Memex Metadata (M2) for Reflective Learning

This paper reports on metadata research and development supporting memory and reflective learning that is being conducted as part of the Memex Metadata (M2) for Student Portfolios project, University of North Carolina at Chapel Hill. The paper reviews learning, memory, and reflective learning strategies; introduces the M2 project; presents a reflective learning scenario for a plant biology class; and reviews two metadata developments underlying the M2 project: 1) A context awareness framework (CAF), and 2) An extended metadata framework. The paper concludes with a brief discussion of future research activities.We would like to acknowledge Microsoft Research and UNC’s Information Technology Services for their support and sponsorship of this research

Mitochondrial DNA mutations in human degenerative diseases and aging

AbstractA wide variety of mitochondrial DNA (mtDNA) mutations have recently been identified in degenerative diseases of the brain, heart, skeletal muscle, kidney and endocrine system. Generally, individuals inheriting these mitochondrial diseases are relatively normal in early life, develop symptoms during childhood, mid-life, or old age depending on the severity of the maternally-inherited mtDNA mutation; and then undergo a progressive decline. These novel features of mtDNA disease are proposed to be the product of the high dependence of the target organs on mitochondrial bioenergetics, and the cumulative oxidative phosphorylation (OXPHOS) defect caused by the inherited mtDNA mutation together with the age-related accumulation mtDNA mutations in post-mitotic tissues

Ischemic stroke risk, smoking, and the genetics of inflammation in a biracial population: the stroke prevention in young women study

<p>Abstract</p> <p>Background</p> <p>Although cigarette smoking is a well-established risk factor for vascular disease, the genetic mechanisms that link cigarette smoking to an increased incidence of stroke are not well understood. Genetic variations within the genes of the inflammatory pathways are thought to partially mediate this risk. Here we evaluate the association of several inflammatory gene single nucleotide polymorphisms (SNPs) with ischemic stroke risk among young women, further stratified by current cigarette smoking status.</p> <p>Methods</p> <p>A population-based case-control study of stroke among women aged 15–49 identified 224 cases of first ischemic stroke (47.3% African-American) and 211 age-comparable control subjects (43.1% African-American). Several inflammatory candidate gene SNPs chosen through literature review were genotyped in the study population and assessed for association with stroke and interaction with smoking status.</p> <p>Results</p> <p>Of the 8 SNPs (across 6 genes) analyzed, only <it>IL6 </it>SNP rs2069832 (allele C, African-American frequency = 92%, Caucasian frequency = 55%) was found to be significantly associated with stroke using an additive model, and this was only among African-Americans (age-adjusted: OR = 2.2, 95% CI = 1.0–5.0, p = 0.049; risk factor adjusted: OR = 2.5, 95% CI = 1.0–6.5, p = 0.05). When stratified by smoking status, two SNPs demonstrated statistically significant gene-environment interactions. First, the T allele (frequency = 5%) of <it>IL6 </it>SNP rs2069830 was found to be protective among non-smokers (OR = 0.30, 95% CI = 0.11–.082, p = 0.02), but not among smokers (OR = 1.63, 95% CI = 0.48–5.58, p = 0.43); genotype by smoking interaction (p = 0.036). Second, the C allele (frequency = 39%) of <it>CD14 </it>SNP rs2569190 was found to increase risk among smokers (OR = 2.05, 95% CI = 1.09–3.86, p = 0.03), but not among non-smokers (OR = 0.93, 95% CI = 0.62–1.39, p = 0.72); genotype by smoking interaction (p = 0.039).</p> <p>Conclusion</p> <p>This study demonstrates that inflammatory gene SNPs are associated with early-onset ischemic stroke among African-American women (<it>IL6</it>) and that cigarette smoking may modulate stroke risk through a gene-environment interaction (<it>IL6 and CD14</it>). Our finding replicates a prior study showing an interaction with smoking and the C allele of <it>CD14 </it>SNP rs2569190.</p

