SELWYN DEWDNEY FONDS

Fonds consists of records illustrating the career of Selwyn Dewdney as writer, artist and pioneer in the field of native rock art, and also contains personal materials and records relating to his background and family. Included are printed editions of published articles and books, source materials, manuscript drafts, sketches, drawings, notes, exhibition catalogues and slides, articles about Dewdney’s rock art studies, financial records, correspondence, notebooks and albums, genealogical charts and notes, photographs, family Christmas cards, and newspaper clippings

Here, there and everywhere: an analysis of reference services in academic archives

The purpose of this study is to investigate how archivists conduct reference services. The investigators administered two surveys to 19 participants at 15 Canadian academic archives to understand archivists’ behaviour while performing reference. There is no standard approach to reference as many archivists use institution-specific tools coupled with their own knowledge. Finding aids are the most frequently accessed tool and are most often used in conjunction with other tools. Limited resources are the primary barrier to the provision of effective reference services. The tools that are employed by archives are archivist focused, which results in reference services that are not user focused

Toward a competency framework for Canadian archivists

The goal of this research project is to establish a foundational competency framework for Canadian archivists. This was achieved by performing a qualitative analysis of established frameworks and generating a foundational competency framework from that analysis. The framework reflects current skills and knowledge requirements. The competency framework is meant to capture all facets of managing an archives, including activities such as governance and human resources. It is intended to strike a balance among all aspects of archival practice. Future iterations should include emergent issues such as emotional labor and regional practices. This competency framework is intended to define and communicate our skills and knowledge. Its acceptance and implementation will benefit our community, our stakeholders, and our collections and will support the longevity and the prosperity of the archival profession

Editorial: From Social Justice to Educational Justice: Challenging Practice, and Finding Hope

The purpose of this Special Issue is to explore, expose and energise issues around the concepts of social justice and education. We recognise that the notion of ‘social justice’ is not static, and is not shaped in a vacuum; it is iterative by nature, and flows across generations and contexts. The multiple historical and ideological perspectives that arise from this flow include education theory, research, and practice. These positionings offer deep insights into the purpose of education; they also raise important questions: are the social and ideological dynamics a force for challenging the status quo, and for rupturing cycles of inequity or perpetuating inequality? Do they interrupt the relations of dominance and subordination

Lung Epithelial Cell Transcriptional Regulation as a Factor in COVID-19 Associated Coagulopathies

SARS-CoV-2 has rapidly become a global pandemic. In addition to the acute pulmonary symptoms of COVID-19 (the disease associated with SARS-CoV-2 infection), pulmonary and distal coagulopathies have caused morbidity and mortality in many patients. Currently, the molecular pathogenesis underlying COVID-19 associated coagulopathies are unknown. Identifying the molecular basis of how SARS-CoV-2 drives coagulation is essential to mitigating short and long term thrombotic risks of sick and recovered COVID-19 patients. We aimed to perform coagulation focused transcriptome analysis of in vitro infected primary respiratory epithelial cells, patient derived bronchial alveolar lavage (BALF) cells, and circulating immune cells during SARS-CoV-2 infection. Our objective was to identify transcription mediated signaling networks driving coagulopathies associated with COVID-19. We analyzed recently published experimentally and clinically derived bulk or single cell RNA sequencing datasets of SARS-CoV-2 infection to identify changes in transcriptional regulation of blood coagulation. We also confirmed that the transcriptional expression of a key coagulation regulator was recapitulated at the protein level. We specifically focused our analysis on lung tissue expressed genes regulating the extrinsic coagulation cascade and the plasminogen activation system. Analyzing transcriptomic data of in vitro infected normal human bronchial epithelial (NHBE) cells and patient derived BALF samples revealed that SARS-CoV-2 infection induces the extrinsic blood coagulation cascade and suppresses the plasminogen activation system. We also performed in vitro SARS-CoV-2 infection experiments on primary human lung epithelial cells to confirm that transcriptional upregulation of Tissue Factor, the extrinsic coagulation cascade master regulator, manifested at the protein level. Further, infection of NHBEs with influenza A virus (IAV) did not drive key regulators of blood coagulation in a similar manner as SARS-CoV-2. Additionally, peripheral blood mononuclear cells (PBMCs) did not differentially express genes regulating the extrinsic coagulation cascade or plasminogen activation system during SARS-CoV-2 infection, suggesting that they are not directly inducing coagulopathy through these pathways. The hyper-activation of the extrinsic blood coagulation cascade and the suppression of the plasminogen activation system in SARS-CoV-2 infected epithelial cells may drive diverse coagulopathies in the lung and distal organ systems. Understanding how hosts drive such transcriptional changes with SARS-CoV-2 infection may enable the design of host-directed therapeutic strategies to treat COVID-19 and other coronaviruses inducing hyper-coagulation

The lung, the niche, and the microbe: Exploring the lung microbiome in cancer and immunity

