Climate action plans: analysis of the effects on form of U.S. cities

This study investigates the effectiveness of community climate action plans (CAPs) and their potential impact on the form of U.S. cities. Greenhouse gas (GHG) mitigation and climate change adaptation strategies enacted by cities have the potential to redirect future public and private investment. Three studies have been prepared to better understand the external policy context that cities are working within, the process and tools they are using, and how climate actions are integrated into their comprehensive plans. Study 1 includes detailed case studies of eight U.S. cities that have completed CAPs. The cities are of various sizes and located in different climate regions. The case studies include a review of state and regional plans and policies; climate action plan technical and policy reports; evaluations of cities’ integration of climate action plans with their comprehensive plans; and interviews with planning project managers. Study 2 includes a national survey population of nearly 200 cities that have completed CAPs. The survey’s independent variables include city fundamentals such as size, location, comprehensive plan requirements, power sources, and political context. Dependent variables are organized into two groups: one for CAP approach and strategies, and the second for policy outcomes that modify the form of cities. Study 3 examines the effectiveness of common strategies utilizing a purpose-built greenhouse gas worksheet calculator. A model town is examined as a baseline community of 50,000 in population that is proposed to double by 2050 to a city of 100,000. A business-as-usual model and two alternatives test mitigation strategies and actions measuring potential effectiveness on GHG emissions. The thesis research findings have significant theoretical and practical implications regarding CAP influence on the future form of U.S. cities. In particular, studies demonstrate the importance of compressing growth into walkable cities with determined and fixed boundaries

Levels of Abnormal Prion Protein in Deer and Elk with Chronic Wasting Disease

Infected deer may pose a higher risk than elk for disease transmission

Characteristics of 263K Scrapie Agent in Multiple Hamster Species

Characteristics correlated better with host factors than with agent strain

The Developmental Transcriptome of the Mosquito Aedes aegypti, an Invasive Species and Major Arbovirus Vector

Mosquitoes are vectors of a number of important human and animal diseases. The development of novel vector control strategies requires a thorough understanding of mosquito biology. To facilitate this, we used RNA-seq to identify novel genes and provide the first high-resolution view of the transcriptome throughout development and in response to blood feeding in a mosquito vector of human disease, Aedes aegypti, the primary vector for Dengue and yellow fever. We characterized mRNA expression at 34 distinct time points throughout Aedes development, including adult somatic and germline tissues, by using polyA+ RNA-seq. We identify a total of 14,238 novel new transcribed regions corresponding to 12,597 new loci, as well as many novel transcript isoforms of previously annotated genes. Altogether these results increase the annotated fraction of the transcribed genome into long polyA+ RNAs by more than twofold. We also identified a number of patterns of shared gene expression, as well as genes and/or exons expressed sex-specifically or sex-differentially. Expression profiles of small RNAs in ovaries, early embryos, testes, and adult male and female somatic tissues also were determined, resulting in the identification of 38 new Aedes-specific miRNAs, and ~291,000 small RNA new transcribed regions, many of which are likely to be endogenous small-interfering RNAs and Piwi-interacting RNAs. Genes of potential interest for transgene-based vector control strategies also are highlighted. Our data have been incorporated into a user-friendly genome browser located at www.Aedes.caltech.edu, with relevant links to Vectorbase (www.vectorbase.org

Prion disease induced alterations in gene expression in spleen and brain prior to clinical symptoms

Prion diseases are fatal neurodegenerative disorders that affect animals and humans. There is a need to gain understanding of prion disease pathogenesis and to develop diagnostic assays to detect prion diseases prior to the onset of clinical symptoms. The goal of this study was to identify genes that show altered expression early in the disease process in the spleen and brain of prion disease-infected mice. Using Affymetrix microarrays, we identified 67 genes that showed increased expression in the brains of prion disease-infected mice prior to the onset of clinical symptoms. These genes function in many cellular processes including immunity, the endosome/lysosome system, hormone activity, and the cytoskeleton. We confirmed a subset of these gene expression alterations using other methods and determined the time course in which these changes occur. We also identified 14 genes showing altered expression prior to the onset of clinical symptoms in spleens of prion disease infected mice. Interestingly, four genes, Atp1b1, Gh, Anp32a, and Grn, were altered at the very early time of 46 days post-infection. These gene expression alterations provide insights into the molecular mechanisms underlying prion disease pathogenesis and may serve as surrogate markers for the early detection and diagnosis of prion disease

Susceptibilities of Nonhuman Primates to Chronic Wasting Disease

A species barrier may protect humans from this disease

Use of a preclinical test in the control of classical scrapie

Scrapie control in Great Britain (GB) was originally based on the National Scrapie Plan's Ram Genotyping scheme aimed at reducing the susceptibility of the national flock. The current official strategy to control scrapie in the national flock involves culling susceptible genotypes in individual, known affected flocks (compulsory scrapie flock scheme or CSFS). However, the recent development of preclinical test candidates means that a strategy based on disease detection may now be feasible. Here, a deterministic within-flock model was used to demonstrate that only large flocks with many home-bred ewes are likely to be a significant risk for flock-to-flock transmission of scrapie. For most other flocks, it was found that the CSFS could be replaced by a strategy using a currently available live test without excessive risk to other farmers, even if the proportion of susceptible genotypes in the flock is unusually large. Even for flocks that represent a high risk of harbouring a high prevalence of infection, there would be limited probability of onward transmission if scrapie is detected soon after disease introduction (typically less than 5 years). However, if detection of disease is delayed, the existing CSFS strategy may be the most appropriate control measure in these cases

Variable tau accumulation in murine models with abnormal prion protein deposits

Rona Barron - ORCID: 0000-0003-4512-9177 https://orcid.org/0000-0003-4512-9177The conversion of cellular prion protein (PrP) into a misfolded isoform is central to the development of prion diseases. However, the heterogeneous phenotypes observed in prion disease may be linked with the presence of other misfolded proteins in the brain. While hyperphosphorylated tau (p.tau) is characteristic of Alzheimer's disease (AD), p.tau is also observed in human prion diseases. To explore this association in the absence of potential effects due to aging, drug treatment, agonal stage and postmortem delay we analyzed p.tau and PrP immunopositivity in mouse models. Analyses were performed on mice inoculated with prion agents, and mice with PrP amyloid in the absence of prion disease. We observed that p.tau was consistently present in animals with prion infectivity (models that transmit disease upon serial passage). In contrast, p.tau was very rarely observed or absent in mice with PrP amyloid plaques in the absence of prion replication. These data indicate that the formation of p.tau is not linked to deposition of misfolded PrP, but suggest that the interaction between replication of infectivity and host factors regulate the formation of p.tau and may contribute to the heterogeneous phenotype of prion diseases.https://doi.org/10.1016/j.jns.2017.10.040383pubpubDecember 201