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Autonomous Exploration and Mapping of Unknown Environments
(2024-05-03) Sarfi, Mohammad Hossein; Bisheban, Mahdis; Thekinen, Joseph Davis; Dankers, Arne
This thesis presents a comprehensive exploration of autonomous exploration and mapping in unknown environments, emphasizing the importance of minimizing exploration time while ensuring high-quality mapping results. It introduces a classical coordinated autonomous exploration strategy inspired by Market-Based task allocation and Ant Colony Optimization techniques. Compared to simpler Market-Based methods, this approach improves efficiency by reducing overlap between robots. The study utilizes a 2D simulation environment to collect training data efficiently, facilitating the evaluation of the proposed methods’ efficiency, adaptability, and generalizability through various experiments. Furthermore, the thesis develops intelligent single-robot autonomous techniques using advanced Deep Reinforcement Learning (DRL) algorithms. Notably, it adopts risk-sensitive strategies, in contrast to traditional risk-neutral approaches in DRL, aiming to enhance exploration efficiency, defined as the time required to complete 95% of the map. The best intelligent policy achieved a significant improvement in exploration efficiency compared to the utility-based classical method. Despite selecting the appropriate DRL algorithm and fine-tuning it accordingly, a comprehensive study and series of experiments are designed to investigate the effects of various state, action, and reward spaces. Moreover, different external features, such as incorporating the Intrinsic Curiosity Module (ICM) or integrating Long-Short Term Memory (LSTM) layers, are considered to further enhance autonomous exploration efficiency. The results demonstrate a significant improvement in autonomous exploration efficiency compared to well-known classical single-robot exploration policies, validating the effectiveness of the suggested novel autonomous exploration strategies. The codes developed for this thesis are available in the Intelligent Dynamics and Control Lab GitHub repository: https://github.com/IDCL-UCalgary
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Open Access
Neutrophil localization during C. rodentium-induced colitis
(2024-05-06) Yoon, Grace Haewon; Cobo, Eduardo; McKay, Derek; Mody, Christopher
Intestinal infections by enteropathogenic bacteria like Escherichia coli pose a significant risk to human health worldwide and can contribute to a wide spectrum of different symptoms and diseases. The infection can result in weight loss, diarrhea, hemorrhagic colitis, dehydration and potentially death. To study enteropathogenic colonization further, a murine Citrobacter rodentium (C. rodentium) model is used in this project to understand the activity of neutrophils, often the first cell line of defense, during infection. While it is known that neutrophils are involved in the eradication of C. rodentium, their presence during different phases of C. rodentium infection and functions at these time points, such as inflammation regulation and clearance, remain unknown, especially in the context of recruitment, location, and time. During an infection within the intestine, pathogens encounter many different obstacles such as the mucus layer, intestinal epithelial cells, and innate immune cells. Neutrophils are innate immune cells that are well recognized as first responders during infections, and they are armed with granules that contain toxic agents such as reactive oxygen species, proteases, and antimicrobial peptides/proteins. In the context of C. rodentium infection, it has been shown that neutrophils preferentially phagocytose the bacteria within the cecal lumen during the steady phase of infection; however, the localization and distribution of neutrophils throughout the progression of the infection remains elusive. Previous studies have alluded to the potential of localization in determining function of neutrophils where neutrophils that have undergone transepithelial migration have more bactericidal capabilities. As such, exploring the localization and distribution throughout the different phases of C. rodentium can shed light on the roles that neutrophils play during the infection. Our findings show that neutrophils are abundantly recruited within the colonic mucosa during the acute inflammation phase (7 dpi) and reach the colonic lumen. Cathelicidin, an antimicrobial peptide, deficiency leads to more neutrophil recruitment than its wildtype counterpart upon infection. Furthermore, the bulk RNA sequencing results show that NET formation and degranulation are upregulated neutrophil functions during C. rodentium infection in both cathelicidin-deficient and wildtype mice. By further understanding the behaviour and activity of neutrophils during infection, it can allow us to harness the microbicidal ability of these cells to use as a potential therapeutic in years to come.
