving T cells to maturity, altering the process of negative selection and ultimately enhancing the survival of potentially diabetogenic T cells resulting in disease susceptibility in these animals.

There is general agreement that biological aging is accompanied by some physiological and cognitive declines. However, there is considerable variability in the nature and rate of such declines. Recently, investigators have begun to consider an individual differences approach to examine factors, other than age, that may account for age-related variance in cognitive functioning. Activity levels have been suggested as one factor that may mediate cognitive changes with age. The current study attempts to employ both aerobic and cognitive activity as interventions, with a group of older adults, to examine whether such interventions can improve cognitive performance or prevent further decline. A total of 54 participants (aged 66-96 years old), engaged in either an aerobic exercise class, a cognitive training class, or a non-intervention control group. Individuals in the treatment groups met three times per week, for one-hour classes, which lasted for 16 weeks. They were administered a battery of cognitive tasks, including memory recall, verbal fluency, and working memory/span measures, as well as questionnaires tapping mood and well-being. Following the intervention period, both the aerobic group and the cognitive group showed improvements on measures of verbal fluency. In addition, the cognitive group evidenced significant improvements on measures of memory recall and the aerobic group showed a decrease in negative affect. The control demonstrated a significant decline in both memory recall and verbal fluency. The results are discussed in terms of the possible mechanisms involved in producing these changes.

Embryonic trichloroethylene (TCE) exposure was previously shown to be associated with an increased incidence of cardiac birth defects. Although embryo data are lacking exposure studies on adult animals show an association between halogenated hydrocarbon exposure and modifications in gene expression. The present study was undertaken to identify embryonic mRNA transcripts differentially expressed following TCE or metabolite exposure. This study identified numerous differentially regulated transcripts following halogenated hydrocarbon exposure. Examples of upregulated transcripts include stress responsive genes (Hsp 70, Hsp 70 cognate), a Ca²⁺-ATPase, calreticulin and serum response factor while downregulated transcripts include Midkine (RARP), numerous ribosomal proteins (8s, 18s, 24s), p137 and vimentin. p137 was a candidate sequence marked for further study to determine whether this sequence could be utilized as a molecular marker of TCE exposure. p137 showed a correlation between increased levels of maternal TCE exposure and decreased levels of transcript expressed in E11 fetal tissue. Immunohistochemical staining using an affinity purified antibody to p137 demonstrates widespread expression in rat E11 and chicken St. 17 embryos. p137 protein is broadly expressed in chicken St. 13 through St. 22 heart, but by St. 29 becomes more restricted in the ventricular myocardium with continued endocardial expression. At stages between St. 13 and St. 17 in chick embryos the ectodermal epithelium, yolk sac epithelium, dermatome, developing optic vesicle and neural tube express p137 protein. To explore potential function of p137, atrioventricular explants were exposed to affinity purified p137 antibody. Results show that p137 antibody treatment blocks epithelial-mesenchymal transformation of endothelial cells in-vitro. This study shows that p137 is expressed during rat and chicken mid-gestation in heart and other epithelial tissue derivatives and appears to play a role in the epithelial-mesenchymal transformation of the cardiac atrioventricular cushions. p137 is identified as a useful marker of developmental exposure to halogenated hydrocarbons and its altered expression may contribute to the phenotype of the affected heart.

Estimation of antemortem body weight is difficult to ascertain from skeletal material. In this analysis, I examine 49 right tali. T-tests run on right and left tali from the same sample show no significant differences between the two sides. Incorporation of data from various individuals, including both males and females, allows for the statistical assessment obtained through Pearson's correlation coefficient between estimated antemortem body weight and 21 measurements conducted on the surface of the talus. All correlations ranged from R = -.1706 to +.4811, suggesting no strong relationship between estimated antemortem body weight and variables utilized in this analysis. A multiple regression was applied and provided an adjusted R square of +.2150. This suggests the measurements incorporated into the statistical run only accounted for twenty-one percent of the total variance in estimated body weight. The surface anatomy of the talus relates more to an interplay between form and function than to weight-bearing.

The effect of the menstrual cycle on energy intake and the dieting habits of adolescents was examined retrospectively for three years in 64 eighth and ninth grade girls. Dieting episodes were found to be evenly distributed across the five menstrual phases with no greater proportion of dieting occurring during the follicular phase. Media, peers, family members, and social pressures have a larger impact on adolescent dieting behaviors as opposed to the menstrual cycle. Comparisons of energy intake between the pre- and postovulatory phases revealed no significant differences in any year. Fifty to eighty percent of the girls' cycles may have been anovulatory the first two years of the study. Variations in energy intake are not observed in anovulatory cycles due to low ovarian hormone levels. Changes in food consumption that correspond to menstrual phases may be observed in girls who are six years or more beyond menarche, when cycles are predominantly ovulatory.

