85 research outputs found

    Documenting change in an urban forest restoration project

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    The West Willamette Restoration Partnership is working to enhance connected natural areas, on both public and private property, in SW Portland to increase functionality as a wildlife corridor with connections to Forest Park to the north and Tryon Creek State Natural Area to the south. To manage the invasive vegetation currently found within strategically selected restoration sites in the Westside Wildlife Corridor, a variety of treatments were conducted and monitored between 2016-2018. Ground ivy (Hedera sp.), canopy weeds (including Clematis vitalba, Hedera sp.), and weedy tree treatments were conducted. Treatments included manual pulling, herbicide treatments, and plantings of native trees and shrubs. Changes in plant species composition and coverage was assessed using the Unified Monitoring Protocol and photo-point monitoring. The current results show promising signs that both long-term community stewardship efforts and short-term high intensity treatments are having the intended effect of decreasing ivy cover and having positive effects on native species diversity. Photo-points of sites of ground ivy and canopy ivy treatments showed noticeable effects: less and dying ivy and new non-invasive plants establishing. More work, and continued maintenance, will be necessary to fully restore these sites to a native plant-dominated condition. The project also utilizes a variety of tools to engage with the public about enhancement efforts

    Variably improved microbial source tracking with digital droplet PCR

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    This study addressed whether digital droplet PCR (ddPCR) could improve sensitivity and specificity of human-associated Bacteroidales genetic markers, BacHum and B. theta, and their quantification in environmental and fecal composite samples. Human markers were quantified by qPCR and ddPCR platforms obtained from the same manufacturer. A total of 180 samples were evaluated by each platform including human and animal feces, sewage, and environmental water. The sensitivity of ddPCR and qPCR marker assays in sewage and human stool was 0.85–1.00 with marginal reduction in human stool by ddPCR relative to qPCR (<10%). The prevalence and distribution of markers across complex sample types was similar (74–100% agreement) by both platforms with qPCR showing higher sensitivity for markers in environmental and composite samples and ddPCR showing greater reproducibility for marker detection in fecal composites. Determination of BacHum prevalence in fecal samples by ddPCR increased specificity relative to qPCR (from 0.58 to 0.88) and accuracy (from 0.77 to 0.94), while the B. theta assay performed similarly on both platforms (specificity = 0.98). In silico analysis indicated higher specificity of ddPCR for BacHum was not solely attributed to reduced sensitivity relative to qPCR. Marker concentrations measured by ddPCR for all sample types were consistently lower than those measured by qPCR, by a factor of 2.6 ± 2.8 for B. theta and 18.7 ± 10.0 for BacHum. We suggest that differences in assay performance on ddPCR and qPCR platforms may be linked to the characteristics of the assay targets (that is, genes with multiple versus single copies and encoding proteins versus ribosomal RNA) however further work is needed to validate these ideas. We conclude that ddPCR is a suitable tool for microbial source tracking, however, other factors such as cost-effectiveness and assay-specific performance should be considered.Fil: Nshimyimana, Jean Pierre. Michigan State University; Estados Unidos. Massachusetts Institute of Technology; Estados Unidos. Nanyang Technological University; SingapurFil: Cruz, Mercedes Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Salta. Instituto de Investigaciones para la Industria Química. Universidad Nacional de Salta. Facultad de Ingeniería. Instituto de Investigaciones para la Industria Química; Argentina. Nanyang Technological University; SingapurFil: Wuertz, Stefan. Nanyang Technological University; SingapurFil: Thompson, Janelle R.. Massachusetts Institute of Technology; Estados Unido

    Expression of Viral Antigen by the Liver Leads to Chronic Infection Through the Generation of Regulatory T Cells

