Showing papers by "University of Illinois at Chicago published in 2022"

An integrated mixed reality system for safety-aware human-robot collaboration using deep learning and digital twin generation

Abstract: For human-robot collaboration (HRC), one of the most practical methods to ensure human safety with a vision-based system is establishing a minimum safe distance. This study proposes a novel integrated mixed reality (MR) system for safety-aware HRC using deep learning and digital twin generation. The proposed approach can accurately measure the minimum safe distance in real-time and provide MR-based task assistance to the human operator. The approach integrates MR with safety-related monitoring by tracking the shared workplace and providing user-centric visualization through smart MR glasses for safe and effective HRC. Two RGB-D sensors are used to reconstruct and track the working environment. One sensor scans one area of the physical environment through 3D point cloud data. The other also scans another area of the environment and tracks the user's 3D skeletal information. In addition, the two partially scanned environments are registered together by applying a fast global registration method to two sets of the 3D point cloud. Furthermore, deep learning-based instance segmentation is applied to the target object's 3D point cloud to increase the registration between the real robot and its virtual robot, the digital twin of the real robot. While only 3D point cloud data are widely used in previous studies, this study proposes a simple yet effective 3D offset-based safety distance calculation method based on the robot's digital twin and the human skeleton. The 3D offset-based method allows for real-time applicability without sacrificing the accuracy of safety distance calculation for HRI. In addition, two comparative evaluations were conducted to confirm the originality and advantage of the proposed MR-based HRC.

SOX2 mediates metabolic reprogramming of prostate cancer cells

Abstract: New strategies are needed to predict and overcome metastatic progression and therapy resistance in prostate cancer. One potential clinical target is the stem cell transcription factor SOX2, which has a critical role in prostate development and cancer. We thus investigated the impact of SOX2 expression on patient outcomes and its function within prostate cancer cells. Analyses of SOX2 expression among a case-control cohort of 1028 annotated tumor specimens demonstrated that SOX2 expression confers a more rapid time to metastasis and decreased patient survival after biochemical recurrence. SOX2 ChIP-Seq analyses revealed SOX2-binding sites within prostate cancer cells which differ significantly from canonical embryonic SOX2 gene targets, and prostate-specific SOX2 gene targets are associated with multiple oncogenic pathways. Interestingly, phenotypic and gene expression analyses after CRISPR-mediated deletion of SOX2 in castration-resistant prostate cancer cells, as well as ectopic SOX2 expression in androgen-sensitive prostate cancer cells, demonstrated that SOX2 promotes changes in multiple metabolic pathways and metabolites. SOX2 expression in prostate cancer cell lines confers increased glycolysis and glycolytic capacity, as well as increased basal and maximal oxidative respiration and increased spare respiratory capacity. Further, SOX2 expression was associated with increased quantities of mitochondria, and metabolomic analyses revealed SOX2-associated changes in the metabolism of purines, pyrimidines, amino acids and sugars, and the pentose phosphate pathway. Analyses of SOX2 gene targets with central functions metabolism (CERK, ECHS1, HS6SDT1, LPCAT4, PFKP, SLC16A3, SLC46A1, and TST) document significant expression correlation with SOX2 among RNA-Seq datasets derived from patient tumors and metastases. These data support a key role for SOX2 in metabolic reprogramming of prostate cancer cells and reveal new mechanisms to understand how SOX2 enables metastatic progression, lineage plasticity, and therapy resistance. Further, our data suggest clinical opportunities to exploit SOX2 as a biomarker for staging and imaging, as well as a potential pharmacologic target.

The Divergent Roles of Symptom and Performance Validity in the Assessment of ADHD.

Abstract: Objective:This study examined concordance between symptom and performance validity among clinically-referred patients undergoing neuropsychological evaluation for Attention-Deficit/Hyperactivity Di...

“All we Wanna do is be Free”: Advocating for Black Liberation in and through K-12 Science Education

Abstract: This paper calls for a critical reimagination of science epistemology and praxis by advocating for a move toward Black liberation in and through K-12 science education. This call is driven by our desires as authors to foster a future of K-12 science teaching and learning that centers, embraces, and promotes historical and contemporary Black scientific innovation and creativity through practices that redress structural anti-Black racism and its implications on Black existence and life. Black Liberatory K-12 Science Education (BLKSE) names the existing challenges with cultivating and empowering Black minds in and through science as a result of anti-Black ideologies that ground and govern K-12 science access, teaching and learning. In naming said challenges as the manifestations of anti-Black ideologies, we shed light on the roles of K-12 science teachers and science teacher education regarding the treatment of Black students given oppressive policies and practices that fail to recognize Black brilliance and innovation. By advocating for a push toward BLKSE, we offer guiding concepts we feel are necessary to begin the process of rooting out anti-Blackness; a process that centers a holistic, heterogenous form of Blackness at the crux of science inquiry and understanding. As a result of this perspective, BLKSE embraces the beauty and creativity of Black youth, naming their positions and ideas as forms of scientific knowledge and inquiry, while disrupting existing mainstream paradigms and practices in science education. Implications for ways to work toward BLKSE in K-12 science teaching and teacher education are provided.

