Infrastructure Engineering - Research Publications
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ItemPrivacy- and context-aware release of trajectory data(ACM, 2020-03)The availability of large-scale spatio-temporal datasets along with the advancements in analytical models and tools have created a unique opportunity to create valuable insights into managing key areas of society from transportation and urban planning to epidemiology and natural disasters management. This has encouraged the practice of releasing/publishing trajectory datasets among data owners. However, an ill-informed publication of such rich datasets may have serious privacy implications for individuals. Balancing privacy and utility, as a major goal in the data exchange process, is challenging due to the richness of spatio-temporal datasets. In this article, we focus on an individual's stops as the most sensitive part of the trajectory and aim to preserve them through spatio-temporal perturbation. We model a trajectory as a sequence of stops and moves and propose an efficient algorithm that either substitutes sensitive stop points of a trajectory with moves from the same trajectory or introduces a minimal detour if no safe Point of Interest (POI) can be found on the same route. This hinders the amount of unnecessary distortion, since the footprint of the original trajectory is preserved as much as possible. Our experiments shows that our method balances user privacy and data utility: It protects privacy through preventing an adversary from making inferences about sensitive stops while maintaining a high level of similarity to the original dataset.
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ItemNo Preview AvailableA predictive model for spatio-temporal variability in stream water quality( 2019-07-23)Abstract. Degraded water quality in rivers and streams can have large economic, societal and ecological impacts. Stream water quality can be highly variable both over space and time. To develop effective management strategies for riverine water quality, it is critical to be able to predict these spatio-temporal variabilities. However, our current capacity to model stream water quality is limited, particularly at large spatial scales across multiple catchments. This is due to a lack of understanding of the key controls that drive spatio-temporal variabilities of stream water quality. To address this, we developed a Bayesian hierarchical statistical model to analyse the spatio-temporal variability in stream water quality across the state of Victoria, Australia. The model was developed based on monthly water quality monitoring data collected at 102 sites over 21 years. The modelling focused on six key water quality constituents: total suspended solids (TSS), total phosphorus (TP), filterable reactive phosphorus (FRP), total Kjeldahl nitrogen (TKN), nitrate-nitrite (NOx), and electrical conductivity (EC). Among the six constituents, the models explained varying proportions of variation in water quality. EC was the most predictable constituent (88.6 % variability explained) and FRP had the lowest predictive performance (19.9 % variability explained). The models were validated for multiple sets of calibration/validation sites and showed robust performance. Temporal validation revealed a systematic change in the TSS model performance across most catchments since an extended drought period in the study region, highlighting potential shifts in TSS dynamics over the drought. Further improvements in model performance need to focus on: (1) alternative statistical model structures to improve fitting for the low concentration data, especially records below the detection limit; and (2) better representation of non-conservative constituents by accounting for important biogeochemical processes. We also recommend future improvements in water quality monitoring programs which can potentially enhance the model capacity, via: (1) improving the monitoring and assimilation of high-frequency water quality data; and (2) improving the availability of data to capture land use and management changes over time.
