95 research outputs found

    ICT use among rural child welfare workers: Implications for LIS education in a global context

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    This presentation will report the research findings on ICT use among rural child welfare workers in North Florida. This study, which represents a collaboration among three different academic units, employed face-to-face interviews and experience sampling via a phone app to collect data about how ICT is being used in the field of child welfare social work and its impact on worker well-being, case outcomes, etc. This research will inform information behavior studies and LIS education interested in research methods as well as information services to the field of social work

    Taxonomy and pathology of Togninia (Diaporthales) and its Phaeoacremonium anamorphs.

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    The genus Togninia (Diaporthales, Togniniaceae) is here monographed along with its Phaeoacremonium (Pm.) anamorphs. Ten species of Togninia and 22 species of Phaeoacremonium are treated. Several new species of Togninia (T.) are described, namely T. argentinensis (anamorph Pm. argentinense), T. austroafricana (anamorph Pm. austroafricanum), T. krajdenii, T. parasitica, T. rubrigena and T. viticola. New species of Phaeoacremonium include Pm. novae-zealandiae (teleomorph T. novae-zealandiae), Pm. iranianum, Pm. sphinctrophorum and Pm. theobromatis. Species can be identified based on their cultural and morphological characters, supported by DNA data derived from partial sequences of the actin and ß-tubulin genes. Phylogenies of the SSU and LSU rRNA genes were used to determine whether Togninia has more affinity with the Calosphaeriales or the Diaporthales. The results confirmed that Togninia had a higher affinity to the Diaporthales than the Calosphaeriales. Examination of type specimens revealed that T. cornicola, T. vasculosa, T. rhododendri, T. minima var. timidula and T. villosa, were not members of Togninia. The new combinations Calosphaeria cornicola, Calosphaeria rhododendri, Calosphaeria transversa, Calosphaeria tumidula, Calosphaeria vasculosa and Jattaea villosa are proposed. Species of Phaeoacremonium are known vascular plant pathogens causing wilting and dieback of woody plants. The most prominent diseases in which they are involved are Petri disease and esca, which occur on grapevines and are caused by a complex of fungi, often including multiple species of Phaeoacremonium. Various Phaeoacremonium species are opportunistic fungi on humans and cause phaeohyphomycosis. The correct and rapid identification of Phaeoacremonium species is important to facilitate the understanding of their involvement in plant as well as human disease. A rapid identification method was developed for the 22 species of Phaeacremonium. It involved the use of 23 species-specific primers, including 20 primers targeting the ß-tubulin gene and three targeting the actin gene. These primers can be used in 14 multiplex reactions. Additionally, a multiple-entry electronic key based on morphological, cultural and ß-tubulin sequence data was developed to facilitate phenotypic and sequence-based species identification of the different Phaeoacremonium species. Separate dichotomous keys are provided for the identification of the Togninia and Phaeoacremonium species. Keys for the identification of Phaeoacremonium-like fungi and the genera related to Togninia are also provided. The mating strategy of several Togninia species was investigated with ascospores obtained from fertile perithecia produced in vitro. Togninia argentinensis and T. novae-zealandiae have homothallic mating systems, whereas T. austroafricana, T. krajdenii, T. minima, T. parasitica, T. rubrigena and T. viticola were heterothallic.

    Minimising fear and anxiety in working dogs:a review

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    The causes of fear and anxiety in working dogs are multifactorial and may include inherited characteristics that differ between individuals (e.g. Goddard and Beilharz, 1982; 1984a,b ), influences of the environment ( Lefebvre et al., 2007 ), and learned experiences during particular sensitive periods ( Appleby et al., 2002 ) and throughout life. Fear-related behavior compromises performance, leads to significant numbers of dogs failing to complete training (e.g., Murphy, 1995; Batt et al., 2008 ), early withdrawals from working roles ( Caron-Lormier et al., 2016 ), and can jeopardize dog and handler safety. Hence, amelioration of fear and anxiety is critical to maintain dogs in working roles and to ensure their well-being. Although current methods of selection and training are seemingly effective at producing many dogs which work in a remarkable array of environments, some dogs do not make the grade, and longevity of service is not always maximized. Programs should strive for optimal efficiency and they need to continually analyze the value of each component of their program, seek evidence for its value and explore potential evidence-based improvements. Here we discuss scientific evidence for methods and strategies which may be of value in reducing the risk of fear behaviors developing in the working dog population and suggest potentially valuable techniques and future research to explore the benefit of these approaches. The importance of environmental influences, learning opportunities, and effects of underlying temperament on the outward expression of fear and anxiety should not be underestimated. Identification of characteristics which predict resilience to stress are valuable, both to enable careful breeding for these traits and to develop predictive tests for puppies and procured animals. It is vitally important to rear animals in optimal environments and introduce them to a range of stimuli in a positive, controlled, and gradual way, as these can all help minimize the number of dogs which develop work-inhibiting fears. Future research should explore innovative methods to best measure the relative resilience of dogs to stressful events. This could include developing optimal exposure protocols to minimize the development of fear and anxiety, and exploring the influence of social learning and the most effective elements of stimulus presentation

    Large-Scale Model-Based Assessment of Deer-Vehicle Collision Risk

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    Ungulates, in particular the Central European roe deer Capreolus capreolus and the North American white-tailed deer Odocoileus virginianus, are economically and ecologically important. The two species are risk factors for deer–vehicle collisions and as browsers of palatable trees have implications for forest regeneration. However, no large-scale management systems for ungulates have been implemented, mainly because of the high efforts and costs associated with attempts to estimate population sizes of free-living ungulates living in a complex landscape. Attempts to directly estimate population sizes of deer are problematic owing to poor data quality and lack of spatial representation on larger scales. We used data on 74,000 deer–vehicle collisions observed in 2006 and 2009 in Bavaria, Germany, to model the local risk of deer–vehicle collisions and to investigate the relationship between deer–vehicle collisions and both environmental conditions and browsing intensities. An innovative modelling approach for the number of deer–vehicle collisions, which allows nonlinear environment–deer relationships and assessment of spatial heterogeneity, was the basis for estimating the local risk of collisions for specific road types on the scale of Bavarian municipalities. Based on this risk model, we propose a new “deer–vehicle collision index” for deer management. We show that the risk of deer–vehicle collisions is positively correlated to browsing intensity and to harvest numbers. Overall, our results demonstrate that the number of deer–vehicle collisions can be predicted with high precision on the scale of municipalities. In the densely populated and intensively used landscapes of Central Europe and North America, a model-based risk assessment for deer–vehicle collisions provides a cost-efficient instrument for deer management on the landscape scale. The measures derived from our model provide valuable information for planning road protection and defining hunting quota. Open-source software implementing the model can be used to transfer our modelling approach to wildlife–vehicle collisions elsewhere

    Genetic mechanisms of critical illness in COVID-19.

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    Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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