MerTK-mediated efferocytosis promotes immune tolerance and tumor progression in osteosarcoma through enhancing M2 polarization and PD-L1 expression

Abstract: The poor progress of immunotherapy on osteosarcoma patients requires deeper delineation of immune tolerance mechanisms in the osteosarcoma microenvironment and a new therapeutic strategy. Clearance of apoptotic cells by phagocytes, a process termed "efferocytosis," is ubiquitous in tumors and mediates the suppression of innate immune inflammatory response. Considering the massive infiltrated macrophages in osteosarcoma, efferocytosis probably serves as a potential target, but is rarely studied in osteosarcoma. Here, we verified M2 polarization and PD-L1 expression of macrophages following efferocytosis. Pharmacological inhibition and genetic knockdown were used to explore the underlying pathway. Moreover, tumor progression and immune landscape were evaluated following inhibition of efferocytosis in osteosarcoma model. Our study indicated that efferocytosis promoted PD-L1 expression and M2 polarization of macrophages. Ëfferocytosis was mediated by MerTK receptor in osteosarcoma and regulated the phenotypes of macrophages through the p38/STAT3 pathway. By establishing the murine osteosarcoma model, we emphasized that inhibition of MerTK suppressed tumor growth and enhanced the T cell cytotoxic function by increasing the infiltration of CD8+ T cells and decreasing their exhaustion. Our findings demonstrate that MerTK-mediated efferocytosis promotes osteosarcoma progression by enhancing M2 polarization of macrophages and PD-L1-induced immune tolerance, which were regulated through the p38/STAT3 pathway.

Outpatient Therapies for COVID-19: How Do We Choose?

Abstract: Several outpatient coronavirus disease 2019 (COVID-19) therapies have reduced hospitalization in randomized controlled trials. The choice of therapy may depend on drug efficacy, toxicity, pricing, availability, and available infrastructure. To facilitate comparative decision-making, we evaluated the efficacy of each treatment in clinical trials and estimated the cost per hospitalization prevented.Wherever possible, we obtained relative risk for hospitalization from published randomized controlled trials. Otherwise, we extracted data from press releases, conference abstracts, government submissions, or preprints. If there was >1 study, the results were meta-analyzed. Using relative risk, we estimated the number needed to treat (NNT), assuming a baseline hospitalization risk of 5%, and compared the cost per hospitalization prevented with the estimate for an average Medicare COVID-19 hospitalization ($21 752). Drug pricing was estimated from GoodRx, from government purchases, or manufacturer estimates. Administrative and societal costs were not included. Results will be updated online as new studies emerge and/or final numbers become available.At a 5% risk of hospitalization, the estimated NNT was 80 for fluvoxamine, 91 for colchicine, 72 for inhaled corticosteroids, 24 for nirmatrelvir/ritonavir, 50 for molnupiravir, 28 for remdesivir, 25 for sotrovimab, 29 for casirivimab/imdevimab, and 29 for bamlanivimab/etesevimab. For drug cost per hospitalization prevented, colchicine, fluvoxamine, inhaled corticosteroids, and nirmatrelvir/ritonavir were below the Medicare estimated hospitalization cost.Many countries are fortunate to have access to several effective outpatient therapies to prevent COVID-19 hospitalization. Given differences in efficacy, toxicity, cost, and administration complexity, this assessment serves as one means to frame treatment selection.

Artificial intelligence guided conformational mining of intrinsically disordered proteins

Abstract: Abstract Artificial intelligence recently achieved the breakthrough of predicting the three-dimensional structures of proteins. The next frontier is presented by intrinsically disordered proteins (IDPs), which, representing 30% to 50% of proteomes, readily access vast conformational space. Molecular dynamics (MD) simulations are promising in sampling IDP conformations, but only at extremely high computational cost. Here, we developed generative autoencoders that learn from short MD simulations and generate full conformational ensembles. An encoder represents IDP conformations as vectors in a reduced-dimensional latent space. The mean vector and covariance matrix of the training dataset are calculated to define a multivariate Gaussian distribution, from which vectors are sampled and fed to a decoder to generate new conformations. The ensembles of generated conformations cover those sampled by long MD simulations and are validated by small-angle X-ray scattering profile and NMR chemical shifts. This work illustrates the vast potential of artificial intelligence in conformational mining of IDPs.

