977 resultados para 660501 Energy transformation


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We obtain stringent bounds in the < r(2)>(K pi)(S)-c plane where these are the scalar radius and the curvature parameters of the scalar K pi form factor, respectively, using analyticity and dispersion relation constraints, the knowledge of the form factor from the well-known Callan-Treiman point m(K)(2)-m(pi)(2), as well as at m(pi)(2)-m(K)(2), which we call the second Callan-Treiman point. The central values of these parameters from a recent determination are accomodated in the allowed region provided the higher loop corrections to the value of th form factor at the second Callan-Treiman point reduce the one-loop result by about 3% with F-K/F-pi = 1.21. Such a variation in magnitude at the second Callan-Treiman point yields 0.12 fm(2) less than or similar to < r(2)>(K pi)(S) less than or similar to 0.21 fm(2) and 0.56 GeV-4 less than or similar to c less than or similar to 1.47 GeV-4 and a strong correlation between them. A smaller value of F-K/F-pi shifts both bounds to lower values.

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Extensive molecular dynamics (MD) simulations have been performed in a B2-NiAl nanowire using an embedded atom method (EAM) potential. We show a stress induced B2 -> body-centered-tetragonal (BCT) phase transformation and a novel temperature and cross-section dependent pseudo-elastic/pseudo-plastic recovery from such an unstable BCT phase with a recoverable strain of similar to 30% as compared to 5-8% in polycrystalline materials. Such a temperature and cross-section dependent pseudo-elastic/pseudo-plastic strain recovery can be useful in various interesting applications of shape memory and strain sensing in nanoscale devices. Effects of size, temperature, and strain rate on the structural and mechanical properties have also been analyzed in detail. For a given size of the nanowire the yield stress of both the B2 and the BCT phases is found to decrease with increasing temperature, whereas for a given temperature and strain rate the yield stress of both the B2 and the BCT phase is found to increase with increase in the cross-sectional dimensions of the nanowire. A constant elastic modulus of similar to 80 GPa of the B2 phase is observed in the temperature range of 200-500 K for nanowires of cross-sectional dimensions in the range of 17.22-28.712 angstrom, whereas the elastic modulus of the BCT phase shows a decreasing trend with an increase in the temperature.

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BACKGROUND OR CONTEXT Laboratories provide the physical spaces for engineering students to connect with theory and have a personal hands-on learning experience. Learning space design and development is well established in many universities however laboratories are often not part of that movement. While active, collaborative and group learning pedagogies are all key words in relation to these new spaces the concepts have always been central to laboratory based learning. The opportunity to build on and strengthen good practice in laboratories is immense. In the 2001 review “Universities in Crisis” many references are made to the decline of laboratories. One such comment in the review was made by Professor Ian Chubb (AVCC), who in 2013, as Chief Scientist for Australia, identifies the national concern about STEM education and presents a strategic plan to address the challenges ahead. What has been achieved and changed in engineering teaching and research laboratories in this time? PURPOSE OR GOAL A large number of universities in Australia and New Zealand own laboratory and other infrastructure designed well for the era they were built but now showing signs of their age, unable to meet the needs of today’s students, limiting the effectiveness of learning outcomes and presenting very low utilisation rates. This paper will present a model for new learning space design that improves student experience and engagement, supporting academic aims and significantly raising the space utilisation rate. APPROACH A new approach in laboratory teaching and research including new management has been adopted by the engineering disciplines at QUT. Flexibility is an underpinning principle along with the modularisation of fixed teaching and learning equipment, high utilisation of spaces and dynamic pedagogical approaches. The revitalised laboratories and workshop facilities are used primarily for the engineering disciplines and increasingly for integrated use across many disciplines in the STEM context. The new approach was built upon a base of an integrated faculty structure from 2005 and realised in 2010 as an associated development with the new Science and Engineering Centre (SEC). Evaluation through student feedback surveys for practical activities, utilisation rate statistics and uptake by academic and technical staff indicate a very positive outcome. DISCUSSION Resulting from this implementation has been increased satisfaction by students, creation of social learning and connecting space and an environment that meets the needs and challenges of active, collaborative and group learning pedagogies. Academic staff are supported, technical operations are efficient and laboratories are effectively utilised. RECOMMENDATIONS/IMPLICATIONS/CONCLUSION Future opportunities for continuous improvement are evident in using the student feedback to rectify faults and improve equipment, environment and process. The model is easily articulated and visible to other interested parties to contribute to sector wide development of learning spaces.

