963 resultados para experimental approach


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Aim A recent Monte Carlo based study has shown that it is possible to design a diode that measures small field output factors equivalent to that in water. This is accomplished by placing an appropriate sized air gap above the silicon chip (1) with experimental results subsequently confirming that a particular Monte Carlo design was accurate (2). The aim of this work was to test if a new correction-less diode could be designed using an entirely experimental methodology. Method: All measurements were performed on a Varian iX at a depth of 5 cm, SSD of 95 cm and field sizes of 5, 6, 8, 10, 20 and 30 mm. Firstly, the experimental transfer of kq,clin,kq,msr from a commonly used diode detector (IBA, stereotactic field diode (SFD)) to another diode detector (Sun Nuclear, unshielded diode, (EDGEe)) was tested. These results were compared to Monte Carlo calculated values of the EDGEe. Secondly, the air gap above the EDGEe silicon chip was optimised empirically. Nine different air gap “tops” were placed above the EDGEe (air depth = 0.3, 0.6, 0.9 mm; air width = 3.06, 4.59, 6.13 mm). The sensitivity of the EDGEe was plotted as a function of air gap thickness for the field sizes measured. Results: The transfer of kq,clin,kq,msr from the SFD to the EDGEe was correct to within the simulation and measurement uncertainties. The EDGEe detector can be made “correction-less” for field sizes of 5 and 6 mm, but was ∼2% from being “correction-less” at field sizes of 8 and 10 mm. Conclusion Different materials will perturb small fields in different ways. A detector is only “correction-less” if all these perturbations happen to cancel out. Designing a “correction-less” diode is a complicated process, thus it is reasonable to expect that Monte Carlo simulations should play an important role.

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Vascular intimal hyperplasia is a major complication following angioplasty. The hallmark feature of this disorder is accumulation of dedifferentiated smooth muscle cells (SMCs) to the luminal side of the injured artery, cellular proliferation, migration, and synthesis of extracellular matrix. This finally results in intimal hyperplasia, which is currently considered an untreatable condition. According to current knowledge, a major part of neointimal cells derive from circulating precursor cells. This has outdated the traditional in vitro cell culture methods of studying neointimal cell migration and proliferation using cultured medial SMCs. Somatostatin and some of its analogs with different selectivity for the five somatostatin receptors (sst1 through sst5) have been shown to have vasculoprotective properties in animal studies. However, clinical trials using analogs selective for sst2/sst3/sst5 to prevent restenosis after percutaneous transluminal coronary angioplasty (PTCA) have failed to show any major benefits. Sirolimus is a cell cycle inhibitor that has been suggested to act synergistically with the protein-tyrosine kinase inhibitor imatinib to inhibit intimal hyperplasia in rat already at well-tolerated submaximal oral doses. The mechanisms behind this synergy and its long-term efficacy are not known. The aim of this study was to set up an ex vivo vascular explant culture model to measure neointimal cell activity without excluding the participation of circulating progenitor cells. Furthermore, two novel potential vasculoprotective treatment strategies were evaluated in detail in rat models of intimal hyperplasia and in the ex vivo explant model: sst1/sst4-selective somatostatin receptor analogs and combination treatment with sirolimus and imatinib. This study shows how whole vessel explants can be used to study the kinetics of neointimal cells and their progenitors, and to evaluate the anti-migratory and anti-proliferative properties of potential vasculoprotective compounds. It also shows how the influx of neointimal progenitor cells occurs already during the first days after vascular injury, how the contribution of cell migration is more important in the injury response than cell proliferation, and how the adventitia actively contribute in vascular repair. The vasculoprotective effect of somatostatin is mediated preferentially through sst4, and through inhibition of cell migration rather than of proliferation, which may explain why sst2/sst3/sst5-selective analogs have failed in clinical trials. Furthermore, a brief early oral treatment with the combination of sirolimus and imatinib at submaximal doses results in long-term synergistic suppression of intimal hyperplasia. The synergy is a result of inhibition of post-operative thrombocytosis and leukocytosis, inhibition of neointimal cell migration to the injury-site, and maintenance of cell integrity by inhibition of apoptosis and SMC dedifferentiation. In conclusion, the influx of progenitor cells already during the first days after injury and the high neointimal cell migratory activity underlines the importance of early therapeutic intervention with anti-migratory compounds to prevent neointimal hyperplasia. Sst4-selective analogs and the combination therapy with sirolimus and imatinib represent potential targets for the development of such vasculoprotective therapies.

