67 research outputs found

    Real-time flood overflow forecasting in Urban Drainage Systems by using time-series multi-stacking of data mining techniques

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    Β© 2023 The Author(s).Overflow forecasting in early warning systems is acknowledged as an essential task for devastating urban flood risk management. Although many machine learning models have been developed recently to forecast water levels in urban drainage systems (UDS), they usually require big and accurate data resources [1]. Alternatively, ensemble data mining models are becoming more popular, in which time-series numerical data are turned into the categorised features that classify wet weather conditions as two classes of overflow and non-overflow conditions [2]. However, the concept of time-series ensemble modelling i.e., blending different data mining techniques for predictions with different timesteps is still new [3]. Furthermore, the application of more advanced models, particularly multi-blending in these types of ensemble modelling requires more investigation. This study aims to introduce a novel multi-stacking model that integrates different decision tree frameworks by developing various base weak learner data mining techniques and associated base model performance indicators in the process of time-series blending of pre-trained stacked ensemble models. The performance of this new approach is compared by several previously developed ensemble models [2] through confusion matrix performance criteria, including hit rate, overestimation, and underestimation. This method is demonstrated by its application to a real case study of UDS located in the northwest of London for performance assessment up to 5hr ahead (i.e., 20 timesteps with 15-min intervals). In total, 140 base-models and 20 stacked models were developed that are stored in the data warehouse to use as real-time early-warning flood overflow forecasting for this case study. These developed models were used through introduced decision three framework that specified stacking blending methodology. Results show that while base models and stacked models suffer from high miss rate, especially for forecasting more than 3hrs ahead (more than 50%), the proposed multi-stacking model could perfectly maintain the miss rate (i.e., sum of over- and under-estimations) of up to 4hr-ahead predictions less than 10%, but this rate dropped to nearly 30% for 5hr-ahead predictions. However, the rate of overflow forecasting remained acceptably near 80% whereas it is recorded to less than 58% for other benchmark models. Using different decision frameworks for determining importance of each stacked model in blending mode of multi-stacking method shows could reduce errors in forecasting rate and take advantage of each model in real-time early warning urban flood forecasting.Peer reviewe

    Enhancing urban flood forecasting in drainage systems using dynamic ensemble-based data mining

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    This study presents a novel approach for urban flood forecasting in drainage systems using a dynamic ensemble-based data mining model which has yet to be utilised properly in this context. The proposed method incorporates an event identification technique and rainfall feature extraction to develop weak learner data mining models. These models are then stacked to create a time-series ensemble model using a decision tree algorithm and confusion matrix-based blending method. The proposed model was compared to other commonly used ensemble models in a real-world urban drainage system in the UK. The results show that the proposed model achieves a higher hit rate compared to other benchmark models, with a hit rate of around 85% vs 70Β % for the next 3Β h of forecasting. Additionally, the proposed smart model can accurately classify various timesteps of flood or non-flood events without significant lag times, resulting in fewer false alarms, reduced unnecessary risk management actions, and lower costs in real-time early warning applications. The findings also demonstrate that two features, "antecedent precipitation history" and "seasonal time occurrence of rainfall," significantly enhance the accuracy of flood forecasting with a hit rate accuracy ranging from 60Β % to 10Β % for a lead time of 15Β min to 3Β h

    Resilience Assessment in Urban Water Infrastructure: A Critical Review of Approaches, Strategies and Applications

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    Urban water infrastructure (UWI) comprises the main systems, including water supply systems (WSS), urban drainage/stormwater systems (UDS) and wastewater systems (WWS). The UWI needs to be resilient to a wide range of shocks and stresses, including structural failures such as pipe breakage and pump breakdown and functional failures such as unmet water demand/quality, flooding and combined sewer overflows. However, there is no general consensus about the resilience assessment of these systems widely presented by various research works. This study aims to critically review the approaches, strategies and applications of the resilience assessment for the complex systems in UWI. This review includes examining bibliometric analysis, developed frameworks related to resilience assessment to help comprehend resilience concepts for the specified UWI systems in urban settings, strategies for improving resilience, resilience indicators and common tools used for modelling resilience assessment in UWI. The results indicate that resilience assessment has primarily been conducted in developed countries, underscoring the macroeconomic significance of UWI. Three key areas have been identified for analysing resilience in UWI: system design, development of resilience concepts and implementation of green infrastructure. Moreover, it has been discovered that although resilience is commonly defined using technical approaches, a more comprehensive understanding of resilience can be gained through a holistic approach. Furthermore, while strategies such as system upgrades, decentralisation, digitalisation and nature-based solutions can enhance UWI resilience, they may be insufficient to fulfil all resilience indicators. To address the challenge of effectively comparing different resilience options, it is crucial to extensively examine comprehensive and sustainability-based indicators in future research