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Sleep is governed by a homeostatic process in which the duration and quality of previous wake regulate the subsequent sleep. Active wakefulness is characterized with high frequency cortical oscillations and depends on stimulating influence of the arousal systems, such as the cholinergic basal forebrain (BF), while cessation of the activity in the arousal systems is required for slow wave sleep (SWS) to occur. The site-specific accumulation of adenosine (a by-product of ATP breakdown) in the BF during prolonged waking /sleep deprivation (SD) is known to induce sleep, thus coupling energy demand to sleep promotion. The adenosine release in the BF is accompanied with increases in extracellular lactate and nitric oxide (NO) levels. This thesis was aimed at further understanding the cellular processes by which the BF is involved in sleep-wake regulation and how these processes are affected by aging. The BF function was studied simultaneously at three levels of organization: 1) locally at a cellular level by measuring energy metabolites 2) globally at a cortical level (the out-put area of the BF) by measuring EEG oscillations and 3) at a behavioral level by studying changes in vigilance states. Study I showed that wake-promoting BF activation, particularly with glutamate receptor agonist N-methyl-D-aspatate (NMDA), increased extracellular adenosine and lactate levels and led to a homeostatic increase in the subsequent sleep. Blocking NMDA activation during SD reduced the high frequency (HF) EEG theta (7-9 Hz) power and attenuated the subsequent sleep. In aging, activation of the BF during SD or experimentally with NMDA (studies III, IV), did not induce lactate or adenosine release and the increases in the HF EEG theta power during SD and SWS during the subsequent sleep were attenuated as compared to the young. These findings implicate that increased or continuous BF activity is important for active wake maintenance during SD as well as for the generation of homeostatic sleep pressure, and that in aging these mechanisms are impaired. Study II found that induction of the inducible NO synthase (iNOS) during SD is accompanied with activation of the AMP-activated protein kinase (AMPK) in the BF. Because decreased cellular energy charge is the most common cause for AMPK activation, this finding implicates that the BF is selectively sensitive to the metabolic demands of SD as increases were not found in the cortex. In aging (study III), iNOS expression and extracellular levels of NO and adenosine were not significantly increased during SD in the BF. Furthermore, infusion of NO donor into the BF did not lead to sleep promotion as it did in the young. These findings indicated that the NO (and adenosine) mediated sleep induction is impaired in aging and that it could at least partly be due to the reduced sensitivity of the BF to sleep-inducing factors. Taken together, these findings show that reduced sleep promotion by the BF contributes to the attenuated homeostatic sleep response in aging.

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Sleep deprivation leads to increased subsequent sleep length and depth and to deficits in cognitive performance in humans. In animals extreme sleep deprivation is eventually fatal. The cellular and molecular mechanisms causing the symptoms of sleep deprivation are unclear. This thesis was inspired by the hypothesis that during wakefulness brain energy stores would be depleted, and they would be replenished during sleep. The aim of this thesis was to elucidate the energy metabolic processes taking place in the brain during sleep deprivation. Endogenous brain energy metabolite levels were assessed in vivo in rats and in humans in four separate studies (Studies I-IV). In the first part (Study I) the effects of local energy depletion on brain energy metabolism and sleep were studied in rats with the use of in vivo microdialysis combined with high performance liquid chromatography. Energy depletion induced by 2,4-dinitrophenol infusion into the basal forebrain was comparable to the effects of sleep deprivation: both increased extracellular concentrations of adenosine, lactate, and pyruvate, and elevated subsequent sleep. This result supports the hypothesis of a connection between brain energy metabolism and sleep. The second part involved healthy human subjects (Studies II-IV). Study II aimed to assess the feasibility of applying proton magnetic resonance spectroscopy (1H MRS) to study brain lactate levels during cognitive stimulation. Cognitive stimulation induced an increase in lactate levels in the left inferior frontal gyrus, showing that metabolic imaging of neuronal activity related to cognition is possible with 1H MRS. Study III examined the effects of sleep deprivation and aging on the brain lactate response to cognitive stimulation. No physiologic, cognitive stimulation-induced lactate response appeared in the sleep-deprived and in the aging subjects, which can be interpreted as a sign of malfunctioning of brain energy metabolism. This malfunctioning may contribute to the functional impairment of the frontal cortex both during aging and sleep deprivation. Finally (Study IV), 1H MRS major metabolite levels in the occipital cortex were assessed during sleep deprivation and during photic stimulation. N-acetyl-aspartate (NAA/H2O) decreased during sleep deprivation, supporting the hypothesis of sleep deprivation-induced disturbance in brain energy metabolism. Choline containing compounds (Cho/H2O) decreased during sleep deprivation and recovered to alert levels during photic stimulation, pointing towards changes in membrane metabolism, and giving support to earlier observations of altered brain response to stimulation during sleep deprivation. Based on these findings, it can be concluded that sleep deprivation alters brain energy metabolism. However, the effects of sleep deprivation on brain energy metabolism may vary from one brain area to another. Although an effect of sleep deprivation might not in all cases be detectable in the non-stimulated baseline state, a challenge imposed by cognitive or photic stimulation can reveal significant changes. It can be hypothesized that brain energy metabolism during sleep deprivation is more vulnerable than in the alert state. Changes in brain energy metabolism may participate in the homeostatic regulation of sleep and contribute to the deficits in cognitive performance during sleep deprivation.