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Backround and Purpose The often fatal (in 50-35%) subarachnoid hemorrhage (SAH) caused by saccular cerebral artery aneurysm (SCAA) rupture affects mainly the working aged population. The incidence of SAH is 10-11 / 100 000 in Western countries and twice as high in Finland and Japan. The estimated prevalence of SCAAs is around 2%. Many of those never rupture. Currently there are, however, no diagnostic methods to identify rupture-prone SCAAs from quiescent, (dormant) ones. Finding diagnostic markers for rupture-prone SCAAs is of primary importance since a SCAA rupture has such a sinister outcome, and all current treatment modalities are associated with morbidity and mortality. Also the therapies that prevent SCAA rupture need to be developed to as minimally invasive as possible. Although the clinical risk factors for SCAA rupture have been extensively studied and documented in large patient series, the cellular and molecular mechanisms how these risk factors lead to SCAA wall rupture remain incompletely known. Elucidation of the molecular and cellular pathobiology of the SCAA wall is needed in order to develop i) novel diagnostic tools that could identify rupture-prone SCAAs or patients at risk of SAH, and to ii) develop novel biological therapies that prevent SCAA wall rupture. Materials and Methods In this study, histological samples from unruptured and ruptured SCAAs and plasma samples from SCAA carriers were compared in order to identify structural changes, cell populations, growth factor receptors, or other molecular markers that would associate with SCAA wall rupture. In addition, experimental saccular aneurysm models and experimental models of mechanical vascular injury were used to study the cellular mechanisms of scar formation in the arterial wall, and the adaptation of the arterial wall to increased mechanical stress. Results and Interpretation Inflammation and degeneration of the SCAA wall, namely loss of mural cells and degradation of the wall matrix, were found to associate with rupture. Unruptured SCAA walls had structural resemblance with pads of myointimal hyperplasia or so called neointima that characterizes early atherosclerotic lesions, and is the repair and adaptation mechanism of the arterial wall after injury or increased mechanical stress. As in pads of myointimal hyperplasia elsewhere in the vasculature, oxidated LDL was found in the SCAA walls. Immunity against OxLDL was demonstrated in SAH patients with detection of circulating anti-oxidized LDL antibodies, which were significantly associated with the risk of rupture in patients with solitary SCAAs. Growth factor receptors associated with arterial wall remodeling and angiogenesis were more expressed in ruptured SCAA walls. In experimental saccular aneurysm models, capillary growth, arterial wall remodeling and neointima formation were found. The neointimal cells were shown to originate from the experimental aneurysm wall with minor contribution from the adjacent artery, and a negligible contribution of bone marrow-derived neointimal cells. Since loss of mural cells characterizes ruptured human SCAAs and likely impairs the adaptation and repair mechanism of ruptured or rupture-prone SCAAs, we investigated also the hypothesis that bone marrow-derived or circulating neointimal precursor cells could be used to enhance neointima formation and compensate the impaired repair capacity in ruptured SCAA walls. However, significant contribution of bone marrow cells or circulating mononuclear cells to neointima formation was not found.

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A semi-experimental approach to solve two-dimensional problems in elasticity is given. The method has been applied to two problems, (i) a square deep beam, and (ii) a bridge pier with a sloping boundary. For the first problem sufficient analytical results are available and hence the accuracy of the method can be verified. Then the method has been extended to the second problem for which sufficient results are not available.

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The Hodgkin and Huxley (HH) model of action potential has become a central paradigm of neuroscience. Despite its ability to predict action potentials with remarkable accuracy, it fails to explain several biophysical findings related to the initiation and propagation of the nerve impulse. The isentropic heat release and optical phenomena demonstrated by various experiments suggest that action potential is accompanied by a transient phase change in the axonal membrane. In this study a method was developed for preparing a giant axon from the crayfish abdominal cord for studying the molecular mechanisms of action potential simultaneously by electrophysiological and optical methods. Also an alternative setup using a single-cell culture of an Aplysia sensory neuron is presented. In addition to the description of the method, the preliminary results on the effect of phloretin, a dipole potential lowering compound, on the excitability of a crayfish giant axon are presented.

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Study of fatigue phenomenon in composites requires a dynamic tool which can detect and identify different failure mechanisms involved. The tool should also be capable of monitoring the cumulative damage progression on-line. Acoustic Emission Technique has been utilized in the experimental investigations on unidirectional carbon fiber reinforced plastic (CFRP) composite specimens subjected to tension-tension fatigue. Amplitude as well as frequency distribution of Acoustic Emission (AE) signals have been studied to detect and characterize different failure mechanisms. For a quantitative measure of degradation of the material with fatigue load cycles, reduction in stiffness of the specimen has been measured intermittently. Ultrasonic imaging could give the information on the changes in the interior status of the material at different stages of fatigue life.