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    Referred to by David E. Kaplan " Does Massive Antigen Burden Allow Hepatic Viruses to Induce Regulatory T Cells and Their Tolerance and Persistence?" CMGH Cellular and Molecular Gastroenterology and Hepatology, Volume 1, Issue 3, May 2015, Pages 259-261International audienceThe constant exposure of the liver to food and bacterial antigens through the mesenteric circulation requires it to maintain tolerance while preserving the ability to mount an effective immune response against pathogens. We investigated the contribution of the liver's tolerogenic nature on the establishment of chronic viral infections. Methods: TTR-NP mice, which express the nucleoprotein (NP) of lymphocytic choriomeningitis virus (LCMV) specifically in hepatocytes under control of a modified transthyretin (TTR) promoter, were infected with the Armstrong (Arm) or WE acute strains of LCMV. Results: The infection persisted for at least 147 days in TTR-NP mice. Expression of NP by the liver induced a strong peripheral tolerance against NP that was mediated by interleukin-10-secreting CD4+ regulatory T cells, leading to high PD-1 (programmed death-1) expression and reduced effector function of virus-specific T cells. Despite an active immune response against LCMV, peripheral tolerance against a single viral protein was sufficient to induce T-cell exhaustion and chronic LCMV Armstrong (Arm) or WE infection by limiting the antiviral T-cell response in an otherwise immunocompetent host. Regulatory T-cell depletion of chronically infected TTR-NP mice led to functional restoration of LCMV-specific CD4+ and CD8+ Tcell responses and viral clearance. Conclusions: Expression of a viral antigen by hepatocytes can induce a state of peripheral tolerance mediated by regulatory Tcells that can lead to the establishment of a chronic viral infection. Strategies targeting regulatory T cells in patients chronically infected with hepatotropic viruses could represent a promising approach to restore functional antiviral immunity and clear infection

    Feature tracking strain analysis detects the onset of regional diastolic dysfunction in territories with acute myocardial injury induced by transthoracic electrical interventions.

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    Electric interventions are used to terminate arrhythmia. However, myocardial injury from the electrical intervention can follow unique pathways and it is unknown how this affects regional ventricular function. This study investigated the impact of transthoracic electrical shocks on systolic and diastolic myocardial deformation. Ten healthy anaesthetized female swine received five transthoracic shocks (5 × 200 J) and six controls underwent a cardiovascular magnetic resonance exam prior to and 5 h after the intervention. Serial transthoracic shocks led to a global reduction in both left (LV, - 15.6 ± 3.3% to - 13.0 ± 3.6%, p < 0.01) and right ventricular (RV, - 16.1 ± 2.3% to - 12.8 ± 4.2%, p = 0.03) peak circumferential strain as a marker of systolic function and to a decrease in LV early diastolic strain rate (1.19 ± 0.35/s to 0.95 ± 0.37/s, p = 0.02), assessed by feature tracking analysis. The extent of myocardial edema (ΔT1) was related to an aggravation of regional LV and RV diastolic dysfunction, whereas only RV systolic function was regionally associated with an increase in T1. In conclusion, serial transthoracic shocks in a healthy swine model attenuate biventricular systolic function, but it is the acute development of regional diastolic dysfunction that is associated with the onset of colocalized myocardial edema

    Adenosine infusion increases plasma levels of VEGF in humans

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    BACKGROUND: Many in vitro studies have shown that adenosine (Ado) can induce vascular endothelial growth factor (VEGF) mRNA and protein expression and stimulate endothelial proliferation. In the present study, we seek to determine whether Ado can increase circulating levels of VEGF protein in the intact human. METHODS: Five outpatients 49.3 ± 6.7 years of age and weighing 88.2 ± 8.5 kg were selected. They were given a 6 min intravenous infusion of Ado (0.14 mg kg(-1 )min(-1)) in conjunction with sestamibi myocardial perfusion scans. Mean blood pressure (MBP, calculated from systolic and diastolic values) and heart rate (HR) were determined before Ado infusion and every 2 min for the next 10 min. Plasma VEGF concentrations (ELISA) were determined immediately before Ado infusion and 1 h, 2 h, and 8 h after the infusion. RESULTS: Plasma VEGF concentration averaged 20.3 ± 2.0 pg ml(-1 )prior to Ado infusion, and increased to 62.7 ± 18.1 pg ml(-1 )at 1 h post- infusion (p < 0.01). VEGF plasma concentration returned to basal levels 2 h after infusion (23.3 ± 3.4 pg ml(-1)). MBP averaged 116 ± 7 mmHg and heart rate averaged 70 ± 7 prior to Ado infusion. MBP decreased by a maximum of ~22% and HR increased by a maximum of ~17% during the infusion. CONCLUSION: We conclude from these preliminary findings that intravenous infusion of adenosine can increase plasma levels of VEGF in humans

