2,902 research outputs found

    Application of large underground seasonal thermal energy storage in district heating system: A model-based energy performance assessment of a pilot system in Chifeng, China

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    Seasonal thermal energy storage (STES) technology is a proven solution to resolve the seasonal discrepancy between heating energy generation from renewables and building heating demands. This research focuses on the performance assessment of district heating (DH) systems powered by low-grade energy sources with large-scale, high temperature underground STES technology. A pilot DH system, located in Chifeng, China that integrates a 0.5 million m3 borehole thermal energy storage system, an on-site solar thermal plant and excess heat from a copper plant is presented. The research in this paper adopts a model-based approach using Modelica to analyze the energy performance of the STES for two district heating system configurations. Several performance indicators such as the extraction heat, the injection heat and the storage coefficient are selected to assess the STES system performance. Results show that a lower STES discharge temperature leads to a better energy performance. A sensitivity analysis of the site properties illustrates that the thermal conductivity of soil is the most influential parameter on the STES system performance. The long-term performance of the STES is also discussed and a shorter stabilization time between one and two years could be achieved by discharging the STES at a lower temperature.This research is part of the seasonal storage for solar and industrial waste heat utilization for urban district heating project funded by the Joint Scientific Thematic Research Programme (JSTP)–Smart Energy in Smart Cities. We gratefully acknowledge the financial support from the Netherlands Organisation for Scientific Research (NWO). We would also like to thank our research partners from Tsinghua University working on the project of the International S&T Cooperation Programof China (ISTCP) (project No. 2015DFG62410). Without their efforts, we would not have been able to obtain the technical data to conduct the case study

    PDGF is a potent initiator of bone formation in a tissue engineered model of pathological ossification

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    Heterotopic ossification (HO) is a debilitating condition defined by the rapid formation of bone in soft tissues. What makes HO fascinating is firstly the rate at which bone is deposited, and secondly the fact that this bone is structurally and compositionally similar to that of a healthy adult. If the mechanisms governing HO are understood, they have the potential to be exploited for the development of potent osteoinductive therapies. With this aim, we utilised a tissue engineered skeletal muscle model to better understand the role of inflammation on this debilitating phenomenon. We showed myoblasts could be divided into two distinct populations, myogenic cells and undifferentiated "reserve" cells. Gene expression analysis of myogenic and osteo-regulatory markers confirmed that "reserve" cells were primed for osteogenic differentiation, but had a reduced capacity for myogenesis. Osteogenic differentiation was significantly enhanced in the presence of PDGF-BB and BMP2, and correlated with conversion to a Sca-1(+) /CD73(+) phenotype. Alizarin red staining showed that PDGF-BB promoted significantly more mineral deposition than BMP2. Finally, we showed that PDGF-induced mineralisation was blocked in the presence of the pro-inflammatory cytokines TNFα and IL1. In conclusion, the present study identified that PDGF-BB is a potent osteoinductive factor in a model of tissue engineered skeletal muscle, and that the osteogenic capacity of this protein was modulated in the presence of pro-inflammatory cytokines. These findings reveal a possible mechanism by which HO develops following trauma. Importantly, these findings have implications for the induction and control of bone formation for regenerative medicine

    Tibetan sheep are better able to cope with low energy intake than Small-tailed Han sheep due to lower maintenance energy requirements and higher nutrient digestibilities

