990 resultados para well failure


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In the case of an ac cable, power transmission is limited by the length of the cable due to the capacitive reactive current component. It is well known that high-voltage direct current (HVDC) cables do not have such limitations. However, insulation-related thermal problems pose a limitation on the power capability of HVDC cables. The author presents a viable theoretical development, a logical extension to Whitehead's theory on thermal limitations of the insulation. The computation of the maximum power-carrying capability of HVDC cables subject to limits on the maximum operable temperature of the insulation is presented. The limitation on the power-carrying capability is closely associated with the electrothermal insulation failure. The effect of environmental interaction by way of external thermal resistance, an important aspect, is also considered in the formulations. The Lagrange multiplier method has been used to handle the ensuing optimization problem. The theory is based on an accepted theory of thermal breakdown in insulation and is an important and a coherent extension of great significance.

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Acute heart failure syndrome represents a prominent and growing health problem all around the world. Ideally, medical treatment for patients admitted to hospital because of this syndrome, in addition to alleviating the acute symptoms, should also prevent myocardial damage, modulate neurohumoral and inflammatory activation, and preserve or even improve renal function. Levosimendan is a cardiac enhancer having both inotropic and vasodilatory effects. It is approved for the short-term treatment of acutely decompensated chronic heart failure, but it has been shown to have beneficial clinical effects also in ischemic heart disease and septic shock as well as in perioperative cardiac support. In the present study, the mechanisms of action of levosimendan were studied in isolated guinea-pig heart preparations: Langendorff-perfused heart, papillary muscle and permeabilized cardiomyocytes as well as in purified phosphodiesterase isoenzyme preparations. Levosimendan was shown to be a potent inotropic agent in isolated Langendorff-perfused heart and right ventricle papillary muscle. In permeabilized cardiomyocytes, it was demonstrated to be a potent calcium sensitizer in contrast to its enantiomer, dextrosimendan. It was additionally shown to be a very selective phosphodiesterase (PDE) type-3 inhibitor, the selectivity factor for PDE3 over PDE4 being 10000 for levosimendan. Irrespective of this very selective PDE3 inhibitory property in purified enzyme preparations, the inotropic effect of levosimendan was demonstrated to be mediated mainly through calcium sensitization in the isolated heart as well as the papillary muscle preparations at clinically relevant concentrations. In the isolated Lagendorff-perfused heart, glibenclamide antagonized the levosimendan-induced increase in coronary flow (CF). Therefore, the main vasodilatory mechanism in coronary veins is believed to be the opening of the ATP-sensitive potassium (KATP) channels. In the paced hearts, CF did not increase in parallel with oxygen consumption (MVO2), thus indicating that levosimendan had a direct vasodilatory effect on coronary veins. The pharmacology of levosimendan was clearly different from that of milrinone, which induced an increase in CF in parallel with MVO2. In conclusion, levosimendan was demonstrated to increase cardiac contractility by binding to cardiac troponin C and sensitizing the myofilament contractile proteins to calcium, and further to induce coronary vasodilatation by opening KATP channels in vascular smooth muscle. In addition, the efficiency of the cardiac contraction was shown to be more advantageous when the heart was perfused with levosimendan in comparison to milrinone perfusion.

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Glaucoma is a multifactorial long-term ocular neuropathy associated with progressive loss of the visual field, retinal nerve fiber structural abnormalities and optic disc changes. Like arterial hypertension it is usually a symptomless disease, but if left untreated leads to visual disability and eventual blindness. All therapies currently used aim to lower intraocular pressure (IOP) in order to minimize cell death. Drugs with new mechanisms of action could protect glaucomatous eyes against blindness. Renin-angiotensin system (RAS) is known to regulate systemic blood pressure and compounds acting on it are in wide clinical use in the treatment of hypertension and heart failure but not yet in ophthalmological use. There are only few previous studies concerning intraocular RAS, though evidence is accumulating that drugs antagonizing RAS can also lower IOP, the only treatable risk factor in glaucoma. The main aim of this experimental study was to clarify the expression of the renin-angiotensin system in the eye tissues and to test its potential oculohypotensive effects and mechanisms. In addition, the possible relationship between the development of hypertension and IOP was evaluated in animal models. In conclusion, a novel angiotensin receptor type (Mas), as well as ACE2 enzyme- producing agonists for Mas, were described for the first time in the eye structures participating in the regulation of IOP. In addition, a Mas receptor agonist significantly reduced even normal IOP. The effect was abolished by a specific receptor antagonist. Intraocular, local RAS would thus to be involved in the regulation of IOP, probably even more in pathological conditions such as glaucoma though there was no unambiguous relationship between arterial and ocular hypertension. The findings suggest the potential as antiglaucomatous drugs of agents which increase ACE2 activity and the formation of angiotensin (1-7), or activate Mas receptors.

