Contours of Inclusion: Inclusive Arts Teaching and Learning

The purpose of this publication is to share models and case examples of the process of inclusive arts curriculum design and evaluation. The first section explains the conceptual and curriculum frameworks that were used in the analysis and generation of the featured case studies (i.e. Understanding by Design, Differentiated Instruction, and Universal Design for Learning). Data for the cases studies was collected from three urban sites (i.e. Los Angeles, San Francisco, and Boston) and included participant observations, student and teacher interviews, curriculum documentation, digital documentation of student learning, and transcripts from discussion forum and teleconference discussions from a professional learning community.The initial case studies by Glass and Barnum use the curricular frameworks to analyze and understand what inclusive practices look like in two case studies of arts-in-education programs that included students with disabilities. The second set of precedent case studies by Kronenberg and Blair, and Jenkins and Agois Hurel uses the frameworks to explain their process of including students by providing flexible arts learning options to support student learning of content standards. Both sets of case studies illuminate curricular design decisions and instructional strategies that supported the active engagement and learning of students with disabilities in educational settings shared with their peers. The second set of cases also illustrate the reflective process of using frameworks like Universal Design for Learning (UDL) to guide curricular design, responsive instructional differentiation, and the use of the arts as a rich, meaningful, and engaging option to support learning. Appended are curriculum design and evaluation tools. (Individual chapters contain references.

Contours of Inclusion: Frameworks and Tools for Evaluating Arts in Education

This collection of essays explores various arts education-specific evaluation tools, as well as considers Universal Design for Learning (UDL) and the inclusion of people with disabilities in the design of evaluation instruments and strategies. Prominent evaluators Donna M. Mertens, Robert Horowitz, Dennie Palmer Wolf, and Gail Burnaford are contributors to this volume. The appendix includes the AEA Standards for Evaluation. (Contains 10 tables, 2 figures, 30 footnotes, and resources for additional reading.) This is a proceedings document from the 2007 VSA arts Research Symposium that preceded the American Evaluation Association's (AEA) annual meeting in Baltimore, MD

VSA Universal Design Access Guide: Every Thing Benefits Every One

The intent of this publication is to provide guidance and resources to VSA staff, contractors, and volunteers regarding implementation of universal design principles in presentations, meeting and conference planning, accessibility services, and web content. The objective of universal design is for everyone to access the same things at the same time, in the same place, and in as close to the same manner as possible. No checklist can produce universal design. In achieving universal design, precision with accessibility standards is only as important as the commitment to embracing inclusion. Universal design manifests only when an understanding of basic accessibility is coupled with a flexible and open mind. Creativity and basic respect make up its foundation. Preparing your organization to embrace self-determination to the fullest extent will foster an atmosphere of universal design. This document briefly describes the Seven Principles of Universal Design. However, Universal Design is more of an ongoing process than a prescription. We hope that you will use this document to foster the habit of using Universal Design principles to guide decision-making. More in-depth information on its history, current applications, and potential can be found by utilizing the resources section of this document

The Progressivity of Social Security

How much does the current social security system really redistribute from rich to poor? We use the PSID to estimate lifetime wage profiles and actual earnings each year for a sample of 1778 individuals, and we use mortality probabilities to calculate expected payroll taxes and social security benefits. For a given set of facts' about the net flows received by each individual, measured progressivity depends on many assumptions. This paper attempts to capture and to quantify all of the individual characteristics that are relevant to determine the progressivity of a life-cycle program like social security. We proceed in seven steps. First, we classify individuals by annual income and use Gini coefficients to find that social security is highly progressive. Second, we reclassify individuals on the basis of lifetime income and find that social security is less progressive. Third, we remove the cap on measured earnings and find that social security is even less progressive. Fourth, we switch from actual to potential lifetime earnings (the present value of the wage rate times 4000 hours each year). This measure captures the value of leisure and home production, so those out of the labor force are less poor, and net payments to them are less progressive. Fifth, we assign to each married individual half of the couple's income. The low-wage spouse is then not so poor less progressive. Sixth, we incorporate mortality probabilities that differ by potential lifetime income. Since the rich live longer and collect benefits longer, social security is no longer progressive. Finally, we increase the discount rate from 2% to 4%, which puts relatively more weight on the earlier-but-regressive payroll tax and less weight on the later-but-progressive benefit schedule. The whole social security system is then regressive.

