Community on Campus: Examining the Impact of Campus Climate, Belonging, and Flourishing on Bystander Behavior Among Diverse University Students

This exploratory, nonexperimental study aimed to investigate the relationships among diverse undergraduate and graduate students’ perceived campus climate, flourishing, and university belonging on bystander intentions and bystander behaviors during the COVID-19 pandemic. The study’s theoretical framework combined the Theory of Planned Behavior and feminist theory, and examined intersectionality through an Identity Risk Index. Data used in the current study were originally collected as part of an institutional Healthy Minds Survey, on health behaviors of college students; responses from n = 171 of the randomly selected participants were used in the current study’s analyses. The majority of participants indicated at least two marginalized social identities and intervened as a bystander at least once in the last year. The results of two MANOVAS indicated significant differences among students with marginalized social identities, and nonsignificant differences by academic level, for flourishing, university belonging, campus climate, and bystander intention. The results of a multilinear regression with a covariate indicated that flourishing, university, and campus climate predict bystander intention more accurately when accounting for students’ marginalized identities. Lastly, a Poisson regression confirmed that bystander intention predicted bystander intervention for university students. Overall, the findings suggest that as university leaders create initiatives and policies aimed to enhance students’ well-being post-COVID-19 pandemic, they should consider systemic implications these decisions may have on students with diverse identities. Inclusive campus climates as well as intentional opportunities to foster university belonging and flourishing, can increase students\u27 intentions to intervene in risky situations, and promote a healthier campus community

Fuzzy logic control of a two degree of freedom parallel robot

Parallel robots differ greatly from their serial counterparts in terms of performance and mechanical ability. Serial robots are open chained mechanisms since each link is connected to an adjacent one and each joint is actuated, while parallel robots implement a closed chained structure. This type of structure consists of having the endpoint of each kinematic chain connected to one another, hence called the common point. There can be a multitude of kinematic chains, but each chain utilizes only one actuator located near the base of the system to perform the desired operation

Ammonium tri-tert-butoxy­silanethiol­ate

The cations and anions of the title salt, NH4 +·C12H27O3SSi−, are linked by N—H⋯S and N—H⋯O hydrogen bonds into a linear chain that runs along the a axis of the monoclinic unit cell. The asymmetric unit contains two cations and two anions

Erythropoietin protects against diabetes through direct effects on pancreatic β cells

In mouse models of type 1 and type 2 diabetes, administration of human erythropoietin protects against disease by acting directly on pancreatic β cells

Immune Cell–Derived C3 Is Required for Autoimmune Diabetes Induced by Multiple Low Doses of Streptozotocin

OBJECTIVE: The complement system contributes to autoimmune injury, but its involvement in promoting the development of autoimmune diabetes is unknown. In this study, our goal was to ascertain the role of complement C3 in autoimmune diabetes. RESEARCH DESIGN AND METHODS: Susceptibility to diabetes development after multiple low-dose streptozotocin treatment in wild-type (WT) and C3-deficient mice was analyzed. Bone marrow chimeras, luminex, and quantitative reverse transcription PCR assays were performed to evaluate the phenotypic and immunologic impact of C3 in the development of this diabetes model. RESULTS: Coincident with the induced elevations in blood glucose levels, we documented alternative pathway complement component gene expression within the islets of the diabetic WT mice. When we repeated the experiments with C3-deficient mice, we observed complete resistance to disease, as assessed by the absence of histologic insulitis and the absence of T-cell reactivity to islet antigens. Studies of WT chimeras bearing C3-deficient bone marrow cells showed that bone marrow cell-derived C3, and not serum C3, is involved in the induction of diabetes in this model. CONCLUSIONS: The data reveal a key role for immune cell-derived C3 in the pathogenesis of murine multiple low-dose streptozotocin-induced diabetes and support the concept that immune cell mediated diabetes is in part complement-dependen

Expression of the NH2-Terminal Fragment of RasGAP in Pancreatic β-Cells Increases Their Resistance to Stresses and Protects Mice From Diabetes

OBJECTIVE: Our laboratory has previously established in vitro that a caspase-generated RasGAP NH(2)-terminal moiety, called fragment N, potently protects cells, including insulinomas, from apoptotic stress. We aimed to determine whether fragment N can increase the resistance of pancreatic beta-cells in a physiological setting. RESEARCH DESIGN AND METHODS: A mouse line, called rat insulin promoter (RIP)-N, was generated that bears a transgene containing the rat insulin promoter followed by the cDNA-encoding fragment N. The histology, functionality, and resistance to stress of RIP-N islets were then assessed. RESULTS: Pancreatic beta-cells of RIP-N mice express fragment N, activate Akt, and block nuclear factor kappaB activity without affecting islet cell proliferation or the morphology and cellular composition of islets. Intraperitoneal glucose tolerance tests revealed that RIP-N mice control their glycemia similarly as wild-type mice throughout their lifespan. Moreover, islets isolated from RIP-N mice showed normal glucose-induced insulin secretory capacities. They, however, displayed increased resistance to apoptosis induced by a series of stresses including inflammatory cytokines, fatty acids, and hyperglycemia. RIP-N mice were also protected from multiple low-dose streptozotocin-induced diabetes, and this was associated with reduced in vivo beta-cell apoptosis. CONCLUSIONS: Fragment N efficiently increases the overall resistance of beta-cells to noxious stimuli without interfering with the physiological functions of the cells. Fragment N and the pathway it regulates represent, therefore, a potential target for the development of antidiabetes tools

