Radical Access: Textiles and Museums

This presentation discusses recent initiatives at Glenbow and Nickle Galleries that endeavor to provide new, radical levels of access to textile collections as a means to build community and affect creativity. While locking textiles away in environmentally controlled rooms and minimizing handling are useful methods for preservation, they are less effective in building vibrant communities or creating future relevance form museum collections. This paper, building on Hemming’s post-colonial textile theory, as well as Onciul’s theories on decolonizing engagement, challenge the apparent dichotomy between access and preservation. It argues that preservation without radical access, without shared community meaning making, without respecting the inherent kinship of museum textiles, is unattainable. This apparent stalemate is a relic of museums’ colonial past where institutional priorities have tended to exclude consideration of source communities’ needs. With textile collections, their physical well-being has been prioritized over their ongoing relationships with cultural groups. The concept of radicalizing access is an approach that both the Nickle Galleries and Glenbow are exploring in order to transform their relationships with the communities they serve. Schmidt will discuss how Glenbow is taking responsibility for previously stripping culture from Indigenous people and how connecting community members with textile collections is affecting reconciliation. A recent project involves connecting Indigenous foster children with textiles, enhancing their awareness and experience of Indigenous Culture. Hardy will discuss ongoing teaching efforts with the Nickle’s Afghan textiles, enhancing awareness of refugee’s experiences of war. Other initiatives involve connecting artists and the Nickle’s textile collections, fostering new creative research. Both sets of examples illustrate how radical access can shift the balance of power between museums and source communities and enable shared meaning making or abrogating that right-enhancing the relevance and ongoing preservation of textiles and communities of textile users

Achilles Tendon Ruptures in Two Male Athletes in NCAA Division I: Report of Two Cases

Major tendon ruptures are rare, with an Achilles tendon rupture (ATR) being the most frequent type. Reported cases most commonly involve male recreational athletes who have increased body mass indexes and are between ages 30 and 50 years. We describe two male athletes in Division I of the National Collegiate Athletic Association who underwent surgical repair for treating an ATR associated with running-related activities. In contrast to other cases, both patients had normal body mass indexes. These two cases identify high-level athletes who underwent operative Achilles tendon repair and returned to their sport at a similar level or high level of post-college athletic activity with promising strength and function

VPg of murine norovirus binds translation initiation factors in infected cells

BACKGROUND: Norovirus genomic and subgenomic RNAs are covalently linked at the 5' nucleotide to a 15 kD protein called VPg. VPg of two human norovirus strains binds translation initiation factor eIF3 and other eIFs in vitro, suggesting VPg functions in initiation of protein synthesis on viral RNA. Human norovirus strains are not cultivable, and thus experimental evidence of interactions between VPg and eIFs in infected cells has been lacking. We used the cultivable murine norovirus MNV-1 as a model to study interactions between VPg and eIFs in infected cells. RESULTS: As shown previously for human norovirus VPg, MNV-1 VPg bound eIF3, eIF4GI, eIF4E, and S6 ribosomal protein in cell extracts by GST pull-down assay. Importantly, MNV-1 VPg co-precipitated eIF4GI and eIF4E from infected macrophages, providing evidence that VPg interacts with components of the translation machinery in norovirus infected cells. CONCLUSION: The interactions between MNV-1 VPg and eIFs completely mimic those reported for the human norovirus VPg, illustrating the utility of MNV-1 as a relevant molecular model to study mechanisms of human norovirus replication

Early vs late string networks from a minimal QCD axion

We propose a new regime of minimal QCD axion dark matter that lies between the pre- and post-inflationary scenarios, such that the Peccei-Quinn (PQ) symmetry is restored only on sufficiently large spatial scales. This leads to a novel cosmological evolution, in which strings and domain walls re-enter the horizon and annihilate later than in the ordinary post-inflationary regime, possibly even after the QCD crossover. Such dynamics can occur if the PQ symmetry is restored by inflationary fluctuations, i.e. the Hubble parameter during inflation HI is larger than the PQ breaking scale fa, but it is not thermally restored afterwards. Solving the Fokker-Planck equation, we estimate the number of inflationary e-folds required for the PQ symmetry to be, on average, restored. Moreover, we show that, in the large parts of parameter space where the radial mode is displaced from the minimum by de Sitter fluctuations, a string network forms due to the radial mode oscillating over the top of its potential after inflation. In both cases we identify order one ranges in HI/fa and in the quartic coupling λ of the PQ potential that lead to the late-string dynamics. In this regime the cosmological dark matter abundance can be reproduced for axion decay constants as low as the astrophysical constraint (108) GeV, corresponding to axion masses up to 10−2 eV, and with miniclusters with masses as large as (10)M⊙

Natural products that reduce rotavirus infectivity identified by a cell-based moderate-throughput screening assay

