46 resultados para loss of crystallinity


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Loss-of-mains protection is an important component of the protection systems of embedded generation. The role of loss-of-mains is to disconnect the embedded generator from the utility grid in the event that connection to utility dispatched generation is lost. This is necessary for a number of reasons, including the safety of personnel during fault restoration and the protection of plant against out-of-synchronism reclosure to the mains supply. The incumbent methods of loss-of-mains protection were designed when the installed capacity of embedded generation was low, and known problems with nuisance tripping of the devices were considered acceptable because of the insignificant consequence to system operation. With the dramatic increase in the installed capacity of embedded generation over the last decade, the limitations of current islanding detection methods are no longer acceptable. This study describes a new method of loss-of-mains protection based on phasor measurement unit (PMU) technology, specifically using a low cost PMU device of the authors' design which has been developed for distribution network applications. The proposed method addresses the limitations of the incumbent methods, providing a solution that is free of nuisance tripping and has a zero non-detection zone. This system has been tested experimentally and is shown to be practical, feasible and effective. Threshold settings for the new method are recommended based on data acquired from both the Great Britain and Ireland power systems.

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In this paper, our previous work on Principal Component Analysis (PCA) based fault detection method is extended to the dynamic monitoring and detection of loss-of-main in power systems using wide-area synchrophasor measurements. In the previous work, a static PCA model was built and verified to be capable of detecting and extracting system faulty events; however the false alarm rate is high. To address this problem, this paper uses a well-known ‘time lag shift’ method to include dynamic behavior of the PCA model based on the synchronized measurements from Phasor Measurement Units (PMU), which is named as the Dynamic Principal Component Analysis (DPCA). Compared with the static PCA approach as well as the traditional passive mechanisms of loss-of-main detection, the proposed DPCA procedure describes how the synchrophasors are linearly
auto- and cross-correlated, based on conducting the singular value decomposition on the augmented time lagged synchrophasor matrix. Similar to the static PCA method, two statistics, namely T2 and Q with confidence limits are calculated to form intuitive charts for engineers or operators to monitor the loss-of-main situation in real time. The effectiveness of the proposed methodology is evaluated on the loss-of-main monitoring of a real system, where the historic data are recorded from PMUs installed in several locations in the UK/Ireland power system.

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To determine the effect of microbial metabolites on the release of root exudates from perennial ryegrass, seedlings were pulse labelled with [14C]-CO2 in the presence of a range of soil micro-organisms. Microbial inoculants were spatially separated from roots by Millipore membranes so that root infection did not occur. Using this technique, only microbial metabolites affected root exudation. The effect of microbial metabolites on carbon assimilation and distribution and root exudation was determined for 15 microbial species. Assimilation of a pulse label varied by over 3.5 fold, dependent on inoculant. Distribution of the label between roots and shoots also varied with inoculant, but the carbon pool that was most sensitive to inoculation was root exudation. In the absence of a microbial inoculant only 1% of assimilated label was exuded. Inoculation of the microcosms always caused an increase in exudation but the percentage exuded varied greatly, within the range of 3-34%. © 1995 Kluwer Academic Publishers.

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The Runx genes function as dominant oncogenes that collaborate potently with Myc or loss of p53 to induce lymphoma when over-expressed. Here we examined the requirement for basal Runx1 activity for tumor maintenance in the Eµ-Myc model of Burkitt's lymphoma. While normal Runx1fl/fl lymphoid cells permit mono-allelic deletion, primary Eµ-Myc lymphomas showed selection for retention of both alleles and attempts to enforce deletion in vivo led to compensatory expansion of p53null blasts retaining Runx1. Surprisingly, Runx1 could be excised completely from established Eµ-Myc lymphoma cell lines in vitro without obvious effects on cell phenotype. Established lines lacked functional p53, and were sensitive to death induced by introduction of a temperature-sensitive p53 (Val135) allele. Transcriptome analysis of Runx1-deleted cells revealed a gene signature associated with lymphoid proliferation, survival and differentiation, and included strong de-repression of recombination-activating (Rag) genes, an observation that was mirrored in a panel of human acute leukemias where RUNX1 and RAG1,2 mRNA expression were negatively correlated. Notably, despite their continued growth and tumorigenic potential, Runx1null lymphoma cells displayed impaired proliferation and markedly increased sensitivity to DNA damage and dexamethasone-induced apoptosis, validating Runx1 function as a potential therapeutic target in Myc-driven lymphomas regardless of their p53 status.

