Seismic retrofitting and health monitoring of school buildings of Cyprus

The vulnerability of existing buildings to seismic forces and their retrofitting is an international problem. The majority of structures in seismic-prone areas worldwide are structures that have been designed either without the consideration of seismic forces, or with previous codes of practice specifying lower levels of seismic forces. In Cyprus, after the three earthquakes that occurred in 1995, 1996, and 1999, the Cyprus State, acting in a pioneering way internationally, has decided the seismic retrofitting of all school buildings, taking into account the sensitivity of the society towards these structures, which house the future generation of the society. In this paper the overall assessment methodology is presented, along with details of the over 10 year ongoing retrofitting program of the school buildings of Cyprus, with emphasis on the description of the program and the development of a wireless monitoring system. In addition, mathematical models of selected school buildings are presented and comparison is made with in-situ measurement

Systems Level Metabolic Phenotype of Methotrexate Administration in the Context of Non-alcoholic Steatohepatitis in the Rat.

Adverse drug reactions (ADRs) represent a significant clinical challenge with respect to patient morbidity and mortality. We investigated the hepatotoxicity and systems level metabolic phenotype of methotrexate (MTX) in the context of a prevalent liver disease; non-alcoholic steatohepatitis (NASH). A nuclear magnetic resonance spectroscopic-based metabonomic approach was employed to analyze the metabolic consequences of MTX (0, 10, 40, and 100 mg/kg) in the urine and liver of healthy rats (control diet) and in a model of NASH (methionine-choline deficient diet). Histopathological analysis confirmed baseline (0 mg/kg) liver necrosis, liver inflammation, and lipid accumulation in the NASH model. Administration of MTX (40 and 100 mg/kg) led to liver necrosis in the control cohort, whereas the NASH cohort also displayed biliary hyperplasia and liver fibrosis (100 mg/kg), providing evidence of the synergistic effect of MTX and NASH. The complementary hepatic and urinary metabolic phenotypes of the NASH model, at baseline, revealed perturbation of multiple metabolites associated with oxidative and energetic stress, and folate homeostasis. Administration of MTX in both diet cohorts showed dose-dependent metabolic consequences affecting gut microbial, energy, nucleobase, nucleoside, and folate metabolism. Furthermore, a unique panel of metabolic changes reflective of the synergistic effect of MTX and NASH was identified, including the elevation of hepatic phenylalanine, urocanate, acetate, and both urinary and hepatic formiminoglutamic acid. This systems level metabonomic analysis of the hepatotoxicity of MTX in the context of NASH provided novel mechanistic insight of potential wider clinical relevance for further understanding the role of liver pathology as a risk factor for ADRs

Seismic Retrofitting of RC Frames with RC Infilling

The effectiveness of seismic retrofitting of multi-storey multi-bay RC-frame buildings, by converting selected bays into new walls through infilling with RC, was studied experimentally at the ELSA facility at JRC, Ispra, and the results are reported here. The full-scale model tested with the pseudo-dynamic method consisted of two parallel frames, linked through 0.15m slabs, having three bays each (8.5m long), with the central bay (2.5m) infilled with RC wall, and being four storeys tall (12m). The frames were designed and detailed for gravity loads only and are typical of similar frames built in Cyprus in the 1970’s. Different connection details and reinforcement percentages for the two infilled frames were used in order to study the effects of these parameters. The results of the pseudo-dynamic and cyclic testing performed are presented and conclusions are drawn.JRC.G.5-European laboratory for structural assessmen

Emission-aware Energy Storage Scheduling for a Greener Grid

Reducing our reliance on carbon-intensive energy sources is vital for reducing the carbon footprint of the electric grid. Although the grid is seeing increasing deployments of clean, renewable sources of energy, a significant portion of the grid demand is still met using traditional carbon-intensive energy sources. In this paper, we study the problem of using energy storage deployed in the grid to reduce the grid's carbon emissions. While energy storage has previously been used for grid optimizations such as peak shaving and smoothing intermittent sources, our insight is to use distributed storage to enable utilities to reduce their reliance on their less efficient and most carbon-intensive power plants and thereby reduce their overall emission footprint. We formulate the problem of emission-aware scheduling of distributed energy storage as an optimization problem, and use a robust optimization approach that is well-suited for handling the uncertainty in load predictions, especially in the presence of intermittent renewables such as solar and wind. We evaluate our approach using a state of the art neural network load forecasting technique and real load traces from a distribution grid with 1,341 homes. Our results show a reduction of >0.5 million kg in annual carbon emissions -- equivalent to a drop of 23.3% in our electric grid emissions.Comment: 11 pages, 7 figure, This paper will appear in the Proceedings of the ACM International Conference on Future Energy Systems (e-Energy 20) June 2020, Australi

The role of thrombospondins in wound healing, ischemia, and the foreign body reaction