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Although grain boundary sliding (GBS) has been recognized as an important process during high-temperature deformation in crystalline materials, there is paucity in experimental data for characterizing a constitutive equation for GBS. High-temperature tensile creep experiments were conducted, together with measurements of GBS at different strains, stresses, grain sizes, and temperatures. Experimental data obtained on a Mg AZ31 alloy demonstrate that, for the first time, dynamic recrystallization during creep does not alter the contribution of GBS to creep during high-temperature deformation. The experimentally observed invariance of the sliding contribution with strain was used together with the creep data for developing a constitutive equation for GBS in a manner similar to the standard creep equation. Using this new approach, it is demonstrated that the stress, grain size, and temperature dependence for creep and GBS are identical. This is rationalized by a model based on GBS controlled by dislocations, within grains or near-grain boundaries. (C) The Minerals, Metals & Materials Society and ASM International 2013

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Adhesives are widely used to execute the assembly of aerospace and automotive structures due to their ability to join dissimilar materials, reduced stress concentration, and improved fatigue resistance. The mechanical behavior of adhesive joints can be studied either using analytical models or by conducting mechanical tests. However, the complexity owing to multiple interfaces, layers with different properties, material and geometric nonlinearity and its three-dimensional nature combine to increase the difficulty in obtaining an overall system of governing equations to predict the joint behavior. On the other hand, experiments are often time consuming and expensive due to a number of parameters involved. Finite element analysis (FEA) is profoundly used in recent years to overcome these limitations. The work presented in this paper involves the finite element modeling and analysis of a composite single lap joint where the adhesive-adherend interface region was modeled using connector elements. The computed stresses were compared with the experimental stresses obtained using digital image correlation technique. The results showed an agreement. Further, the failure load predicted using FEA was found to be closer to the actual failure load obtained by mechanical tests.

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This paper presents an experimental procedure to determine the acoustic and vibration behavior of an inverter-fed induction motor based on measurements of the current spectrum, acoustic noise spectrum, overall noise in dB, and overall A-weighted noise in dBA. Measurements are carried out on space-vector modulated 8-hp and 3-hp induction motor drives over a range of carrier frequencies at different modulation frequencies. The experimental data help to distinguish between regions of high and low acoustic noise levels. The measurements also bring out the impact of carrier frequency on the acoustic noise. The sensitivity of the overall noise to carrier frequency is indicative of the relative dominance of the high-frequency electromagnetic noise over mechanical and aerodynamic components of noise. Based on the measured current and acoustic noise spectra, the ratio of dynamic deflection on the stator surface to the product of fundamental and harmonic current amplitudes is obtained at each operating point. The variation of this ratio of deflection to current product with carrier frequency indicates the resonant frequency clearly and also gives a measure of the amplification of vibration at frequencies close to the resonant frequency. This ratio is useful to predict the magnitude of acoustic noise corresponding to significant time-harmonic currents flowing in the stator winding.

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Understanding recolonization processes of intertidal fish assemblages is integral for predicting the consequences of significant natural or anthropogenic impacts on the intertidal zone. Recolonization of experimentally defaunated intertidal rockpools by fishes at Bass Point, New South Wales (NSW), Australia, was assessed quantitatively by using one long-term and two short-term studies. Rockpools of similar size and position at four sites within the intertidal zone were repeatedly defaunated of their fish fauna after one week, one month, and three months during two shortterm studies in spring and autumn (5 months each), and every six months for the long-term study (12 months). Fish assemblages were highly resilient to experimental perturbations—recolonizing to initial fish assemblage structure within 1−3 months. This recolonization was primarily due to subadults (30−40 mm TL) and adults (>40 mm TL) moving in from adjacent rockpools and presumably to abundant species competing for access to vacant habitat. The main recolonizers were those species found in highest numbers in initial samples, such as Bathygobius cocosensis, Enneapterygius rufopileus, and Girella elevata. Defaunation did not affect the size composition of fishes, except during autumn and winter when juveniles (<30 mm TL) recruited to rockpools. It appears that Bass Point rockpool fish assemblages are largely controlled by postrecruitment density-dependent mechanisms that indicate that recolonization may be driven by deterministic mechanisms.