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ItemCharacterizing dominant hydrological processes under uncertainty: evaluating the interplay between model structure, parameter sampling, error metrics, and data information content(Copernicus Publications, 2020-03-23)<p>Hydrological models are conventionally evaluated in terms of their response surface or likelihood surface constructed with the model parameter space. To evaluate models as hypotheses, we developed the method of <em>Flux Mapping</em> to construct a hypothesis space based on model process representation. Here we defined the hypothesis space based on dominant runoff generating mechanisms, and acceptable model runs are defined as total simulated flow with similar (and minimal) model error simulated by distinct combinations of runoff components. We demonstrate that the hypothesis space in each modeling case is the result of interplay between the factors of model structure, parameter sampling, choice of error metric, and data information content. The aim of this study is to disentangle the role of each factor in this interplay. We used two model structures (SACRAMENTO and SIMHYD), two parameter sampling approaches (small samples based on guided-search and large samples based on Latin Hypercube Sampling), three widely used error metrics (NSE, KGE, and WIA &#8212; Willmott&#8217;s Index of Agreement), and hydrological data from a range of Australian catchments. First, we characterized how the three error metrics behave under different error regimes independent of any modeling. We then conducted a series of controlled experiments, i.e. a type of one-factor-at-a-time sensitivity analysis, to unpack the role of each factor in runoff simulation. We show that KGE is a more reliable error metric compared to NSE and WIA for model evaluation. We also argue that robust error metrics and sufficient parameter sampling are necessary conditions for evaluating models as hypotheses under uncertainty. We particularly argue that sampling sufficiency, regardless of the sampling strategy, should be further evaluated based on its interaction with other modeling factors determining the model response. We conclude that the interplay of these modeling factors is complex and unique to each modeling case, and hence generalizing model-based inferences should be done with caution particularly in characterizing hydrological processes in large-sample hydrology.</p>
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ItemNo Preview AvailableThe acceptability and uptake of smartphone tracking for COVID-19 in Australia(Center for Open Science, 2020)
In response to the COVID-19 pandemic, many Governments are instituting mobile tracking technologies to perform rapid contact tracing. However, these technologies are only effective if the public is willing to use them, implying that their perceived public health benefits must outweigh personal concerns over privacy and security. The Australian federal government recently launched the `COVIDSafe' app, designed to anonymously register nearby contacts. If a contact later identifies as infected with COVID-19, health department officials can rapidly followup with their registered contacts to stop the virus' spread. The current study assessed attitudes towards three tracking technologies (telecommunication network tracking, a government app, and Apple and Google's Bluetooth exposure notification system) in two representative samples of the Australian public prior to the launch of COVIDSafe. We compared these attitudes to usage of the COVIDSafe app after its launch in a further two representative samples of the Australian public. Using Bayesian methods, we find widespread acceptance for all tracking technologies, however, observe a large intention-behaviour gap between people’s stated attitudes and actual uptake of the COVIDSafe app. We consider the policy implications of these results for Australia and the world at large.
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ItemSatellite cell-specific ablation of Cdon impairs integrin activation, FGF signalling, and muscle regeneration.(Wiley, 2020-08)BACKGROUND: Perturbation in cell adhesion and growth factor signalling in satellite cells results in decreased muscle regenerative capacity. Cdon (also called Cdo) is a component of cell adhesion complexes implicated in myogenic differentiation, but its role in muscle regeneration remains to be determined. METHODS: We generated inducible satellite cell-specific Cdon ablation in mice by utilizing a conditional Cdon allele and Pax7 CreERT2 . To induce Cdon ablation, mice were intraperitoneally injected with tamoxifen (tmx). Using cardiotoxin-induced muscle injury, the effect of Cdon depletion on satellite cell function was examined by histochemistry, immunostaining, and 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay. Isolated myofibers or myoblasts were utilized to determine stem cell function and senescence. To determine pathways related to Cdon deletion, injured muscles were subjected to RNA sequencing analysis. RESULTS: Satellite cell-specific Cdon ablation causes impaired muscle regeneration with fibrosis, likely attributable to decreased proliferation, and senescence, of satellite cells. Cultured Cdon-depleted myofibers exhibited 32 ± 9.6% of EdU-positive satellite cells compared with 58 ± 4.4% satellite cells in control myofibers (P < 0.05). About 32.5 ± 3.7% Cdon-ablated myoblasts were positive for senescence-associated β-galactosidase (SA-β-gal) while only 3.6 ± 0.5% of control satellite cells were positive (P < 0.001). Transcriptome analysis of muscles at post-injury Day 4 revealed alterations in genes related to mitogen-activated protein kinase signalling (P < 8.29 e-5 ) and extracellular matrix (P < 2.65 e-24 ). Consistent with this, Cdon-depleted tibialis anterior muscles had reduced phosphorylated extracellular signal-regulated kinase (p-ERK) protein levels and expression of ERK targets, such as Fos (0.23-fold) and Egr1 (0.31-fold), relative to mock-treated control muscles (P < 0.001). Cdon-depleted myoblasts exhibited impaired ERK activation in response to basic fibroblast growth factor. Cdon ablation resulted in decreased and/or mislocalized integrin β1 activation in satellite cells (weak or mislocalized integrin1 in tmx = 38.7 ± 1.9%, mock = 21.5 ± 6%, P < 0.05), previously linked with reduced fibroblast growth factor (FGF) responsiveness in aged satellite cells. In mechanistic studies, Cdon interacted with and regulated cell surface localization of FGFR1 and FGFR4, likely contributing to FGF responsiveness of satellite cells. Satellite cells from a progeria model, Zmpste24-/- myofibers, showed decreased Cdon levels (Cdon-positive cells in Zmpste24-/- = 63.3 ± 11%, wild type = 90 ± 7.7%, P < 0.05) and integrin β1 activation (weak or mislocalized integrin β1 in Zmpste24-/- = 64 ± 6.9%, wild type = 17.4 ± 5.9%, P < 0.01). CONCLUSIONS: Cdon deficiency in satellite cells causes impaired proliferation of satellite cells and muscle regeneration via aberrant integrin and FGFR signalling.