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Permeation of gases through single surfactant stabilized aqueous films has previously been studied in view of the potentiality of foam to separate gaseous mixtures. The earlier analysis assumed that the gas phase was well mixed and that the mass-transfer process was completely controlled by the liquid film. Permeabilities evaluated from single film data based on such analysis failed to predict the mass-transfer data obtained on permeation through two films. It is shown that the neglect of gas-phase resistance and the effect of film movement is the reason for the failure of the well-mixed gas models. An exact analysis of diffusion through two films is presented. It successfully predicts the experimental data on two films based on parameters evaluated from single film data.

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A quantitative expression has been obtained for the equivalent resistance of an internal short in rechargeable cells under constant voltage charging.

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This project built upon the successful outcomes of a previous project (TU02005) by adding to the database of salt tolerance among warm season turfgrass cultivars, through further hydroponic screening trials. Hydroponic screening trials focussed on new cultivars or cultivars that were not possible to cover in the time available under TU02005, including: 11 new cultivars of Paspalum vaginatum; 13 cultivars of Cynodon dactylon; six cultivars of Stenotaphrum secundatum; one accession of Cynodon transvaalensis; 12 Cynodon dactylon x transvaalensis hybrids; two cultivars of Sporobolus virginicus; five cultivars of Zoysia japonica; one cultivar of Z. macrantha, one common form of Z. tenuifolia and one Z. japonica x tenuifolia hybrid. The relative salinity tolerance of different turfgrasses is quantified in terms of their growth response to increasing levels of salinity, often defined by the salt level that equates to a 50% reduction in shoot yield, or alternatively the threshold salinity. The most salt tolerant species in these trials were Sporobolus virginicus and Paspalum vaginatum, consistent with the findings from TU02005 (Loch, Poulter et al. 2006). Cynodon dactylon showed the largest range in threshold values with some cultivars highly sensitive to salt, while others were tolerant to levels approaching that of the more halophytic grasses. Coupled with the observational and anecdotal evidence of high drought tolerance, this species and other intermediately tolerant species provide options for site specific situations in which soil salinity is coupled with additional challenges such as shade and high traffic conditions. By recognising the fact that a salt tolerant grass is not the complete solution to salinity problems, this project has been able to further investigate sustainable long-term establishment and management practices that maximise the ability of the selected grass to survive and grow under a particular set of salinity and usage parameters. Salt-tolerant turf grasses with potential for special use situations were trialled under field conditions at three sites within the Gold Coast City Council, while three sites, established under TU02005 within the Redland City Council boundaries were monitored for continued grass survival. Several randomised block experiments within Gold Coast City were established to compare the health and longevity of seashore paspalum (Paspalum vaginatum), Manila grass (Zoysia matrella), as well as the more tolerant cultivars of other species like buffalo grass (Stenotaphrum secundatum) and green couch (Cynodon dactylon). Whilst scientific results were difficult to achieve in the field situation, where conditions cannot be controlled, these trials provided valuable observational evidence of the likely survival of these species. Alternatives to laying full sod such as sprigging were investigated, and were found to be more appropriate for areas of low traffic as the establishment time is greater. Trials under controlled and protected conditions successfully achieved a full cover of Paspalum vaginatum from sprigs in a 10 week time frame. Salt affected sites are often associated with poor soil structure. Part of the research investigated techniques for the alleviation of soil compaction frequently found on saline sites. Various methods of soil de-compaction were investigated on highly compacted heavy clay soil in Redlands City. It was found that the heavy duplex soil of marine clay sediments required the most aggressive of treatments in order to achieve limited short-term effects. Interestingly, a well constructed sports field showed a far greater and longer term response to de-compaction operations, highlighting the importance of appropriate construction in the successful establishment and management of turfgrasses on salt affected sites. Fertiliser trials in this project determined plant demand for nitrogen (N) to species level. This work produced data that can be used as a guide when fertilising, in order to produce optimal growth and quality in the major turf grass species used in public parkland. An experiment commenced during TU02005 and monitored further in this project, investigated six representative warm-season turfgrasses to determine the optimum maintenance requirements for fertiliser N in south-east Queensland. In doing so, we recognised that optimum level is also related to use and intensity of use, with high profile well-used parks requiring higher maintenance N than low profile parks where maintaining botanical composition at a lower level of turf quality might be acceptable. Kikuyu (Pennisetum clandestinum) seemed to require the greatest N input (300-400 kg N/ha/year), followed by the green couch (Cynodon dactylon) cultivars ‘Wintergreen’ and ‘FLoraTeX’ requiring approximately 300 kg N/ha/year for optimal condition and growth. ‘Sir Walter’ (Stenotaphrum secundatum) and ‘Sea Isle 1’ (Paspalum vaginatum) had a moderate requirement of approximately 200 kg/ha/year. ‘Aussiblue’ (Digitaria didactyla)maintained optimal growth and quality at 100-200 kg N/ha/year. A set of guidelines has been prepared to provide various options from the construction and establishment of new grounds, through to the remediation of existing parklands by supporting the growth of endemic grasses. They describe a best management process through which salt affected sites should be assessed, remediated and managed. These guidelines, or Best Management Practices, will be readily available to councils. Previously, some high salinity sites have been turfed several times over a number of years (and Council budgets) for a 100% failure record. By eliminating this budgetary waste through targeted workable solutions, local authorities will be more amenable to investing appropriate amounts into these areas. In some cases, this will lead to cost savings as well as resulting in better quality turf. In all cases, however, improved turf quality will be of benefit to ratepayers, directly through increased local use of open space in parks and sportsfields and indirectly by attracting tourists and other visitors to the region bringing associated economic benefits. At the same time, environmental degradation and erosion of soil in bare areas will be greatly reduced.