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Open Access
Elucidating the role of prolactin receptor during β cell adaptation to metabolic stressors
(2024-05-06) Lee, Daniel; Huang, Carol; Hemberger, Myriam; Shemanko, Carrie
The role of prolactin receptor (PRLR) during β cell adaptation to pregnancy has been extensively studied. Human epidemiological studies have revealed a potential role of prolactin outside pregnancy in maintaining glucose homeostasis. In this study, we discovered that the absence of PRLR in pancreatic β cells leads to impaired glucose tolerance in multiparous mice challenged with a high-fat diet (HFD). Unlike during pregnancy, where PRLR regulates β cell mass expansion, we observed that PRLR had a smaller role in regulating β cell mass in this model. Pancreatic islets from our knockout mice had a similar insulin secretory capacity as the wild-type mice in vitro, suggesting that an in vivo factor was responsible for the difference in glucose homeostasis. Interestingly, a difference in in vivo insulin secretion was observed when mice were challenged with oral but not intraperitoneal glucose, suggesting a defect in the incretin effect. The incretin effect, where oral glucose administration elicits a greater insulin secretory response compared to intravenous administration, is mediated by incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). We found a reduction in mRNA expressions of both incretin hormone receptors, GIP receptor (Gipr) and GLP-1 receptor (Glp-1r), in the pancreatic islets of our islet-specific PRLR knockout mice in comparison to wild-type controls after 12 weeks of HFD. Additionally, the mRNA expression of transcription factors, E2F transcription factor 1 (E2f1) and peroxisome proliferator-activated receptor-γ (Pparg), which have been shown to regulate the expressions of Gipr and Glp-1r and are downstream of PRLR, were downregulated. Together, these results suggest PRLR may have a role in the maintaining incretin effect during metabolic stress outside of pregnancy. Our findings contribute to our understanding of the complexity of PRLR in maintaining glucose homeostasis outside of pregnancy.
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Open Access
Probing the activity of the inhibitor of growth 1a (ING1a) gene promoter under conditions of cellular stress
(2024-04-30) Hill, Alexander William; Riabowol, Karl; Billon, Pierre; Williams, Gareth; Shutt, Timothy
The INhibitor of Growth (ING) family of proteins was initially characterized in 1996 when subtractive hybridization studies revealed a novel type II tumor suppressor, which the authors called ING1. Since then, additional members of the family have been discovered and characterized as important epigenetic regulators, influencing various cellular processes such as stemness, growth, and development. Previous studies have demonstrated that one of the main isoforms of ING1, named ING1a, shows increased expression in senescent cells, with overexpression of the protein resulting in the premature senescence of young fibroblasts. Classically, senescence is a phenotype that occurs as a result of telomere attrition, causing a DNA damage response that ultimately puts the cell in growth arrest. More recent work has shown that the application of various cellular stressors can induce senescence in cells which have otherwise not reached their replicative lifespan, termed stress-induced premature senescence (SIPS). Currently, the relationship between ING1a and cellular stress is incompletely understood, especially at the level of transcriptional control. In the current work, analysis of predicted transcription factors was performed for the ING1a promoter in addition to other stress and senescence-related promoters, demonstrating great overlap between ING1a and senescence marker p16. qPCR analysis of predicted factors showed decreased expression of FOXD1, FOXL1, and MAZ in senescent fibroblasts. ChIP-qPCR against MAZ was performed, validating the transcription factor prediction and showing that MAZ binds to the ING1a promoter. Comparison between promoter-driven constructs and the endogenous promoters revealed that there is likely considerable epigenetic regulation controlling the expression of ING1a, though transcriptional elements sensitive to oxidative stress are likely present.
Item
Embargo
Temperature Distribution and Gradient Effects on Steel-Concrete Composite Girder Bridge
(2024-04-23) Nayeem, Mostansir Billah; Billah, AHM Muntasir; El-Badry, Mamdouh; Hassan, Quazi Khalid
Thermal loads are a crucial environmental component that significantly affects the performance of bridges, especially under extreme climate conditions. Previous research suggests that under extreme climate situations, the impact of temperature may surpass that of dead and live loads, hence emphasizing the need to study the temperature gradient effect. While numerous studies have investigated the effects of temperature variations on concrete or steel bridges, relatively limited exploration has been conducted on the thermal effects experienced by steel-concrete composite bridges. Given substantial disparities in thermal performance between steel and concrete, understanding the temperature field and gradient effect in steel-concrete composite box girder bridges is paramount for both engineers and researchers. However, determining the temperature field within composite bridges requires more sophisticated modeling and analysis. Analytical methods often face challenges in providing accurate temperature field results due to the complex geometry and boundary conditions in real structures. Consequently, numerical simulation has emerged as the most effective approach to estimating the temperature field of bridge structures. The overall objective of this research is to investigate the impact of temperature field and local climatic conditions on the thermal response of steel-concrete composite girder. This study involves developing an efficient Finite Element (FE) model of a dimensionally reduced steel-concrete composite bridge girder to assess the structural effects of a 24-hour simulated temperature field through a sequentially coupled thermo-mechanical analysis technique in Abaqus. The three-dimensional numerical model is validated against existing experimental results conducted in a laboratory environment. Results demonstrate that under similar thermal boundary conditions, composite bridge girder specimens with varying concrete strengths exhibit discernible variations in stress values. Additionally, this study also presents a refined simulation approach utilizing Canadian location-specific historical weather and climate data to analyze the temperature field of a steel-concrete composite girder bridge in Calgary. The utilization of historical meteorological data ensures that the simulated thermal responses closely align with the actual environmental conditions experienced by the bridge. This finite element model can be used as an effective tool for predicting temperature fields by accounting for the unique climatic data of individual bridge locations.