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    Visiting Fellow Heena Akbar

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    <p>Dr Heena Akbar’s research is shaping how  is used to address the health and well-being of Maori & Pacific peoples, particularly women with type 2 diabetes. Her research seeks to understand the socio-cultural determinants that contribute to health and well-being, integrating community participatory action research and indigenous perspectives and knowledge systems with social justice principles. Heena has been awarded several grants and fellowship that focused on Pacific and Indigenous health and wellbeing. Her co-developed solutions lead to Heena being awarded the auDA Foundation fellowship in 2017 to co-design an e-health family-centred, diabetes self-management intervention with Maori and Pacific Communities in Queensland. Heena recently received a 2021 Women’s Health Translational Research Network (WHTRN) Early Middle Career Research Award to pilot the Pasifika Wellness Program in Queensland. Her research serves to reduce the social and economic burden from diabetes and its related complications, and impact policy development that translates to better health outcomes for Maori & Pacific peoples in Australia. Heena’s research now develops community-based strategies that provide access to affordable food for a healthy and active life so as to reduce the burden of chronic diseases for Maori & Pacific families and communities.</p&gt

    Investigating the Role of Formate Oxidation in Shewanella oneidensis MR-1

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    Faculty adviser: Jeffrey GralnickThis research was supported by the Undergraduate Research Opportunities Program (UROP).Joo, Heena. (2015). Investigating the Role of Formate Oxidation in Shewanella oneidensis MR-1. Retrieved from the University Digital Conservancy, https://hdl.handle.net/11299/169607

    Data, Data Everywhere: But Not a Drop to Analyze

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    Heena Santry, M.D., M.S. will discuss the challenges she faced as a researcher in converting two decades worth of trauma registry data into usable form for analysis. Dr. Santry is Assistant Professor of Surgery and Quantitative Health Sciences where she also serves as Director of Trauma Outcomes Research and Quality Assessment. She is also a UMass Clinical Research Scholar funded through the CTSA

    2010 K12 Awardees: Overview of Research Projects

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    Two UMCCTS Clinical Research Scholars (K awardees) describe their research projects and professional growth as junior faculty: - Sarah Cutrona on "Electronic Transmission of Health Information across Networks" - Heena Santry on "Career Development for an Academic Acute Care Surgeon and Acute Care Surgery Practice Patterns: A Tale of Two Complexities

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    Kinetics of Spontaneous and EF-G-Accelerated Rotation of Ribosomal Subunits

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    SummaryRibosome dynamics play an important role in translation. The rotation of the ribosomal subunits relative to one another is essential for tRNA-mRNA translocation. An important unresolved question is whether subunit rotation limits the rate of translocation. Here, we monitor subunit rotation relative to peptide bond formation and translocation using ensemble kinetics and single-molecule FRET. We observe that spontaneous forward subunit rotation occurs at a rate of 40 s−1, independent of the rate of preceding peptide bond formation. Elongation factor G (EF-G) accelerates forward subunit rotation to 200 s−1. tRNA-mRNA movement is much slower (10–40 s−1), suggesting that forward subunit rotation does not limit the rate of translocation. The transition back to the non-rotated state of the ribosome kinetically coincides with tRNA-mRNA movement. Thus, large-scale movements of the ribosome are intrinsically rapid and gated by its ligands such as EF-G and tRNA

    The role of airway tissue-resident memory T Cells in severe asthma

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    The growing realisation that severe asthma encompasses a collection of clinical phenotypes and endotypes, plus the variable response to current asthma therapies suggest underlying pathophysiological heterogeneity and complex immune molecular pathways.T cells are critical orchestrators of airway inflammation. However, the role of tissue-resident memory T (TRM) cells, localised to sites of inflammation in the airway epithelium, in the pathogenesis of severe asthma remains unknown. Therefore, this thesis aims to investigate the molecular heterogeneity of airway CD4+ and CD8+ TRM cells in severe asthma pathogenesis and extend this characterisation to the underlying clinical phenotypic nature of severe asthma compared to mild asthma.In the first section of this thesis, I undertook extensive clinical phenotypic characterisation of participants with difficult/severe and mild asthma (Chapter 3). Subsequent separate K-means clustering analysis of the difficult/severe and mild asthma cohorts identified 6 clinically relevant difficult/severe asthma clusters and 2 mild asthma clusters, reflecting severe disease heterogeneity (Chapter 4).For the second section of this thesis, bronchoalveolar (BAL) fluid samples collected from a proportion of severe and mild asthma participants were immunophenotyped using flow cytometry. This analysis suggested that CD103+CD4+ TRM and CD103+CD8+ TRM cells represented the dominant population in asthma. Subsequent bulk and single-cell RNA-seq of BAL memory CD4+ (Chapter 5) and CD8+ (Chapter 6) T cell populations were completed to investigate the molecular profiles of these cells in relation to asthma severity. The transcriptional profiling of BAL CD4+ T cells highlighted a novel population of cytotoxic CD103+CD4+ TRM cells enriched for transcripts linked to TCR activation, TH1-like cytotoxicity and pro-inflammatory molecular features, which was associated with increasing asthma severity in the male adult-onset severe asthma phenotype. In contrast, the transcriptional profiling of BAL CD8+ T cells revealed 9 transcriptionally distinct putative airway CD103+CD8+ TRM cell states across the spectrum of asthma severity, thus highlighting significant molecular heterogeneity. Strikingly, 3 airway CD8+ TRM cell states were unique to severe asthma and appeared to be highly proliferative with enhanced cytotoxicity, glucocorticoid insensitivity and pro-inflammatory molecular properties. Such superior functional properties of cytotoxic CD103+CD4+ TRM and CD103+CD8+ TRM cells suggest their role as key drivers of persistent airway inflammation, remodelling and glucocorticoid insensitivity in severe asthma.In conclusion, these novel findings indicate the need to look beyond the traditional T2 model of severe asthma to better understand disease heterogeneity. Future work will aim towards completing functional studies in vivo to better understand the molecular role of airway CD4+ and CD8+ TRM cell populations and their interactions in severe asthma
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