10 research outputs found

    Wildlife-Vehicle Collisions in Utah: An Analysis of Wildlife Road Mortality Hotspots, Economic Impacts and Implications for Mitigation and Management

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    In the US, the roaded landscape has had serious ecological effects. We studied wildlife-vehicle collisions occurring on the 248 state routes in Utah from 1992 to 2002. We tracked trends and patterns in deer-vehicle collisions, evaluated all routes for frequency of deer kills, and identified hotspots ( segments of road with high concentrations of collisions per mile). We found pronounced patterns: e.g., 61.15% of all collisions occurred on only 10 routes. We studied the effects of posted speed limit and annual average daily traffic flow and found that no relationship existed between traffic volume and/or posted speed limit and the number of wildlife-vehicle collisions that occurred. We put the economic costs associated with wildlife vehicle collisions into a public safety perspective and confirmed that associated costs, damage, injuries, and loss of resources are significant aspects of DVCs that require attention and justify mitigation

    Locations of Deer–Vehicle Collisions are Unrelated to Traffic Volume or Posted Speed Limit

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    Consensus is lacking regarding the influence of vehicle speed and traffic volume on deer–vehicle collision (DVC) rates. Yet, annual average daily traffic fl ow (AADT) and posted speed limit (PSL) typically are used to measure these variables. To resolve this conflict, we studied the effects of traffic volume and vehicle speed on DVCs in Utah. Our results showed no relationship between AADT or PSL and DVC occurrence. There are at least 3 explanations for our results: (1) no causal relationship exists; (2) AADT and PSL, as measured, actually explain little of the variation; and (3) data quality problems exist. We discuss the likelihood for each explanation. We argue that even though traffic speed and volume have been used to predict DVC occurrence and may be useful explanatory variables, the metrics AADT and PSL are poor surrogate variables. Thus, uses of these variables to predict risk will likely provide unreliable results

    Assessment of costs associated with deer–vehicle collisions: human death and injury, vehicle damage, and deer loss

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    Collisions between large vertebrates and vehicles along roadways are an increasing concern, not only because of ecological consequences, but also because of associated economic and social costs. We used a large-scale, long-term data set comprising several databases from Utah to summarize and analyze these costs. The overall cost for 13,020 collisions from 1996 to 2001 in Utah was approximately 45,175,454,resultinginanestimatedaverageperyearcostofabout45,175,454, resulting in an estimated average per year cost of about 7,529,242 and a mean collision cost of 3,470.Thesefiguresincludehumanfatalitycostsof3,470. These figures include human fatality costs of 24 million (53% of total costs); vehicle damage costs of 18million(3918 million (39%); loss of deer, valued at 2.7 million (6%); and human injury costs of $1 million (2%). Cost-benefit analyses have shown that mitigation efforts, which are prioritized based on road-kill data, can produce positive net economic gains and also increase driver safety

    MPN patients harbor recurrent truncating mutations in transcription factor NF-E2

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    Item does not contain fulltextThe molecular etiology of myeloproliferative neoplasms (MPNs) remains incompletely understood, despite recent advances incurred through the discovery of several different mutations in MPN patients. We have recently described overexpression of the transcription factor NF-E2 in MPN patients and shown that elevated NF-E2 levels in vivo cause an MPN phenotype and predispose to leukemic transformation in transgenic mice. We report the presence of acquired insertion and deletion mutations in the NF-E2 gene in MPN patients. These result in truncated NF-E2 proteins that enhance wild-type (WT) NF-E2 function and cause erythrocytosis and thrombocytosis in a murine model. NF-E2 mutant cells acquire a proliferative advantage, witnessed by clonal dominance over WT NF-E2 cells in MPN patients. Our data underscore the role of increased NF-E2 activity in the pathophysiology of MPNs