The consequences of nuclear transfer for mammalian foetal development and offspring survival : a mitochondrial DNA perspective

Review of the articleThe introduction of nuclear transfer (NT) and other technologies that involve embryo reconstruction require us to reinvestigate patterns of mitochondrial DNA (mtDNA) transmission, transcription and replication. MtDNA is a 16.6 kb genome located within each mitochondrion. The number of mitochondria and mtDNA copies per organelle is specific to each cell type. MtDNA is normally transmitted through the oocyte to the offspring. However, reconstructed oocytes often transmit both recipient oocyte mtDNA and mtDNA associated with the donor nucleus. We argue that the transmission of two populations of mtDNA may have implications for offspring survival as only one allele might be actively transcribed. This could result in the offspring phenotypically exhibiting mtDNA depletion-type syndromes. A similar occurrence could arise when nucleo-cytoplasmic interactions fail to regulate mtDNA transcription and replication, especially as the initiation of mtDNA replication post-implantation is a key developmental event. Furthermore, failure of the donor somatic nucleus to be reprogrammed could result in the early initiation of replication and the loss of cellular mtDNA specificity. We suggest investigations should be conducted to enhance our understanding of nucleo-cytoplasmic interactions in order to improve NT efficiency

Practitioner\u27s Guide to Technology, Pedagogy, and Content Knowledge (TPACK): Rich Media Cases of Teacher Knowledge

The goal of the TPACK Practitioners Guide is simple--to offer exemplary cases of technology integration efforts that result in curriculum-based student learning in each of the following nine content areas and grade level contexts: Elementary Science, Elementary Math, Elementary Social Studies, Elementary Reading, Middle School Language Arts, Secondary Science, Secondary Math, Secondary Social Studies, and, Secondary English.https://scholarworks.wm.edu/book/1000/thumbnail.jp

Editorial: Implementing the Teacher Education Initiative

Representatives from ten specialty professional associations affiliated with the National Technology Leadership Coalition (NTLC) are collaborating with Microsoft Corporation to develop an innovative professional development opportunity for teacher educators—the Teacher Education Initiative (TEI). The goal of the initiative is to enhance preparation of future teachers to use technology in effective ways to teach students across grades and academic disciplines. This effort builds upon initiatives such as Preparing Tomorrow’s Teachers to Use Technology (PT3) and Microsoft’s Partners in Learning (PIL) program. The goals of TEI are described in more detail in a previously published overview, “Preparing Teachers for Tomorrow’s Technologies” (Dilworth et al., 2012). The current article describes planned implementation strategies designed to advance more effective integration of technology in teacher preparation. TEI is grounded in the framework of technology, pedagogy, and content knowledge (TPACK; referred to as technological pedagogical content knowledge in Mishra & Koehler, 2006). Representatives of teacher education associations from a number of academic disciplines have assumed responsibility for the development of teacher education resources for each discipline. Representatives from associations related to special education, instructional technology, and teacher education at large are developing resources for non-discipline-specific teacher educators. In order to facilitate a systematic, coordinated approach within each TEI college or university representatives from the American Association of Colleges for Teacher Education (AACTE) are developing related materials for the leaders of schools, colleges and departments of teacher education

