模糊滑动控制的一般方法(英文)

陈述了一种新的模糊逻辑控制方法,它可消除滑动控制所固有的抖动问题。方法的推导是将多开关滑动控制问题简化成等效的单开关问题。控制规律显示它是一种模糊滑动控制的一般方法。文献中的其他方法可由此法导出。模糊推理规则由两个输入变量组成。第一个输入变量是系统状态到所预定的状态空间中的超平面之间的方向距离;第二个输入变量的选择可根据应用而定,例如方向距离的导数、控制设计者所感兴趣的特定变量,或者某些状态变量的加权之和。这个新方法易于在高阶系统中实现,并且可以直接而明确地控制系统的动态过程。它消除了滑动控制和经典模糊滑动控制中的抖动问题。此外。新方法比其他类似方法的控制要简单。稳定性和性能分析显示了此法的有效性。此法已用于一带有典型驱动和反馈传感器的工业直流电机的位置控制之中。     

Improved immunogenicity of a peptide epitope after fusion to hepatitis B core protein

Synthetic vaccines for viral diseases can use defined regions of viral proteins as immunogens: the peptide sequence of amino acids 141-160 of the VP1 protein of foot and mouth disease virus (FMDV) elicits virus-neutralizing antibodies to protect guinea pigs, cattle and pigs either when coupled to a carrier protein or when administered in liposomes or in incomplete Freund's adjuvant. The immune response to these peptides is much lower than that to complete virus particles and the same sequence fused to the N terminus of beta-galactosidase did not produce a more potent immunogen than synthetic peptide alone. We report here an expression system for immunogenic epitopes linked to a carrier protein, hepatitis B core antigen, to form part of a virus-like complex which can present these epitopes to the immune system at high density. The immunogenicity of these structures approaches that of FMDV particles.     

Nuclear inositides: inconsistent consistencies

It is now clear that phosphoinositides, which play a major role in the regulation of a variety of cellular processes in the cytoplasm, are found within the nucleus. Their role in this subcellular compartment is still contentious: however, data has suggested that nuclear inositides generate substrates, such as PtdIns(4,5)P2, utilised by a number of nuclear signalling pathways: for example, nuclear phospholipase C and the PtdIns 3-kinase cascade. There is also evidence that PtdIns(4,5)P2 may play a role in the localisation and regulation of a number of nuclear proteins such as the BAF complex, which is involved in the regulation of chromatin structure. Although the presence of nuclear inositides has been demonstrated in a number of different cell types, suggesting that it is ubiquitous, there are many inconsistencies within the literature concerning the locations and isotypes of enzymes that are involved in their regulation and in the potential second messengers which are generated by them. This review aims to highlight some of these inconsistencies in order to focus on areas that need further characterisation.     

A one-hit model of cell death in inherited neuronal degenerations

In genetic disorders associated with premature neuronal death, symptoms may not appear for years or decades. This delay in clinical onset is often assumed to reflect the occurrence of age-dependent cumulative damage. For example, it has been suggested that oxidative stress disrupts metabolism in neurological degenerative disorders by the cumulative damage of essential macromolecules. A prediction of the cumulative damage hypothesis is that the probability of cell death will increase over time. Here we show in contrast that the kinetics of neuronal death in 12 models of photoreceptor degeneration, hippocampal neurons undergoing excitotoxic cell death, a mouse model of cerebellar degeneration and Parkinson's and Huntington's diseases are all exponential and better explained by mathematical models in which the risk of cell death remains constant or decreases exponentially with age. These kinetics argue against the cumulative damage hypothesis; instead, the time of death of any neuron is random. Our findings are most simply accommodated by a 'one-hit' biochemical model in which mutation imposes a mutant steady state on the neuron and a single event randomly initiates cell death. This model appears to be common to many forms of neurodegeneration and has implications for therapeutic strategies.     

Effects of hypophysectomy, bilateral adrenalectomy and hormone replacement therapy upon organ monoamine oxidase activity.

Changes in MAO activity after hypophysectomy (HX) are not due to adrenal insufficiency. ACTH failed to reverse the effects of HX and enhanced the depression of cardiac and spleenic MAO. The data suggests both facilitatory and inhibitory effects of pituitary hormones on MAO activity.