16 resultados para Growth mechanism

em University of Queensland eSpace - Australia


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Tungsten oxide microtubules, arrayed in a radial flower-like structure, were synthesized by simply using W powders reacting with Ni(NO3)(2) center dot 6H(2)O at a elevated temperature. The formed microtubules, with lengths more than 100 pin and outer diameters of 1-5 mu m, have irregular open ends, showing clear grooves along the growth direction on the tubule surface. A novel aggregation mechanism based on chemical-vapor-deposit process was proposed to describe the growth process of the synthesized tubules, and the possible mechanism for the arrangement of the radial flower-like morphology was discussed.

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During the growth of GaAs nanowires on the {111}B GaAs substrate, truncated triangular GaAs nanowires were commonly observed in the bottom region of nanowires. Through detailed structural analysis by electron microscopy, we have determined the growth mechanism of truncated triangular GaAs nanowires.

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Multi-layer hydrogen storage thin films with Mg and MmNi(3.5)(CoAlMn)(1.5) (here Mm denotes La-rich mischmetal) as alternative layers were prepared by direct current magnetron sputtering. Transmission electron microscopy investigation shows that the microstructure of the MmNi(3.5)(CoAlMn)(1.5) and Mg layers are significantly different although their deposition conditions are the same. The MmNi(3.5)(CoAlMn)(1.5) layer is composed of two regions: one is an amorphous region approximately 4 nm thick at the bottom of the layer and the other is a nanocrystalline region on top of the amorphous region. The Mg layer is also composed of two regions: one is a randomly orientated nanocrystalline region 50 nm thick at the bottom of the layer and the other is a columnar crystallite region on top of the nanocrystalline region. These Mg columnar crystallites have their [001] directions parallel to the growth direction and the average lateral size of these columnar crystallites is about 100 nm. A growth mechanism of the multi-layer thin films is discussed based on the experiment results. Wiley-Liss, Inc.

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High-resolution transmission electron microscopy (HRTEM) was used to study the olivine to spinel transformation. HRTEM structure images of Mg2GeO4 olivine deformed under a pressure of 6 GPa at 600 degreesC clearly show that a shear mechanism dominates the transformation. The transformation is not a nucleation and growth mechanism. It also differs in certain crucial aspects from the type of martensitic transformation proposed before. During the transformation, it is a shear movement that brings the oxygen anions to their positions in the spinel structure. An edge dislocation following each shear then puts the cations in their spinel sites. The Burgers' vector of each dislocation is perpendicular to the anion shear direction. (C) 2004 American Institute of Physics.

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Based on phage display optimization studies with human growth hormone (GH), it is thought that the biopotency of GH cannot be increased. This is proposed to be a result of the affinity of the first receptor for hormone far exceeding that which is required to trap the hormone long enough to allow diffusion of the second receptor to form the ternary complex, which initiates signaling. We report here that despite similar site 1 kinetics to the hGH/hGH receptor interaction, the potency of porcine GH for its receptor can be increased up to 5-fold by substituting hGH residues involved in site 1 binding into pGH. Based on extensive mutations and BIAcore studies, we show that the higher potency and site 1 affinity of hGH for the pGHR is primarily a result of a decreased off-rate associated with residues in the extended loop between helices 1 and 2 that interact with the two key tryptophans Trp(104) and Trp(169) in the receptor binding hot spot. Our mutagenic analysis has also identified a second determinant (Lys(165)), which in addition to His(169), restricts the ability of non-primate hormones to activate hGH receptor. The increased biopotency of GH that we observe can be explained by a model for GH receptor activation where subunit alignment is critical for effective signaling.

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Listeria monocytogenes is a food-borne Gram-positive bacterium that is responsible for a variety of infections (worldwide) annually. The organism is able to survive a variety of environmental conditions and stresses, however, the mechanisms by which L. monocytogenes adapts to environmental change are yet to be fully elucidated. An understanding of the mechanism(s) by which L. monocytogenes survives unfavourable environmental conditions will aid in developing new food processing methods to control the organism in foodstuffs. We have utilized a proteomic approach to investigate the response of L. monocytogenes batch cultures to the transition from exponential to stationary growth phase. Proteomic analysis showed that batch cultures of L. monocytogenes perceived stress and began preparations for stationary phase much earlier (approximately A(600) = 0.75, mid-exponential) than predicted by growth characteristics alone. Global analysis of the proteome revealed that the expression levels of more than 50% of all proteins observed changed significantly over a 7-9 h period during this transition phase. We have highlighted ten proteins in particular whose expression levels appear to be important in the early onset of the stationary phase. The significance of these findings in terms of functionality and the mechanistic picture are discussed.

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One of the first and most enduring roles identified for the plant hormone auxin is the mediation of apical dominance. Many reports have claimed that reduced stem indole-3-acetic acid (IAA) levels and/ or reduced basipetal IAA transport directly or indirectly initiate bud growth in decapitated plants. We have tested whether auxin inhibits the initial stage of bud release, or subsequent stages, in garden pea (Pisum sativum) by providing a rigorous examination of the dynamics of auxin level, auxin transport, and axillary bud growth. We demonstrate that after decapitation, initial bud growth occurs prior to changes in IAA level or transport in surrounding stem tissue and is not prevented by an acropetal supply of exogenous auxin. We also show that auxin transport inhibitors cause a similar auxin depletion as decapitation, but do not stimulate bud growth within our experimental time- frame. These results indicate that decapitation may trigger initial bud growth via an auxin-independent mechanism. We propose that auxin operates after this initial stage, mediating apical dominance via autoregulation of buds that are already in transition toward sustained growth.

