501 research outputs found

    From Farm Results Demonstrations to Multistate Impact Designs: Cooperative Extension Navigates its Way Through Evaluation Pathways

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    This article explores how evaluation has been developed and expanded within the Cooperative Extension system, from the beginning of agricultural education in America in 1800 to the present day. Important periods across the history of Extension evaluation have been identified and categorized according to major themes and significant contributions of Extension individuals and organizations. Challenges for the future of evaluation within Extension are discussed

    Risk Assessment Matrices for Workplace Hazards: Design for Usability

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    In occupational safety and health (OSH), the process of assessing risks of identified hazards considers both the (i) foreseeable events and exposures that can cause harm and (ii) the likelihood or probability of occurrence. To account for both, a table format known as a risk assessment matrix uses rows and columns for ordered categories of the foreseeable severity of harm and likelihood/ probability of that occurrence. The cells within the table indicate level of risk. Each category has a text description separate from the matrix as well as a word or phrase heading each row and column. Ideally, these header terms will help the risk assessment team distinguish among the categories. A previous project provided recommended sets of header terms for common matrices based on findings from a survey of undergraduate OSH students. This paper provides background on risk assessment matrices, discusses usability issues, and presents findings from a survey of people with OSH-related experience. The aim of the survey was to confirm or improve the prior recommended sets of terms. The prior recommendations for severity, likelihood, and extent of exposure were confirmed with minor modifications. Improvements in the probability terms were recommended

    Mutations in AKAP5 Disrupt Dendritic Signaling Complexes and Lead to Electrophysiological and Behavioral Phenotypes in Mice

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    AKAP5 (also referred to as AKAP150 in rodents and AKAP79 in humans) is a scaffolding protein that is highly expressed in neurons and targets a variety of signaling molecules to dendritic membranes. AKAP5 interacts with PKA holoenzymes containing RIIα or RIIβ as well as calcineurin (PP2B), PKC, calmodulin, adenylyl cyclase type V/VI, L-type calcium channels, and β-adrenergic receptors. AKAP5 has also been shown to interact with members of the MAGUK family of PSD-scaffolding proteins including PSD95 and SAP97 and target signaling molecules to receptors and ion channels in the postsynaptic density (PSD). We created two lines of AKAP5 mutant mice: a knockout of AKAP5 (KO) and a mutant that lacks the PKA binding domain of AKAP5 (D36). We find that PKA is delocalized in both the hippocampus and striatum of KO and D36 mice indicating that other neural AKAPs cannot compensate for the loss of PKA binding to AKAP5. In AKAP5 mutant mice, a significant fraction of PKA becomes localized to dendritic shafts and this correlates with increased binding to microtubule associated protein-2 (MAP2). Electrophysiological and behavioral analysis demonstrated more severe deficits in both synaptic plasticity and operant learning in the D36 mice compared with the complete KO animals. Our results indicate that the targeting of calcineurin or other binding partners of AKAP5 in the absence of the balancing kinase, PKA, leads to a disruption of synaptic plasticity and results in learning and memory defects

    Detection and molecular characterisation of Cryptosporidium parvum in British European hedgehogs (Erinaceus europaeus)

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    Surveillance was conducted for the occurrence of protozoan parasites of the genus Cryptosporidium in European hedgehogs (Erinaceus europaeus) in Great Britain. In total, 108 voided faecal samples were collected from hedgehogs newly admitted to eight wildlife casualty treatment and rehabilitation centres. Terminal large intestinal (LI) contents from three hedgehog carcasses were also analysed. Information on host and location variables, including faecal appearance, body weight, and apparent health status, was compiled. Polymerase Chain Reaction (PCR) targeting the 18S ribosomal RNA gene, confirmed by sequencing, revealed an 8% (9/111) occurrence of Cryptosporidium parvum in faeces or LI contents, with no significant association between the host or location variables and infection. Archived small intestinal (SI) tissue from a hedgehog with histological evidence of cryptosporidiosis was also positive for C. parvum by PCR and sequence analysis of the 18S rRNA gene. No other Cryptosporidium species were detected. PCR and sequencing of the glycoprotein 60 gene identified three known zoonotic C. parvum subtypes not previously found in hedgehogs: IIdA17G1 (n=4), IIdA19G1 (n=1) and IIdA24G1 (n=1). These subtypes are also known to infect livestock. Another faecal sample contained C. parvum IIcA5G3j which has been found previously in hedgehogs, and for which there is one published report in a human, but is not known to affect livestock. The presence of zoonotic subtypes of C. parvum in British hedgehogs highlights a potential public health concern. Further research is needed to better understand the epidemiology and potential impacts of Cryptosporidium infection in hedgehogs

    Global, regional, and national burden of neurological disorders, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016

