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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ItemThe carbon footprint of treating patients with septic shock in the intensive care unit(College of Intensive Care Medicine of Australia and New Zealand, 2018-12-01)OBJECTIVE: To use life cycle assessment to determine the environmental footprint of the care of patients with septic shock in the intensive care unit (ICU). DESIGN, SETTING AND PARTICIPANTS: Prospective, observational life cycle assessment examining the use of energy for heating, ventilation and air conditioning; lighting; machines; and all consumables and waste associated with treating ten patients with septic shock in the ICU at BarnesJewish Hospital, St. Louis, MO, United States (US-ICU) and ten patients at Footscray Hospital, Melbourne, Vic, Australia (Aus-ICU). MAIN OUTCOME MEASURES: Environmental footprint, particularly greenhouse gas emissions. RESULTS: Energy use per patient averaged 272 kWh/day for the US-ICU and 143 kWh/day for the Aus-ICU. The average daily amount of single-use materials per patient was 3.4 kg (range, 1.0-6.3 kg) for the US-ICU and 3.4 kg (range, 1.2-8.7 kg) for the Aus-ICU. The average daily particularly greenhouse gas emissions arising from treating patients in the US-ICU was 178 kg carbon dioxide equivalent (CO2-e) emissions (range, 165-228 kg CO2-e), while for the Aus-ICU the carbon footprint was 88 kg CO2-e (range, 77-107 kg CO2-e). Energy accounted for 155 kg CO2-e in the US-ICU (87%) and 67 kg CO2-e in the Aus-ICU (76%). The daily treatment of one patient with septic shock in the US-ICU was equivalent to the total daily carbon footprint of 3.5 Americans' CO2-e emissions, and for the Aus-ICU, it was equivalent to the emissions of 1.5 Australians. CONCLUSION: The carbon footprints of the ICUs were dominated by the energy use for heating, ventilation and air conditioning; consumables were relatively less important, with limited effect of intensity of patient care. There is large opportunity for reducing the ICUs' carbon footprint by improving the energy efficiency of buildings and increasing the use of renewable energy sources.
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ItemNo Preview AvailableEditorial(Informa UK Limited, 2015-06-01)
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ItemA Novel Approach for 3D Modeling and Geovisualization of Easement Rights in Apartments(CMV Verlag, 2018-12-01)
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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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ItemAntibiotic use and abuse: a threat to mitochondria and chloroplasts with impact on research, health, and environment.(Wiley, 2015-10)Recently, several studies have demonstrated that tetracyclines, the antibiotics most intensively used in livestock and that are also widely applied in biomedical research, interrupt mitochondrial proteostasis and physiology in animals ranging from round worms, fruit flies, and mice to human cell lines. Importantly, plant chloroplasts, like their mitochondria, are also under certain conditions vulnerable to these and other antibiotics that are leached into our environment. Together these endosymbiotic organelles are not only essential for cellular and organismal homeostasis stricto sensu, but also have an important role to play in the sustainability of our ecosystem as they maintain the delicate balance between autotrophs and heterotrophs, which fix and utilize energy, respectively. Therefore, stricter policies on antibiotic usage are absolutely required as their use in research confounds experimental outcomes, and their uncontrolled applications in medicine and agriculture pose a significant threat to a balanced ecosystem and the well-being of these endosymbionts that are essential to sustain health.
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ItemGrowth differentiation factor 15 is a myomitokine governing systemic energy homeostasis.(Rockefeller University Press, 2017-01-02)Reduced mitochondrial electron transport chain activity promotes longevity and improves energy homeostasis via cell-autonomous and -non-autonomous factors in multiple model systems. This mitohormetic effect is thought to involve the mitochondrial unfolded protein response (UPRmt), an adaptive stress-response pathway activated by mitochondrial proteotoxic stress. Using mice with skeletal muscle-specific deficiency of Crif1 (muscle-specific knockout [MKO]), an integral protein of the large mitoribosomal subunit (39S), we identified growth differentiation factor 15 (GDF15) as a UPRmt-associated cell-non-autonomous myomitokine that regulates systemic energy homeostasis. MKO mice were protected against obesity and sensitized to insulin, an effect associated with elevated GDF15 secretion after UPRmt activation. In ob/ob mice, administration of recombinant GDF15 decreased body weight and improved insulin sensitivity, which was attributed to elevated oxidative metabolism and lipid mobilization in the liver, muscle, and adipose tissue. Thus, GDF15 is a potent mitohormetic signal that safeguards against the onset of obesity and insulin resistance.