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ItemMitochondrial Quality Control in the Heart: New Drug Targets for Cardiovascular Disease.(The Korean Society of Cardiology, 2020-05)Despite considerable efforts to prevent and treat cardiovascular disease (CVD), it has become the leading cause of death worldwide. Cardiac mitochondria are crucial cell organelles responsible for creating energy-rich ATP and mitochondrial dysfunction is the root cause for developing heart failure. Therefore, maintenance of mitochondrial quality control (MQC) is an essential process for cardiovascular homeostasis and cardiac health. In this review, we describe the major mechanisms of MQC system, such as mitochondrial unfolded protein response and mitophagy. Moreover, we describe the results of MQC failure in cardiac mitochondria. Furthermore, we discuss the prospects of 2 drug candidates, urolithin A and spermidine, for restoring mitochondrial homeostasis to treat CVD.
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ItemZNF746/PARIS overexpression induces cellular senescence through FoxO1/p21 axis activation in myoblasts.(Springer Science and Business Media LLC, 2020-05-12)Various stresses, including oxidative stress, impair the proliferative capacity of muscle stem cells leading to declined muscle regeneration related to aging or muscle diseases. ZNF746 (PARIS) is originally identified as a substrate of E3 ligase Parkin and its accumulation is associated with Parkinson's disease. In this study, we investigated the role of PARIS in myoblast function. PARIS is expressed in myoblasts and decreased during differentiation. PARIS overexpression decreased both proliferation and differentiation of myoblasts without inducing cell death, whereas PARIS depletion enhanced myoblast differentiation. Interestingly, high levels of PARIS in myoblasts or fibroblasts induced cellular senescence with alterations in gene expression associated with p53 signaling, inflammation, and response to oxidative stress. PARIS overexpression in myoblasts starkly enhanced oxidative stress and the treatment of an antioxidant Trolox attenuated the impaired proliferation caused by PARIS overexpression. FoxO1 and p53 proteins are elevated in PARIS-overexpressing cells leading to p21 induction and the depletion of FoxO1 or p53 reduced p21 levels induced by PARIS overexpression. Furthermore, both PARIS and FoxO1 were recruited to p21 promoter region and Trolox treatment attenuated FoxO1 recruitment. Taken together, PARIS upregulation causes oxidative stress-related FoxO1 and p53 activation leading to p21 induction and cellular senescence of myoblasts.
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ItemGrowth differentiation factor 15 protects against the aging-mediated systemic inflammatory response in humans and mice.(Wiley, 2020-08)Mitochondrial dysfunction is associated with aging-mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and type 2 diabetes. Growth differentiation factor 15 (GDF15) is an important mitokine generated in response to mitochondrial stress and dysfunction; however, the implications of GDF15 to the aging process are poorly understood in mammals. In this study, we identified a link between mitochondrial stress-induced GDF15 production and protection from tissue inflammation on aging in humans and mice. We observed an increase in serum levels and hepatic expression of GDF15 as well as pro-inflammatory cytokines in elderly subjects. Circulating levels of cell-free mitochondrial DNA were significantly higher in elderly subjects with elevated serum levels of GDF15. In the BXD mouse reference population, mice with metabolic impairments and shorter survival were found to exhibit higher hepatic Gdf15 expression. Mendelian randomization links reduced GDF15 expression in human blood to increased body weight and inflammation. GDF15 deficiency promotes tissue inflammation by increasing the activation of resident immune cells in metabolic organs, such as in the liver and adipose tissues of 20-month-old mice. Aging also results in more severe liver injury and hepatic fat deposition in Gdf15-deficient mice. Although GDF15 is not required for Th17 cell differentiation and IL-17 production in Th17 cells, GDF15 contributes to regulatory T-cell-mediated suppression of conventional T-cell activation and inflammatory cytokines. Taken together, these data reveal that GDF15 is indispensable for attenuating aging-mediated local and systemic inflammation, thereby maintaining glucose homeostasis and insulin sensitivity in humans and mice.
