95 research outputs found

    Optimal Emission Policy under the Risk of Irreversible Pollution

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    We consider an optimal consumption and pollution problem that has two important features. Environmental damages due to economic activities may be irreversible and the level at which the degradation becomes irreversible is unknown. Particular attention is paid to the situation where agents are relatively impatient and/or do not care a lot about the environment and/or Nature regenerates at low rate. We show that the optimal policy of the uncertain problem drives the economy in the long run toward a steady state while, when ignoring irreversibility, the economy follows a balanced growth path accompanied by a perpetual decrease in environmental quality and consumption, both asymptotically converging toward zero. Therefore, accounting for the risk of irreversibility induces more conservative decisions regarding consumption and polluting emissions. In general, however, we cannot rule out situations where the economy will optimally follow an irreversible path and consequently, will also be left, in the long run, with an irreversibly degraded environment.Optimal Control, Irreversibility Threshold, Uncertainty, Optimal Reversible, Irreversible Policy

    Automated retrieval of 3D CAD model objects in construction range images

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    Optimisation Of Controller Parameters For Adaptive Building Envelopes Through A Co-Simulation Interface: A Case Study

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    Adaptive building envelopes can dynamically adapt to environmental changes, often supported by a control system. While building performance simulation (BPS) tools can be employed to test different design alternatives, representing control strategies within current BPS tools can be challenging, especially for systems with a fast, dynamic response. Another challenge in current BPS tools is the ability to tune and select parameters for the particular use case. In this study, a modelling approach is presented for the integrated analysis of control strategies of adaptive building envelopes linking thermal performance and control with an optimisation algorithm. The proposed modelling approach was evaluated using a case study with an automated motorised blind with two distinct control strategies. Simulation results suggest that the window heat gains were 72.7 % lower when the controller model was coupled with an optimiser to identify optimised controller parameters compared to a baseline control strategy. The results of this study are suggestive of the benefits that can be obtained from adjusting the dynamic aspects of the building envelope. The results support the thesis of using optimisation as standard building envelope design practice in the future

    Automated Damage Index Estimation of Reinforced Concrete Columns for Post-Earthquake Evaluations

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    In emergency scenarios, immediate reconnaissance efforts are necessary. These efforts often take months to complete in full. While underway, building occupants are unable to return to their homes/businesses, and thus, the impact on the society of the disaster-stricken region is increased. In order to mitigate the impact, researchers have focused on creating a more efficient means of assessing the condition of buildings in the post-disaster state. In this paper, a machine vision-based methodology for real-time post-earthquake safety assessment is presented. A novel method of retrieving spalled properties on reinforced concrete (RC) columns in RC frame buildings using image data is presented. In this method, the spalled region is detected using a local entropy-based approach. Following this, the depth properties are retrieved using contextual information pertaining to the amount and type of reinforcement which is exposed. The method is validated using a dataset of damaged RC column images.This material is based in part upon work supported by the National Science Foundation under Grant Numbers CMMI-1034845 and CMMI-0738417.This is the accepted manuscript. The final version is available from ASCE at http://dx.doi.org/10.1061/(ASCE)ST.1943-541X.000120

    Optimal emission policy under the risk of irreversible pollution

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    International audienceWe consider an optimal consumption and pollution problem that has two important features. Environmental damages due to economic activities may be irreversible and the level at which the degradation becomes irreversible is unknown. Particular attention is paid to the situation where agents are relatively impatient and/or do not care a lot about the environment and/or Nature regenerates at low rate. We show that the optimal policy of the uncertain problem drives the economy in the long run toward a steady state while, when ignoring irreversibility, the economy follows a balanced growth path accompanied by a perpetual decrease in environmental quality and consumption, both asymptotically converging toward zero. Therefore, accounting for the risk of irreversibility induces more conservative decisions regarding consumption and polluting emissions. In general, however, we cannot rule out situations where the economy will optimally follow an irreversible path and consequently, will also be left, in the long run, with an irreversibly degraded environment

    The contribution of bone marrow-derived cells to angiogenesis and lymphangiogenesis in murine models of carcinogenesis