    Selective modulation of subtype III IP3R by Akt regulates ER Ca2+ release and apoptosis

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    Ca2+ transfer from endoplasmic reticulum (ER) to mitochondria can trigger apoptotic pathways by inducing release of mitochondrial pro-apoptotic factors. Three different types of inositol 1,4,5-trisphosphate receptor (IP3R) serve to discharge Ca2+ from ER, but possess some peculiarities, especially in apoptosis induction. The anti-apoptotic protein Akt can phosphorylate all IP3R isoforms and protect cells from apoptosis, reducing ER Ca2+ release. However, it has not been elucidated which IP3R subtypes mediate these effects. Here, we show that Akt activation in COS7 cells, which lack of IP3R I, strongly suppresses IP3-mediated Ca2+ release and apoptosis. Conversely, in SH-SY 5Y cells, which are type III-deficient, Akt is unable to modulate ER Ca2+ flux, losing its anti-apoptotic activity. In SH-SY 5Y-expressing subtype III, Akt recovers its protective function on cell death, by reduction of Ca2+ release. Moreover, regulating Ca2+ flux to mitochondria, Akt maintains the mitochondrial integrity and delays the trigger of apoptosis, in a type III-dependent mechanism. These results demonstrate a specific activity of Akt on IP3R III, leading to diminished Ca2+ transfer to mitochondria and protection from apoptosis, suggesting an additional level of cell death regulation mediated by Akt

    Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

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    Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as β€˜accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. β€˜Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death

    Transglutaminase 2 Contributes to Apoptosis Induction in Jurkat T Cells by Modulating Ca(2+) Homeostasis via Cross-Linking RAP1GDS1

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    BACKGROUND: Transglutaminase 2 (TG2) is a protein cross-linking enzyme known to be associated with the in vivo apoptosis program of T cells. However, its role in the T cell apoptosis program was not investigated yet. RESULTS: Here we report that timed overexpression of both the wild type (wt) and the cross-linking mutant of TG2 induced apoptosis in Jurkat T cells, the wt being more effective. Part of TG2 colocalised with mitochondria. WtTG2-induced apoptosis was characterized by enhanced mitochondrial Ca(2+) uptake. Ca(2+)-activated wtTG2 cross-linked RAP1, GTP-GDP dissociation stimulator 1, an unusual guanine exchange factor acting on various small GTPases, to induce a yet uncharacterized signaling pathway that was able to promote the Ca(2+) release from the endoplasmic reticulum via both Ins3P and ryanodine sensitive receptors leading to a consequently enhanced mitochondrial Ca(2+)uptake. CONCLUSIONS: Our data indicate that TG2 might act as a Ca(2+) sensor to amplify endoplasmic reticulum-derived Ca(2+) signals to enhance mitochondria Ca(2+) uptake. Since enhanced mitochondrial Ca(2+) levels were previously shown to sensitize mitochondria for various apoptotic signals, our data demonstrate a novel mechanism through which TG2 can contribute to the induction of apoptosis in certain cell types. Since, as compared to knock out cells, physiological levels of TG2 affected Ca(2+) signals in mouse embryonic fibroblasts similar to Jurkat cells, our data might indicate a more general role of TG2 in the regulation of mitochondrial Ca(2+) homeostasis

    Selective regulation of IP3-receptor-mediated Ca2+ signaling and apoptosis by the BH4 domain of Bcl-2 versus Bcl-Xl