DER OKONOMISCHE EFFEKT EINER ERHOHUNG DER ARBEITSLOSENLEISTUNGEN : NEUBETRACHT UNTER VERWENDUNG DES ATKINSON MODELLS

In der zweiten Halfte der 1970er begannen sich wirtschaftliche Kennziffern industrialisierter Staaten rapide zu verschlechtern. Gleichzeitig ruckte der Wohlfahrtsstaat als Ursache in das Zentrum der Kritik. Einige Wirtschaftswissenschaftler, insbesondere die deutschen Neo- Liberalisten, hatten bereits seit den 1950ern eine kritische Haltung zum wohlfahrtsstaatlichen Konzept eingenommen. Seit den 1970ern gesellten sich zu diesen Liberalisten auch viele Wirtschaftswissenschaftler, die zuvor den Wohlfahrtsstaat unterstutzt hatten. A.B. Atkinson wies jedoch daraufhin, daB viele der verwandten okonomischen Analysen auf un- fundierten theoretischen Modellen basierten, die die eigentlichen Merkmale des sozialen Wohlfahrtsprogramms auBer Acht lieBen. In der vorliegenden Arbeit gehen wir daher, den wirtschaftlichen Auswirkungen der Arbeitslosenversicherung in Einklang mit Atkinsons Kritik nach. Es gelang ihm gegenteilige Ergebnisse zu dem popularen Shapiro und Stiglitz Shirking Modell, durch Einfuhrung zweier Annahmen, d.h. Arbeitslosenleistungen werden identifizierten Shirkern vorenthalten und Arbeitslosenleistungen werden generell nur fur einen bestimmten Zeitraum angeboten, nachzuweisen. In der vorliegenden Arbeit zeigen wir, daB Gehalt basierende Arbeitslosenleistungen sich positiv auf Produktivitat und Beschaftigung auswirken. Zeitliche Begrenzung und eine ansteigende Sockelleistung alleine haben nicht die gleichen Ergebnisse im Shapiro und Stiglitz Modell

Common data elements for clinical research in mitochondrial disease: a National Institute for Neurological Disorders and Stroke project

Objectives The common data elements (CDE) project was developed by the National Institute of Neurological Disorders and Stroke (NINDS) to provide clinical researchers with tools to improve data quality and allow for harmonization of data collected in different research studies. CDEs have been created for several neurological diseases; the aim of this project was to develop CDEs specifically curated for mitochondrial disease (Mito) to enhance clinical research. Methods Nine working groups (WGs), composed of international mitochondrial disease experts, provided recommendations for Mito clinical research. They initially reviewed existing NINDS CDEs and instruments, and developed new data elements or instruments when needed. Recommendations were organized, internally reviewed by the Mito WGs, and posted online for external public comment for a period of eight weeks. The final version was again reviewed by all WGs and the NINDS CDE team prior to posting for public use

Expert Panel Curation of 113 Primary Mitochondrial Disease Genes for the Leigh Syndrome Spectrum

OBJECTIVE: Primary mitochondrial diseases (PMDs) are heterogeneous disorders caused by inherited mitochondrial dysfunction. Classically defined neuropathologically as subacute necrotizing encephalomyelopathy, Leigh syndrome spectrum (LSS) is the most frequent manifestation of PMD in children, but may also present in adults. A major challenge for accurate diagnosis of LSS in the genomic medicine era is establishing gene-disease relationships (GDRs) for this syndrome with >100 monogenic causes across both nuclear and mitochondrial genomes. METHODS: The Clinical Genome Resource (ClinGen) Mitochondrial Disease Gene Curation Expert Panel (GCEP), comprising 40 international PMD experts, met monthly for 4 years to review GDRs for LSS. The GCEP standardized gene curation for LSS by refining the phenotypic definition, modifying the ClinGen Gene-Disease Clinical Validity Curation Framework to improve interpretation for LSS, and establishing a scoring rubric for LSS. RESULTS: The GDR with LSS across the nuclear and mitochondrial genomes was classified as definitive for 31/114 gene-disease relationships curated (27%); moderate for 38 (33%); limited for 43 (38%); and 2 as disputed (2%). Ninety genes were associated with autosomal recessive inheritance, 16 were maternally inherited, 5 autosomal dominant, and 3 X-linked. INTERPRETATION: GDRs for LSS were established for genes across both nuclear and mitochondrial genomes. Establishing these GDRs will allow accurate variant interpretation, expedite genetic diagnosis of LSS, and facilitate precision medicine, multi-system organ surveillance, recurrence risk counselling, reproductive choice, natural history studies and eligibility for interventional clinical trials. This article is protected by copyright. All rights reserved