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Candida yeast species are widespread opportunistic microbes, which are usually innocent opportunists unless the systemic or local defense system of the host becomes compromised. When they adhere on a fertile substrate such as moist and warm, protein-rich human mucosal membrane or biomaterial surface, they become activated and start to grow pseudo and real hyphae. Their growth is intricately guided by their ability to detect surface defects (providing secure hiding , thigmotropism) and nutrients (source of energy, chemotropism). The hypothesis of this work was that body mobilizes both non-specific and specific host defense against invading candidal cells and that these interactions involve resident epithelial cells, rapidly responding non-specific protector neutrophils and mast cells as well as the antigen presenting and responding den-dritic cell lymphocyte plasma cell system. It is supposed that Candida albicans, as a result of dar-winistic pressure, has developed or is utilizing strategies to evade these host defense reactions by e.g. adhering to biomaterial surfaces and biofilms. The aim of the study was to assess the host defense by taking such key molecules of the anti-candidal defense into focus, which are also more or less characteristic for the main cellular players in candida-host cell interactions. As a model for candidal-host interaction, sections of chronic hyperplastic candidosis were used and compared with sections of non-infected leukoplakia and healthy tissue. In this thesis work, neutrophil-derived anti-candidal α-defensin was found in the epithelium, not only diffusely all over in the epithelium, but as a strong α-defensin-rich superficial front probably able to slow down or prevent penetration of candida into the epithelium. Neutrophil represents the main host defence cell in the epithelium, to which it can rapidly transmigrate from the circulation and where it forms organized multicellular units known as microabscesses (study I). Neutrophil chemotactic inter-leukin-8 (IL-8) and its receptor (IL-8R) were studied and were surprisingly also found in the candidal cells, probably helping the candida to keep away from IL-8- and neutrophil-rich danger zones (study IV). Both leukocytes and resident epithelial cells contained TLR2, TLR4 and TLR6 receptors able to recognize candidal structures via utilization of receptors similar to the Toll of the banana fly. It seems that candida can avoid host defence via stimulation of the candida permissive TLR2 instead of the can-dida injurious TLR4 (study V). TLR also provides the danger signal to the immune system without which it will not be activated to specifically respond against candidal antigens. Indeed, diseased sites contained receptor activator of nuclear factor kappa B ligand (RANKL; II study), which is important for the antigen capturing, processing and presenting dendritic cells and for the T lymphocyte activation (study III). Chronic hyperplastic candidosis provides a disease model that is very useful to study local and sys-temic host factors, which under normal circumstances restrain C. albicans to a harmless commensal state, but failure of which in e.g. HIV infection, cancer and aging may lead to chronic infection.