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Charge changing processes of MeV ions penetrating through liquid spray is confirmed to be abundant source of various energetic negative ion and neutral atom beams its generic nature is demonstrated.

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We performed fluorescent in situ hybridization (FISH) for 16q23 abnormalities in 861 patients with newly diagnosed multiple myeloma and identified deletion of 16q [del(16q)] in 19.5%. In 467 cases in which demographic and survival data were available, del(16q) was associated with a worse overall survival (OS). It was an independent prognostic marker and conferred additional adverse survival impact in cases with the known poor-risk cytogenetic factors t(4;14) and del(17p). Gene expression profiling and gene mapping using 500K single-nucleotide polymorphism (SNP) mapping arrays revealed loss of heterozygosity (LOH) involving 3 regions: the whole of 16q, a region centered on 16q12 (the location of CYLD), and a region centered on 16q23 (the location of the WW domain-containing oxidoreductase gene WWOX). CYLD is a negative regulator of the NF-kappaB pathway, and cases with low expression of CYLD were used to define a "low-CYLD signature." Cases with 16q LOH or t(14;16) had significantly reduced WWOX expression. WWOX, the site of the translocation breakpoint in t(14;16) cases, is a known tumor suppressor gene involved in apoptosis, and we were able to generate a "low-WWOX signature" defined by WWOX expression. These 2 genes and their corresponding pathways provide an important insight into the potential mechanisms by which 16q LOH confers poor prognosis.

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Scavenger receptor BI (SR-BI) is the major receptor for high-density lipoprotein (HDL)
cholesterol (HDL-C). In humans, high amounts of HDL-C in plasma are associated with a
lower risk of coronary heart disease (CHD). Mice that have depleted Scarb1 (SR-BI
knockout mice) have markedly elevated HDL-C levels but, paradoxically, increased
atherosclerosis. The impact of SR-BI on HDL metabolism and CHD risk in humans remains
unclear. Through targeted sequencing of coding regions of lipid-modifying genes in 328
individuals with extremely high plasma HDL-C levels, we identified a homozygote for a lossof-function
variant, in which leucine replaces proline 376 (P376L), in SCARB1, the gene
encoding SR-BI. The P376L variant impairs posttranslational processing of SR-BI and
abrogates selective HDL cholesterol uptake in transfected cells, in hepatocyte-like cells
derived from induced pluripotent stem cells from the homozygous subject, and in mice.
Large population-based studies revealed that subjects who are heterozygous carriers of
the P376L variant have significantly increased levels of plasma HDL-C. P376L carriers have
a profound HDL-related phenotype and an increased risk of CHD (odds ratio = 1.79, which is
statistically significant).

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Poly-L-Lactide is a bioresorbable polymer which degrades through hydrolysis of its ester linkage influenced by initial molecular weight and degree of crystallinity. Polymers belonging to the aliphatic polyester family currently represent the most attractive group of polymers that meet the medical and physical demands for safe clinical applications. Compression moulded PLLA pellets were produced as rods, sterilized and degraded both in vitro and in vivo (sub-dermal implantation model). The material molecular weight, crystallinity, mechanical strength and thermal properties were evaluated. In both in vitro and in vivo environments, degradation proceeded at the same rate and followed the general sequence of aliphatic polyester degradation, ruling out enzymes accelerating the degradation rate in vivo. By 44 weeks duration of implantation the PLLA rods were still biocompatible, before any mass loss was observed.

