Analyzing The Impact Of The 2012 Ford Focus Target Hunt: Can Student Managed Projects Accomplish Both Academic And Corporate Objectives?

Student-managed business projects offer students the opportunity to garner valuable real world experience while businesses can fulfill corporate responsibilities utilizing relatively inexpensive manpower. This paper describes an event marketing/social media marketing project completed in conjunction with Jackson-Dawson Communications, representing the Ford Motor Company, and a Midwestern University chapter of the American Marketing Association. Through the successful implementation of the AIDA-IMC promotion model, a committed AMA Chapter, and a number of very cooperative business partnerships, a host of corporate and academic objectives were accomplished while participants gained valuable insight into event marketing principles

Public Talks and Science Listens: A Community-Based Participatory Approach to Characterizing Environmental Health Risk Perceptions and Assessing Recovery Needs in the Wake of Hurricanes Katrina and Rita

In response to the human health threats stemming from Hurricanes Katrina and Rita, inter-disciplinary working groups representing P30-funded Centers of the National Institute Environmental Health Sciences were created to assess threats posed by mold, harmful alga blooms, chemical toxicants, and various infectious agents at selected sites throughout the hurricane impact zone. Because of proximity to impacted areas, UTMB NIEHS Center in Environmental Toxicology was charged with coordinating direct community outreach efforts, primarily in south Louisiana. In early October 2005, UTMB/NIEHS Center Community Outreach and Education Core, in collaboration with outreach counterparts at The University of Texas MD Anderson Cancer Center @ Smithville TX/Center for Research in Environmental Disease sent two groups into southern Louisiana. One group used Lafourche Parish as a base to deliver humanitarian aid and assess local needs for additional supplies during local recovery/reclamation. A second group, ranging through New Iberia, New Orleans, Chalmette, rural Terrebonne, Lafourche and Jefferson Parishes and Baton Rouge met with community environmental leaders, emergency personnel and local citizens to 1) sample public risk perceptions, 2) evaluate the scope and reach of ongoing risk communication efforts, and 3) determine how the NIEHS could best collaborate with local groups in environmental health research and local capacity building efforts. This scoping survey identified specific information gaps limiting efficacy of risk communication, produced a community “wish list” of potential collaborative research projects. The project provided useful heuristics for disaster response and management planning and a platform for future collaborative efforts in environmental health assessment and risk communication with local advocacy groups in south Terrebonne-Lafourche parishes

Phosphorylation of GFAP is associated with injury in the neonatal pig hypoxic-ischemic brain

Glial fibrillary acidic protein (GFAP) is an intermediate filament protein expressed in the astrocyte cytoskeleton that plays an important role in the structure and function of the cell. GFAP can be phosphorylated at six serine (Ser) or threonine (Thr) residues but little is known about the role of GFAP phosphorylation in physiological and pathophysiological states. We have generated antibodies against two phosphorylated GFAP (pGFAP) proteins: p8GFAP, where GFAP is phosphorylated at Ser-8 and p13GFAP, where GFAP is phosphorylated at Ser-13. We examined p8GFAP and p13GFAP expression in the control neonatal pig brain and at 24 and 72 h after an hypoxic-ischemic (HI) insult. Immunohistochemistry demonstrated pGFAP expression in astrocytes with an atypical cytoskeletal morphology, even in control brains. Semi-quantitative western blotting revealed that p8GFAP expression was significantly increased at 24 h post-insult in HI animals with seizures in frontal, parietal, temporal and occipital cortices. At 72 h post-insult, p8GFAP and p13GFAP expression were significantly increased in HI animals with seizures in brain regions that are vulnerable to cellular damage (cortex and basal ganglia), but no changes were observed in brain regions that are relatively spared following an HI insult (brain stem and cerebellum). Increased pGFAP expression was associated with poor neurological outcomes such as abnormal encephalography and neurobehaviour, and increased histological brain damage. Phosphorylation of GFAP may play an important role in astrocyte remodelling during development and disease and could potentially contribute to the plasticity of the central nervous system