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    Tibetan sheep are indigenous to the Qinghai-Tibetan Plateau (QTP) and are well-adapted to and even thrive under the harsh alpine conditions. Small-tailed Han sheep were introduced to the plateau because of their high prolificacy and are maintained mainly in feedlots. Because of their different backgrounds, we hypothesised that Tibetan and Small-tailed Han sheep would differ in their utilization of energy intake and predicted that Tibetan sheep would cope better with low energy intake than Small-tailed Han sheep. To test this prediction, we determined nutrient digestibilities, energy requirements for maintenance and blood metabolite and hormone concentrations involved in energy metabolism in these breeds. Sheep of each breed (n = 24 of each, all wethers and 1.5 years of age) were distributed randomly into one of four groups and offered ad libitum diets of different digestible energy (DE) densities: 8.21, 9.33, 10.45 and 11.57 MJ DE/kg Dry matter (DM). Following 42 d of measuring feed intake, a 1-week digestion and metabolism experiment was done. DM intakes did not differ between breeds nor among treatments but, by design, DE intake increased linearly in both breeds as dietary energy level increased (P < 0.001). The average daily gain (ADG) was significantly greater in the Tibetan than Small-tailed Han sheep (P = 0.003) and increased linearly in both breeds (P < 0.001). In addition, from the regression analysis of ADG on DE intake, daily DE maintenance requirements were lower for Tibetan than for Small-tailed Han sheep (0.41 vs 0.50 MJ/BW0.75, P < 0.05). The DE and metabolizable energy (ME) digestibilities were higher in the Tibetan than Small-tailed Han sheep (P < 0.001) and increased linearly as the energy level increased in the diet (P < 0.001). At the lowest energy treatment, Tibetan sheep when compared with Small-tailed Han sheep, had: 1) higher serum glucose and glucagon, but lower insulin concentrations (P < 0.05), which indicated a higher capacity for gluconeogenesis and ability to regulate glucose metabolism; and 2) higher non-esterified fatty acids (NEFA) and lower very low density lipoprotein (VLDL) and triglyceride (TG) concentrations (P < 0.05), which indicated a higher capacity for NEFA oxidation but lower ability for triglyceride (TG) synthesis. We concluded that our prediction was supported as these differences between breeds conferred an advantage for Tibetan over Small-tailed Han sheep to cope better with low energy diets

    Renal pericytes: regulators of medullary blood flow

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    Regulation of medullary blood flow (MBF) is essential in maintaining normal kidney function. Blood flow to the medulla is supplied by the descending vasa recta (DVR), which arise from the efferent arterioles of juxtamedullary glomeruli. DVR are composed of a continuous endothelium, intercalated with smooth muscle-like cells called pericytes. Pericytes have been shown to alter the diameter of isolated and in situ DVR in response to vasoactive stimuli that are transmitted via a network of autocrine and paracrine signalling pathways. Vasoactive stimuli can be released by neighbouring tubular epithelial, endothelial, red blood cells and neuronal cells in response to changes in NaCl transport and oxygen tension. The experimentally described sensitivity of pericytes to these stimuli strongly suggests their leading role in the phenomenon of MBF autoregulation. Because the debate on autoregulation of MBF fervently continues, we discuss the evidence favouring a physiological role for pericytes in the regulation of MBF and describe their potential role in tubulo-vascular cross-talk in this region of the kidney. Our review also considers current methods used to explore pericyte activity and function in the renal medulla

    Evaluation of the BCS Approximation for the Attractive Hubbard Model in One Dimension

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    The ground state energy and energy gap to the first excited state are calculated for the attractive Hubbard model in one dimension using both the Bethe Ansatz equations and the variational BCS wavefunction. Comparisons are provided as a function of coupling strength and electron density. While the ground state energies are always in very good agreement, the BCS energy gap is sometimes incorrect by an order of magnitude, particularly at half-filling. Finite size effects are also briefly discussed for cases where an exact solution in the thermodynamic limit is not possible. In general, the BCS result for the energy gap is poor compared to the exact result.Comment: 25 pages, 5 Postscript figure

    Identifying the cellular mechanisms leading to heterotopic ossification

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    Heterotopic ossification (HO) is a debilitating condition defined by the de novo development of bone within non-osseous soft tissues, and can be either hereditary or acquired. The hereditary condition, fibrodysplasia ossificans progressiva is rare but life threatening. Acquired HO is more common and results from a severe trauma that produces an environment conducive for the formation of ectopic endochondral bone. Despite continued efforts to identify the cellular and molecular events that lead to HO, the mechanisms of pathogenesis remain elusive. It has been proposed that the formation of ectopic bone requires an osteochondrogenic cell type, the presence of inductive agent(s) and a permissive local environment. To date several lineage-tracing studies have identified potential contributory populations. However, difficulties identifying cells in vivo based on the limitations of phenotypic markers, along with the absence of established in vitro HO models have made the results difficult to interpret. The purpose of this review is to critically evaluate current literature within the field in an attempt identify the cellular mechanisms required for ectopic bone formation. The major aim is to collate all current data on cell populations that have been shown to possess an osteochondrogenic potential and identify environmental conditions that may contribute to a permissive local environment. This review outlines the pathology of endochondral ossification, which is important for the development of potential HO therapies and to further our understanding of the mechanisms governing bone formation