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Studies suggest that activation of phosphoinositide 3-kinase-Akt may protect against neuronal cell death in Alzheimer's disease (AD). Here, however, we provide evidence of increased Akt activation, and hyperphosphorylation of critical Akt substrates in AD brain, which link to AD pathogenesis, suggesting that treatments aiming to activate the pathway in AD need to be considered carefully. A different distribution of Akt and phospho-Akt was detected in AD temporal cortex neurons compared with control neurons, with increased levels of active phosphorylated-Akt in particulate fractions, and significant decreases in Akt levels in AD cytosolic fractions, causing increased activation of Akt (phosphorylated-Akt/total Akt ratio) in AD. In concordance, significant increases in the levels of phosphorylation of total Akt substrates, including: GSK3ßSer9, tauSer214, mTORSer2448, and decreased levels of the Akt target, p27kip1, were found in AD temporal cortex compared with controls. A significant loss and altered distribution of the major negative regulator of Akt, PTEN (phosphatase and tensin homologue deleted on chromosome 10), was also detected in AD neurons. Loss of phosphorylated-Akt and PTEN-containing neurons were found in hippocampal CA1 at end stages of AD. Taken together, these results support a potential role for aberrant control of Akt and PTEN signalling in AD.

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Given currently high rates of extinction, it is critical to be able to predict how ecosystems will respond to loss of species and consequent changes in community structure. Much previous research in this area has been based on terrestrial systems, using synthetically assembled communities. There has beer! much less research on inter-trophic effects in different systems, using in situ removal experiments. Problems with the design of early experiments have made it difficult to determine whether reductions in ecosystem functioning in low diversity treatments were due to the number of species present or merely to the reduced likelihood of including particular (

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The rate of species loss is increasing on a global scale and predators are most at risk from human-induced extinction. The effects of losing predators are difficult to predict, even with experimental single species removals, because different combinations of species interact in unpredictable ways. We tested the effects of the loss of groups of common predators on herbivore and algal assemblages in a model benthic marine system. The predator groups were fish, shrimp and crabs. Each group was represented by at least two characteristic species based on data collected at local field sites. We examined the effects of the loss of predators while controlling for the loss of predator biomass. The identity, not the number of predator groups, affected herbivore abundance and assemblage structure. Removing fish led to a large increase in the abundance of dominant herbivores, such as Ampithoids and Caprellids. Predator identity also affected algal assemblage structure. It did not, however, affect total algal mass. Removing fish led to an increase in the final biomass of the least common taxa (red algae) and reduced the mass of the dominant taxa (brown algae). This compensatory shift in the algal assemblage appeared to facilitate the maintenance of a constant total algal biomass. In the absence of fish, shrimp at higher than ambient densities had a similar effect on herbivore abundance, showing that other groups could partially compensate for the loss of dominant predators. Crabs had no effect on herbivore or algal populations, possibly because they were not at carrying capacity in our experimental system. These findings show that contrary to the assumptions of many food web models, predators cannot be classified into a single functional group and their role in food webs depends on their identity and density in 'real' systems and carrying capacities.

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The focus of this study was to disentangle the effects of multiple stressors on biodiversity, ecosystem functioning and stability. This project examined the effects of anthropogenic increased nutrient loads on the diversity of coastal ecosystems and the effects of loss of species on ecosystem functioning. Specifically, the direct effect of sewage outfalls on benthic communities was assessed using a fully replicated survey that incorporated spatial and temporal variation. In addition, two field experiments examined the effects of loss of species at multiple trophic levels, and tested for potential interactive effects with enhanced nutrient concentration conditions on benthic assemblage structure and ecosystem functioning. This research addressed priority issues outlined in the Biodiversity Knowledge Programme for Ireland (2006) and also aimed to deliver information relevant to European Union (EU) directives (the Water Framework Directive [WFD], the Habitats Directive and the Marine Strategy Framework Directive).