In aging vertebrates, subpopulations of limbic and periventricular astrocytes accumulate peroxidase-positive cytoplasmic inclusions distinct from lipofuscin. In rodent brain, chronic estrogenization accelerates the appearance of this senescent glial phenotype. Identical inclusions are rapidly induced in primary neuroglial cultures by cysteamine exposure. Abnormal mitochondria replete with redox-active iron and other transition metals are the subcellular precursors of the inclusions in situ and in cysteamine-treated cultures. The objective of this thesis was to elucidate mechanisms responsible for the biogenesis of these glial inclusions in the aging nervous system. / We determined that the accumulation of astrocytic inclusions in cysteamine-treated rat glial cultures occurs in the context of an antecedent cellular stress response characterized by (i) the upregulation of heat shock proteins (HSP) 27, 72, 90, ubiquitin and heme oxygenase-1, and (ii) enhanced resistance of cysteamine-stressed astroglia to subsequent oxidative injury. Furthermore, multiple injections of cysteamine or estradiol valerate in adult male rats induced robust overexpression of stress proteins and an accretion of identical peroxidase-positive granules in GFAP-positive astroglia. Both in situ and in cysteamine-treated cultures, HSP27, ubiquitin, glucose-regulated protein 94 and to a lesser extent, HSP72 (but not HSP90 or $ alpha$B-crystallin) exhibited immunolocalization to these astrocytic "stress" inclusions. We observed that exogenous $ rm H sb2O sb2$ induces identical inclusions in cultured astroglia and that cysteamine-derived $ rm H sb2O sb2$ promotes lipid peroxidation in isolated astroglial mitochondria. These data indicate that sustained oxidative stress may represent a "final common pathway" leading to the transformation of normal mitochondria to peroxidase-positive astrocytic inclusions in the aging nervous system. / The metal-dependent peroxidase activity of these glial inclusions has been shown to oxidize dopamine and other catechols to neurotoxic free radicals in vitro, implicating these cells in the pathogenesis of parkinsonism and other free radical-related neurodegenerations. Since peroxidase-positive astroglia have been identified in aging human striatum, the findings presented here suggest that antioxidant therapy coupled with pharmacological inhibition of metal sequestration by "stressed" astroglial mitochondria may prove useful in the management of Parkinson's disease and other age-associated neurodegenerative afflictions.

There is evidence that amyloid deposition within the brain is of major importance in the pathogenesis of Alzheimer's disease (AD), but the mechanism of this deposition is not known, and several theories are currently under great debate. The present study of intraneuronal changes in the human brain with age and disease suggests a new explanation for amyloid plaque formation in the pathogenesis of AD. / This work indicates that intraneuronal inclusions originally observed by Rees (1975), may contain amyloid peptide (Abeta), the beta-pleated form of which is the major component of the amyloid plaques in AD. We have therefore called them amylosomes. Using the techniques of histology, immunohistochemistry, computerized morphology, as well as protein isolation and analysis, we examined the distribution, size, density and chemical composition of amylosomes in the human brain throughout life. Amylosomes appear during early childhood and remain constant in size and number until advanced old age. Their protein content and immunostaining characteristics indicate they contain Abeta, and their dendritic location in regions where AD plaques form suggested a possible role in Abeta transport from the brain to the CSF. We therefore isolated and quantified human brain microtubule proteins (MT) and the dendritic microtubule-associated protein 2 (MAP2), assessed their ability to polymerize in vitro, quantified the MAP2 mRNA with age, and related these results to the apolipoprotein E (APOE) genotype, which is known to modulate the risk of AD. There was an age-related decrease in MT proteins and MAP2 and in their ability to polymerize, that was accelerated in individuals with APOE epsilon4 allele(s), the group at greatest risk of AD. These results are consistent with the proposal that amylosomes play a role in Abeta metabolism, and an age-related decrease in the dendritic MT transport system could lead to retention of amylosomes, within the brain, with deposition of the Abeta and plaque formation as a consequence. This theory can account for most of the important features of AD, and resolves a number of contradictory hypotheses, as well as suggesting relevant area for further investigation. A better understanding of the pathogenesis will hopefully reveal strategies for prevention and treatment of this common and presently incurable disease.

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There are increasing numbers of preterm children of very low and extremely low birth weights surviving due to advances in neonatal care. The majority of these children attend mainstream classrooms and perform in the low average range on cognitive measures compared to peers. However, outcome studies document a range of subtle, clinically important impairments in their motor, visual-motor and visual perceptual performance compared to peers. The impact of these impairments on a complex, occupational task such as handwriting performance has never been investigated in the preterm population using an objective measure, except through parent or teacher questionnaires. / The primary objective of this doctoral thesis was to characterize and compare handwriting performance in preterm children (birth weight of ≤1250 grams) attending Grade One, to typically developing peers matched by age, gender and classroom. Standardized outcome measures were used to examine handwriting performance, sensorimotor component skills and psychosocial factors. Preterm survivors demonstrated significantly lower handwriting legibility and slower speed scores compared to matched peers. Visual perception and motor accuracy were identified as predictors of legibility; and in-hand manipulation (translation) and finger identification were associated with handwriting speed in preterm children. However, in typically developing children, legibility was associated with upper extremity steadiness, visual motor control and in-hand manipulation (rotation); and speed was associated with in-hand manipulation (translation) and upper limb speed and dexterity. These findings have important implications for clinical practice in guiding both evaluation approaches and intervention strategies. Clearly, preterm survivors are at high risk for developing handwriting difficulties at school-age. Increasing awareness may help with early identification and intervention with a view towards minimizing the negative effects on self-esteem and academic achievement often documented in children with handwriting difficulty.