62 resultados para Cellular telephony


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Cellular automaton (CA) was used to simulate dynamic recrystallization (DRX) during thermomechanical deformation. Initial grain size, initial grain orientation and dislocation density were used as input data to the CA model. Flow curve, dislocation density, final grain size and orientation, and DRX volume fraction were the output data which were compared with experimental data to validate the model. The model proposed in this work considered the thermomechanical parameters (e.g., temperature and strain rate) and their role on the nucleation and growth kinetics during DRX. It was shown that the CA model can predict the final microstructure and flow curve to a high degree of accuracy and was able to successfully simulate the volume fraction of DRX as a function of strain for a wide range of deformation conditions.

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Engineering contributions have played an important role in the rise and evolution of cellular biology. Engineering technologies have helped biologists to explore the living organisms at cellular and molecular levels, and have created new opportunities to tackle the unsolved biological problems. There is now a growing demand to further expand the role of engineering in cellular biology research. For an engineer to play an effective role in cellular biology, the first essential step is to understand the cells and their components. However, the stumbling block of this step is to comprehend the information given in the cellular biology literature because it best suits the readers with a biological background. This paper aims to overcome this bottleneck by describing the human cell components as micro-plants that form cells as micro-bio-factories. This concept can accelerate the engineers’ comprehension of the subject. In this paper, first the structure and function of different cell components are described. In addition, the engineering attempts to mimic various cell components through numerical modelling or physical implementation are highlighted. Next, the interaction of different cell components that facilitate complicated chemical processes, such as energy generation and protein synthesis, are described. These complex interactions are translated into simple flow diagrams, generally used by engineers to represent multi-component processes.

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The paper presents a framework to design robust transmit power controllers in cellular radio systems. The robust controllers designed are able to guarantee the quality of service (QoS) by keeping the carrier-to-inference-plus-noise ratio (CIRN) above a desired level in face of network link gain variations. The controller design problem is solved by solving a noncooperative dynamic game between the controller and unknown link gain variations.

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Eccentrically biased exercise results in skeletal muscle damage and stimulates adaptations in muscle, whereby indexes of damage are attenuated when the exercise is repeated. We hypothesized that changes in ultrastructural damage, inflammatory cell infiltration, and markers of proteolysis in skeletal muscle would come about as a result of repeated eccentric exercise and that gender may affect this adaptive response. Untrained male (n = 8) and female (n = 8) subjects performed two bouts (bout 1 and bout 2), separated by 5.5 wk, of 36 repetitions of unilateral, eccentric leg press and 100 repetitions of unilateral, eccentric knee extension exercises (at 120% of their concentric single repetition maximum), the subjects' contralateral nonexercised leg served as a control (rest). Biopsies were taken from the vastus lateralis from each leg 24 h postexercise. After bout 2, the postexercise force deficit and the rise in serum creatine kinase (CK) activity were attenuated. Women had lower serum CK activity compared with men at all times (P < 0.05), but there were no gender differences in the relative magnitude of the force deficit. Muscle Z-disk streaming, quantified by using light microscopy, was elevated vs. rest only after bout 1 (P < 0.05), with no gender difference. Muscle neutrophil counts were significantly greater in women 24 h after bout 2 vs. rest and bout 1 (P < 0.05) but were unchanged in men. Muscle macrophages were elevated in men and women after bout 1 andbout 2 (P < 0.05). Muscle protein content of the regulatory calpain subunit remained unchanged whereas ubiquitin-conjugated protein content was increased after both bouts (P < 0.05), with a greater increase after bout 2. We conclude that adaptations to eccentric exercise are associated with attenuated serum CK activity and, potentially, an increase in the activity of the ubiquitin proteosome proteolytic pathway.

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The Alzheimer’s disease Aβ peptide can increase the levels of cell-associated amyloid precursor protein (APP) in vitro. To determine the specificity of this response for Aβ and whether it is related to cytotoxicity, we tested a diverse range of fibrillar peptides including amyloid-β (Aβ), the fibrillar prion peptides PrP106–126 and PrP178–193 and human islet-cell amylin. All these peptides increased the levels of APP and amyloid precursor-like protein 2 (APLP2) in primary cultures of astrocytes and neurons. Specificity was shown by a lack of change to amyloid precursor-like protein 1, τ-1 and cellular prion protein (PrPc) levels. APP and APLP2 levels were elevated only in cultures exposed to fibrillar peptides as assessed by electron microscopy and not in cultures treated with non-fibrillogenic peptide variants or aggregated lipoprotein. We found that PrP106–126 and the non-toxic but fibril-forming PrP178–193 increased APP levels in cultures derived from both wild-type and PrPc-deficient mice indicating that fibrillar peptides up-regulate APP through a non-cytotoxic mechanism and irrespective of parental protein expression. Fibrillar PrP106–126 and Aβ peptides bound recombinant APP and APLP2 suggesting the accumulation of these proteins was mediated by direct binding to the fibrillated peptide. This was supported by decreased APP accumulation following extensive washing of the cultures to remove fibrillar aggregates. Pre-incubation of fibrillar peptide with recombinant APP18–146, the putative fibril binding site, also abrogated the accumulation of APP. These findings show that diverse fibrillogenic peptides can induce accumulation of APP and APLP2 and this mechanism could contribute to pathogenesis in neurodegenerative disorders.

