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The problem of output feedback stabilization of linear systems based on a reduced‐order model is addressed in this paper. New reduced‐order models are proposed for the output feedback design of linear systems with a singular perturbation model. An output feedback controller with a zero steady‐state gain matrix is proposed for stabilizing this kind of system. It is shown that with the proposed controller the reduced‐order model based feedback design can guarantee the actual closed‐loop stability for the sufficiently small perturbation parameter. This approach can overcome the difficulties in the existing design method using the so‐called zeroth‐order approximation model, whose validity is highly dependent on the value of the perturbation parameter.  相似文献   
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Jurkat T cells undergo rapid apoptosis upon stimulation of the Fas/APO-1 (CD95) receptor. We examined the role of the mitogen-activated protein kinase (MAPK) cascade as a negative regulator of Fas-mediated apoptosis. To this end, we used both physiologic and artificial activators of MAPK, all of which activate MAPK by distinct routes. MAPK activity could be efficiently elevated by two T cell mitogens, the lectin PHA and an agonistic Ab to the T cell receptor complex as well as by the type 1 and 2A phosphatase inhibitor, calyculin A, and the protein kinase C-activating phorbol ester, tetradecanoyl phorbol acetate. All these treatments were effective in preventing the characteristic early and late features of Fas-mediated apoptosis, including activation of caspases. Our results indicate that the elevated MAPK activities intervene upstream of caspase activation. The degree of MAPK activation by the different stimuli used in our study corresponds well to their potency to inhibit apoptosis, indicating that MAPK activation serves as an efficient modulator of Fas-mediated apoptosis. The role of MAPK in modulation of Fas-mediated apoptosis was further corroborated by transient transfection with constitutively active MAPK kinase, resulting in complete inhibition of the Fas response, whereas transfection with a dominant negative form of MAPK kinase had no effect. Furthermore, the apoptosis inhibitory effect of the MAPK activators could be abolished by the specific MAPK kinase inhibitor PD 098059. Modulation of Fas responses by MAPK signaling may determine the persistence of an immune response and may explain the insensitivity of recently activated T cells to Fas receptor stimulation.  相似文献   
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Fatigue and fracture mechanisms in Nb fiber-reinforced MoSi2 composites are elucidated in this article. The effects of fiber diameter on fracture and crack-tip shielding mechanisms are discussed after a review of micromechanical models which are applied to the prediction of residual stress levels, toughening, and microcracking phenomena. Toughening is shown to occur by a combination of crack bridging and crack-tip blunting under monotonic and cyclic loading. However, the observed failure mechanisms are different under monotonic and cyclic loading. Composites with smaller (250-μm) fiber diameters are shown to have better fatigue resistance and lower fracture toughness than composites with larger (750-μm) fiber diameters. The occurrence of slower fatigue crack growth rates in the composites reinforced with smaller diameter Nb fibers is rationalized by assessing the combined effects of fiber spacing and interfacial crack growth on the average crack growth rates within the composites.  相似文献   
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Two measures of weight cycling and indexes of psychological functioning were examined in a large sample of dieters. History of weight cycling was assessed to include number of dieting attempts, total lifetime weight lost and regained, and number of weight cycles over 20 lb (9.1 kg). Experience of weight cycling measured perception of being a yo-yo dieter and perceived success at maintaining past weight losses. Experience was more strongly related than history to all psychological measures. Further, when controlling for the effects of age, body mass index, and experience, the relation between history and the psychological variables was nonsignificant. This finding suggests that an individual's perception of being a weight cycler may be more related to psychological problems than the actual number of pounds lost and regained over dine. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   
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A profile of respiratory complications has been associated with the onset and development of obesity in humans. Similar phenotypes have been routinely demonstrated in genetic animal models of obesity such as the ob mouse (C57BL/6J-Lepob). The objective of the present study was to test the hypothesis that a constellation of respiratory complications are attenuated with leptin (i.e., protein product of the ob gene) replacement. Daily leptin administration during a 6-wk period was conducted to control body weight of mutant ob mice similar to genotypic control groups. During the treatment period, repeated baseline ventilatory measurements were assessed by using whole body plethysmography while quasistatic pressure-volume curves were performed to further explore the role of leptin in improving lung mechanics. Diaphragmatic myosin heavy chain (MHC) isoform phenotype was examined to determine proportional changes in MHC composition. In room air, breathing frequency and minute ventilation were significantly (P < 0.01) different among ob treatment groups, suggesting that leptin opposed the development of a rapid breathing pattern observed in vehicle-treated ob mice. Quasistatic deflation curves indicated that the lung volume of leptin-treated ob mice was significantly (P < 0.05) greater relative to vehicle-treated ob mice at airway pressures between 0 and 30 cmH2O. Diaphragm MHC composition of leptin-treated ob mice was restored significantly (P < 0.05) to resemble the control phenotype. In this genetic mouse model of obesity, the results suggested that respiratory complications associated with the obese phenotype, including rapid breathing pattern at baseline, diminished lung compliance, and abnormal respiratory muscle adaptations, are attenuated with prolonged leptin treatment.  相似文献   
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Cells of the innate immune system secrete cytokines early in immune responses that guide maturing T helper (Th) cells along appropriate lineages. This study investigates the role of cytokine networks, bridging the innate and acquired immune systems, in the pathogenesis of an organ specific autoimmune disease. Experimental allergic encephalomyelitis (EAE), a demyelinating disease of the central nervous system, is widely used as an animal model for multiple sclerosis. We demonstrate that interleukin (IL)-12 is essential for the generation of the autoreactive Th1 cells that induce EAE, both in the presence and absence of interferon gamma. The disease-promoting effects of IL-12 are antagonized by IL-10 produced by an antigen nonspecific CD4+ T cell which, in turn, is regulated by the endogenous production of IL-12. This unique immunoregulatory circuit appears to play a critical role in controlling Th cell differentiation and provides a mechanism by which microbial triggers of the innate immune system can modulate autoimmune disease.  相似文献   
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