Standard SANC modules for NLO QCD Radiative Corrections to Single-top Production

It this paper we present the results obtained with the newly created Standard SANC modules for calculation of the NLO QCD corrections to single top production processes in s and t channels at the partonic level, as well as top-decays. The main aim of these results is to prove the correct work of modules. A comprehensive comparison with results of the CompHEP system is given, where possible. These modules are intended to be used in Monte Carlo generators for single top production processes at the LHC. As in our recent paper, devoted to the electroweak corrections to these processes, we study the regularization of the top-legs associated infrared divergences with aid of the complex mass of the top quark. A comparison of QCD corrections with those computed by the conventional method is presented both for top production and decays. For s channel production we give an analytic proof of equivalence of the two methods in the limit of low top width.Comment: 21 pages, 2 figures, 17 table

L-infinity algebra connections and applications to String- and Chern-Simons n-transport

We give a generalization of the notion of a Cartan-Ehresmann connection from Lie algebras to L-infinity algebras and use it to study the obstruction theory of lifts through higher String-like extensions of Lie algebras. We find (generalized) Chern-Simons and BF-theory functionals this way and describe aspects of their parallel transport and quantization. It is known that over a D-brane the Kalb-Ramond background field of the string restricts to a 2-bundle with connection (a gerbe) which can be seen as the obstruction to lifting the PU(H)-bundle on the D-brane to a U(H)-bundle. We discuss how this phenomenon generalizes from the ordinary central extension U(1) -> U(H) -> PU(H) to higher categorical central extensions, like the String-extension BU(1) -> String(G) -> G. Here the obstruction to the lift is a 3-bundle with connection (a 2-gerbe): the Chern-Simons 3-bundle classified by the first Pontrjagin class. For G = Spin(n) this obstructs the existence of a String-structure. We discuss how to describe this obstruction problem in terms of Lie n-algebras and their corresponding categorified Cartan-Ehresmann connections. Generalizations even beyond String-extensions are then straightforward. For G = Spin(n) the next step is "Fivebrane structures" whose existence is obstructed by certain generalized Chern-Simons 7-bundles classified by the second Pontrjagin class.Comment: 100 pages, references and clarifications added; correction to section 5.1 and further example to 9.3.1 adde

Meta-analysis of epigenetic aging in schizophrenia reveals multifaceted relationships with age, sex, illness duration, and polygenic risk

Background: The study of biological age acceleration may help identify at-risk individuals and reduce the rising global burden of age-related diseases. Using DNA methylation (DNAm) clocks, we investigated biological aging in schizophrenia (SCZ), a mental illness that is associated with an increased prevalence of age-related disabilities and morbidities. In a whole blood DNAm sample of 1090 SCZ cases and 1206 controls across four European cohorts, we performed a meta-analysis of differential aging using three DNAm clocks (i.e., Hannum, Horvath, and Levine). To dissect how DNAm aging contributes to SCZ, we integrated information on duration of illness and SCZ polygenic risk, as well as stratified our analyses by chronological age and biological sex. Results: We found that blood-based DNAm aging is significantly altered in SCZ independent from duration of the illness since onset. We observed sex-specific and nonlinear age effects that differed between clocks and point to possible distinct age windows of altered aging in SCZ. Most notably, intrinsic cellular age (Horvath clock) is decelerated in SCZ cases in young adulthood, while phenotypic age (Levine clock) is accelerated in later adulthood compared to controls. Accelerated phenotypic aging was most pronounced in women with SCZ carrying a high polygenic burden with an age acceleration of + 3.82 years (CI 2.02–5.61, P = 1.1E−03). Phenotypic aging and SCZ polygenic risk contributed additively to the illness and together explained up to 14.38% of the variance in disease status. Conclusions: Our study contributes to the growing body of evidence of altered DNAm aging in SCZ and points to intrinsic age deceleration in younger adulthood and phenotypic age acceleration in later adulthood in SCZ. Since increased phenotypic age is associated with increased risk of all-cause mortality, our findings indicate that specific and identifiable patient groups are at increased mortality risk as measured by the Levine clock. Our study did not find that DNAm aging could be explained by the duration of illness of patients, but we did observe age- and sex-specific effects that warrant further investigation. Finally, our results show that combining genetic and epigenetic predictors can improve predictions of disease outcomes and may help with disease management in schizophrenia.</p