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The mitochondrion is an organelle of outmost importance, and the mitochondrial network performs an array of functions that go well beyond ATP synthesis. Defects in mitochondrial performance lead to diseases, often affecting nervous system and muscle. Although many of these mitochondrial diseases have been linked to defects in specific genes, the molecular mechanisms underlying the pathologies remain unclear. The work in this thesis aims to determine how defects in mitochondria are communicated within - and interpreted by - the cells, and how this contributes to disease phenotypes. Fumarate hydratase (FH) is an enzyme of the citrate cycle. Recessive defects in FH lead to infantile mitochondrial encephalopathies, while dominant mutations predispose to tumor formation. Defects in succinate dehydrogenase (SDH), the enzyme that precedes FH in the citrate cycle, have also been described. Mutations in SDH subunits SDHB, SDHC and SDHD are associated with tumor predisposition, while mutations in SDHA lead to a characteristic mitochondrial encephalopathy of childhood. Thus, the citrate cycle, via FH and SDH, seems to have essential roles in mitochondrial function, as well as in the regulation of processes such as cell proliferation, differentiation or death. Tumor predisposition is not a typical feature of mitochondrial energy deficiency diseases. However, defects in citrate cycle enzymes also affect mitochondrial energy metabolism. It is therefore necessary to distinguish what is specific for defects in citrate cycle, and thus possibly associated with the tumor phenotype, from the generic consequences of defects in mitochondrial aerobic metabolism. We used primary fibroblasts from patients with recessive FH defects to study the cellular consequences of FH-deficiency (FH-). Similarly to the tumors observed in FH- patients, these fibroblasts have very low FH activity. The use of primary cells has the advantage that they are diploid, in contrast with the aneuploid tumor cells, thereby enabling the study of the early consequences of FH- in diploid background, before tumorigenesis and aneuploidy. To distinguish the specific consequences of FH- from typical consequences of defects in mitochondrial aerobic metabolism, we used primary fibroblasts from patients with MELAS (mitochondrial encephalopathy with lactic acidosis and stroke-like episodes) and from patients with NARP (neuropathy, ataxia and retinitis pigmentosa). These diseases also affect mitochondrial aerobic metabolism but are not known to predispose to tumor formation. To study in vivo the systemic consequences of defects in mitochondrial aerobic metabolism, we used a transgenic mouse model of late-onset mitochondrial myopathy. The mouse contains a transgene with an in-frame duplication of a segment of Twinkle, the mitochondrial replicative helicase, whose defects underlie the human disease progressive external ophthalmoplegia. This mouse model replicates the phenotype in the patients, particularly neuronal degeneration, mitochondrial myopathy, and subtle decrease of respiratory chain activity associated with mtDNA deletions. Due to the accumulation of mtDNA deletions, the mouse was named deletor. We first studied the consequences of FH- and of respiratory chain defects for energy metabolism in primary fibroblasts. To further characterize the effects of FH- and respiratory chain malfunction in primary fibroblasts at transcriptional level, we used expression microarrays. In order to understand the in vivo consequences of respiratory chain defects in vivo, we also studied the transcriptional consequences of Twinkle defects in deletor mice skeletal muscle, cerebellum and hippocampus. Fumarate accumulated in the FH- homozygous cells, but not in the compound heterozygous lines. However, virtually all FH- lines lacked cytoplasmic FH. Induction of glycolysis was common to FH-, MELAS and NARP fibroblasts. In deletor muscle glycolysis seemed to be upregulated. This was in contrast with deletor cerebellum and hippocampus, where mitochondrial biogenesis was in progress. Despite sharing a glycolytic pattern in energy metabolism, FH- and respiratory chain defects led to opposite consequences in redox environment. FH- was associated with reduced redox environment, while MELAS and NARP displayed evidences of oxidative stress. The deletor cerebellum had transcriptional induction of antioxidant defenses, suggesting increased production of reactive oxygen species. Since the fibroblasts do not represent the tissues where the tumors appear in FH- patients, we compared the fibroblast array data with the data from FH- leiomyomas and normal myometrium. This allowed the determination of the pathways and networks affected by FH-deficiency in primary cells that are also relevant for myoma formation. A key pathway regulating smooth muscle differentiation, SRF (serum response factor)-FOS-JUNB, was found to be downregulated in FH- cells and in myomas. While in the deletor mouse many pathways were affected in a tissue-specific basis, like FGF21 induction in the deletor muscle, others were systemic, such as the downregulation of ALAS2-linked heme synthesis in all deletor tissues analyzed. However, interestingly, even a tissue-specific response of FGF21 excretion could elicit a global starvation response. The work presented in this thesis has contributed to a better understanding of mitochondrial stress signalling and of pathways interpreting and transducing it to human pathology.