    Cystamine/cysteamine rescues the dopaminergic system and shows neurorestorative properties in an animal model of Parkinson's disease.

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    The neuroprotective properties of cystamine identified in pre-clinical studies have fast-tracked this compound to clinical trials in Huntington's disease, showing tolerability and benefits on motor symptoms. We tested whether cystamine could have such properties in a Parkinson's disease murine model and now provide evidence that it can not only prevent the neurodegenerative process but also can reverse motor impairments created by a 6-hydroxydopamine lesion 3weeks post-surgery. Importantly, we report that cystamine has neurorestorative properties 5weeks post-lesion as seen on the number of nigral dopaminergic neurons which is comparable with treatments of cysteamine, the reduced form of cystamine used in the clinic, as well as rasagiline, increasingly prescribed in early parkinsonism. All three compounds induced neurite arborization of the remaining dopaminergic cells which was further confirmed in ex vivo dopaminergic explants derived from Pitx3-GFP mice. The disease-modifying effects displayed by cystamine/cysteamine would encourage clinical testing

    Cerebrovascular and blood-brain barrier impairments in Huntington's disease: Potential implications for its pathophysiology: Vascular impairments in HD

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    ObjectiveAlthough the underlying cause of Huntington's disease (HD) is well established, the actual pathophysiological processes involved remain to be fully elucidated. In other proteinopathies such as Alzheimer's and Parkinson's diseases, there is evidence for impairments of the cerebral vasculature as well as the blood–brain barrier (BBB), which have been suggested to contribute to their pathophysiology. We investigated whether similar changes are also present in HD.MethodsWe used 3‐ and 7‐Tesla magnetic resonance imaging as well as postmortem tissue analyses to assess blood vessel impairments in HD patients. Our findings were further investigated in the R6/2 mouse model using in situ cerebral perfusion, histological analysis, Western blotting, as well as transmission and scanning electron microscopy.ResultsWe found mutant huntingtin protein (mHtt) aggregates to be present in all major components of the neurovascular unit of both R6/2 mice and HD patients. This was accompanied by an increase in blood vessel density, a reduction in blood vessel diameter, as well as BBB leakage in the striatum of R6/2 mice, which correlated with a reduced expression of tight junction‐associated proteins and increased numbers of transcytotic vesicles, which occasionally contained mHtt aggregates. We confirmed the existence of similar vascular and BBB changes in HD patients.InterpretationTaken together, our results provide evidence for alterations in the cerebral vasculature in HD leading to BBB leakage, both in the R6/2 mouse model and in HD patients, a phenomenon that may, in turn, have important pathophysiological implications. Ann Neurol 2015;78:160–17

    Christopher Hollis. The Monstrous Regiment, 1929

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    Janelle Pierre. Christopher Hollis. The Monstrous Regiment, 1929. In: Revue des Sciences Religieuses, tome 11, fascicule 3, 1931. pp. 502-508

    Christopher Hollis. The Monstrous Regiment, 1929

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    Janelle Pierre. Christopher Hollis. The Monstrous Regiment, 1929. In: Revue des Sciences Religieuses, tome 11, fascicule 3, 1931. pp. 502-508

    Herbert Leslie Stewart, A century of anglo-catholicism

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    Janelle Pierre. Herbert Leslie Stewart, A century of anglo-catholicism. In: Revue des Sciences Religieuses, tome 10, fascicule 4, 1930. pp. 712-717
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