Thrombospondin (TSP) 1 and TSP2 have been implicated in the regulation of several processes during tissue repair. Due to their matricellular nature, these proteins are thought to modulate cell-matrix interactions through a variety of mechanisms specific to the spatio-temporal context of their expression. Most notably, TSP1 and TSP2 appear to play distinct, non-overlapping roles in the healing of skin wounds. In contrast, both proteins have been implicated as regulators of ischemia-induced angiogenesis. Moreover, TSP2 has been shown to be a critical regulator of angiogenesis in the foreign body response (FBR). In this review, we discuss the role of TSPs in tissue repair and examine the mechanistic data regarding the ability of the thrombospondins to modulate cell-matrix interactions in this context

Vulnerability assessment and feasibility analysis of seismic strengthening of school buildings

The majority of structures in seismic-prone areas worldwide are structures that have been designed either without seismic design considerations, or using codes of practice that are seriously inadequate in the light of current seismic design principles. In Cyprus, after a series of earthquakes that occurred between 1995 and 1999, it was decided to carry out an unprecedented internationally seismic retrofitting of all school buildings, taking into account the sensitivity of the society towards these structures. In this paper representative school buildings are analysed in both their pristine condition and after applying retrofitting schemes typical of those implemented in the aforementioned large-scale strengthening programme. Non-linear analysis is conducted on calibrated analytical models of the selected buildings and fragility curves are derived for typical reinforced concrete and unreinforced masonry structures. These curves are then used to carry out a feasibility study, including both benefit-cost and life-cycle analysis, and evaluate the effectiveness of the strengthening programme

Thrombospondin-2 and SPARC/osteonectin are critical regulators of bone remodeling

Thrombospondin-2 (TSP2) and osteonectin/BM-40/SPARC are matricellular proteins that are highly expressed by bone cells. Mice deficient in either of these proteins show phenotypic alterations in the skeleton, and these phenotypes are most pronounced under conditions of altered bone remodeling. For example, TSP2-null mice have higher cortical bone volume and are resistant to bone loss associated with ovariectomy, whereas SPARC-null mice have decreased trabecular bone volume and fail to demonstrate an increase in bone mineral density in response to a bone-anabolic parathyroid hormone treatment regimen. In vitro, marrow stromal cell (MSC) osteoprogenitors from TSP2-null mice have increased proliferation but delayed formation of mineralized matrix. Similarly, in cultures of SPARC-null MSCs, osteoblastic differentiation and mineralized matrix formation are decreased. Overall, both TSP2 and SPARC positively influence osteoblastic differentiation. Intriguingly, both of these matricellular proteins appear to impact MSC fate through mechanisms that could involve the Notch signaling system. This review provides an overview of the role of TSP2 and SPARC in regulating bone structure, function, and remodeling, as determined by both in vitro and in vivo studies

The interaction of Thrombospondins with extracellular matrix proteins

The thrombospondins (TSPs) are a family of five matricellular proteins that appear to function as adapter molecules to guide extracellular matrix synthesis and tissue remodeling in a variety of normal and disease settings. Various TSPs have been shown to bind to fibronectin, laminin, matrilins, collagens and other extracellular matrix (ECM) proteins. The importance of TSP-1 in this context is underscored by the fact that it is rapidly deposited at the sites of tissue damage by platelets. An association of TSPs with collagens has been known for over 25 years. The observation that the disruption of the TSP-2 gene in mice leads to collagen fibril abnormalities provided important in vivo evidence that these interactions are physiologically important. Recent biochemical studies have shown that TSP-5 promotes collagen fibril assembly and structural studies suggest that TSPs may interact with collagens through a highly conserved potential metal ion dependent adhesion site (MIDAS). These interactions are critical for normal tissue homeostasis, tumor progression and the etiology of skeletal dysplasias

E2F-1 Directly Regulates Thrombospondin 1 Expression

Thrombospondin 1 (TSP1) has been shown to play a critical role in inhibiting angiogenesis, resulting in inhibition of tumor growth and metastases. To figure out TSP1's regulators will lead to reveal its biological function mechanistically. In this study, we show that E2F-1 could activate the transcription of TSP1 by both promoter assays and Northern blot. Analysis of various TSP1 promoter mutant constructs showed that a sequence located −144/−137 up-stream of the transcriptional initiation site, related to the consensus E2F-responsive sequence, is necessary for the activation. In consistence with up-regulation of TSP-1 activity by over-expression of E2F-1, the knockdown of endogenous E2F-1 inhibited TSP-1 promoter activity significantly, implying that E2F-1 mediated regulation of TSP-1 is relevant in vivo. In addition, E2F-1 could also directly bind to the TSP1 promoter region covering −144/−137 region as revealed by ChIP assays. Furthermore, the E2F-1-induced activation of TSP1 gene transcription is suppressed by pRB1 in a dose-dependent manner. Taken together, the results demonstrate that TSP1 is a novel target for E2F1, which might imply that E2F-1 can affect angiogenesis by modulating TSP1 expression