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    Background Neurological disorders are increasingly recognised as major causes of death and disability worldwide. The aim of this analysis from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 is to provide the most comprehensive and up-to-date estimates of the global, regional, and national burden from neurological disorders. Methods We estimated prevalence, incidence, deaths, and disability-adjusted life-years (DALYs; the sum of years of life lost [YLLs] and years lived with disability [YLDs]) by age and sex for 15 neurological disorder categories (tetanus, meningitis, encephalitis, stroke, brain and other CNS cancers, traumatic brain injury, spinal cord injury, Alzheimer’s disease and other dementias, Parkinson’s disease, multiple sclerosis, motor neuron diseases, idiopathic epilepsy, migraine, tension-type headache, and a residual category for other less common neurological disorders) in 195 countries from 1990 to 2016. DisMod-MR 2.1, a Bayesian meta-regression tool, was the main method of estimation of prevalence and incidence, and the Cause of Death Ensemble model (CODEm) was used for mortality estimation. We quantified the contribution of 84 risks and combinations of risk to the disease estimates for the 15 neurological disorder categories using the GBD comparative risk assessment approach. Findings Globally, in 2016, neurological disorders were the leading cause of DALYs (276 million [95% UI 247–308]) and second leading cause of deaths (9·0 million [8·8–9·4]). The absolute number of deaths and DALYs from all neurological disorders combined increased (deaths by 39% [34–44] and DALYs by 15% [9–21]) whereas their agestandardised rates decreased (deaths by 28% [26–30] and DALYs by 27% [24–31]) between 1990 and 2016. The only neurological disorders that had a decrease in rates and absolute numbers of deaths and DALYs were tetanus, meningitis, and encephalitis. The four largest contributors of neurological DALYs were stroke (42·2% [38·6–46·1]), migraine (16·3% [11·7–20·8]), Alzheimer’s and other dementias (10·4% [9·0–12·1]), and meningitis (7·9% [6·6–10·4]). For the combined neurological disorders, age-standardised DALY rates were significantly higher in males than in females (male-to-female ratio 1·12 [1·05–1·20]), but migraine, multiple sclerosis, and tension-type headache were more common and caused more burden in females, with male-to-female ratios of less than 0·7. The 84 risks quantified in GBD explain less than 10% of neurological disorder DALY burdens, except stroke, for which 88·8% (86·5–90·9) of DALYs are attributable to risk factors, and to a lesser extent Alzheimer’s disease and other dementias (22·3% [11·8–35·1] of DALYs are risk attributable) and idiopathic epilepsy (14·1% [10·8–17·5] of DALYs are risk attributable). Interpretation Globally, the burden of neurological disorders, as measured by the absolute number of DALYs, continues to increase. As populations are growing and ageing, and the prevalence of major disabling neurological disorders steeply increases with age, governments will face increasing demand for treatment, rehabilitation, and support services for neurological disorders. The scarcity of established modifiable risks for most of the neurological burden demonstrates that new knowledge is required to develop effective prevention and treatment strategies

    Global, regional, and national burden of meningitis, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016

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    Background Acute meningitis has a high case-fatality rate and survivors can have severe lifelong disability. We aimed to provide a comprehensive assessment of the levels and trends of global meningitis burden that could help to guide introduction, continuation, and ongoing development of vaccines and treatment programmes.AA received funding from Department of Science and Technology, Government of India, New Delhi, through INSPIRE Faculty Award Scheme. HB was financially supported by Mazandaran University of Medical Sciences, Sari, Iran. AB received support for research from the Project of Ministry of Education, Science and Technology of the Republic of Serbia (No. III45005). TWB was supported by the Alexander von Humboldt Foundation through the Alexander von Humboldt Professor award, funded by the Federal Ministry of Education and Research. FC reports European Union (FEDER funds POCI/01/0145/FEDER/007728 and POCI/01/0145/ FEDER/007265) and National Funds (FCT/MEC, Fundação para a Ciência e a Tecnologia and Ministério da Educação e Ciência) under the Partnership Agreements PT2020 UID/MULTI/04378/2013 and PT2020 UID/QUI/50006/2013. HF was financially supported by Urmia University of Medical sciences, Urmia, Iran. EF reports European Union (FEDER funds POCI/01/0145/FEDER/007728 and POCI/01/0145/FEDER/007265) and National Funds (FCT/MEC, Fundação para a Ciência e a Tecnologia and Ministério da Educação e Ciência) under the Partnership Agreements PT2020 UID/MULTI/04378/2013 and PT2020 UID/QUI/50006/2013. JK has received research funding from Merck Pharmaceuticals. AM acknowledges that Imperial College London is grateful for support from the NW London National Institute of Health and Research Collaboration for Leadership in Applied Health Research and Care. UOM acknowledges funding from the German National Cohort Study Federal Ministry of Education and Research Grant #01ER1511/D. AMS was supported by a fellowship from the Egyptian Fulbright Mission Program. MSM acknowledges the support from the Ministry of Education, Science and Technological Development, Republic of Serbia (Contract No. 175087). KBT acknowledges funding supports from the Maurice Wilkins Centre for Biodiscovery, Cancer Society of New Zealand, Health Research Council, Gut Cancer Foundation, and the University of Auckland. CSW’s work is funded by the South African Medical Research Council and the National Research Foundation of South Africa (Grant Numbers: 106035 and 108571)
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