Directions for 21st Century Lifelong Learning Institutes: Elucidating Questions from Osher Lifelong Learning Institute Studies

The literature regarding lifelong learning is robust, while the literature on lifelong learning institutions, centers, and programs remain under-researched in comparison. This article draws insights from a specific network of lifelong learning institutes with a rich history and high rapport in the United States: the Osher Lifelong Learning Institute (OLLI) network. Sixty articles regarding OLLIs are catalogued and highlighted to elucidate twelve thematic areas and twelve questions for future research and practice. In particular, these themes are related to adult education, healthy aging, and educational gerontology. The article concludes by reflecting on trends in and needs for institutional research and practice.Les publications portant sur l’éducation permanente sont nombreuses, contrairement à celles touchant les institutions, centres et programmes d’éducation permanente qui, en comparaison, demeurent généralement mal connus. Cet article recueille des idées d’un réseau d’instituts d’éducation permanente ayant un passé riche et de bons rapports aux États-Unis : le réseau Osher Lifelong Learning Institute (OLLI). Soixante articles portant sur OLLI ont été catalogués et analysés pour faire ressortir douze thèmes et douze questions pour la recherche et la pratique à l’avenir. Ces thèmes se rattachent à l’éducation des adultes, le vieillissement sain et la gérontologie éducative. L’article se termine par des réflexions sur des tendances et des besoins relatifs à la recherche et la pratique institutionnelles.Mots clés : recherche institutionnelle, éducation permanente, ainés, éducation des adultes, universités adaptées aux personnes âgée

Cotton Production in Far West Texas with Emphasis on Irrigation and Fertilization.

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Vaccine conjugate

Describes a method of producing active immunity against a viral disease in an animal subject. It comprises of administering a vaccine conjugate consisting essentially of a live virus and a neutralizing factor bound to the live virus to the subject. The neutralizing factor is selected from the group consisting of antibodies and antibody fragments. The live virus is one capable of producing disease in the subject, and the antibody or antibody fragment is one capable of neutralizing the live virus

Method of treating viral diseases in animals

Describes a method of producing active immunity against a viral disease in an animal subject. It comprises of administering a vaccine conjugate consisting essentially of a live virus and a neutralizing factor bound to the live virus to the subject. The neutralizing factor is selected from the group consisting of antibodies and antibody fragments. The live virus is one capable of producing disease in the subject, and the antibody or antibody fragment is one capable of neutralizing the live virus. Preferred subjects are birds, a preferred virus is Infectious Bursal Disease Virus, and a preferred route of administration to birds is by in ovo administration

Method of treatment

Describes a method of producing active immunity against a viral disease in an animal subject. It comprises of administering a vaccine conjugate consisting essentially of a live virus and a neutralizing factor bound to the live virus to the subject. The neutralizing factor is selected from the group consisting of antibodies and antibody fragments. The live virus is one capable of producing disease in the subject, and the antibody or antibody fragment is one capable of neutralizing the live virus. Preferred subjects are birds, a preferred virus is Infectious Bursal Disease Virus, and a preferred route of administration to birds is by in ovo administration

Vaccine conjugate for treatment of avian diseases

A method of producing active immunity against infectious bursal disease virus in an avian subject comprises administering to the subject a vaccine conjugate consisting essentially of a live virus and a neutralizing factor bound to the live virus. The neutralizing factor is selected from the group consisting of antibodies and antibody fragments. The live virus is one capable of producing disease in the subject, and the antibody or antibody fragment is one capable of neutralizing the live virus. A preferred route of administration to birds is by in ovo administration

Maternal neurofascin-specific autoantibodies bind to structures of the fetal nervous system during pregnancy, but have no long term effect on development in the rat

