The windy city : harnessing power in the neighborhood landscape

Thesis (M.C.P.)--Massachusetts Institute of Technology, Dept. of Urban Studies and Planning, 2008.This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.Includes bibliographical references.As wind power has spread in North America, so has an awareness that community acceptance will largely determine whether this renewable energy source continues to grow. Despite apparently widespread popular support for wind energy, a number of proposals for wind farms in rural and offshore locations have been derailed by local concerns. Meanwhile, several towns and cities have begun to explore another possibility: siting wind projects in urban areas. This thesis provides a framework to help readers compare the stories told about wind power in cities to the experiences in rural or "pristine" locations. It asks: 1) What are the motivations for wind power development in the urban context? 2) Does the community and political response to wind power in towns and cities differ from the experience in rural or offshore settings? To answer these questions, I investigated wind energy projects in Hull (Boston, MA region), Toronto (ON), Palmdale (Los Angeles, CA region), and Lackawanna (Buffalo, NY region). Based on a review of existing literature on rural wind siting controversies, I anticipated that local opinions about urban wind power would be formed primarily by expectations about the urban skyline and natural landscape, choice of ownership models, and the extent of meaningful community participation in the planning process. I found that while many of the factors highlighted in research on rural wind siting did affect community acceptance in the four cases, the greater social and spatial complexity of the "local" urban environment created new challenges. I conclude that 1) stories about urban wind power's costs and benefits diverged at the neighborhood scale and city scale;(cont.) 2) the use of degraded and industrial sites helped in siting turbines, but did not guarantee success due to the multiple interpretations of even these sites; 3) "local" ownership did not necessarily quell controversies over siting; and 4) political dynamics that were largely unrelated to the specific projects strongly influenced communities' receptiveness to proposed wind development. I suggest several strategies to help cities plan for urban wind power initiatives at a larger scale that are equitable and provide meaningful environmental and economic benefits.by Jonathan S. Cherry.M.C.P

Differential regulation of the SMN2 gene by individual HDAC proteins

Spinal muscular atrophy (SMA) is an autosomal recessive neurodegenerative disorder that is the leading genetic cause of infantile death. SMA is caused by homozygous deletion or mutation of the survival of motor neuron 1 gene (SMN1). The SMN2 gene is nearly identical to SMN1, however is alternatively spliced. The close relationship to SMN1 results in SMN2 being a very power genetic modifier of SMA disease severity and a target for therapies. We sought to identify the regulatory role individual HDAC proteins use to control expression of full length protein from the SMN2 genes. We used quantitative PCR to determine the effects shRNA silencing of individual HDACs on the steady state levels of a SMN2-luciferase reporter transcripts. We determined that reduction of individual HDAC proteins was sufficient to increase SMN protein levels in a transgenic reporter system. Knockdown of class I HDAC proteins preferentially activated the reporter by increased promoter transcription. Silencing of class II HDAC proteins maintained transcriptional activity; however silencing of HDAC 5 and 6 also appeared to enhance inclusion of an alternatively spliced exon. This work highlights HDAC proteins 2 and 6 as excellent investigative targets. These data are important to the basic understanding of SMN expression regulation and the refinements of current therapeutic compounds as well as the development of novel SMA therapeutics

Insecurity and the invisible : the challenge of spiritual (in)security

CITATION: Fisher, J. & Leonardi, C. 2020. Insecurity and the invisible : the challenge of spiritual (in)security. Security Dialogue, 52(5):383–400, doi:10.1177/0967010620973540.The original publication is available at https://journals.sagepub.comThe search for security has become an almost permanent feature of the contemporary lived experience and what Brian Massumi has called an ‘operative logic’ for states across the globe. The modern study – and practice – of security has, nonetheless, been largely concerned with the protection, preservation and sustaining of the material, the tangible and the visible. For many people around the world, however, feelings of security also derive from understandings of an individual or community’s relationships with invisible and spiritual forces. Religious devotion and divine protection represent a central plank of security for many, just as fears of divine retribution, demonic possession or witchcraft feature as a central dimension of insecurity for many others. This remains, however, a significant blindspot in much of security studies – and, indeed, often eludes and challenges state authority as much as it intersects with and enhances it. Drawing on fieldwork undertaken in northwestern Uganda, this study reflects critically on the provenance and implications of this blindspot and argues for an expanded understanding of what ‘counts’ as (in)security. In doing so, the article emphasizes the global character of spiritual (in)security and the challenges an understanding of (in)security that encompasses this pose to longstanding scholarly and practitioner associations of (in)security with state authority.https://journals.sagepub.com/doi/full/10.1177/0967010620973540Publisher's versio

Differences of Cycling Experiences and Perceptions between E-Bike and Bicycle Users in the United States

E-bikes are bicycles that provide pedal-assistance to aid people in cycling. Because of the potential of promoting sustainable transportation, more attention has been focused on the e-bike market. This paper investigates the differences of the cycling experience and perceptions between e-bike and conventional bicycle users, using samples drawn from independent bicycle dealer customers. A total of 806 respondents in the United States took the on-line survey, including 363 e-bike-owning respondents. The results show that e-bikes play a more important role in utilitarian travel, such as commuting and running errands, compared to a conventional bicycle. Conventional bicycle-owning respondents use their bicycles more for recreation and exercise. Also, e-bike owners tend to bike longer distances and take more trips per week. Both e-bike respondents and bicycle respondents stated that improved health was a key factor for cycling, while Millennials and Generation X respondents cycle to save time and improve the environment. Finally, an ordered logit model is proposed for evaluating factors that influence interest in future e-bike ownership. Travel purpose, e-bike familiarity, annual household income, and education level are statistically significant factors in the model. These findings begin to provide insight and a profile of potential new markets for e-bikes in the United States

