椭圆管道与连接器过盈装配应力有限元分析

基于组合厚壁圆筒理论和管道与连接器过盈装配有限元计算,分析了海底椭圆管道与机械连接器水下过盈装配的应力问题。采用数值模拟的方法分析过盈装配过程中的产生的极值有效应力并引入椭圆度应力系数大小衡量应力集中效应强弱。结果表明,管道接触应力与等效过盈量密切相关,而椭圆度影响过盈面接触应力分布的均匀性。椭圆度应力系数越大,管道应力集中效应越明显,承载的应力越大。随着椭圆度增大,通过适当增加等效过盈量的办法,即可增大过盈装配应力的承载能力。     

Aluminium in Alzheimer’s disease: are we still at a crossroad?

Aluminium, an environmentally abundant non-redox trivalent cation has long been implicated in the pathogenesis of Alzheimers disease (AD). However, the definite mechanism of aluminium toxicity in AD is not known. Evidence suggests that trace metal homeostasis plays a crucial role in the normal functioning of the brain, and any disturbance in it can exacerbate events associated with AD. The present paper reviews the scientific literature linking aluminium with AD. The focus is on aluminium levels in brain, region-specific and subcellular distribution, its relation to neurofibrillary tangles, amyloid beta, and other metals. A detailed mechanism of the role of aluminium in oxidative stress and cell death is highlighted. The importance of complex speciation chemistry of aluminium in relation to biology has been emphasized. The debatable role of aluminium in AD and the cross-talk between aluminium and genetic susceptibility are also discussed. Finally, it is concluded based on extensive literature that the neurotoxic effects of aluminium are beyond any doubt, and aluminium as a factor in AD cannot be discarded. However, whether aluminium is a sole factor in AD and whether it is a factor in all AD cases still needs to be understood.Received 22 July 2004; received after revision 3 September 2004; accepted 16 September 2004     

Functional relationship of cytochrome c(6) and plastocyanin in Arabidopsis

Photosynthetic electron carriers are important in converting light energy into chemical energy in green plants. Although protein components in the electron transport chain are largely conserved among plants, algae and prokaryotes, there is thought to be a major difference concerning a soluble protein in the thylakoid lumen. In cyanobacteria and eukaryotic algae, both plastocyanin and cytochrome c(6) mediate electron transfer from cytochrome b(6)f complex to photosystem I. In contrast, only plastocyanin has been found to play the same role in higher plants. It is widely accepted that cytochrome c(6) has been evolutionarily eliminated from higher-plant chloroplasts. Here we report characterization of a cytochrome c(6)-like protein from Arabidopsis (referred to as Atc6). Atc6 is a functional cytochrome c localized in the thylakoid lumen. Electron transport reconstruction assay showed that Atc6 replaced plastocyanin in the photosynthetic electron transport process. Genetic analysis demonstrated that neither plastocyanin nor Atc6 was absolutely essential for Arabidopsis growth and development. However, plants lacking both plastocyanin and Atc6 did not survive.     

Comparative cytological study after prolonged cultural regime of bacteria-free crown gall tumour and its corresponding normal tissue ofAlthaea rosea isolated from the same plant

Zusammenfassung Kulturen von Tumorgewebe (Crown Gall) und normalen Explantaten vonAlthaea rosea wurden nach mehr als 10jähriger Kultivierung zytologisch verglichen.     

Steroidal peptides

Zusammenfassung Es wird die Möglichkeit erwogen, dass Steroide mit geeignet gebauten Peptidseitenketten am Aufbau oder Transport von Hormonen beteiligt sein könnten. Über die erstmalige Darstellung von Steroidpeptiden wird berichtet. Als Beispiele werden die Synthesen der beiden geschützten Steroidpeptide III und IV beschrieben.

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Part XXIV of a series entitledSteroids and Related Natural Products. For the preceding contribution see:J. P. Kutney, W. Cretney, G. R. Pettit, andJ. C. Knight, Tetrahedron, in press.

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A preliminary report of this study was presented (April 9, 1964) at the Third International Symposium on the Chemistry of Natural Products, Kyoto (Japan).

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This investigation was supported by National Science Foundation Research Grant GB-249.     

Design and implementation of a wideband HF channel simulator

The paper presents a wideband high frequency (HF) channel simulator.The simulation consists of a software simulation of a direct-sequence spread-spectrum (DSSS) HF system with RAKE receiver.The validity of the HF channel simulator is demonstrated by the analysis of the scattering function and example results of the simulator.The performance of DS system under HF channel and noise are also presented.The simulation results and theoretical analysis show that a straightforward DS system may properly mitigate the intersymbol interference (ISI) distortion of the HF channel while perform badly under the HF noise and interference.     

Loss of Omi mitochondrial protease activity causes the neuromuscular disorder of mnd2 mutant mice

The mouse mutant mnd2 (motor neuron degeneration 2) exhibits muscle wasting, neurodegeneration, involution of the spleen and thymus, and death by 40 days of age. Degeneration of striatal neurons, with astrogliosis and microglia activation, begins at around 3 weeks of age, and other neurons are affected at later stages. Here we have identified the mnd2 mutation as the missense mutation Ser276Cys in the protease domain of the nuclear-encoded mitochondrial serine protease Omi (also known as HtrA2 or Prss25). Protease activity of Omi is greatly reduced in tissues of mnd2 mice but is restored in mice rescued by a bacterial artificial chromosome transgene containing the wild-type Omi gene. Deletion of the PDZ domain partially restores protease activity to the inactive recombinant Omi protein carrying the Ser276Cys mutation, suggesting that the mutation impairs substrate access or binding to the active site pocket. Loss of Omi protease activity increases the susceptibility of mitochondria to induction of the permeability transition, and increases the sensitivity of mouse embryonic fibroblasts to stress-induced cell death. The neurodegeneration and juvenile lethality in mnd2 mice result from this defect in mitochondrial Omi protease.     

Microscopic electronic inhomogeneity in the high-Tc superconductor Bi2Sr2CaCu2O8+x

The parent compounds of the copper oxide high-transition-temperature (high-Tc) superconductors are unusual insulators (so-called Mott insulators). Superconductivity arises when they are 'doped' away from stoichiometry. For the compound Bi2Sr2CaCu2O8+x, doping is achieved by adding extra oxygen atoms, which introduce positive charge carriers ('holes') into the CuO2 planes where the superconductivity is believed to originate. Aside from providing the charge carriers, the role of the oxygen dopants is not well understood, nor is it clear how the charge carriers are distributed on the planes. Many models of high-Tc superconductivity accordingly assume that the introduced carriers are distributed uniformly, leading to an electronically homogeneous system as in ordinary metals. Here we report the presence of an electronic inhomogeneity in Bi2Sr2CaCu2O8+x, on the basis of observations using scanning tunnelling microscopy and spectroscopy. The inhomogeneity is manifested as spatial variations in both the local density of states spectrum and the superconducting energy gap. These variations are correlated spatially and vary on the surprisingly short length scale of approximately 14 A. Our analysis suggests that this inhomogeneity is a consequence of proximity to a Mott insulator resulting in poor screening of the charge potentials associated with the oxygen ions left in the BiO plane after doping, and is indicative of the local nature of the superconducting state.