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    Cancer is a class of diseases in which a group of cells display uncontrolled growth (division beyond the normal limits), invasion (intrusion on and destruction of adjacent tissues), and sometimes metastasis (spread to other locations in the body via the circulatory system). In addition to tumor cell-intrinsic genetic and epigenetic alterations, the tumor stroma, i.e. endothelial cells, pericytes, fibroblasts and a diverse immune cell infiltrate, might substantially contribute to tumor progression, metastatic potential and resistance to therapy. I therefore investigated the influence of immune cells on the growth of tumors in the Rip1Tag2 mouse insulinoma model of multistage carcinogenesis. I detected a strong infiltration of myeloid cells, i.e. macrophages and granulocytes, into insulinomas. Functional experiments in vivo revealed that depletion of macrophages in tumors led to reduced angiogenesis but did not affect tumor growth. During the characterization of the immune cell contribution to tumor growth in the Rip1Tag2 tumor model, I detected bone marrow-derived cells at unexpected sites. In particular, when I analyzed the spatial contribution of GFP-tagged bone marrow cells in tumors of lymphangiogenic Rip1Tag2;RipVEGF-C mice, I detected bone marrow-derived cells in lymphatic endothelium surrounding the tumors. Detailed analysis of the integrated GFP+-cells revealed the expression of a complete set of markers that are characteristic for lymphatic endothelial cells, the cell surface proteins LYVE-1 and Podoplanin, as well as the homeo-box transcription factor Prox-1. Depending on the analysis technique applied, either confocal microscopy followed by 3D reconstitution or flow cytometry, between 3 and 9% of lymphatic endothelial cells in tumors are derived from the bone marrow. These studies were expanded to a second tumor model, the subcutaneous growth of TRAMP-C1 prostate cancer cells in syngenic mice, which confirmed the findings made in Rip1Tag2; RipVEGF-C mice, and allowed to further substantiate the suggested ontogeny of the integrated, bone marrow-derived cells. Cell sorting and genetic lineage tracing experiments indicated that the bone marrow-derived tumor lymphatic endothelial cells were at least partially derived from the myeloid lineage. Tumor mice were adoptively transferred with labeled myeloid (progenitor) cells, and subsequent integration of these cells into tumor lymphatic endothelium was detected. Cre/Lox technology resulting in myeloid-specific marker gene expression was employed to come to similar conclusions in a pure genetic experimental system without bone marrow cell-transfer or irradiation. In a loss-of-function approach, macrophages were pharmacologically depleted in Rip1Tag2;RipVEGF-C mice. Peritumoral lymphatic vessel coverage was found to be reduced in 2 macrophage-depleted mice as compared to control mice. Expression level analysis of the lymphangiogenic factors VEGF-C and VEGF-D by tumor-infiltrating macrophages indicated that their contribution to lymphangiogenesis by supplying growth factors is negligible and that the reduced lymphangiogenesis might indeed come from the reduced availability of macrophages as building blocks of lymphatic endothelia. The same plasticity of myeloid cells I detected in vivo was also observed in vitro, where bone marrow-derived macrophages start forming tube like structures and also start expressing lymphatic endothelial markers, when cultured under pro-inflammatory and endothelial specific conditions. In conclusion, this data indicates a myeloid origin of cells that trans-differentiate into lymphatic endothelial cells in an inflammatory tumor environment. The increasing use of non-invasive imaging technologies prompted us to evaluate an approach resulting in bioluminescent pancreatic insulinoma, principally an improved Rip1Tag2 tumor model of multistage pancreatic β-cell carcinogenesis. I therefore constructed a bicistronic expression cassette in which SV40 early region is followed by an internal ribosomal entry site and a firefly luciferase coding sequence, under the transcriptional control of the Rat insulin promoter 1. Transgenic expression in mice resulted in β-cell carcinogenesis that could be monitored noninvasively by in vivo bioluminescence. Numerous tumors of different malignancy stages can be detected in individual mice, indicating that this model recapitulates multistage carcinogenesis. In addition, in this mouse strain called RL-1 (RipTag-IRES-Luciferase line 1), due to the very stringent expression exclusively in the β-cells of Langerhans islets, we could determine micro-metastasis in liver via luciferase expression of metastatic cells. This mouse line will be of value to study antitumoral therapeutic approaches in real-time, as well as to define roles for tumor-promoting as well as metastasis-related genes when crossed to other transgenic or gene-targeted mice

    Integration of passive RFID location tracking for real-time visualization in building information models (BIM)

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    Navigation through large and unfamiliar facilities with labyrinths of corridors and rooms is difficult and often results in a person being lost. Additionally, locating a specific utility within a facility is often a tough task. The hypothesis tested in this research is that integrating real-time automated sensing technology and a Building Information Model will provide real time visualization that can assist in localization and navigation of a facility. The scope of this research is facility maintenance management during the Operation and Maintenance (O&M) phase of a facility. The thesis demonstrates how the integration of passive Radio Frequency Identification (RFID) tracking technology and Building Information Modeling (BIM) can assist in facilities maintenance management. The objectives of this research included 1) developing a framework that utilizes the integration of commercially-available RFID and a BIM model; 2) evaluating the framework for real-time resource location tracking within an indoor environment; and 3) developing an algorithm for real-time localization and visualization in a BIM model. A prototype application has been developed that simultaneously connects the RFID readers, a database, and a BIM model. The goal of this system is to have a real-time localization accuracy of 3 meters at 95% confidence. Testing was conducted in laboratory conditions, and the results show that the system error was within the 3 meters goal.M.S

