复数,实数及实对称数据下Bruun FFT算法的实现

本文在复数、实数以及实对称数据下研究和实现了Ｂｒｕｕｎ ＦＦＴ算法。文章分析和评价了各种数据下ＢｒｕｕｎＦＦＴ的运算量和特点，提出了算法的实现结构和方法。最后给了ＴＭＳ３２０Ｃ３０上的运算时间，我们实现的算法比基２ＦＦＴ速度提高３５％。     

Étude biochimique des poissons: 1. Variations semestrielles de la teneur en eau et en protéines du tissu musculaire de la truite Arc-en-ciel (Salmo gairdnerii Rich)

Summary The authors have noted, during the reproductive cycle of the Rainbow trout (Salmo gairdnerii Rich), important variations concerning water and total proteins content. This study shows a great correlation between the biological process and biochemical variations.     

Crystal structure of enteropathogenic Escherichia coli intimin-receptor complex

Intimin and its translocated intimin receptor (Tir) are bacterial proteins that mediate adhesion between mammalian cells and attaching and effacing (A/E) pathogens. Enteropathogenic Escherichia coli (EPEC) causes significant paediatric morbidity and mortality world-wide. A related A/E pathogen, enterohaemorrhagic E. coli (EHEC; O157:H7) is one of the most important food-borne pathogens in North America, Europe and Japan. A unique and essential feature of A/E bacterial pathogens is the formation of actin-rich pedestals beneath the intimately adherent bacteria and localized destruction of the intestinal brush border. The bacterial outer membrane adhesin, intimin, is necessary for the production of the A/E lesion and diarrhoea. The A/E bacteria translocate their own receptor for intimin, Tir, into the membrane of mammalian cells using the type III secretion system. The translocated Tir triggers additional host signalling events and actin nucleation, which are essential for lesion formation. Here we describe the the crystal structures of an EPEC intimin carboxy-terminal fragment alone and in complex with the EPEC Tir intimin-binding domain, giving insight into the molecular mechanisms of adhesion of A/E pathogens.     

Die Hämagglutination des Influenzavirus A2-Hongkong

Summary A₂-Hongkong influenza virus does not agglutinate the erythrocytes of the cow, the calf, the horse, the pony and the spiny mouse at room temperature, while the A₂-Asia influenza virus causes agglutination. At a temperature of 4 °C A₂-Hongkong was able to agglutinate the erythrocytes of all species examined except those of the spiny mouse. Whether the A₂-Hongkong virus does or does not agglutinate the erythrocytes of the chicken, the donkey, the goat, the spiny mouse and the horse at room temperature could depend on the speed of elution.     

Inhibition of caspase-1 slows disease progression in a mouse model of Huntington's disease.

Huntington's disease is an autosomal-dominant progressive neurodegenerative disorder resulting in specific neuronal loss and dysfunction in the striatum and cortex. The disease is universally fatal, with a mean survival following onset of 15-20 years and, at present, there is no effective treatment. The mutation in patients with Huntington's disease is an expanded CAG/polyglutamine repeat in huntingtin, a protein of unknown function with a relative molecular mass of 350,000 (M(r) 350K). The length of the CAG/polyglutamine repeat is inversely correlated with the age of disease onset. The molecular pathways mediating the neuropathology of Huntington's disease are poorly understood. Transgenic mice expressing exon 1 of the human huntingtin gene with an expanded CAG/polyglutamine repeat develop a progressive syndrome with many of the characteristics of human Huntington's disease. Here we demonstrate evidence of caspase-1 activation in the brains of mice and humans with the disease. In this transgenic mouse model of Huntington's disease, expression of a dominant-negative caspase-1 mutant extends survival and delays the appearance of neuronal inclusions, neurotransmitter receptor alterations and onset of symptoms, indicating that caspase-1 is important in the pathogenesis of the disease. In addition, we demonstrate that intracerebroventricular administration of a caspase inhibitor delays disease progression and mortality in the mouse model of Huntington's disease.     

西部农业信息化建设问题的探讨

西部农业信息化水平低下制约着西部农业的发展。物质基础薄弱、信息意识淡薄、信息人才及资金短缺是造成西部农业信息化水平低下的原因。为加快西部信息化农业建设，应该从更新观念、加大政府支持力度、利用有限资源进行信息化基础建设、重视人才资源的开发、培育信息产品市场、加强农业应用系统和信息化农业技术的研究、加强示范应用体系等方面入手。