442 research outputs found

    Alien Registration- Bell, Kathleen D. (Portland, Cumberland County)

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    https://digitalmaine.com/alien_docs/24146/thumbnail.jp

    WILLINGNESS TO PAY FOR LOCAL COHO SALMON ENHANCEMENT IN COASTAL COMMUNITIES

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    Salmon restoration and enhancement are dominant environmental policy issues in Oregon and Washington. In response to salmon species listings under the Endangered Species Act, salmon protection and recovery actions are being implemented throughout the Pacific Northwest at substantial opportunity costs. In this paper, we examine the willingness to pay (WTP) of coastal residents for local coho salmon enhancement programs. A contingent valuation study is completed using survey responses from five rural, coastal communities of Oregon and Washington, where coho salmon are prevalent. Our empirical results indicate that coastal residents are willing to pay for local coho salmon enhancement and that WTP varies considerably with individual opinions of the merit of the enhancement program.Resource /Energy Economics and Policy,

    Sustainability Science: A Call to Collaborative Action

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    Sustainability science is an emerging field directed at advancing sustainable development. Informed by recent scholarship and institutional experiments, we identify key roles for economists and encourage their greater participation in this research. Our call to collaborative action comes from positive experiences with the Sustainability Solutions Initiative based at the University of Maine, where economists collaborate with other experts and diverse stakeholders on real-world problems involving interactions between natural and human systems. We articulate a mutually beneficial setting where economists’ methods, skills, and norms add value to the problem-focused, interdisciplinary research of sustainability science and where resources, opportunities, and challenges from science bolster economic research specifically and land/sea grant institutions broadly

    Analysis of Apparel Structural Characteristics to Determine Effects on Fit, Performance, and Cost of Womens’ Athletic Shirts

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    Erica Bell is an undergraduate student in the School of Human Ecology at Louisiana Tech University. D’Atra McFarland is an undergraduate student in the School of Human Ecology at Louisiana Tech University. Janay Williams is an undergraduate student in the School of Human Ecology at Louisiana Tech University. Kathleen Heiden is an Associate Professor in the School of Human Ecology at Louisiana Tech University

    Amantadine Did Not Positively Impact Cognition in Chronic Traumatic Brain Injury: A Multi-Site, Randomized, Controlled Trial

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    Despite limited evidence to support the use of amantadine to enhance cognitive function after traumatic brain injury (TBI), the clinical use for this purpose is highly prevalent and is often based on inferred belief systems. The aim of this study was to assess effect of amantadine on cognition among individuals with a history of TBI and behavioral disturbance using a parallel-group, randomized, double-blind, placebo-controlled trial of amantadine 100 mg twice-daily versus placebo for 60 days. Included in the study were 119 individuals with two or more neuropsychological measures greater than 1 standard deviation below normative means from a larger study of 168 individuals with chronic TBI (>6 months post-injury) and irritability. Cognitive function was measured at treatment days 0, 28, and 60 with a battery of neuropsychological tests. Composite indices were generated: General Cognitive Index (included all measures), a Learning Memory Index (learning/memory measures), and Attention/Processing Speed Index (attention and executive function measures). Repeated-measures analysis of variance revealed statistically significant between-group differences favoring the placebo group at day 28 for General Cognitive Index (p = 0.002) and Learning Memory Index (p = 0.001), but not Attention/Processing Speed Index (p = 0.25), whereas no statistically significant between-group differences were found at day 60. There were no statistically significant between-group differences on adverse events. Cognitive function in individuals with chronic TBI is not improved by amantadine 100 mg twice-daily. In the first 28 days of use, amantadine may impede cognitive processing. However, the effect size was small and mean scores for both groups were generally within expectations for persons with history of complicated mild-to-severe TBI, suggesting that changes observed across assessments may not have functional significance. The use of amantadine to enhance cognitive function is not supported by these findings

    Pharmacological And Genetic Reversal Of Age-Dependent Cognitive Deficits Attributable To Decreased Presenilin Function

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    Alzheimer\u27s disease (AD) is the leading cause of cognitive loss and neurodegeneration in the developed world. Although its genetic and environmental causes are not generally known, familial forms of the disease (FAD) are attributable to mutations in a single copy of the Presenilin (PS) and amyloid precursor protein genes. The dominant inheritance pattern of FAD indicates that it may be attributable to gain or change of function mutations. Studies of FAD-linked forms of presenilin (psn) in model organisms, however, indicate that they are loss of function, leading to the possibility that a reduction in PS activity might contribute to FAD and that proper psn levels are important for maintaining normal cognition throughout life. To explore this issue further, we have tested the effect of reducing psn activity during aging in Drosophila melanogaster males. We have found that flies in which the dosage of psn function is reduced by 50% display age-onset impairments in learning and memory. Treatment with metabotropic glutamate receptor (mGluR) antagonists or lithium during the aging process prevented the onset of these deficits, and treatment of aged flies reversed the age-dependent deficits. Genetic reduction of Drosophila metabotropic glutamate receptor (DmGluRA), the inositol trisphosphate receptor (InsP(3)R), or inositol polyphosphate 1-phosphatase also prevented these age-onset cognitive deficits. These findings suggest that reduced psn activity may contribute to the age-onset cognitive loss observed with FAD. They also indicate that enhanced mGluR signaling and calcium release regulated by InsP(3)R as underlying causes of the age-dependent cognitive phenotypes observed when psn activity is reduced

    Potential Impact of Amantadine on Aggression in Chronic Traumatic Brain Injury

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    Objective: To assess the effects of amantadine on anger and aggression among individuals with a chronic traumatic brain injury (TBI). Methods: A cohort of 118 persons with chronic TBI (>6 months postinjury) and moderate-severe aggression selected from a larger cohort of 168 participants enrolled in a parallel-group, randomized, double-blind, placebo-controlled trial of amantadine 100 mg twice daily (n = 82) versus placebo (n = 86) for treatment of irritability were studied. Anger and aggression were measured at treatment days 0, 28, and 60 using observer-rated and participant-rated State-Trait Anger Expression Inventory-2 (STAXI-2) and Neuropsychiatric Inventory-Agitation/Aggression domain (NPI-A) Most Problematic and Distress scores. Results: Participant-rated day 60 NPI-A Most Problematic (adjusted P = .0118) and NPI-A Distress (adjusted P = .0118) were statistically significant between the 2 groups, but STAXI-2 differences were not significant after adjustment for multiple comparisons. Substantial improvements were noted in both amantadine and placebo groups (70% vs 56% improving at least 3 points on day 60 Observer NPI-A; P = .11). Conclusion: Amantadine 100 mg twice daily in this population with chronic TBI appears to be beneficial in decreasing aggression from the perspective of the individual with TBI. No beneficial impact on anger was found

    DNA fragility in the parallel evolution of pelvic reduction in stickleback fish

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    Evolution generates a remarkable breadth of living forms, but many traits evolve repeatedly, by mechanisms that are still poorly understood. A classic example of repeated evolution is the loss of pelvic hindfins in stickleback fish (Gasterosteus aculeatus). Repeated pelvic loss maps to recurrent deletions of a pelvic enhancer of the Pitx1 gene. Here, we identify molecular features contributing to these recurrent deletions. Pitx1 enhancer sequences form alternative DNA structures in vitro and increase double-strand breaks and deletions in vivo. Enhancer mutability depends on DNA replication direction and is caused by TG-dinucleotide repeats. Modeling shows that elevated mutation rates can influence evolution under demographic conditions relevant for sticklebacks and humans. DNA fragility may thus help explain why the same loci are often used repeatedly during parallel adaptive evolution
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