Does Stress Matter? Findings from a Self-Report Survey of Contract Cheating Behaviours of Canadian College Students

Presentation for the International Centre of Academic Integrity Annual Conference, March 2023.Othe

How Stressed are Students and What Can We Do About It? Findings from a Self-report Survey of Contract Cheating Behaviours and the Stressful Events College Students Experience

Empirical research on contract cheating in Canada has been limited (Eaton, 2022) and tends to focus on the university (Eaton, 2019; Stoesz & Los, 2019; Thacker, 2022) while there has been relatively little research on academic integrity and contract cheating in community colleges and other non-university higher education institutions (Bretag & Harper, 2020). To address this gap, in 2021, researchers collected data on student engagement in academic integrity violation behaviour and the stress they experienced as they were completing their programs at one Canadian community college. Using self-report survey methodology and utilizing students as partners in research, we found students engaged in a variety of contract cheating behaviours, and experienced a myriad of stressful events both in and outside the college context, including traumatic life events. In this presentation, we explore the link between stress and contract cheating behaviour and address how we can respond at all levels of our institutions to better support students and promote academic integrity.    &nbsp

Strata-bound vein array in the basal Pierre Shale, Lake Francis Case, South Dakota, U.S.A

A distinctive strata-bound vein array occurs in the basal Pierre Shale exposed along the shores of Lake Francis Case, a reservoir on the Missouri River in south-central South Dakota. Typically 2–4 meters in thickness, the array consistently outcrops over a \u3e50-km distance, a significant areal footprint. Ash layers define the upper and lower bounds of the vein array. Two, suborthogonal, preferred directions of vertical veins (northeast and southeast strike) define a regional pattern. By volume, vertical veins comprise 1–2% of the rock. Thinner, more discontinuous, and irregular horizontal veins also occur. Comparisons between array orientations and the joint/vein pattern in the immediately underlying marls of the top of the Niobrara Chalk identify distinct differences. Traverse data suggest that the vein arrays are characterized by uniform horizontal extension. Vertical veins in the array are typically 1–2 centimeters thick and contain massive jarosite, selenite, and fibrous gypsum. The abundance of jarosite and fibrous gypsum distinctly correlates with position in the weathering profile, and these phases are interpreted as due to replacement of original selenite during modern weathering. However, for initial vein array formation, the following suggests that they are not related to modern weathering and formed at depth: (1) a lack of correlation of vein width/frequency with position in the weathering profile; (2) the regional extent; (3) the consistent preferred orientations; (4) the uniform horizontal extension; and (5) the coarse-grained character of the selenite. The consistent strike pattern suggests influence of a regional stress field. The mechanism/timing of vein array formation is unclear. Formation due to diagenetic processes, which are especially significant in mud rocks, would explain the strata-bound character and isotropic horizontal strain and is considered most likely. Formation during glacial loading is one intriguing possibility. Localization of the vein array may be due to the organic-rich character of the host Burning Brule Member of the Sharon Springs Formation

The role of different microbiota in metastatic brain tumors

View full abstracthttps://openworks.mdanderson.org/leading-edge/1005/thumbnail.jp