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Loss of biodiversity and nutrient enrichment are two of the main human impacts on ecosystems globally, yet we understand very little about the interactive effects of multiple stressors on natural communities and how this relates to biodiversity and ecosystem functioning. Advancing our understanding requires the following: (1) incorporation of processes occurring within and among trophic levels in natural ecosystems and (2) tests of context-dependency of species loss effects. We examined the effects of loss of a key predator and two groups of its prey on algal assemblages at both ambient and enriched nutrient conditions in a marine benthic system and tested for interactions between the loss of functional diversity and nutrient enrichment on ecosystem functioning. We found that enrichment interacted with food web structure to alter the effects of species loss in natural communities. At ambient conditions, the loss of primary consumers led to an increase in biomass of algae, whereas predator loss caused a reduction in algal biomass (i.e. a trophic cascade). However, contrary to expectations, we found that nutrient enrichment negated the cascading effect of predators on algae. Moreover, algal assemblage structure varied in distinct ways in response to mussel loss, grazer loss, predator loss and with nutrient enrichment, with compensatory shifts in algal abundance driven by variation in responses of different algal species to different environmental conditions and the presence of different consumers. We identified and characterized several context-dependent mechanisms driving direct and indirect effects of consumers. Our findings highlight the need to consider environmental context when examining potential species redundancies in particular with regard to changing environmental conditions. Furthermore, non-trophic interactions based on empirical evidence must be incorporated into food web-based ecological models to improve understanding of community responses to global change.

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Our knowledge of the effects of consumer species loss on ecosystem functioning is limited by a paucity of manipulative field studies, particularly those that incorporate inter-trophic effects. Further, given the ongoing transformation of natural habitats by anthropogenic activities, studies should assess the relative importance of biodiversity for ecosystem processes across different environmental contexts by including multiple habitat types. We tested the context-dependency of the effects of consumer species loss by conducting a 15-month field experiment in two habitats (mussel beds and rock pools) on a temperate rocky shore, focussing on the responses of algal assemblages following the single and combined removals of key gastropod grazers (Patella vulgata, P. ulyssiponensis, Littorina littorea and Gibbula umbilicalis). In both habitats, the removal of limpets resulted in a larger increase in macroalgal richness than that of either L. littorea or G. umbilicalis. Further, by the end of the study, macroalgal cover and richness were greater following the removal of multiple grazer species compared to single species removals. Despite substantial differences in physical properties and the structure of benthic assemblages between mussel beds and rock pools, the effects of grazer loss on macroalgal cover, richness, evenness and assemblage structure were remarkably consistent across both habitats. There was, however, a transient habitat-dependent effect of grazer removal on macroalgal assemblage structure that emerged after three months, which was replaced by non-interactive effects of grazer removal and habitat after 15 months. This study shows that the effects of the loss of key consumers may transcend large abiotic and biotic differences between habitats in rocky intertidal systems. While it is clear that consumer diversity is a primary driver of ecosystem functioning, determining its relative importance across multiple contexts is necessary to understand the consequences of consumer species loss against a background of environmental change.

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This paper investigates the effects of polyethylene glycol (PEG), on the mechanical and thermal properties of nalidixic acid/ploy ε-caprolactone (NA)/PCL blends prepared by hot melt extrusion. The blends were characterized by tensile and flexural analysis, dynamic mechanical analysis, differential scanning calorimetry, thermogravimetric analysis and X-ray diffraction. Experimental data indicated that the addition of NA caused loss of the tensile strength and toughness of PCL. Thermal analysis of the PCL showed that on addition of the thermally unstable NA, thermal degradation occurred early and was autocatalytic. However, the NA did benefit from the heat shielding provided by the PCL matrix resulting in more thermally stable NA particles. Results show that loading PEG in the PCL had a detrimental effect on the tensile strength and toughness of the blends, reducing them by 20-40%. The partial miscibility of the PCL-PEG system, causes an increase in Tg. While increases in the crystallinity is attributed to the plasticisation effect of PEG and the nucleation effect of NA. The average crystal size increased by 8% upon PEG addition.