Next generation immuno-oncology tumor profiling using a rapid, non-invasive, computational biophysics biomarker in early-stage breast cancer

BackgroundImmuno-oncology (IO) therapies targeting the PD-1/PD-L1 axis, such as immune checkpoint inhibitor (ICI) antibodies, have emerged as promising treatments for early-stage breast cancer (ESBC). Despite immunotherapy's clinical significance, the number of benefiting patients remains small, and the therapy can prompt severe immune-related events. Current pathologic and transcriptomic predictions of IO response are limited in terms of accuracy and rely on single-site biopsies, which cannot fully account for tumor heterogeneity. In addition, transcriptomic analyses are costly and time-consuming. We therefore constructed a computational biomarker coupling biophysical simulations and artificial intelligence-based tissue segmentation of dynamic contrast-enhanced magnetic resonance imaging (DCE-MRIs), enabling IO response prediction across the entire tumor.MethodsBy analyzing both single-cell and whole-tissue RNA-seq data from non-IO-treated ESBC patients, we associated gene expression levels of the PD-1/PD-L1 axis with local tumor biology. PD-L1 expression was then linked to biophysical features derived from DCE-MRIs to generate spatially- and temporally-resolved atlases (virtual tumors) of tumor biology, as well as the TumorIO biomarker of IO response. We quantified TumorIO within patient virtual tumors (n = 63) using integrative modeling to train and develop a corresponding TumorIO Score.ResultsWe validated the TumorIO biomarker and TumorIO Score in a small, independent cohort of IO-treated patients (n = 17) and correctly predicted pathologic complete response (pCR) in 15/17 individuals (88.2% accuracy), comprising 10/12 in triple negative breast cancer (TNBC) and 5/5 in HR+/HER2- tumors. We applied the TumorIO Score in a virtual clinical trial (n = 292) simulating ICI administration in an IO-naïve cohort that underwent standard chemotherapy. Using this approach, we predicted pCR rates of 67.1% for TNBC and 17.9% for HR+/HER2- tumors with addition of IO therapy; comparing favorably to empiric pCR rates derived from published trials utilizing ICI in both cancer subtypes.ConclusionThe TumorIO biomarker and TumorIO Score represent a next generation approach using integrative biophysical analysis to assess cancer responsiveness to immunotherapy. This computational biomarker performs as well as PD-L1 transcript levels in identifying a patient's likelihood of pCR following anti-PD-1 IO therapy. The TumorIO biomarker allows for rapid IO profiling of tumors and may confer high clinical decision impact to further enable personalized oncologic care

Expansion and Characterization of Human Melanoma Tumor-Infiltrating Lymphocytes (TILs)

Various immunotherapeutic strategies for cancer are aimed at augmenting the T cell response against tumor cells. Adoptive cell therapy (ACT), where T cells are manipulated ex vivo and subsequently re-infused in an autologous manner, has been performed using T cells from various sources. Some of the highest clinical response rates for metastatic melanoma have been reported in trials using tumor-infiltrating lymphocytes (TILs). These protocols still have room for improvement and furthermore are currently only performed at a limited number of institutions. The goal of this work was to develop TILs as a therapeutic product at our institution.TILs from 40 melanoma tissue specimens were expanded and characterized. Under optimized culture conditions, 72% of specimens yielded rapidly proliferating TILs as defined as at least one culture reaching ≥3×10(7) TILs within 4 weeks. Flow cytometric analyses showed that cultures were predominantly CD3+ T cells, with highly variable CD4+:CD8+ T cell ratios. In total, 148 independent bulk TIL cultures were assayed for tumor reactivity. Thirty-four percent (50/148) exhibited tumor reactivity based on IFN-γ production and/or cytotoxic activity. Thirteen percent (19/148) showed specific cytotoxic activity but not IFN-γ production and only 1% (2/148) showed specific IFN-γ production but not cytotoxic activity. Further expansion of TILs using a 14-day "rapid expansion protocol" (REP) is required to induce a 500- to 2000-fold expansion of TILs in order to generate sufficient numbers of cells for current ACT protocols. Thirty-eight consecutive test REPs were performed with an average 1865-fold expansion (+/- 1034-fold) after 14 days.TILs generally expanded efficiently and tumor reactivity could be detected in vitro. These preclinical data from melanoma TILs lay the groundwork for clinical trials of ACT