Elucidating the Role of Microbiome in Low- and High-Grade Glioma

https://openworks.mdanderson.org/sumexp22/1117/thumbnail.jp

Power analysis for generalized linear mixed models in ecology and evolution

Power analysis for generalized linear mixed models in ecology and evolution. Methods in Ecology and Evolution, 6(2 University of Basel, Petersplatz 1, Basel CH-4003, Switzerland Summary 1. 'Will my study answer my research question?' is the most fundamental question a researcher can ask when designing a study, yet when phrased in statistical terms -'What is the power of my study?' or 'How precise will my parameter estimate be?' -few researchers in ecology and evolution (EE) try to answer it, despite the detrimental consequences of performing under-or over-powered research. We suggest that this reluctance is due in large part to the unsuitability of simple methods of power analysis (broadly defined as any attempt to quantify prospectively the 'informativeness' of a study) for the complex models commonly used in EE research. With the aim of encouraging the use of power analysis, we present simulation from generalized linear mixed models (GLMMs) as a flexible and accessible approach to power analysis that can account for random effects, overdispersion and diverse response distributions. 2. We illustrate the benefits of simulation-based power analysis in two research scenarios: estimating the precision of a survey to estimate tick burdens on grouse chicks and estimating the power of a trial to compare the efficacy of insecticide-treated nets in malaria mosquito control. We provide a freely available R function, sim.glmm, for simulating from GLMMs. 3. Analysis of simulated data revealed that the effects of accounting for realistic levels of random effects and overdispersion on power and precision estimates were substantial, with correspondingly severe implications for study design in the form of up to fivefold increases in sampling effort. We also show the utility of simulations for identifying scenarios where GLMM-fitting methods can perform poorly. 4. These results illustrate the inadequacy of standard analytical power analysis methods and the flexibility of simulation-based power analysis for GLMMs. The wider use of these methods should contribute to improving the quality of study design in EE

Sleep in wildland firefighters: what do we know and why does it matter?

Wildland firefighters perform physical work while being subjected to multiple stressors and adverse, volatile working environments for extended periods. Recent research has highlighted sleep as a significant and potentially modifiable factor impacting operational performance. The aim of this review was to (1) examine the existing literature on firefighters’ sleep quantity and quality during wildland firefighting operations; (2) synthesise the operational and environmental factors that impact on sleep during wildland firefighting; and (3) assess how sleep impacts aspects of firefighters’ health and safety, including mental and physical health, physical task performance, physical activity and cognitive performance. Firefighters’ sleep is restricted during wildfire deployments, particularly when shifts have early start times, are of long duration and when sleeping in temporary accommodation. Shortened sleep impairs cognitive but not physical performance under simulated wildfire conditions. The longer-term impacts of sleep restriction on physiological and mental health require further research. Work shifts should be structured, wherever possible, to provide regular and sufficient recovery opportunities (rest during and sleep between shifts), especially in dangerous working environments where fatigue-related errors have severe consequences. Fire agencies should implement strategies to improve and manage firefighters’ sleep and reduce any adverse impacts on firefighters’ work

Improving cardiometabolic health with diet, physical activity, and breaking up sitting: what about sleep?

Cardiometabolic disease poses a serious health and economic burden worldwide and its prevalence is predicted to increase. Prolonged sitting, lack of physical activity, poor diet, and short sleep duration are ubiquitous behaviors in modern society, and all are independent risk factors in the development of cardiometabolic disease. Existing evidence demonstrates that breaking up prolonged periods of sitting is beneficial for cardiometabolic health, however, studies have not controlled for prior sleep duration. This article examines how prolonged sitting and short sleep duration independently contribute to cardiometabolic risk, and how breaking up sitting and obtaining adequate sleep may reduce this risk. We suggest that as prolonged sitting and short sleep duration influence the same cardiometabolic parameters, there is potential for short sleep to attenuate the positive impact of breaking up prolonged sitting with physical activity. Likewise, breaking up prolonged sitting and obtaining adequate sleep together could improve predictors of cardiometabolic disease, i.e., the combined effect may be stronger than either alone. To explore these perspectives, we propose a research agenda to investigate the relationship between breaking up prolonged sitting with physical activity and short sleep duration. This will provide an evidence-base for informing the design of interventions to reduce the burden of cardiometabolic disease on communities worldwide

Chronic Kidney Disease Severity Is Associated With Selective Expansion of a Distinctive Intermediate Monocyte Subpopulation