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Electronic excitation in H2O, H2S, H2Se and H2Te molecules has been studied by the EELS technique. Spectra of H2S and H2Se are remarkably similar with the 1b1-nd transition most intense. The intensity of the first transition 1b1-nsa1 decreases through H2O to H2Se and this transition is absent in H2Te. Transitions observed by EELS have been compared with optical absorption studies. A correlation diagram of the occupied and the excited states has been provided for these four molecules by making use of UVPES and EELS.

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The dynamics of reactions with low internal barriers are studied both analytically and numerically for two different models. Exact expressions for the average rate,kI, are obtained by solving the associated first passage time problems. Both the average rate constant, kI, and the numerically calculated long-time rate constant, kL, show a fractional power law dependence on the barrier height for very low barriers. The crossover of the reaction dynamics from low to high barrier is investigated.

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An integrated approach to energy planning, when applied to large hydroelectric projects, requires that the energy-opportunity cost of the land submerged under the reservoir be incorporated into the planning methodology. Biomass energy lost from the submerged land has to be compared to the electrical energy generated, for which we develop four alternative formulations of the net-energy function. The design problem is posed as an LP problem and is solved for two sites in India. Our results show that the proposed designs may not be viable in net-energy terms, whereas a marginal reduction in the generation capacity could lead to an optimal design that gives substantial savings in the submerged area. Allowing seasonal variations in the hydroelectric generation capacity also reduces the reservoir size. A mixed hydro-wood generation system is then examined and is found to be viable.

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The effect of rapid solidification on the ordering reaction in Fe---Si and Fe---Al alloys has been reported. It is shown that rapid solidification can influence the ordering reaction in alloys with higher critical ordering temperatures. For ordering reactions at lower temperatures, the effect is similar to that of solid-state quenching. Different factors influencing the ordering reactions and domain structures during rapid solidification of iron-based alloys are discussed.

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Complexes of I2 with diethyl ether and triethylamine and of Br, with diethyl ether have been investigated in the vapor phase for the first time by employing electron energy loss spectroscopy. Besides the CT bands, blue-shifted vacuum-UV bands of the halogens have been assigned; the amine-I, system appears to exhibit two CT bands,associated with two different excited states of the complex.

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An indigenous electron energy loss spectrometer has been designed and fabricated for the study of free molecules. The spectrometer enables the recording of low-resolution electronic spectra of molecules inthe vapour phase with ready access to the vacuum ultraviolet region. Electron energy loss spectra of aliphatic alcohols and carbonyl compounds as wellas of benzene derivatives have been recorded with the indigenous spectrometer and the electronic transitions in these molecules discussed.

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Increase water use efficiency and productivity, and reduce energy and water usage and costs, of dairy and fodder enterprises, to reduce costs of milk production.