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Growth hormone is believed to activate the growth hormone receptor (GHR) by dimerizing two identical receptor subunits, leading to activation of JAK2 kinase associated with the cytoplasmic domain. However, we have reported previously that dimerization alone is insufficient to activate full-length GHR. By comparing the crystal structure of the liganded and unliganded human GHR extracellular domain, we show here that there is no substantial change in its conformation on ligand binding. However, the receptor can be activated by rotation without ligand by inserting a defined number of alanine residues within the transmembrane domain. Fluorescence resonance energy transfer ( FRET), bioluminescence resonance energy transfer (BRET) and coimmunoprecipitation studies suggest that receptor subunits undergo specific transmembrane interactions independent of hormone binding. We propose an activation mechanism involving a relative rotation of subunits within a dimeric receptor as a result of asymmetric placement of the receptor-binding sites on the ligand.

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Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists are increasingly used in patients with diabetes, and small studies have suggested a beneficial effect on renal function, but their effects on. extracellular matrix (ECM) turnover are unknown. The aims of this study were to investigate the effects of the PPAR-gamma agonist pioglitazone on growth and matrix production in human cortical fibroblasts (CF). Cell growth and ECM production and turnover were measured in human CF in the presence and absence of 1 and 3 muM pioglitazone. Exposure of CF to pioglitazone caused an antiproliferative (P < 0.0001) and hypertrophic (P < 0.0001) effect; reduced type IV collagen secretion (P < 0.01), fibronectin secretion (P < 0.0001), and proline incorporation (P < 0.0001); decreased MMP-9 activity (P < 0.05); and reduced tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2 secretion (P < 0.001 and P < 0.0001, respectively). These effects were independent of TGF-beta1. A reduction in ECM production was similarly observed when CF were exposed to a selective PPAR-gamma agonist (L-805645) in concentrations that caused no toxicity, confirming the antifibrotic effects of pioglitazone were mediated through a PPAR-gamma-dependent mechanism. Exposure of CF to high glucose conditions induced an increase in the expression of collagen IV (P < 0.05), which was reversed both in the presence of pioglitazone (1 and 3 muM) and by L-805645. In summary, exposure of human CIF to pioglitazone causes an antiproliferative effect and reduces ECM production through mechanisms that include reducing TIMP activity, independent of TGF-beta1. These studies suggest that the PPAR-gamma agonists may have a specific role in ameliorating the course of progressive tubulointerstitial fibrosis under both normoglycemic and hyperglycemic states.

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Fibroblast growth factor (FGF) receptors (FGFRs) signal to modulate diverse cellular functions, including epithelial cell morphogenesis. In epithelial cells, E-cadherin plays a key role in cell-cell adhesion, and its function can be regulated through endocytic trafficking. In this study, we investigated the location, trafficking, and function of FGFR1 and E-cadherin and report a novel mechanism, based on endocytic trafficking, for the coregulation of E-cadherin and signaling from FGFR1. FGF induces the internalization of surface FGFR1 and surface E-cadherin, followed by nuclear translocation of FGFR1. The internalization of both proteins is regulated by common endocytic machinery, resulting in cointernalization of FGFR1 and E-cadherin into early endosomes. By blocking endocytosis, we show that this is a requisite, initial step for the nuclear translocation of FGFR1. Overexpression of E-cadherin blocks both the coendocytosis of E-cadherin and FGFR1, the nuclear translocation of FGFR1 and FGF-induced signaling to the mitogen-activated protein kinase pathway. Furthermore, stabilization of surface adhesive E-cadherin, by overexpressing p120(ctn), also blocks internalization and nuclear translocation of FGFR1. These data reveal that conjoint endocytosis and trafficking is a novel mechanism for the coregulation of E-cadherin and FGFR1 during cell signaling and morphogenesis.

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The mechanism of bainite growth has been investigated using in situ transmission electron microscopy observations. It was found that, in a number of alloys studied, a bainitic embryo is made of basic transformation units. These units are either a group of stacking faults or, in two dimensions, a series of parallelograms of different sizes. Thickening/widening of the bainite embryo takes place through shear along the stacking fault planes or twining planes. The bainite embryo is elongated by the formation of new transformation units at both tips of the bainite plate. The three-dimensional morphology of bainite is a convex tens-like lath. It is believed that the bainite embryo grows by shearing, which is controlled by the diffusion of solute atoms during the transformation. As the growth rate is much lower than that of martensite, it is therefore detectable. (c) 2006 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.

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Listeria monocytogenes has previously been shown to adapt to a wide variety of environmental niches, principally those associated with low pH, and this compromises its control in food environments. An understanding of the mechanism(s) by which L. monocytogenes survives unfavourable environmental conditions will aid in developing new food processing methods to control the organism in foodstuffs. The present Study aimed to gain a further understanding of the physiological basis for the differential effects of one control strategy, namely the use of the lantibiotic nisin. Using propidium iodide (PI) to probe membrane integrity it was shown that L. monocytogenes Scott A was sensitive to nisin (8 ng mL(-1)) but this was growth phase dependent with stationary phase cells (OD600=1.2) being much more resistant than exponential phase cells (OD600=0.38). We demonstrate that, using a combination of techniques including fluorescence activated cell sorting (FACS), the membrane adaptations underpinning nisin resistance are triggered much earlier (OD600 < 0.5) than the onset of stationary phase. The significance of these findings in terms of mechanism and application are discussed. (c) 2005 Elsevier B.V.All rights reserved.