Transcriptional Repression by FoxM1 Suppresses Tumor Differentiation and Promotes Metastasis of Breast Cancer

Abstract: Abstract The transcription factor Forkhead box M1 (FoxM1) is overexpressed in breast cancers and correlates with poor prognosis. Mechanistically, FoxM1 associates with CBP to activate transcription and with Rb to repress transcription. Although the activating function of FoxM1 in breast cancer has been well documented, the significance of its repressive activity is poorly understood. Using CRISPR–Cas9 engineering, we generated a mouse model that expresses FoxM1-harboring point mutations that block binding to Rb while retaining its ability to bind CBP. Unlike FoxM1-null mice, mice harboring Rb-binding mutant FoxM1 did not exhibit significant developmental defects. The mutant mouse line developed PyMT-driven mammary tumors that were deficient in lung metastasis, which was tumor cell-intrinsic. Single-cell RNA-seq of the tumors revealed a deficiency in prometastatic tumor cells and an expansion of differentiated alveolar type tumor cells, and further investigation identified that loss of the FoxM1/Rb interaction caused enhancement of the mammary alveolar differentiation program. The FoxM1 mutant tumors also showed increased Pten expression, and FoxM1/Rb was found to activate Akt signaling by repressing Pten. In human breast cancers, expression of FoxM1 negatively correlated with Pten mRNA. Furthermore, the lack of tumor-infiltrating cells in FoxM1 mutant tumors appeared related to decreases in pro-metastatic tumor cells that express factors required for infiltration. These observations demonstrate that the FoxM1/Rb-regulated transcriptome is critical for the plasticity of breast cancer cells that drive metastasis, identifying a prometastatic role of Rb when bound to FoxM1. Significance: This work provides new insights into how the interaction between FoxM1 and Rb facilitates the evolution of metastatic breast cancer cells by altering the transcriptome.

A Search for Millilensing Gamma-Ray Bursts in the Observations of Fermi GBM

Abstract: Abstract Millilensing of gamma-ray bursts (GRBs) is expected to manifest as multiple emission episodes in a single triggered GRB with similar light-curve patterns and similar spectrum properties. Identifying such lensed GRBs could help improve constraints on the abundance of compact dark matter. Here we present a systemic search for millilensing among 3000 GRBs observed by the Fermi GBM up to 2021 April. Eventually we find four interesting candidates by performing an autocorrelation test, hardness test, and time-integrated/resolved spectrum test. GRB 081126A and GRB 090717A are ranked as the first-class candidates based on their excellent performance in both temporal and spectrum analysis. GRB 081122A and GRB 110517B are ranked as the second-class candidates (suspected candidates), mainly because their two emission episodes show clear deviations in part of the time-resolved spectrum or in the time-integrated spectrum. Considering a point-mass model for the gravitational lens, our results suggest that the density parameter of lens objects with mass M L ∼ 10 6 M ⊙ is larger than 1.5 × 10 −3 .

Impact of Perceived Social Support on Mental Health, Quality of Life, and Disability in Post–9/11 U.S. Military Veterans:

Abstract: This study examined the impact of perceived social support on mental health and psychosocial functioning in combat veterans after military deployment, including veterans with post-traumatic stress ...

Salmonella enterica serovar Typhimurium chitinases modulate the intestinal glycome and promote small intestinal invasion

Abstract: Salmonella enterica serovar Typhimurium ( S . Typhimurium) is one of the leading causes of food-borne illnesses worldwide. To colonize the gastrointestinal tract, S . Typhimurium produces multiple virulence factors that facilitate cellular invasion. Chitinases have been recently emerging as virulence factors for various pathogenic bacterial species, and the S . Typhimurium genome contains two annotated chitinases: STM0018 ( chiA ) and STM0233 . However, the role of these chitinases during S . Typhimurium pathogenesis is unknown. The putative chitinase STM0233 has not been studied previously, and only limited data exists on ChiA. Chitinases typically hydrolyze chitin polymers, which are absent in vertebrates. However, chiA expression was detected in infection models and purified ChiA cleaved carbohydrate subunits present on mammalian surface glycoproteins, indicating a role during pathogenesis. Here, we demonstrate that expression of chiA and STM0233 is upregulated in the mouse gut and that both chitinases facilitate epithelial cell adhesion and invasion. S . Typhimurium lacking both chitinases showed a 70% reduction in invasion of small intestinal epithelial cells in vitro . In a gastroenteritis mouse model, chitinase-deficient S . Typhimurium strains were also significantly attenuated in the invasion of small intestinal tissue. This reduced invasion resulted in significantly delayed S . Typhimurium dissemination to the spleen and the liver, but chitinases were not required for systemic survival. The invasion defect of the chitinase-deficient strain was rescued by the presence of wild-type S . Typhimurium, suggesting that chitinases are secreted. By analyzing N -linked glycans of small intestinal cells, we identified specific N-acetylglucosamine-containing glycans as potential extracellular targets of S . Typhimurium chitinases. This analysis also revealed a differential abundance of Lewis X/A-containing glycans that is likely a result of host cell modulation due to the detection of S . Typhimurium chitinases. Similar glycomic changes elicited by chitinase deficient strains indicate functional redundancy of the chitinases. Overall, our results demonstrate that S . Typhimurium chitinases contribute to intestinal adhesion and invasion through modulation of the host glycome.