2,032 research outputs found

    Boom Boom

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    This music clip is from the CD entitled Transformation. The band was directed by Chris Merz.https://scholarworks.uni.edu/jazzband/1023/thumbnail.jp

    Celebration Jig

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    This music clip is from the CD entitled Leap of Faith. The band was directed by Dr. Robert Washut.https://scholarworks.uni.edu/jazzband/1030/thumbnail.jp

    Disentangling Pathways of Adolescent Sexual Risk from Problem Behavior Syndrome

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    Understanding the development of adolescent sexual risk behavior is complicated by the co-occurrence of sexual risk with substance use and delinquency, conceptualized as “problem behavior syndrome,” with common causes and influences underlying all three problem behaviors (Jessor & Jessor, 1977). Explaining the development of sexual risk becomes even more complex given the changing patterns of adaptation and maladaptation over the course of adolescence (Sroufe & Rutter, 1984). Research also suggests that multiple pathways may forecast adolescent engagement in sexual risk behavior, underscoring the ideas of equifinality and multifinality in developmental psychopathology (Cicchetti & Rogosh, 1996). To understand the diverse nature of sexual risk taking, researchers must identify these pathways and disentangle co-occurring problem behaviors from sexual risk. Revealing the course of sexual risk taking and the early risk and protective processes through which problem behavior develops allows researchers to identify the developmental periods that would be most amenable to intervention efforts (Rolf et al., 1990). Using data from the National Longitudinal Survey of Youth (NLSY79), this study aimed to disentangle problem behavior syndrome by identifying the unique developmental pathways of adolescent sexual risk, alcohol use and delinquency. This study also investigated how early adolescent processes of risk and protection were associated with the growth of these risk behaviors during adolescence. Using a developmental psychopathology and resilience framework, risk trajectories were measured with adolescents aged 15 to 24, and antecedents were measured with early adolescents ages 10 to 14 (N= 1778). Using Latent Class Growth Analyses (LCGA), joint trajectory analyses revealed five distinct adolescent risk taking groups: high sex and alcohol, moderate problem behavior, problem behavior, alcohol-only, and alcohol and delinquency experimentation. Early adolescent externalizing problems were particularly important in understanding adolescent risk group membership. The co-occurrence between sexual risk and alcohol use, the diversity of problem behavior syndrome, and potential intervention and prevention efforts are discussed

    Estimating the Location and Spatial Extent of a Covert Anthrax Release

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    Rapidly identifying the features of a covert release of an agent such as anthrax could help to inform the planning of public health mitigation strategies. Previous studies have sought to estimate the time and size of a bioterror attack based on the symptomatic onset dates of early cases. We extend the scope of these methods by proposing a method for characterizing the time, strength, and also the location of an aerosolized pathogen release. A back-calculation method is developed allowing the characterization of the release based on the data on the first few observed cases of the subsequent outbreak, meteorological data, population densities, and data on population travel patterns. We evaluate this method on small simulated anthrax outbreaks (about 25–35 cases) and show that it could date and localize a release after a few cases have been observed, although misspecifications of the spore dispersion model, or the within-host dynamics model, on which the method relies can bias the estimates. Our method could also provide an estimate of the outbreak's geographical extent and, as a consequence, could help to identify populations at risk and, therefore, requiring prophylactic treatment. Our analysis demonstrates that while estimates based on the first ten or 15 observed cases were more accurate and less sensitive to model misspecifications than those based on five cases, overall mortality is minimized by targeting prophylactic treatment early on the basis of estimates made using data on the first five cases. The method we propose could provide early estimates of the time, strength, and location of an aerosolized anthrax release and the geographical extent of the subsequent outbreak. In addition, estimates of release features could be used to parameterize more detailed models allowing the simulation of control strategies and intervention logistics

    Modeling the Incubation Period of Anthrax

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    Models of the incubation period of anthrax are important to public health planners because they can be used to predict the delay before outbreaks are detected, the size of an outbreak and the duration of time that persons should remain on antibiotics to prevent disease. The difficulty is that there is little direct data about the incubation period in humans. The objective of this paper is to develop and apply models for the incubation period of anthrax. Mechanistic models that account for the biology of spore clearance and germination are developed based on a competing risks formulation. The models predict that the incubation period distribution depends critically on the rate that spores are cleared from the lung and to a lesser extent on the dose of inhaled spores. The models are used in a statistical analysis of data from an anthrax outbreak that occurred in Sverdlovsk, Russia. The analysis suggests that spores are cleared from the lung at a rate between 8% per day, and 14% per day, which is in good agreement with experimental studies of animals. The analysis suggests that at low doses, the overall median incubation period time is about 10 days, which includes a median lag of about 2 days between spore germination and onset of symptoms. Male gender and younger ages were associated with longer incubation periods as was lower dose of inhaled spores

    BED Estimates of HIV Incidence: Resolving the Differences, Making Things Simpler

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    Objective: Develop a simple method for optimal estimation of HIV incidence using the BED capture enzyme immunoassay. Design: Use existing BED data to estimate mean recency duration, false recency rates and HIV incidence with reference to a fixed time period, T. Methods: Compare BED and cohort estimates of incidence referring to identical time frames. Generalize this approach to suggest a method for estimating HIV incidence from any cross-sectional survey. Results: Follow-up and BED analyses of the same, initially HIV negative, cases followed over the same set time period T, produce estimates of the same HIV incidence, permitting the estimation of the BED mean recency period for cases who have been HIV positive for less than T. Follow-up of HIV positive cases over T, similarly, provides estimates of the false-recent rate appropriate for T. Knowledge of these two parameters for a given population allows the estimation of HIV incidence during T by applying the BED method to samples from cross-sectional surveys. An algorithm is derived for providing these estimates, adjusted for the false-recent rate. The resulting estimator is identical to one derived independently using a more formal mathematical analysis. Adjustments improve the accuracy of HIV incidence estimates. Negative incidence estimates result from the use of inappropriate estimates of the false-recent rate and/or from sampling error, not from any error in the adjustment procedure

    FORECASTING THE GLOBAL BURDEN OF ALZHEIMER\u27S DISEASE

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    Background: The goal was to forecast the global burden of Alzheimer’s disease and evaluate the potential impact of interventions that delay disease onset or progression. Methods: A stochastic multi-state model was used in conjunction with U.N. worldwide population forecasts and data from epidemiological studies on risks of Alzheimer’s disease. Findings: In 2006 the worldwide prevalence of Alzheimer’s disease was 26.6 million. By 2050, prevalence will quadruple by which time 1 in 85 persons worldwide will be living with the disease. We estimate about 43% of prevalent cases need a high level of care equivalent to that of a nursing home. If interventions could delay both disease onset and progression by a modest 1 year, there would be nearly 9.2 million fewer cases of disease in 2050 with nearly all the decline attributable to decreases in persons needing high level of care. Interpretation: We face a looming global epidemic of Alzheimer’s disease as the world’s population ages. Modest advances in therapeutic and preventive strategies that lead to even small delays in Alzheimer’s onset and progression can significantly reduce the global burden of the disease
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