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ItemComparisons of cancer-associated fibroblasts in the intratumoral stroma and invasive front in colorectal cancer.(Ovid Technologies (Wolters Kluwer Health), 2019-05)The aim of this study was to evaluate the cytomorphologic maturity and molecular activation of cancer-associated fibroblasts (CAFs) in the intratumoral stroma and invasive front in colorectal cancer and understand how they affect cancer invasion and long-term oncological outcomes.The cytomorphologic maturity of and α-smooth muscle actin (α-SMA), fibroblast activation protein α (FAPα), and fibroblast-specific protein 1 (FSP-1) expression in CAFs in the intratumoral stroma (CAF) and the invasive front (CAF) of colorectal cancer tissues were compared (n = 147). The correlations between CAF maturation, molecular activity markers, and cancer invasion were evaluated by network analysis. Overall survival and systemic recurrence were analyzed to assess the oncological effects of CAF properties.The cytomorphologic maturation rate was comparable between CAF and CAF. The presence of mature CAFs was related to epidermal growth factor receptor overexpression in cancer cells. Expression rates of α-SMA (96.6%-98.0%) and FAPα (18.6%-22.9%) were similar between CAF and CAF. FSP-1 expression was more frequent in CAF than in CAF (66.4% vs 58.2%, P = .038). There was a significant decrease in FSP-1 expression in CAF and CAF in higher stages. The infiltrating growth pattern of the tumor was more frequent in the immature CAF. In colorectal cancer with perineural invasion and lymph node metastasis, FSP-1 expression in CAF was significantly lower. On multivariate analysis using the Cox proportional hazards model, immature CAF was found to be an independent prognostic factor of overall survival. In non-metastatic (stage I-III) colorectal cancer patients, CAF maturity was not a prognostic factor for systemic recurrence.Cytomorphologic maturity and molecular activation markers were similar between CAFs in the intratumoral stroma and invasive front of colorectal cancer.
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ItemCancer-Associated Fibroblasts and Desmoplastic Reactions Related to Cancer Invasiveness in Patients With Colorectal Cancer.(Korean Society of Coloproctology, 2019-02)PURPOSE: We evaluated the relationship of cancer-associated fibroblasts (CAFs) and desmoplastic reactions with cancer invasiveness and long-term outcomes in patients with colorectal cancer (CRC). METHODS: Histologic evaluation of mature CAFs and desmoplasia was performed by observing the collagen fiber structure and fibroblast cytomorphology in the intratumoral stroma and invasive front of CRC tissues. Cancer-cell invasiveness was evaluated using lymphatic invasion, vascular invasion, perineural invasion, tumor budding, and tumor growth patterns. Overall survival and systemic recurrence were analyzed. A network analysis was performed between CAF maturation, desmoplastic reaction, and cancer invasiveness. RESULTS: The proportions of mature CAFs in the intratumoral stroma and the invasive front were 57.6% and 60.3%, respectively. Epidermal growth factor receptor (EGFR) overexpression was significantly higher in the mature CAFs in the invasive front as compared to immature CAFs. Lymphatic invasion increased as the number of mature fibroblasts in the intratumoral stroma increased. Tumor budding was observed in almost half of both mature and immature stroma samples and occurred more frequently in infiltrating tumors. On network analysis, well-connected islands were identified that was associated with EGFR overexpression, CAF maturation, and infiltrating tumor growth patterns leading to tumor budding. CONCLUSION: The maturity of CAFs and desmoplastic reactions were associated with cancer invasion. However, the cytomorphologic characteristics of CAFs were insufficient as an independent prognostic factor for patients with CRC.