Neurofascin was recently reported as a target for axopathic autoantibodies in patients with multiple sclerosis (MS), a response that will exacerbate axonal pathology and disease severity in an animal model of multiple sclerosis. As transplacental transfer of maternal autoantibodies can permanently damage the developing nervous system we investigated whether intrauterine exposure to this neurofascin-specific response had any detrimental effect on white matter tract development. To address this question we intravenously injected pregnant rats with either a pathogenic anti-neurofascin monoclonal antibody or an appropriate isotype control on days 15 and 18 of pregnancy, respectively, to mimic the physiological concentration of maternal antibodies in the circulation of the fetus towards the end of pregnancy. Pups were monitored daily with respect to litter size, birth weight, growth and motor development. Histological studies were performed on E20 embryos and pups sacrificed on days 2, 10, 21, 32 and 45 days post partum. Results: Immunohistochemistry for light and confocal microscopy confirmed passively transferred anti-neurofascin antibody had crossed the placenta to bind to distinct structures in the developing cortex and cerebellum. However, this did not result in any significant differences in litter size, birth weight, or general physical development between litters from control mothers or those treated with the neurofascin-specific antibody. Histological analysis also failed to identify any neuronal or white matter tract abnormalities induced by the neurofascin-specific antibody. Conclusions: We show that transplacental transfer of circulating anti-neurofascin antibodies can occur and targets specific structures in the CNS of the developing fetus. However, this did not result in any pre- or post-natal abnormalities in the offspring of the treated mothers. These results assure that even if anti-neurofascin responses are detected in pregnant women with multiple sclerosis these are unlikely to have a negative effect on their children

International Evidence Based Reappraisal of Genes Associated With Arrhythmogenic Right Ventricular Cardiomyopathy Using the Clinical Genome Resource Framework

Background - Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disease characterized by ventricular arrhythmias and progressive ventricular dysfunction. Genetic testing is recommended and a pathogenic variant in an ARVC-associated gene is a major criterion for diagnosis according to the 2010 Task Force Criteria (TFC). As incorrect attribution of a gene to ARVC can contribute to misdiagnosis, we assembled an international multidisciplinary ARVC ClinGen Gene Curation Expert Panel to reappraise all reported ARVC genes. / Methods - Following a comprehensive literature search, six two-member teams conducted blinded independent curation of reported ARVC genes using the semi-quantitative ClinGen framework. /Results - Of 26 reported ARVC genes, only six (PKP2, DSP, DSG2, DSC2, JUP, TMEM43) had strong evidence and were classified as definitive for ARVC causation. There was moderate evidence for two genes, DES and PLN. The remaining 18 genes had limited or no evidence. RYR2 was refuted as an ARVC gene since clinical data and model systems exhibited a catecholaminergic polymorphic ventricular tachycardia (CPVT) phenotype. In ClinVar, only 5 pathogenic / likely pathogenic (P/LP) variants (1.1%) in limited evidence genes had been reported in ARVC cases in contrast to 450 desmosome gene variants (97.4%). / Conclusions - Using the ClinGen approach to gene-disease curation, only eight genes, (PKP2, DSP, DSG2, DSC2, JUP, TMEM43, PLN, DES) had definitive or moderate evidence for ARVC and these genes accounted for nearly all P/LP ARVC variants in ClinVar. Therefore, only P/LP variants in these eight genes should yield a major criterion for ARVC diagnosis. P/LP variants identified in other genes in a patient should prompt further phenotyping as variants in many of these genes are associated with other cardiovascular conditions

Beyond gene-disease validity: capturing structured data on inheritance, allelic-requirement, disease-relevant variant classes, and disease mechanism for inherited cardiac conditions

Background: As the availability of genomic testing grows, variant interpretation will increasingly be performed by genomic generalists, rather than domain-specific experts. Demand is rising for laboratories to accurately classify variants in inherited cardiac condition (ICC) genes, including secondary findings. Methods: We analyse evidence for inheritance patterns, allelic requirement, disease mechanism and disease-relevant variant classes for 65 ClinGen-curated ICC gene-disease pairs. We present this information for the first time in a structured dataset, CardiacG2P, and assess application in genomic variant filtering. Results: For 36/65 gene-disease pairs, loss of function is not an established disease mechanism, and protein truncating variants are not known to be pathogenic. Using the CardiacG2P dataset as an initial variant filter allows for efficient variant prioritisation whilst maintaining a high sensitivity for retaining pathogenic variants compared with two other variant filtering approaches. Conclusions: Access to evidence-based structured data representing disease mechanism and allelic requirement aids variant filtering and analysis and is a pre-requisite for scalable genomic testing