Distributional Impacts of Proposed Changes to the Social Security System

In this paper we assess the degree to which the current social security system redistributes income from rich to poor. We then estimate the impact of various proposed changes to social security on the overall redistributive effect of the system. Our analysis takes a steady state approach in which we assume participants work their entire lives and retire under a given system. Redistribution is measured on a lifetime basis using estimated earnings profiles for a sample of people taken from the PSID. We account for differential mortality, not only by gender and race, but also be lifetime income. Our results indicate that the current social security system redistributes less than is generally perceived, mainly because people with higher lifetime income live longer and therefore draw benefits longer. Remaining progressivity is reduced and even reversed by an increase in the assumed discount rate, since regressive taxes become more important relative to later progressive benefits. We find that many of the proposed changes to social security have surprising little effect on the redistribution inherent in the system.

Double-labelled HIV-1 particles for study of virus–cell interaction

AbstractHuman immunodeficiency virus (HIV) delivers its genome to a host cell through fusion of the viral envelope with a cellular membrane. While the viral and cellular proteins involved in entry have been analyzed in detail, the dynamics of virus–cell fusion are largely unknown. Single virus tracing (SVT) provides the unique opportunity to visualize viral particles in real time allowing direct observation of the dynamics of this stochastic process. For this purpose, we developed a double-coloured HIV derivative carrying a green fluorescent label attached to the viral matrix protein combined with a red label fused to the viral Vpr protein designed to distinguish between complete virions and subviral particles lacking MA after membrane fusion. We present here a detailed characterization of this novel tool together with exemplary live cell imaging studies, demonstrating its suitability for real-time analyses of HIV–cell interaction

Dopamine Neuron Stimulating Actions of a GDNF Propeptide

BACKGROUND: Neurotrophic factors, such as glial cell line-derived neurotrophic factor (GDNF), have shown great promise for protection and restoration of damaged or dying dopamine neurons in animal models and in some Parkinson's disease (PD) clinical trials. However, the delivery of neurotrophic factors to the brain is difficult due to their large size and poor bio-distribution. In addition, developing more efficacious trophic factors is hampered by the difficulty of synthesis and structural modification. Small molecules with neurotrophic actions that are easy to synthesize and modify to improve bioavailability are needed. METHODS AND FINDINGS: Here we present the neurobiological actions of dopamine neuron stimulating peptide-11 (DNSP-11), an 11-mer peptide from the proGDNF domain. In vitro, DNSP-11 supports the survival of fetal mesencephalic neurons, increasing both the number of surviving cells and neuritic outgrowth. In MN9D cells, DNSP-11 protects against dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA)-induced cell death, significantly decreasing TUNEL-positive cells and levels of caspase-3 activity. In vivo, a single injection of DNSP-11 into the normal adult rat substantia nigra is taken up rapidly into neurons and increases resting levels of dopamine and its metabolites for up to 28 days. Of particular note, DNSP-11 significantly improves apomorphine-induced rotational behavior, and increases dopamine and dopamine metabolite tissue levels in the substantia nigra in a rat model of PD. Unlike GDNF, DNSP-11 was found to block staurosporine- and gramicidin-induced cytotoxicity in nutrient-deprived dopaminergic B65 cells, and its neuroprotective effects included preventing the release of cytochrome c from mitochondria. CONCLUSIONS: Collectively, these data support that DNSP-11 exhibits potent neurotrophic actions analogous to GDNF, making it a viable candidate for a PD therapeutic. However, it likely signals through pathways that do not directly involve the GFRalpha1 receptor

Antibiotics in Feed Induce Prophages in Swine Fecal Microbiomes

Antibiotics are a cost-effective tool for improving feed efficiency and preventing disease in agricultural animals, but the full scope of their collateral effects is not understood. Antibiotics have been shown to mediate gene transfer by inducing prophages in certain bacterial strains; therefore, one collateral effect could be prophage induction in the gut microbiome at large. Here we used metagenomics to evaluate the effect of two antibiotics in feed (carbadox and ASP250 [chlortetracycline, sulfamethazine, and penicillin]) on swine intestinal phage metagenomes (viromes). We also monitored the bacterial communities using 16S rRNA gene sequencing. ASP250, but not carbadox, caused significant population shifts in both the phage and bacterial communities. Antibiotic resistance genes, such as multidrug resistance efflux pumps, were identified in the viromes, but in-feed antibiotics caused no significant changes in their abundance. The abundance of phage integrase-encoding genes was significantly increased in the viromes of medicated swine over that in the viromes of nonmedicated swine, demonstrating the induction of prophages with antibiotic treatment. Phage-bacterium population dynamics were also examined. We observed a decrease in the relative abundance of Streptococcus bacteria (prey) when Streptococcus phages (predators) were abundant, supporting the “kill-the-winner” ecological model of population dynamics in the swine fecal microbiome. The data show that gut ecosystem dynamics are influenced by phages and that prophage induction is a collateral effect of in-feed antibiotics