关于直译和意译新定义的研究

给出了直译和意译的新定义,它体现了直译和意译的本质特征,较好地划清了二者之间的界限。     

Bacterial suicide through stress

Outside of the laboratory, bacterial cells are constantly exposed to stressful conditions, and an ability to resist those stresses is essential to their survival. However, the degree of stress required to bring about cell death varies with growth phase, amongst other parameters. Exponential phase cells are significantly more sensitive to stress than stationary phase ones, and a novel hypothesis has recently been advanced to explain this difference in sensitivity, the suicide response. Essentially, the suicide response predicts that rapidly growing and respiring bacterial cells will suffer growth arrest when subjected to relatively mild stresses, but their metabolism will continue: a burst of free-radical production results from this uncoupling of growth from metabolism, and it is this free-radical burst that is lethal to the cells, rather than the stress per se. The suicide response hypothesis unifies a variety of previously unrelated empirical observations, for instance induction of superoxide dismutase by heat shock, alkyl-hydroperoxide reductase by osmotic shock and catalase by ethanol shock. The suicide response also has major implications for current [food] processing methods. Received 29 March 1999; received after revision 14 May 1999; accepted 17 May 1999     

强半无爪图的完全圈可扩性

证明了连通局部连通的强半无爪图是完全圈可扩的．从而推广了Oberly D，Sumner D，Clark L，Hendry G R T等的相关结果．     

Age-related lipid peroxidation in the digestive gland of mussels: The role of the antioxidant defence systems

Summary The main cellular defence systems against free radical-mediated oxidative stress are significantly reduced in the dige⁺ive gland of aged (>10 years old) compared to younger (2–4 years old) mussels (Mytilus edulis L.). Moreover, the concentration of lipid peroxidation products (malondialdehyde) is increased in the same age group with respect to younger animals. The obtained data indicate that an impairment of the antioxidant defence systems would render the older animals more susceptible to peroxidative stress, thus supporting the general significance of the free radical theory of aging.     

松散物料力学的若干理论和实践

本文讨论了松散物料力学的一些基本问题:屈服轨迹,静屈服轨迹和动屈服轨迹;在它上面没有切应力和正应力的自由表面;有效屈服轨迹和时间效应;主动应力状态和被动应力状态;松散物料的主应力轨迹,拱的理论等。在每个问题中,既讨论了理论问题,也讨论了实践问题。     

Role of <Emphasis Type="Italic">N</Emphasis>-linked polymannose oligosaccharides in targeting glycoproteins for endoplasmic reticulum-associated degradation

Misfolded or incompletely assembled multisubunit glycoproteins undergo endoplasmic reticulum-associated degradation (ERAD) regulated in large measure by their N-linked polymannose oligosaccharides. In this quality control system lectin interaction with Glc₃Man₉GlcNAc₂ glycans after trimming with endoplasmic reticulum (ER) -glucosidases and -mannosidases sorts out persistently unfolded glycoproteins for N-deglycosylation and proteolytic degradation. Monoglucosylated (Glc₁Man₉GlcNAc₂) glycoproteins take part in the calnexin/calreticulin glucosylation-deglucosylation cycle, while the Man₈GlcNAc₂ isomer B product of ER mannosidase I interacts with EDEM. Proteasomal degradation requires retrotranslocation into the cytosol through a Sec61 channel and deglycosylation by peptide: N-glycosidase (PNGase); in alternate models both PNGase and proteasomes may be either free in the cytosol or ER membrane-imbedded/attached. Numerous proteins appear to undergo nonproteasomal degradation in which deglycosylation and proteolysis take place in the ER lumen. The released free oligosaccharides (OS) are transported to the cytosol as OS-GlcNAc₂ along with similar components produced by the hydrolytic action of the oligosaccharyltransferase, where they together with OS from the proteasomal pathway are trimmed to Man₅GlcNAc₁ by the action of cytosolic endo--N-acetylglucosaminidase and -mannosidase before entering the lysosomes. Some misfolded glycoproteins can recycle between the ER, intermediate and Golgi compartments, where they are further processed before ERAD. Moreover, properly folded glycoproteins with mannose-trimmed glycans can be deglucosylated in the Golgi by endomannosidase, thereby releasing calreticulin and permitting formation of complex OS. A number of regulatory controls have been described, including the glucosidase-glucosyltransferase shuttle, which controls the level of Glc₃Man₉GlcNAc₂-P-P-Dol, and the unfolded protein response, which enhances synthesis of components of the quality control system.Received 26 January 2004; accepted 25 February 2004     

卡尔·桑德堡的诗歌风格

卡尔·桑德堡的诗歌,一方面,从内容到形式上继承了沃尔特·惠特曼的创作风格:内容上,桑德堡使自己的诗歌成为"人民的声音";形式上,他采用自由体诗,打破传统的十四行诗的韵律,像惠特曼一样采用长句、重复、叠韵、罗列等技巧表达自己的情感。另一方面,卡尔·桑德堡紧跟时代脉搏,成为意象派诗人的一员,正是他短小精悍、浑然一体的意象诗使他名垂青史。     

电磁场数值分析的无单元Galerkin方法

阐述了移动最小二乘无单元Galerkin方法的基本原理及实现过程,给出了权函数的选取原则,和基于Lagrange乘子法的边界条件处理方法,结合算例说明了该方法用于电磁场分析的有效性和计算特点,并着重研究了影响半径对计算结果的影响,计算结果表明,对于非均匀媒质,影响半径应在一个与高斯积分点有关的范围内取值,以避免媒质作用的“扩散”而降低计算精度。     

4-Hydroxynonenal-modified amyloid-beta peptide inhibits the proteasome: possible importance in Alzheimer's disease

The amyloid β-peptide (Aβ) is a 4-kDa species derived from the amyloid precursor protein, which accumulates in the brains of patients with Alzheimer’s disease. Although we lack full understanding of the etiology and pathogenesis of selective neuron death, considerable data do imply roles for both the toxic Aβ and increased oxidative stress. Another significant observation is the accumulation of abnormal, ubiquitin-conjugated proteins in affected neurons, suggesting dysfunction of the proteasome proteolytic system in these cells. Recent reports have indicated that Aβ can bind and inhibit the proteasome, the major cytoslic protease for degrading damaged and ubiquitin-conjugated proteins. Earlier results from our laboratory showed that moderately oxidized proteins are preferentially recognized and degraded by the proteasome; however, severely oxidized proteins cannot be easily degraded and, instead, inhibit the proteasome. We hypothesized that oxidatively modified Aβ might have a stronger (or weaker) inhibitory effect on the proteasome than does native Aβ. We therefore also investigated the proteasome inhibitory action of Aβ _1–40 (a peptide comprising the first 40 residues of Aβ) modified by the intracellular oxidant hydrogen peroxide, and by the lipid peroxidation product 4-hydroxynonenal (HNE). H₂O₂ modification of Aβ _1–40 generates a progressively poorer inhibitor of the purified human 20S proteasome. In contrast, HNE modification of Aβ _1–40 generates a progressively more selective and efficient inhibitor of the degradation of fluorogenic peptides and oxidized protein substrates by human 20S proteasome. This interaction may contribute to certain pathological manifestations of Alzheimer’s disease Received 26 September 2000; accepted 26 September 2000