Debakarn Koorliny Wangkiny: steady walking and talking using first nations-led participatory action research methodologies to build relationships

Aboriginal participatory action research (APAR) has an ethical focus that corrects the imbalances of colonisation through participation and shared decision-making to position people, place, and intention at the centre of research. APAR supports researchers to respond to the community's local rhythms and culture. APAR supports researchers to respond to the community's local rhythms and culture. First Nations scholars and their allies do this in a way that decolonises mainstream approaches in research to disrupt its cherished ideals and endeavours. How these knowledges are co-created and translated is also critically scrutinised. We are a team of intercultural researchers working with community and mainstream health service providers to improve service access, responsiveness, and Aboriginal client outcomes. Our article begins with an overview of the APAR literature and pays homage to the decolonising scholarship that champions Aboriginal ways of knowing, being, and doing. We present a research program where Aboriginal Elders, as cultural guides, hold the research through storying and cultural experiences that have deepened relationships between services and the local Aboriginal community. We conclude with implications of a community-led engagement framework underpinned by a relational methodology that reflects the nuances of knowledge translation through a co-creation of new knowledge and knowledge exchange

Lung adenocarcinoma with peculiar growth to the pulmonary artery and thrombus formation: report of a case

<p>Abstract</p> <p>Background</p> <p>Cases of pulmonary artery masses have only rarely been reported, and the optimal type of the diagnosis and treatment is controversial.</p> <p>Case Presentation</p> <p>An 81-year-old woman was found to have an abnormal shadow on chest X-ray film. Computed tomography showed an irregularly bordered tumor centered in the hilar region extending from segment 6 to the middle lobe of the right lung. Pulmonary angiography showed complete occlusion of the trunk at the periphery proximal to the bifurcation of the posterior ascending branch. Based on bronchoscopic biopsy of the tumor, an adenocarcinoma was diagnosed. Middle and lower lobectomy was performed. Histopathologically, the adenocarcinoma had invaded the tunica intima of the pulmonary artery and also replaced the endothelium in the same region. Although a large thrombus was found at the vessel invasion site of the adenocarcinoma in the pulmonary artery, there were no malignant findings in the thrombus itself.</p> <p>Conclusions</p> <p>This is the first reported case of radical resection of a lung cancer with invasion along the pulmonary artery wherein a benign thrombus had formed. In general, surgery would be the treatment of choice for a pulmonary artery mass.</p

IL23 differentially regulates the Th1/Th17 balance in ulcerative colitis and Crohn’s disease

ABSTRACT Background: A novel T helper (Th) cell lineage, Th17, that exclusively produces the proinflammatory cytokine interleukin 17 (IL17) has been reported to play important roles in various inflammatory diseases. IL23 is also focused upon for its potential to promote Th17. Here, the roles of the IL23/IL17 axis in inflammatory bowel diseases such as ulcerative colitis (UC) and Crohn&apos;s disease (CD) were investigated. Methods: Mucosal samples were obtained from surgically resected specimens (controls, n = 12; UC, n = 17; CD, n = 22). IL17 production by isolated peripheral blood (PB) and lamina propria (LP) CD4 + cells was examined. Quantitative PCR amplification was performed to determine the mRNA expression levels of IL17, interferon c (IFNc), IL23 receptor (IL23R) and retinoic acid-related orphan receptor c (RORC) in LP CD4 + cells, and IL12 family members, such as IL12p40, IL12p35 and IL23p19, in whole mucosal specimens. The effects of exogenous IL23 on IL17 production by LP CD4 + cells were also examined. Results: IL17 production was higher in LP CD4 + cells than in PB. Significant IL17 mRNA upregulation in LP CD4 + cells was found in UC, while IFNc was increased in CD. IL23R and RORC were upregulated in LP CD4 + cells isolated from both UC and CD. IL17 production was significantly increased by IL23 in LP CD4 + cells from UC but not CD. Upregulated IL23p19 mRNA expression was correlated with IL17 in UC and IFNc in CD. Conclusions: IL23 may play important roles in controlling the differential Th1/Th17 balance in both UC and CD, although Th17 cells may exist in both diseases. Crohn&apos;s disease (CD) and ulcerative colitis (UC) are the two major forms of inflammatory bowel disease (IBD). Although the aetiology of IBD remains unclear, accumulating evidence suggests that dysfunction of the mucosal immune system plays important roles in IBD pathogenesis

2015-2016 Music for the Mind

https://spiral.lynn.edu/conservatory_otherseasonalconcerts/1004/thumbnail.jp

The Impact of Digital Storytelling on Social Agency: Early Experience at an Online University