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This study concerns the implementation of steering by contracting in health care units and in the work of the doctors employed by them. The study analyses how contracting as a process is being implemented in hospital district units, health centres and in the work of their doctors, as well as how these units carry out their operations and patient care within the restrictions set by the contracts. Based on interviews with doctors, the study analyses the realisation of operations within the units from the doctors perspective and through their work. The key result of the study is that the steering impact of contracting was not felt at the level of practical work. The contracting was implemented by assigning the related tasks to management only. The management implemented the contract by managing their resources rather than by intervening in doctors activities or the content of their tasks. The steering did not extend to improving practical care processes. This allowed the unchanged continuation of core operations in an autonomous manner and in part, protected from the impacts of contracting. In health centres, the contract concluded was viewed as merely steering the operations of the hospital district and its implementation did not receive the support of the centres. The fact that primary health care and specialised health care constitute separate contracting parties had adverse effects on the contract s implementation and the integration of care. A theoretical review unveiled several reasons for the failure of steering by contracting to alter operations within units. These included the perception steering by contracting as a weak change incentive. The doctors shunned the introduction of an economic logic and ideology into health care and viewed steering by contracting as a hindrance to delivering care to patients and a disturbance to their work and patient relationships. Contracting caused tensions between representatives of the financial administration and health care professionals. It also caused internal tensions, while it had varying impacts on different specialities, including the introduction of varying potential to influence contracts. Most factors preventing the realisation of the steering objective could have been ameliorated through positive leadership. There is a need to bridge the gap between financial steering and patient work. Key measures include encouraging the commitment of middle management, supporting leadership expertise and identifying the right methods of contributing to a mutual understanding between the cultures of financing, administration and health care. Criticism of the purchasers expertise and the view that undersized orders are due to the purchaser s financial difficulties underlines the importance of the purchaser s size. Overly detailed, product-based contracts seemed to place the focus on the quantities and costs of services rather than health impacts and efficiency of operations. Bundling contracts into larger service packages would encourage the enhancement of operations. Steering by contracting represents unexploited potential: it could function as a forum for integrated regional planning of services, and the prioritisation and integration of care, and offer an opportunity and an incentive for developing core operations.

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Developmental dyslexia is a specific reading disability, which is characterised by unexpected difficulty in reading, spelling and writing despite adequate intelligence, education and social environment. It is the most common childhood learning disorder affecting 5-10 % of the population and thus constitutes the largest portion of all learning disorders. It is a persistent developmental failure although it can be improved by compensation. According to the most common theory, the deficit is in phonological processing, which is needed in reading when the words have to be divided into phonemes, or distinct sound elements. This occurs in the lowest level of the hierarchy of the language system and disturbs processes in higher levels, such as understanding the meaning of words. Dyslexia is a complex genetic disorder and previous studies have found nine locations in the genome that associate with it. Altogether four susceptibility genes have been found and this study describes the discovery of the first two of them, DYX1C1 and ROBO1. The first clues were obtained from two Finnish dyslexic families that have chromosomal translocations which disrupt these genes. Genetic analyses supported their role in dyslexia: DYX1C1 associates with dyslexia in the Finnish population and ROBO1 was linked to dyslexia in a large Finnish pedigree. In addition a genome-wide scan in Finnish dyslexic families was performed. This supported the previously detected dyslexia locus on chromosome 2 and revealed a new locus on chromosome 7. Dyslexia is a neurological disorder and the neurobiological function of the susceptibility genes DYX1C1 and ROBO1 are consistent with this. ROBO1 is an axon guidance receptor gene, which is involved in axon guidance across the midline in Drosophila and axonal pathfinding between the two hemispheres via the corpus callosum, as well as neuronal migration in the brain of mice. The translocation and decreased ROBO1 expression in dyslexic individuals indicate that two functional copies of ROBO1 gene are required in reading. DYX1C1 was a new gene without a previously known function. Inhibition of Dyx1c1 expression showed that it is needed in normal brain development in rats. Without Dyx1c1 protein, the neurons in the developing brain will not migrate to their final position in the cortex. These two dyslexia susceptibility genes DYX1C1 and ROBO1 revealed two distinct neurodevelopmental mechanisms of dyslexia, axonal pathfinding and neuronal migration. This study describes the discovery of the genes and our research to clarify their role in developmental dyslexia.

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It is shown that a leaky aquifer model can be used for well field analysis in hard rock areas, treating the upper weathered and clayey layers as a composite unconfined aquitard overlying a deeper fractured aquifer. Two long-duration pump test studies are reported in granitic and schist regions in the Vedavati river basin. The validity of simplifications in the analytical solution is verified by finite difference computations.