Identification of Novel Compounds That Increase SMN Protein Levels Using an Improved SMN2 Reporter Cell Assay

Spinal muscular atrophy (SMA) is a neurodegenerative disorder that is characterized by progressive loss of motor neuron function. It is caused by the homozygous loss of the SMN1 (survival of motor neuron 1) gene and a decrease in full-length SMN protein. SMN2 is a nearly identical homolog of SMN1 that, due to alternative splicing, expresses predominantly truncated SMN protein. SMN2 represents an enticing therapeutic target. Increasing expression of full-length SMN from the SMN2 gene might represent a treatment for SMA. We describe a newly designed cell-based reporter assay that faithfully and reproducibly measures full-length SMN expression from the SMN2 gene. This reporter can detect increases of SMN protein by an array of compounds previously shown to regulate SMN2 expression and by the overexpression of proteins that modulate SMN2 splicing. It also can be used to evaluate changes at both the transcriptional and splicing level. This assay can be a valuable tool for the identification of novel compounds that increase SMN2 protein levels and the optimization of compounds already known to modulate SMN2 expression. We present here preliminary data from a high-throughput screen using this assay to identify novel compounds that increase expression of SMN2

A Step Closer to Meeting the Threat of Avian Influenza

Schultz-Cherry discusses a new study that describes the generation of live, attenuated H5N1 influenza viruses that may be suitable candidates for use in humans

Galactic Cosmic Radiation Leads to Cognitive Impairment and Increased Aβ Plaque Accumulation in a Mouse Model of Alzheimer’s Disease

Galactic Cosmic Radiation consisting of high-energy, high-charged (HZE) particles poses a significant threat to future astronauts in deep space. Aside from cancer, concerns have been raised about late degenerative risks, including effects on the brain. In this study we examined the effects of $^{56}$Fe particle irradiation in an APP/PS1 mouse model of Alzheimer’s disease (AD). We demonstrated 6 months after exposure to 10 and 100 cGy $^{56}$Fe radiation at 1 GeV/µ, that APP/PS1 mice show decreased cognitive abilities measured by contextual fear conditioning and novel object recognition tests. Furthermore, in male mice we saw acceleration of Aβ plaque pathology using Congo red and 6E10 staining, which was further confirmed by ELISA measures of Aβ isoforms. Increases were not due to higher levels of amyloid precursor protein (APP) or increased cleavage as measured by levels of the β C-terminal fragment of APP. Additionally, we saw no change in microglial activation levels judging by CD68 and Iba-1 immunoreactivities in and around Aβ plaques or insulin degrading enzyme, which has been shown to degrade Aβ. However, immunohistochemical analysis of ICAM-1 showed evidence of endothelial activation after 100 cGy irradiation in male mice, suggesting possible alterations in Aβ trafficking through the blood brain barrier as a possible cause of plaque increase. Overall, our results show for the first time that HZE particle radiation can increase Aβ plaque pathology in an APP/PS1 mouse model of AD

Differential gene expression in the cortical sulcus compared to the gyral crest within the early stages of chronic traumatic encephalopathy

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative tauopathy found in individuals with a history of repetitive head impacts (RHI). Previous work has demonstrated that neuroinflammation is involved in CTE pathogenesis, however, the specific inflammatory mechanisms are still unclear. Here, using RNA-sequencing and gene set enrichment analysis (GSEA), we investigated the genetic changes found in tissue taken from the region CTE pathology is first found, the cortical sulcus, and compared it to neighboring gryal crest tissue to identify what pathways were directly related to initial hyperphosphorylated tau (p-tau) deposition. 21 cases were chosen for analysis: 6 cases had no exposure to RHI or presence of neurodegenerative disease (Control), 5 cases had exposure to RHI but no presence of neurodegenerative disease (RHI), and 10 cases had exposure to RHI and low stage CTE (CTE). Two sets of genes were identified: genes that changed in both the sulcus and crest and genes that changed specifically in the sulcus relative to the crest. When examining genes that changed in both the sulcus and crest, GSEA demonstrated an increase in immune related processes and a decrease in neuronal processes in RHI and CTE groups. Sulcal specific alterations were observed to be driven by three mechanisms: anatomy, RHI, or p-tau. First, we observed consistent sulcal specific alterations in immune, extracellular matrix, vascular, neuronal, and endocytosis/exocytosis categories across all groups, suggesting the sulcus has a unique molecular signature compared to the neighboring crest independent of pathology. Second, individuals with a history of RHI demonstrated impairment in metabolic and mitochondrial related processes. Finally, in individuals with CTE, we observed impairment of immune and phagocytic related processes. Overall, this work provides the first observation of biological processes specifically altered in the sulcus that could be directly implicated in CTE pathogenesis and provide novel targets for biomarkers and therapies