    Deformed Oscillator Algebras and Higher-Spin Gauge Interactions of Matter Fields in 2+1 Dimensions

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    We formulate a non-linear system of equations which describe higher-spin gauge interactions of massive matter fields in 2+1 dimensional space-time and explain some properties of the deformed oscillator algebra which underlies this formulation. In particular we show that the parameter of mass MM of matter fields is related to the deformation parameter in this algebra.Comment: LaTex, 12 pages, no figures; Invited talk at the International Seminar Supersymmetry and Quantum Field Theory dedicated to the memory of Dmitrij V. Volkov; Kharkov, January 1997; to appear in the proceeding

    Defining the balance between regeneration and pathological ossification in skeletal muscle

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    Heterotopic ossification (HO) is characterised by the formation of bone at atypical sites. This type of ectopic bone formation is most prominent in skeletal muscle, most frequently resulting as a consequence of physical trauma and associated with aberrant tissue regeneration. The condition is debilitating, reducing a patient’s range of motion and potentially causing severe pathologies resulting from nerve and vascular compression. Despite efforts to understand the pathological processes governing HO, there remains a lack of consensus regarding the micro-environmental conditions conducive to its formation, and attempting to define the balance between muscle regeneration and pathological ossification remains complex. The development of HO is thought to be related to a complex interplay between factors released both locally and systemically in response to trauma. It develops as skeletal muscle undergoes significant repair and regeneration, and is likely to result from the misdirected differentiation of endogenous or systemically derived progenitors in response to biochemical and/or environmental cues. The process can be sequentially delineated by the presence of inflammation, tissue breakdown, adipogenesis, hypoxia, neo-vasculogenesis, chondrogenesis and ossification. However, exactly how each of these stages contributes to the formation of HO is at present not well understood. Our previous review examined the cellular contribution to HO. Therefore, the principal aim of this review will be to comprehensively outline changes in the local tissue micro-environment following trauma, and identify how these changes can alter the balance between skeletal muscle regeneration and ectopic ossification. An understanding of the mechanisms governing this condition is required for the development and advancement of HO prophylaxis and treatment, and may even hold the key to unlocking novel methods for engineering hard tissues

    Defining the balance between regeneration and pathological ossification in skeletal muscle

    Get PDF
    Heterotopic ossification (HO) is characterised by the formation of bone at atypical sites. This type of ectopic bone formation is most prominent in skeletal muscle, most frequently resulting as a consequence of physical trauma and associated with aberrant tissue regeneration. The condition is debilitating, reducing a patient’s range of motion and potentially causing severe pathologies resulting from nerve and vascular compression. Despite efforts to understand the pathological processes governing HO, there remains a lack of consensus regarding the micro-environmental conditions conducive to its formation, and attempting to define the balance between muscle regeneration and pathological ossification remains complex. The development of HO is thought to be related to a complex interplay between factors released both locally and systemically in response to trauma. It develops as skeletal muscle undergoes significant repair and regeneration, and is likely to result from the misdirected differentiation of endogenous or systemically derived progenitors in response to biochemical and/or environmental cues. The process can be sequentially delineated by the presence of inflammation, tissue breakdown, adipogenesis, hypoxia, neo-vasculogenesis, chondrogenesis and ossification. However, exactly how each of these stages contributes to the formation of HO is at present not well understood. Our previous review examined the cellular contribution to HO. Therefore, the principal aim of this review will be to comprehensively outline changes in the local tissue micro-environment following trauma, and identify how these changes can alter the balance between skeletal muscle regeneration and ectopic ossification. An understanding of the mechanisms governing this condition is required for the development and advancement of HO prophylaxis and treatment, and may even hold the key to unlocking novel methods for engineering hard tissues
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