27 research outputs found

    Illinois Waterfowl Surveys and Investigations W-43-R-63 Annual Progress Report FY2016 Period: 1 July 2015 – 30 June 2016

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    Objectives 1) Inventory abundance and distribution of waterfowl and other waterbirds (a minimum of 10 species and guilds) during autumn migration at a minimum of 30 sites along the Illinois and central Mississippi rivers of Illinois, 2) Estimate waterfowl and other waterbird population sizes (a minimum of 10 species and guilds) during autumn migration using an aerial quadrat survey along the central Illinois River for comparison with aerial inventories (Objective 1), 3) Investigate the ecology of up to 50 gadwall and 50 American green-winged teal during spring migration in and near the central Illinois River valley of Illinois, 4) Determine breeding bird use of and nest density in a minimum of 10 moist-soil wetlands managed for waterfowl during summer in central Illinois, 5) Investigate the breeding ecology of a minimum of 50 sandhill cranes during spring and summer in northeastern Illinois consistent with an ongoing research project, 6) Investigate movements and home range size of a minimum of 10 Canada geese during winter in and near the Greater Chicago Metropolitan Area of Illinois, and 7) Determine habitat quality of a minimum of 100 wetlands and deepwater habitats during spring, summer, and early autumn for migrating dabbling ducks, breeding wetland birds, and migrating shorebirds in Illinois.Illinois Department of Natural Resources, Division of Wildlife & U.S. Fish and Wildlife Service Contract Number: RC09-13FWUIUCunpublishednot peer reviewedOpe

    Accounts from developers of generic health state utility instruments explain why they produce different QALYs: a qualitative study

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    Purpose and setting: Despite the label generic health state utility instruments (HSUIs), empirical evidence shows that different HSUIs generate different estimates of Health-Related Quality of Life (HRQoL) in the same person. Once a HSUI is used to generate a QALY, the difference between HSUIs is often ignored, and decision-makers act as if \u27a QALY is a QALY is a QALY\u27. Complementing evidence that different generic HSUIs produce different empirical values, this study addresses an important gap by exploring how HSUIs differ, and processes that produced this difference. 15 developers of six generic HSUIs used for estimating the QOL component of QALYs: Quality of Well-Being (QWB) scale; 15 Dimension instrument (15D); Health Utilities Index (HUI); EuroQol EQ-5D; Short Form-6 Dimension (SF-6D), and the Assessment of Quality of Life (AQoL) were interviewed in 2012-2013. Principal findings: We identified key factors involved in shaping each instrument, and the rationale for similarities and differences across measures. While HSUIs have a common purpose, they are distinctly discrete constructs. Developers recalled complex developmental processes, grounded in unique histories, and these backgrounds help to explain different pathways taken at key decision points during the HSUI development. The basis for the HSUIs was commonly not equivalent conceptually: differently valued concepts and goals drove instrument design and development, according to each HSUI\u27s defined purpose. Developers drew from different sources of knowledge to develop their measure depending on their conceptualisation of HRQoL. Major conclusions/contribution to knowledge: We generated and analysed first-hand accounts of the development of the HSUIs to provide insight, beyond face value, about how and why such instruments differ. Findings enhance our understanding of why the six instruments developed the way they did, from the perspective of key developers of those instruments. Importantly, we provide additional, original explanation for why a QALY is not a QALY is not a QALY

    Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

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    IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

    Data from: A set of plastid loci for use in multiplex fragment length genotyping for intraspecific variation in Pinus (Pinaceae)

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    Premise of the study: Recently released Pinus plastome sequences support characterization of 15 plastid Simple Sequence Repeat (ptSSR) loci originally published for P. contorta and P. thunbergii. This allows selection of loci for single-tube PCR multiplexed genotyping in any subsection of the genus. Methods: Unique placement of primers and primer conservation across the genus were investigated, and a set of six loci were selected for single-tube multiplexing. We compare interspecific variation between ptSSRs and nucleotide sequences of ycf1 then test intraspecific variation for ptSSRs using 911 samples in the P. ponderosa species complex. Results: The ptSSR loci contain mononucleotide and complex repeats with additional length variation in flanking regions. They are not located in hypervariable regions and most primers are conserved across the genus. A single PCR per sample multiplexed for six loci yielded 45 alleles in 911 samples. Discussion: The protocol allows efficient genotyping of many samples. The ptSSR loci are too variable for Pinus phylogenies but are useful for the study of genetic structure within and among populations. The multiplex method could easily be extended to other plant groups by choosing primers for ptSSR loci in a plastome alignment for the target group