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    Antiapoptotic B-cell lymphoma 2 (Bcl-2) targets the inositol 1,4,5-trisphosphate receptor (IP3R) via its BH4 domain, thereby suppressing IP3R Ca2+-flux properties and protecting against Ca2+-dependent apoptosis. Here, we directly compared IP3R inhibition by BH4-Bcl-2 and BH4-Bcl-Xl. In contrast to BH4-Bcl-2, BH4-Bcl-Xl neither bound the modulatory domain of IP3R nor inhibited IP3-induced Ca2+ release (IICR) in permeabilized and intact cells. We identified a critical residue in BH4-Bcl-2 (Lys17) not conserved in BH4-Bcl-Xl (Asp11). Changing Lys17 into Asp in BH4-Bcl-2 completely abolished its IP3R-binding and -inhibitory properties, whereas changing Asp11 into Lys in BH4-Bcl-Xl induced IP3R binding and inhibition. This difference in IP3R regulation between BH4-Bcl-2 and BH4-Bcl-Xl controls their antiapoptotic action. Although both BH4-Bcl-2 and BH4-Bcl-Xl had antiapoptotic activity, BH4-Bcl-2 was more potent than BH4-Bcl-Xl. The effect of BH4-Bcl-2, but not of BH4-Bcl-Xl, depended on its binding to IP(3)Rs. In agreement with the IP3R-binding properties, the antiapoptotic activity of BH4-Bcl-2 and BH4-Bcl-Xl was modulated by the Lys/Asp substitutions. Changing Lys17 into Asp in full-length Bcl-2 significantly decreased its binding to the IP3R, its ability to inhibit IICR and its protection against apoptotic stimuli. A single amino-acid difference between BH4-Bcl-2 and BH4-Bcl-Xl therefore underlies differential regulation of IP(3)Rs and Ca2+-driven apoptosis by these functional domains. Mutating this residue affects the function of Bcl-2 in Ca2+ signaling and apoptosis

    TESS hunt for young and maturing exoplanets (THYME). III. A two-planet system in the 400 Myr Ursa major group

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    A.W.M. was supported through NASA's Astrophysics Data Analysis Program (80NSSC19K0583). M.L.W. was supported by a grant through NASA's K2 GO program (80NSSC19K0097). This material is based on work supported by the National Science Foundation Graduate Research Fellowship Program under grant No. DGE-1650116 to P.C.T. A.V.'s work was performed under contract with the California Institute of Technology/Jet Propulsion Laboratory funded by NASA through the Sagan Fellowship Program executed by the NASA Exoplanet Science Institute. D.D. acknowledges support from NASA through Caltech/JPL grant RSA-1006130 and through the TESS Guest Investigator Program grant 80NSSC19K1727.Exoplanets can evolve significantly between birth and maturity, as their atmospheres, orbits, and structures are shaped by their environment. Young planets (<1 Gyr) offer an opportunity to probe the critical early stages of this evolution, where planets evolve the fastest. However, most of the known young planets orbit prohibitively faint stars. We present the discovery of two planets transiting HD 63433 (TOI 1726, TIC 130181866), a young Sun-like (Mβˆ—=0.99Β±0.03) star. Through kinematics, lithium abundance, and rotation, we confirm that HD 63433 is a member of the Ursa Major moving group (Ο„=414Β±23 Myr). Based on the TESS light curve and updated stellar parameters, we estimate the planet radii are 2.15Β±0.10RβŠ• and 2.67Β±0.12RβŠ•, the orbital periods are 7.11 and 20.55 days, and the orbital eccentricities are lower than about 0.2. Using HARPS-N velocities, we measure the Rossiter-McLaughlin signal of the inner planet, demonstrating that the orbit is prograde. Since the host star is bright (V=6.9), both planets are amenable to transmission spectroscopy, radial velocity measurements of their masses, and more precise determination of the stellar obliquity. This system is therefore poised to play an important role in our understanding of planetary system evolution in the first billion years after formation.PostprintPeer reviewe

    Recurrent Signature Patterns in HIV-1 B Clade Envelope Glycoproteins Associated with either Early or Chronic Infections

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    Here we have identified HIV-1 B clade Envelope (Env) amino acid signatures from early in infection that may be favored at transmission, as well as patterns of recurrent mutation in chronic infection that may reflect common pathways of immune evasion. To accomplish this, we compared thousands of sequences derived by single genome amplification from several hundred individuals that were sampled either early in infection or were chronically infected. Samples were divided at the outset into hypothesis-forming and validation sets, and we used phylogenetically corrected statistical strategies to identify signatures, systematically scanning all of Env. Signatures included single amino acids, glycosylation motifs, and multi-site patterns based on functional or structural groupings of amino acids. We identified signatures near the CCR5 co-receptor-binding region, near the CD4 binding site, and in the signal peptide and cytoplasmic domain, which may influence Env expression and processing. Two signatures patterns associated with transmission were particularly interesting. The first was the most statistically robust signature, located in position 12 in the signal peptide. The second was the loss of an N-linked glycosylation site at positions 413–415; the presence of this site has been recently found to be associated with escape from potent and broad neutralizing antibodies, consistent with enabling a common pathway for immune escape during chronic infection. Its recurrent loss in early infection suggests it may impact fitness at the time of transmission or during early viral expansion. The signature patterns we identified implicate Env expression levels in selection at viral transmission or in early expansion, and suggest that immune evasion patterns that recur in many individuals during chronic infection when antibodies are present can be selected against when the infection is being established prior to the adaptive immune response
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