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The defoThe deformation behaviors and energy absorption characteristics of constructed cellular aluminums were investigated by compressive tests. Constructed cellular aluminum specimens with two kinds of thickness in the cold-pressed panel and various numbers of layers bonded together have been tested. The plateau stress and the energy absorption have been measured and furthermore, the deformation behaviors have been evaluated. Results indicate that superior mechanical properties with constructed cellular aluminums can be achieved when the distribution of material at cell level is properly selected. Excellent energy absorption per unit mass can be obtained by only changing the thickness of the original aluminum sheet.nnation behaviors and energy absorption characteristics of constructed cellular aluminums were investigated by compressive tests. Constructed cellular aluminum specimens with two kinds of thickness in the cold-pressed panel and various numbers of layers bonded together have been tested. The plateau stress and the energy absorption have been measured and furthennore, the defonnation behaviors have been evaluated. Results indicate that superior mechanical properties with constructed cellular aluminums can be achieved when the distribution of material at cell level is properly selected. Excellent energy absorption per unit mass can be obtained by only changing the thickness of the original aluminum sheet.

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This project investigated how plants respond to invading pathogens using microscopic, biochemical and genetic approaches. The development of transgenic plants containing the green fluorescent protein cloned from jellyfish enabled a new approach to studying plant defence genes. In particular, the role and involvement of the plant gene PAL1 was analysed.

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A 2D cellular automation approach was used to simulate microstructure evolution during and after hot deformation. Initial properties of the microstructure and dislocation density were used as input data to the cellular automation model. The flow curve and final grain size were the output data for the dynamic recrystallization simulation, and softening kinetics curves were the output data of static and metadynamic recrystallization simulations. The model proposed in this work considered the effect of thermomechanical parameters (e.g., temperature and strain rate) on the nucleation and growth kinetics during dynamic recrystallization. The dynamic recrystallized microstructures at different strains, temperatures, and strain rates were used as input data for static and metadynamic recrystallization simulations. It was shown that the cellular automation approach can model the final microstructure and flow curve successfully in dynamic recrystallization conditions. The postdeformation simulation results showed that the time for 50% recrystallization decreases with increasing strain for a given initial grain size and that dynamic recrystallization slows the postdeformation recrystallization kinetics compared to a model without dynamic recrystallization.

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We report here on the use of a Sindbis virus-based DNA-launch RNA replicon vector (pSIN-HA) that expresses influenza hemagglutinin (HA) as an immunogen. Immunization of mice with pSIN-HA generated anti-HA antibody and CTL responses and resulted in lower lung viral titers after influenza challenge when compared to controls. Importantly, immunization with a low dose of pSIN-HA mediated significantly reduced lung viral titers following challenge at 43 weeks after the final immunization. In contrast, immunization with a non-replicon DNA vector expressing HA failed to mediate reduced lung viral titer at the same dose. This demonstrated the dose-sparing capacity of the SIN vector system and its ability to stimulate long-term memory responses, properties that are highly desirable in any vaccine formulation.

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Oxidative stress plays a central role in neuronal injury and cell death in acute and chronic pathological conditions. The cellular responses to oxidative stress embrace changes in mitochondria and other organelles, notably endoplasmic reticulum, and can lead to a number of cell death paradigms, which cover a spectrum from apoptosis to necrosis and include autophagy. In Alzheimer's disease, and other pathologies including Parkinson's disease, protein aggregation provides further cellular stresses that can initiate or feed into the pathways to cell death engendered by oxidative stress. Specific attention is paid here to mitochondrial dysfunction and programmed cell death, and the diverse modes of cell death mediated by mitochondria under oxidative stress. Novel insights into cellular responses to neuronal oxidative stress from a range of different stressors can be gained by detailed transcriptomics analyses. Such studies at the cellular level provide the key for understanding the molecular and cellular pathways whereby neurons respond to oxidative stress and undergo injury and death. These considerations underpin the development of detailed knowledge in more complex integrated systems, up to the intact human bearing the neuropathology, facilitating therapeutic advances.