    A Set of Plastid Loci for Use in Multiplex Fragment Length Genotyping for Intraspecific Variation in <i>Pinus</i> (Pinaceae)

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    Premise of the study: Recently released Pinus plastome sequences support characterization of 15 plastid simple sequence repeat (cpSSR) loci originally published for P. contorta and P. thunbergii. This allows selection of loci for single-tube PCR multiplexed genotyping in any subsection of the genus. Methods: Unique placement of primers and primer conservation across the genus were investigated, and a set of six loci were selected for single-tube multiplexing. We compared interspecific variation between cpSSRs and nucleotide sequences ofycf1 and tested intraspecific variation for cpSSRs using 911 samples in the P. ponderosa species complex. Results: The cpSSR loci contain mononucleotide and complex repeats with additional length variation in flanking regions. They are not located in hypervariable regions, and most primers are conserved across the genus. A single PCR per sample multiplexed for six loci yielded 45 alleles in 911 samples. Discussion: The protocol allows efficient genotyping of many samples. The cpSSR loci are too variable for Pinus phylogenies but are useful for the study of genetic structure within and among populations. The multiplex method could easily be extended to other plant groups by choosing primers for cpSSR loci in a plastome alignment for the target group

    Alignment of 15 cpSSR primer pairs with Pinus plastomes

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    The published nucleotide sequences for 15 cpSSR primer pairs located within the aligned plastomes of 107 species of Pinus and six Pinaceae outgroups (TreeBase S12640)

    Interdisciplinary Expansions: Applying Recovery-Informed Theory to Interdisciplinary Areas of Recovery Science Research

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    © 2020 Taylor & Francis. To understand how persons with substance use disorders (SUDs) achieve and maintain wellness, it is necessary to expand recovery science research. The experiences of individuals in recovery are rarely reflected in SUD research which, at times, discounts subjective experiences of recovery. Recovery-informed theory (RIT) offers new lines of inquiry into various aspects of recovery, which may lead to innovative approaches to how SUDs are understood within clinical, professional, and community contexts. This paper reviews three preliminary areas to apply RIT: recovery measurement, identity processes, and systems engagement. Such advancement can impact the collective understanding of how individuals recover from SUD

    IL-1α/IL-1R1 expression in chronic obstructive pulmonary disease and mechanistic relevance to smoke-induced neutrophilia in mice.

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    BACKGROUND: Cigarette smoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD), a major cause of morbidity and mortality worldwide. Despite this, the cellular and molecular mechanisms that contribute to COPD pathogenesis are still poorly understood. METHODOLOGY AND PRINCIPAL FINDINGS: The objective of this study was to assess IL-1 α and β expression in COPD patients and to investigate their respective roles in perpetuating cigarette smoke-induced inflammation. Functional studies were pursued in smoke-exposed mice using gene-deficient animals, as well as blocking antibodies for IL-1α and β. Here, we demonstrate an underappreciated role for IL-1α expression in COPD. While a strong correlation existed between IL-1α and β levels in patients during stable disease and periods of exacerbation, neutrophilic inflammation was shown to be IL-1α-dependent, and IL-1β- and caspase-1-independent in a murine model of cigarette smoke exposure. As IL-1α was predominantly expressed by hematopoietic cells in COPD patients and in mice exposed to cigarette smoke, studies pursued in bone marrow chimeric mice demonstrated that the crosstalk between IL-1α+ hematopoietic cells and the IL-1R1+ epithelial cells regulates smoke-induced inflammation. IL-1α/IL-1R1-dependent activation of the airway epithelium also led to exacerbated inflammatory responses in H1N1 influenza virus infected smoke-exposed mice, a previously reported model of COPD exacerbation. CONCLUSIONS AND SIGNIFICANCE: This study provides compelling evidence that IL-1α is central to the initiation of smoke-induced neutrophilic inflammation and suggests that IL-1α/IL-1R1 targeted therapies may be relevant for limiting inflammation and exacerbations in COPD
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