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The stress corrosion cracking (SCC) characteristics of agr-titanium sheets in a bromine-methanol solution have been studied in the annealed and cold-rolled conditions using longitudinal and transverse specimens. The times to failure for annealed longitudinal specimens were longer than those for similarly tested transverse specimens. The cold-rolled specimens developed resistance to SCC, but failed by cleavage when notched, unlike the intergranular separation in annealed titanium. The apparent activation energy was found to be texture dependent and was in the range 30 to 51 kJ mol–1 for annealed titanium, and 15kJ mol–1 for cold-rolled titanium. The dependence of SCC behaviour on the texture is related to the changes in the crack initiation times. These are caused by changes in the passivation and repassivation characteristics of the particular thickness plane. The thickness planes are identified with the help of X-ray pole figures obtained on annealed and cold-rolled material. On the basis of the activation energy and the electrochemical measurements, the mechanism of SCC in annealed titanium is identified to be the one involving stress-aided anodic dissolution. On the other hand, the results on the cold-rolled titanium are in support of the hydrogen embrittlement mechanism consisting of hydride precipitation. The cleavage planes identified from the texture data match with the reported habit planes for hydride formation.

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Mulibrey nanism is a hereditary developmental disorder, characterized by prenatal onset growth failure without postnatal catch-up growth, distinctive craniofacial features, progressive cardiopathy and failure of sexual maturation. In addition, the patients develop insulin resistance syndrome and type 2 diabetes and they have an increased risk of developing tumors. The TRIM37 gene that underlies mulibrey nanism encodes for a member of the tripartite motif (TRIM) protein family. The physiological function of TRIM37 and the pathogenetic mechanisms leading from TRIM37 dysfunction to the mulibrey nanism phenotype are unknown. However, TRIM37 localizes at least partially to peroxisomes, and possesses ubiquitin E3-ligase activity. Thus, it may mediate ubiquitin dependent protein degradation, suggesting that accumulation of yet unknown substrate proteins may underlie the disease pathogenesis. In this study, the TRIM37 gene was characterized in detail. A transcription initiation window, with several separate transcription start sites, was identified and the putative promoter region immediately upstream from the transcription initiation window was shown to possess basal promoter activity. Further, several alternative splice variants of the gene were identified, including a highly expressed testis specific variant, encoding for an identical protein product with the main transcript. Expression of TRIM37 mRNA was detected in several different tissues, with highest expression seen in testis and in brain, when the expression patterns of the two major transcripts in different human tissues were studied by quantitative real-time PCR. Several mulibrey nanism patients were studied and thirteen novel mutations in TRIM37 were found, including three mutations (p.Gly322Val, p.Cys109Ser, p.Glu271_Ser287), that are likely to express mutant TRIM37 proteins. These mutations were further shown to alter the subcellular localization of the mutant proteins. Most of the mulibrey nanism associated mutations however, lead to premature termination codons and degradation of mRNA. All the TRIM37 mutations identified to date predict loss-of-function alleles, and thus no phenotype-genotype correlation is seen among the patients. In order to understand the pathogenetic mechanisms underlying mulibrey nanism, an animal model for the disorder is needed. For the development of a Trim37 knock-out mouse, the mouse Trim37 gene was characterized. Alternative splice variants, were identified, including a testis specific variant predicting a longer protein product. Further, a strictly tissue and cell-specific pattern of Trim37 expression was observed in developing and adult mouse tissues, when studied by immunohistochemical methods. This distribution of Trim37 expression in mouse tissues is in agreement with the clinical findings in human mulibrey nanism patients. This thesis work gives new tools for the diagnostics of mulibrey nanism as well as for studying the molecular pathogenesis behind this interesting disorder.

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Out-of-plane behaviour of mortared and mortarless masonry walls with various forms of reinforcement, including unreinforced masonry as a base case is examined using a layered shell element based explicit finite element modelling method. Wall systems containing internal reinforcement, external surface reinforcement and intermittently laced reinforced concrete members and unreinforced masonry panels are considered. Masonry is modelled as a layer with macroscopic orthotropic properties; external reinforcing render, grout and reinforcing bars are modelled as distinct layers of the shell element. Predictions from the layered shell model have been validated using several out-of-plane experimental datasets reported in the literature. The model is used to examine the effectiveness of two retrofitting schemes for an unreinforced masonry wall.