Chronic kidney disease (CKD) affects 11–13% of the world's population and greatly increases risk of atherosclerotic cardiovascular disease (ASCVD) and death. It is characterized by systemic inflammation and disturbances in the blood leukocytes that remain incompletely understood. In particular, abnormalities in the numbers and relative proportions of the three major monocyte subsets—classical, intermediate, and non-classical—are described in CKD and end-stage renal disease. In this study, we characterized absolute numbers of blood leukocyte subtypes in adults with renal function varying from normal to advanced CKD. The primary aim was to identify monocyte subpopulations that associated most closely with current estimated glomerular filtration rate (eGFR) and subsequent rate of eGFR decline. Leucocyte and monocyte populations were enumerated by multi-color flow cytometry of whole blood and peripheral blood mononuclear cell (PBMC) samples from adults with CKD stage 1–5 (n = 154) and healthy adults (n = 33). Multiple-linear regression analyses were performed to identify associations between numbers of leucocyte and monocyte populations and clinical characteristics including eGFR and rate of eGFR decline with adjustment for age and gender. In whole blood, total monocyte and neutrophil, but not lymphocyte, numbers were higher in adults with CKD 1-5 compared to no CKD and were significantly associated with current eGFR even following correction for age. In PBMC, classical and intermediate monocyte numbers were higher in CKD 1-5 but only intermediate monocyte numbers were significantly associated with current eGFR in an age-corrected analysis. When intermediate monocytes were further sub-divided into those with mid- and high-level expression of class II MHC (HLA-DRmid and HLA-DRhi intermediate monocytes) it was found that only DRhi intermediate monocytes were increased in number in CKD 1-5 compared to no CKD and were significantly associated with eGFR independently of age among the total (No CKD + CKD 1-5) study cohort as well as those with established CKD (CKD 1-5 only). Furthermore, blood number of DRhi intermediate monocytes alone proved to be significantly associated with subsequent rate of renal functional decline. Together, our data confirm neutrophil and monocyte subset dysregulation in CKD and identify a distinct subpopulation of intermediate monocytes that is associated with higher rate of loss of kidney function

T Cell Receptor-Independent, CD31/IL-17A-Driven Inflammatory Axis Shapes Synovitis in Juvenile Idiopathic Arthritis

T cells are considered autoimmune effectors in juvenile idiopathic arthritis (JIA), but the antigenic cause of arthritis remains elusive. Since T cells comprise a significant proportion of joint-infiltrating cells, we examined whether the environment in the joint could be shaped through the inflammatory activation by T cells that is independent of conventional TCR signaling. We focused on the analysis of synovial fluid (SF) collected from children with oligoarticular and rheumatoid factor-negative polyarticular JIA. Cytokine profiling of SF showed dominance of five molecules including IL-17A. Cytometric analysis of the same SF samples showed enrichment of αβT cells that lacked both CD4 and CD8 co-receptors [herein called double negative (DN) T cells] and also lacked the CD28 costimulatory receptor. However, these synovial αβT cells expressed high levels of CD31, an adhesion molecule that is normally employed by granulocytes when they transit to sites of injury. In receptor crosslinking assays, ligation of CD31 alone on synovial CD28nullCD31+ DN αβT cells effectively and sufficiently induced phosphorylation of signaling substrates and increased intracytoplasmic stores of cytokines including IL-17A. CD31 ligation was also sufficient to induce RORγT expression and trans-activation of the IL-17A promoter. In addition to T cells, SF contained fibrocyte-like cells (FLC) expressing IL-17 receptor A (IL-17RA) and CD38, a known ligand for CD31. Stimulation of FLC with IL-17A led to CD38 upregulation, and to production of cytokines and tissue-destructive molecules. Addition of an oxidoreductase analog to the bioassays suppressed the CD31-driven IL-17A production by T cells. It also suppressed the downstream IL-17A-mediated production of effectors by FLC. The levels of suppression of FLC effector activities by the oxidoreductase analog were comparable to those seen with corticosteroid and/or biologic inhibitors to IL-6 and TNFα. Collectively, our data suggest that activation of a CD31-driven, αβTCR-independent, IL-17A-mediated T cell-FLC inflammatory circuit drives and/or perpetuates synovitis. With the notable finding that the oxidoreductase mimic suppresses the effector activities of synovial CD31+CD28null αβT cells and IL-17RA+CD38+ FLC, this small molecule could be used to probe further the intricacies of this inflammatory circuit. Such bioactivities of this small molecule also provide rationale for new translational avenue(s) to potentially modulate JIA synovitis