    Var gene diversity and their serological recognition by naturally exposed individuals

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    Plasmodium falciparum causes the worst form of human malaria and leads to 1-2 million deaths annually, most of them children below the age of 5 living in subsaharan Africa. Morbidity varies from asymptomatic infections with no symptoms to severe malaria accompanied by organ failure, severe anemia and coma. Most of these clinical presentations are associated with sequestration of infected red blood cells (iRBC) on host endothelium. By attaching the parasitized erythrocyte to host receptors such as CD36, ICAM or CSA the parasite prevents the cell from being cleared by the spleen and therefore prolongs its own survival. A key protein involved in this process is the variant surface antigen Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) which is a parasite derived protein transported to the RBC surface to mediate cytoadherence. With this process exposes the parasite itself to the host immune system leading to the production of specific antibodies. In order to evade this host immune response the parasite undergoes antigenic variation by switching to another member of the same protein family. PfEMP1 is encoded by approximately 60 var genes per haploid genome and is expressed at the surface in a mutually exclusive manner, i.e. only 1 of the 60 proteins is expressed and exposed at any one time whilst the others remain silenced. Protection against severe malaria is thought to be mediated to a large degree by the piecemeal acquisition of anti-PfEMP1 antibodies during early childhood, since adults still get infected but rarely develop severe malaria symptoms. Recent observations suggest that not all PfEMP1 proteins expressed by a parasite are equally virulent, but only a subset of distinct var genes might render a parasite more pathogenic than parasites expressing different var gene variants. To generate potential anti-severe disease interventions members of this particular subset need to be identified. To date, only 6 studies have been published investigating the repertoire of expressed var genes in vivo. We have further used samples collected in Papua New Guinea from a case control study and analyzed var transcripts by RT-PCR followed by cloning and sequencing. We determined the 3 main groups of 5’UTR and analysed the data with respect to the clinical presentation of the children they were collected from. The detected number of different var group B and C transcipts was not significantly different between asymptomatic, mild or severe malaria cases, whereas an increase of group A var genes was observed in symptomatic cases when compared to children without any malaria symptoms. We identified an amino acid substitution mainly occurring in asymptomatic children with high parasitemia that might influence the binding affinity of parasites expressing these variants. However, using phylogenetic analyses we were not able to identify other distinct var genes or subsets associated with severe malaria. Blasting DBL1α domains against the 3D7 genome to obtain information on the upstream region was found to be suitable for group A var genes only, whereas 28% of group B and 62% of group C sequences were assigned to the wrong subgroup using this method. Even though we observed a 7% sequence overlap, bioinformatic analyses estimated the var gene repertoire in this region of PNG to be unlimited. It has previously been shown, that isolates causing severe disease are recognized more frequently than those causing mild malaria. In the second part of this thesis, we wanted to obtain information on the importance of distinct PfEMP1 domains in the recognition by the host immune system. For that purpose, fragments of 2 representative var genes shown to be associated with severe malaria were recombinantly expressed in E.coli and analyzed for their recognition by naturally exposed sera of different origin. Analysis of synthetic peptides using the same sera served to complement the results of ELISAs using recombinant proteins if expression of distinct domains was not possible. ELISA and Western blot analysis determined that 3 recombinant fragments and 2 synthetic peptides harbor epitopes that might play a role in the generation of protective antibodies. However, since sample size was small further investigations are required to confirm these findings. In the third part of this thesis, we tested the usefulness of the GeneMapper® analysis software to genotype var genes. It has been successfully established for genotyping the polymorphic marker gene msp2 and since var genes also show some length polymorphism it was investigated whether this technique could replace tedious cloning and sequencing approaches, used so far to dissect var gene diversity. Therefore, purified PCR products of UTR-DBL domains generated during the sequence analysis were reamplified with fluorescently labeled DBL-specific primers and analyzed by GeneMapper®. The results were then compared to the sequencing data. GeneMapper® sizing was highly accurate with a mean deviation of 1bp and showed a high consistency with sequencing data. Furthermore, GeneMapper® detected 141 sequences which were not identified with the sequencing approach, whereas vice verca, this was only the case for 16 sequences. However, a significant proportion of var genes could not be distinguished because the analyzed DBL domains were identical in size. Despite this shortcoming, we belive that GeneMapper® would greatly facilitate the analysis of expressed var genes and their dynamics
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