Digital Storytelling\u27 is a term often used to refer to a number of different types of digital narrative including web-based stories, hypertexts, videoblogs and computer games. This emergent form of creative work has found an outlet in a wide variety of different domains ranging from community social history, to cookbooks, to the classroom. It is the latter domain that provides the focus for this paper, specifically the online classroom at the tertiary level...Early feedback from students suggests that listening to and telling \u27true stories\u27 was a compelling and emotionally-engaging experience, providing an opportunity for \u27transformative reflection\u27 (Lambert 2000). By including multimedia, learners were able to build upon the fundamentals, presenting content in an easy-to-absorb and compelling way. In terms of team assignments students learned to become more effective actors in collaborative work environments

Evolution of Highly Polymorphic T Cell Populations in Siblings with the Wiskott-Aldrich Syndrome

Population level evolutionary processes can occur within a single organism when the germ line contains a mutation that confers a cost at the level of the cell. Here we describe how multiple compensatory mutations arose through a within-individual evolutionary process in two brothers with the immune deficiency Wiskott-Aldrich Syndrome (WAS). As a result, both brothers have T lymphocyte populations that are highly polymorphic at the locus of the germ line defect, and no single allele achieves fixation. WASP, the gene product affected in this disease, is specific to white blood cells where it is responsible for regulating actin cytoskeleton dynamics in a wide range of cellular responses. The brothers inherited a rare allele predicted to result in truncated WASP lacking the carboxy-terminal VCA domains, the region that directly catalyzes actin filament generation. Although the brothers' T cell populations are highly polymorphic, all share a corrective effect relative to the inherited allele in that they restore the VCA domain. This indicates massive selection against the truncated germ line allele. No single somatic allele becomes fixed in the circulating T cell population of either brother, indicating that a regulated step in maturation of the affected cell lineage is severely compromised by the germ line allele. Based on the finding of multiple somatic mutations, the known maturation pathway for T-lineage cells and the known defects of T cells and precursor thymocytes in mice with truncated WASP, we hypothesize that the presence of truncated WASP (WASPΔVCA) confers an extreme disadvantage in early developing thymocytes, above and beyond the known cost of absence of full-length WASP, and that the disadvantage likely occurs through dominant negative competition of WASPΔVCA with N-WASP, a protein that otherwise partially compensates for WASP absence in developing thymocytes

Impact of Intestinal Microbiota on Intestinal Luminal Metabolome

Low–molecular-weight metabolites produced by intestinal microbiota play a direct role in health and disease. In this study, we analyzed the colonic luminal metabolome using capillary electrophoresis mass spectrometry with time-of-flight (CE-TOFMS) —a novel technique for analyzing and differentially displaying metabolic profiles— in order to clarify the metabolite profiles in the intestinal lumen. CE-TOFMS identified 179 metabolites from the colonic luminal metabolome and 48 metabolites were present in significantly higher concentrations and/or incidence in the germ-free (GF) mice than in the Ex-GF mice (p < 0.05), 77 metabolites were present in significantly lower concentrations and/or incidence in the GF mice than in the Ex-GF mice (p < 0.05), and 56 metabolites showed no differences in the concentration or incidence between GF and Ex-GF mice. These indicate that intestinal microbiota highly influenced the colonic luminal metabolome and a comprehensive understanding of intestinal luminal metabolome is critical for clarifying host-intestinal bacterial interactions

Intestinal Epithelial Cell-Specific Deletion of PLD2 Alleviates DSS-Induced Colitis by Regulating Occludin

Ulcerative colitis is a multi-factorial disease involving a dysregulated immune response. Disruptions to the intestinal epithelial barrier and translocation of bacteria, resulting in inflammation, are common in colitis. The mechanisms underlying epithelial barrier dysfunction or regulation of tight junction proteins during disease progression of colitis have not been clearly elucidated. Increase in phospholipase D (PLD) activity is associated with disease severity in colitis animal models. However, the role of PLD2 in the maintenance of intestinal barrier integrity remains elusive. We have generated intestinal specific Pld2 knockout mice (Pld2 IEC-KO) to investigate the mechanism of intestinal epithelial PLD2 in colitis. We show that the knockout of Pld2 confers protection against dextran sodium sulphate (DSS)-induced colitis in mice. Treatment with DSS induced the expression of PLD2 and downregulated occludin in colon epithelial cells. PLD2 was shown to mediate phosphorylation of occludin and induce its proteasomal degradation in a c-Src kinase-dependent pathway. Additionally, we have shown that treatment with an inhibitor of PLD2 can rescue mice from DSS-induced colitis. To our knowledge, this is the first report showing that PLD2 is pivotal in the regulation of the integrity of epithelial tight junctions and occludin turn over, thereby implicating it in the pathogenesis of colitis