Meta-analysis of epigenetic aging in schizophrenia reveals multifaceted relationships with age, sex, illness duration, and polygenic risk

Background: The study of biological age acceleration may help identify at-risk individuals and reduce the rising global burden of age-related diseases. Using DNA methylation (DNAm) clocks, we investigated biological aging in schizophrenia (SCZ), a mental illness that is associated with an increased prevalence of age-related disabilities and morbidities. In a whole blood DNAm sample of 1090 SCZ cases and 1206 controls across four European cohorts, we performed a meta-analysis of differential aging using three DNAm clocks (i.e., Hannum, Horvath, and Levine). To dissect how DNAm aging contributes to SCZ, we integrated information on duration of illness and SCZ polygenic risk, as well as stratified our analyses by chronological age and biological sex. Results: We found that blood-based DNAm aging is significantly altered in SCZ independent from duration of the illness since onset. We observed sex-specific and nonlinear age effects that differed between clocks and point to possible distinct age windows of altered aging in SCZ. Most notably, intrinsic cellular age (Horvath clock) is decelerated in SCZ cases in young adulthood, while phenotypic age (Levine clock) is accelerated in later adulthood compared to controls. Accelerated phenotypic aging was most pronounced in women with SCZ carrying a high polygenic burden with an age acceleration of + 3.82 years (CI 2.02–5.61, P = 1.1E−03). Phenotypic aging and SCZ polygenic risk contributed additively to the illness and together explained up to 14.38% of the variance in disease status. Conclusions: Our study contributes to the growing body of evidence of altered DNAm aging in SCZ and points to intrinsic age deceleration in younger adulthood and phenotypic age acceleration in later adulthood in SCZ. Since increased phenotypic age is associated with increased risk of all-cause mortality, our findings indicate that specific and identifiable patient groups are at increased mortality risk as measured by the Levine clock. Our study did not find that DNAm aging could be explained by the duration of illness of patients, but we did observe age- and sex-specific effects that warrant further investigation. Finally, our results show that combining genetic and epigenetic predictors can improve predictions of disease outcomes and may help with disease management in schizophrenia.</p

LD Hub:a centralized database and web interface to perform LD score regression that maximizes the potential of summary level GWAS data for SNP heritability and genetic correlation analysis

Motivation: LD score regression is a reliable and efficient method of using genome-wide association study (GWAS) summary-level results data to estimate the SNP heritability of complex traits and diseases, partition this heritability into functional categories, and estimate the genetic correlation between different phenotypes. Because the method relies on summary level results data, LD score regression is computationally tractable even for very large sample sizes. However, publicly available GWAS summary-level data are typically stored in different databases and have different formats, making it difficult to apply LD score regression to estimate genetic correlations across many different traits simultaneously. Results: In this manuscript, we describe LD Hub - a centralized database of summary-level GWAS results for 173 diseases/traits from different publicly available resources/consortia and a web interface that automates the LD score regression analysis pipeline. To demonstrate functionality and validate our software, we replicated previously reported LD score regression analyses of 49 traits/diseases using LD Hub; and estimated SNP heritability and the genetic correlation across the different phenotypes. We also present new results obtained by uploading a recent atopic dermatitis GWAS meta-analysis to examine the genetic correlation between the condition and other potentially related traits. In response to the growing availability of publicly accessible GWAS summary-level results data, our database and the accompanying web interface will ensure maximal uptake of the LD score regression methodology, provide a useful database for the public dissemination of GWAS results, and provide a method for easily screening hundreds of traits for overlapping genetic aetiologies

Genetic risk for autism spectrum disorders and neuropsychiatric variation in the general population

Almost all genetic risk factors for autism spectrum disorders (ASDs) can be found in the general population, but the effects of that risk are unclear in people not ascertained for neuropsychiatric symptoms. Using several large ASD consortia and population based resources, we find genetic links between ASDs and typical variation in social behavior and adaptive functioning. This finding is evidenced through both inherited and de novo variation, indicating that multiple types of genetic risk for ASDs influence a continuum of behavioral and developmental traits, the severe tail of which can result in an ASD or other neuropsychiatric disorder diagnosis. A continuum model should inform the design and interpretation of studies of neuropsychiatric disease biology