BACKGROUND: There is widespread interest in the use of innate immune modulators as a defense strategy against infectious pathogens. Using rotavirus as a model system, we developed a cell-based, moderate-throughput screening (MTS) assay to identify compounds that reduce rotavirus infectivity in vitro, toward a long-term goal of discovering immunomodulatory agents that enhance innate responses to viral infection. RESULTS: A natural product library consisting of 280 compounds was screened in the assay and 15 compounds that significantly reduced infectivity without cytotoxicity were identified. Time course analysis of four compounds with previously characterized effects on inflammatory gene expression inhibited replication with pre-treatment times as minimal as 2 hours. Two of these four compounds, α-mangostin and 18-β-glycyrrhetinic acid, activated NFκB and induced IL-8 secretion. The assay is adaptable to other virus systems, and amenable to full automation and adaptation to a high-throughput format. CONCLUSION: Identification of several compounds with known effects on inflammatory and antiviral gene expression that confer resistance to rotavirus infection in vitro suggests the assay is an appropriate platform for discovery of compounds with potential to amplify innate antiviral responses

Rotavirus infection activates the UPR but modulates its activity

<p>Abstract</p> <p>Background</p> <p>Rotaviruses are known to modulate the innate antiviral defense response driven by IFN. The purpose of this study was to identify changes in the cellular proteome in response to rotavirus infection in the context of the IFN response. We also sought to identify proteins outside the IFN induction and signaling pathway that were modulated by rotavirus infection.</p> <p>Methods</p> <p>2D-DIGE and image analysis were used to identify cellular proteins that changed in levels of expression in response to rotavirus infection, IFN treatment, or IFN treatment prior to infection. Immunofluorescence microscopy was used to determine the subcellular localization of proteins associated with the unfolded protein response (UPR).</p> <p>Results</p> <p>The data show changes in the levels of multiple proteins associated with cellular stress in infected cells, including levels of ER chaperones GRP78 and GRP94. Further investigations showed that GRP78, GRP94 and other proteins with roles in the ER-initiated UPR including PERK, CHOP and GADD34, were localized to viroplasms in infected cells.</p> <p>Conclusions</p> <p>Together the results suggest rotavirus infection activates the UPR, but modulates its effects by sequestering sensor, transcription factor, and effector proteins in viroplasms. The data consequently also suggest that viroplasms may directly or indirectly play a fundamental role in regulating signaling pathways associated with cellular defense responses.</p

Morita Duality and Noncommutative Wilson Loops in Two Dimensions

We describe a combinatorial approach to the analysis of the shape and orientation dependence of Wilson loop observables on two-dimensional noncommutative tori. Morita equivalence is used to map the computation of loop correlators onto the combinatorics of non-planar graphs. Several nonperturbative examples of symmetry breaking under area-preserving diffeomorphisms are thereby presented. Analytic expressions for correlators of Wilson loops with infinite winding number are also derived and shown to agree with results from ordinary Yang-Mills theory.Comment: 32 pages, 9 figures; v2: clarifying comments added; Final version to be published in JHE

Unraveling the directional link between adiposity and inflammation: a bidirectional mendelian randomization approach

&lt;b&gt;Context&lt;/b&gt;: Associations between adiposity and circulating inflammation markers are assumed to be causal, although the direction of the relationship has not been proven. &lt;b&gt;Objective&lt;/b&gt;: The aim of the study was to explore the causal direction of the relationship between adiposity and inflammation using a bidirectional Mendelian randomization approach. &lt;b&gt;Methods&lt;/b&gt;: In the PROSPER study of 5804 elderly patients, we related C-reactive protein (CRP) single nucleotide polymorphisms (SNPs) (rs1800947 and rs1205) and adiposity SNPs (FTO and MC4R) to body mass index (BMI) as well as circulating levels of CRP and leptin. We gave each individual two allele scores ranging from zero to 4, counting each pair of alleles related to CRP levels or BMI. &lt;b&gt;Results&lt;/b&gt;: With increasing CRP allele score, there was a stepwise decrease in CRP levels (P for trend &#60; 0.0001) and a 1.98 mg/liter difference between extremes of the allele score distribution, but there was no associated change in BMI or leptin levels (P ≥ 0.89). By contrast, adiposity allele score was associated with 1) an increase in BMI (1.2 kg/m2 difference between extremes; P for trend 0.002); 2) an increase in circulating leptin (5.77 ng/ml difference between extremes; P for trend 0.0027); and 3) increased CRP levels (1.24 mg/liter difference between extremes; P for trend 0.002). &lt;b&gt;Conclusions&lt;/b&gt;: Greater adiposity conferred by FTO and MC4R SNPs led to higher CRP levels, with no evidence for any reverse pathway. Future studies should extend our findings to other circulating inflammatory parameters. This study illustrates the potential power of Mendelian randomization to dissect directions of causality between intercorrelated metabolic factors