    Clinical and genetic characteristics of late-onset Huntington's disease

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    Background: The frequency of late-onset Huntington's disease (>59 years) is assumed to be low and the clinical course milder. However, previous literature on late-onset disease is scarce and inconclusive. Objective: Our aim is to study clinical characteristics of late-onset compared to common-onset HD patients in a large cohort of HD patients from the Registry database. Methods: Participants with late- and common-onset (30\u201350 years)were compared for first clinical symptoms, disease progression, CAG repeat size and family history. Participants with a missing CAG repeat size, a repeat size of 6435 or a UHDRS motor score of 645 were excluded. Results: Of 6007 eligible participants, 687 had late-onset (11.4%) and 3216 (53.5%) common-onset HD. Late-onset (n = 577) had significantly more gait and balance problems as first symptom compared to common-onset (n = 2408) (P <.001). Overall motor and cognitive performance (P <.001) were worse, however only disease motor progression was slower (coefficient, 120.58; SE 0.16; P <.001) compared to the common-onset group. Repeat size was significantly lower in the late-onset (n = 40.8; SD 1.6) compared to common-onset (n = 44.4; SD 2.8) (P <.001). Fewer late-onset patients (n = 451) had a positive family history compared to common-onset (n = 2940) (P <.001). Conclusions: Late-onset patients present more frequently with gait and balance problems as first symptom, and disease progression is not milder compared to common-onset HD patients apart from motor progression. The family history is likely to be negative, which might make diagnosing HD more difficult in this population. However, the balance and gait problems might be helpful in diagnosing HD in elderly patients

    The New Conspiracy to Support an Idea

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    Clinical and genetic characteristics of late-onset Huntington's disease

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    Background: The frequency of late-onset Huntington's disease (>59 years) is assumed to be low and the clinical course milder. However, previous literature on late-onset disease is scarce and inconclusive. Objective: Our aim is to study clinical characteristics of late-onset compared to common-onset HD patients in a large cohort of HD patients from the Registry database. Methods: Participants with late- and common-onset (30–50 years)were compared for first clinical symptoms, disease progression, CAG repeat size and family history. Participants with a missing CAG repeat size, a repeat size of ≤35 or a UHDRS motor score of ≤5 were excluded. Results: Of 6007 eligible participants, 687 had late-onset (11.4%) and 3216 (53.5%) common-onset HD. Late-onset (n = 577) had significantly more gait and balance problems as first symptom compared to common-onset (n = 2408) (P <.001). Overall motor and cognitive performance (P <.001) were worse, however only disease motor progression was slower (coefficient, −0.58; SE 0.16; P <.001) compared to the common-onset group. Repeat size was significantly lower in the late-onset (n = 40.8; SD 1.6) compared to common-onset (n = 44.4; SD 2.8) (P <.001). Fewer late-onset patients (n = 451) had a positive family history compared to common-onset (n = 2940) (P <.001). Conclusions: Late-onset patients present more frequently with gait and balance problems as first symptom, and disease progression is not milder compared to common-onset HD patients apart from motor progression. The family history is likely to be negative, which might make diagnosing HD more difficult in this population. However, the balance and gait problems might be helpful in diagnosing HD in elderly patients

    Cognitive decline in Huntington's disease expansion gene carriers

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    Reduced Cancer Incidence in Huntington's Disease: Analysis in the Registry Study

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    Background: People with Huntington's disease (HD) have been observed to have lower rates of cancers. Objective: To investigate the relationship between age of onset of HD, CAG repeat length, and cancer diagnosis. Methods: Data were obtained from the European Huntington's disease network REGISTRY study for 6540 subjects. Population cancer incidence was ascertained from the GLOBOCAN database to obtain standardised incidence ratios of cancers in the REGISTRY subjects. Results: 173/6528 HD REGISTRY subjects had had a cancer diagnosis. The age-standardised incidence rate of all cancers in the REGISTRY HD population was 0.26 (CI 0.22-0.30). Individual cancers showed a lower age-standardised incidence rate compared with the control population with prostate and colorectal cancers showing the lowest rates. There was no effect of CAG length on the likelihood of cancer, but a cancer diagnosis within the last year was associated with a greatly increased rate of HD onset (Hazard Ratio 18.94, p < 0.001). Conclusions: Cancer is less common than expected in the HD population, confirming previous reports. However, this does not appear to be related to CAG length in HTT. A recent diagnosis of cancer increases the risk of HD onset at any age, likely due to increased investigation following a cancer diagnosis
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