The lung is a complex and unique organ system whose biology is strongly influenced by environmental exposure, oxygen abundance, connection to extrapulmonary systems via a dense capillary network, and an array of immune cells that reside in the tissue at steady state. The lung also harbors a low biomass community of commensal microorganisms that are dynamic during both health and disease with the capacity to modulate regulatory immune responses during diseases such as cancer. Lung cancer is the third most common cancer worldwide with the highest mortality rate amongst cancers due to the difficulty of an early diagnosis. This review discusses the current body of work addressing the interactions between the lung microbiota and the immune system, and how these two components of the pulmonary system are linked to lung cancer development and outcomes. Bringing in lessons from broader studies examining the effects of the gut microbiota on cancer outcomes, we highlight many challenges and gaps in this nascent field

Bacterial production of transparent exopolymer particles during static and laboratory-based cross-flow experiments

Open Access Article. This article is licensed under a Creative Commons Attribution 3.0 Unported Licence.Biofouling of seawater reverse osmosis (SWRO) membranes represents one of the leading causes of performance deterioration in the desalination industry. This work investigates the biofouling potential of microbial communities present in a reverse osmosis (RO) feed tank. As an example, water from the RO feed tank of the Penneshaw desalination plant (Kangaroo Island, South Australia) was used in a static biofilm formation experiment. Cultures of the indigenous biofilms formed during the static experiment showed that α-Proteobacteria and γ-Proteobacteria accounted for nearly 80% of the classes of bacteria present in the RO feed tank. Pseudomonas sp. was identified as the major species and isolated for testing in static and laboratory-based cross flow biofilm formation experiments. Results showed that the volume of TEPs generated by Pseudomonas sp. during the laboratory-based cross-flow experiment was 10 fold higher to that produced during the static experiment for the same time period, while both experiments were inoculated with cell concentrations of the same order of magnitude. The availability of nutrients was also shown to be a key driver in TEP production, particularly for the static experiments. This study provides insights into the phenomenon of biofouling by assessing the production of biofouling precursors from one of the main genera of biofilm-forming bacteria, namely Pseudomonas sp

Rapid Pathogen-Induced Apoptosis: A Mechanism Used by Dendritic Cells to Limit Intracellular Replication of Legionella pneumophila

Dendritic cells (DCs) are specialized phagocytes that internalize exogenous antigens and microbes at peripheral sites, and then migrate to lymphatic organs to display foreign peptides to naïve T cells. There are several examples where DCs have been shown to be more efficient at restricting the intracellular replication of pathogens compared to macrophages, a property that could prevent DCs from enhancing pathogen dissemination. To understand DC responses to pathogens, we investigated the mechanisms by which mouse DCs are able to restrict replication of the intracellular pathogen Legionella pneumophila. We show that both DCs and macrophages have the ability to interfere with L. pneumophila replication through a cell death pathway mediated by caspase-1 and Naip5. L. pneumophila that avoided Naip5-dependent responses, however, showed robust replication in macrophages but remained unable to replicate in DCs. Apoptotic cell death mediated by caspase-3 was found to occur much earlier in DCs following infection by L. pneumophila compared to macrophages infected similarly. Eliminating the pro-apoptotic proteins Bax and Bak or overproducing the anti-apoptotic protein Bcl-2 were both found to restore L. pneumophila replication in DCs. Thus, DCs have a microbial response pathway that rapidly activates apoptosis to limit pathogen replication

Surviving Deadly Lung Infections: Innate Host Tolerance Mechanisms in the Pulmonary System

Much research on infectious diseases focuses on clearing the pathogen through the use of antimicrobial drugs, the immune response, or a combination of both. Rapid clearance of pathogens allows for a quick return to a healthy state and increased survival. Pathogen-targeted approaches to combating infection have inherent limitations, including their pathogen-specific nature, the potential for antimicrobial resistance, and poor vaccine efficacy, among others. Another way to survive an infection is to tolerate the alterations to homeostasis that occur during a disease state through a process called host tolerance or resilience, which is independent from pathogen burden. Alterations in homeostasis during infection are numerous and include tissue damage, increased inflammation, metabolic changes, temperature changes, and changes in respiration. Given its importance and sensitivity, the lung is a good system for understanding host tolerance to infectious disease. Pneumonia is the leading cause of death for children under five worldwide. One reason for this is because when the pulmonary system is altered dramatically it greatly impacts the overall health and survival of a patient. Targeting host pathways involved in maintenance of pulmonary host tolerance during infection could provide an alternative therapeutic avenue that may be broadly applicable across a variety of pathologies. In this review, we will summarize recent findings on tolerance to host lung infection. We will focus on the involvement of innate immune responses in tolerance and how an initial viral lung infection may alter tolerance mechanisms in leukocytic, epithelial, and endothelial compartments to a subsequent bacterial infection. By understanding tolerance mechanisms in the lung we can better address treatment options for deadly pulmonary infections