与顶点C-划分有关的上可嵌入图类

图的顶点C-划分是指：G的顶点划分{V1，V2…，Vk}，使得每个G[Vi]为多重完全图(1≤i≤k)。结合图的顶点C-划分的条件，确定了一类点的度在modulo4下值为0或3的上可嵌入图类，综合已有结果，较完整地刻画了这类图的上可嵌入情况。     

物理疗法干预睡眠障碍研究进展

物理疗法是干预睡眠、提高人群睡眠质量的重要手段。对物理因子中光、声、温度、振动、电磁场、压力刺激手段来改善睡眠的办法进行了综述：总结了各物理因子手段改善睡眠的效应和机制,介绍了基于物理因子治疗睡眠疾病的国内外研究进展和相关物理治疗仪器、设备。为制定科学合理的睡眠障碍物理疗治方案提供理论依据。     

消费需求不足的原因分析与对策

消费需求是总需求的重要组成部分,是促进经济增长的重要动力.但是我国目前市场消费需求不足,已成为经济增长的主要制约因素.在分析影响消费需求的原因之后,提出了扩大消费需求的综合对策.     

Chitotriosidase: the yin and yang

The enzyme chitotriosidase (ChT), the human analogue of chitinases from non-vertebrate species, is one of the most abundant and indicative proteins secreted by activated macrophages. Its enzymatic activity is elevated in serum of patients suffering from Gaucher’s disease type 1 and in some other inherited lysosomal storage disorders, as well as in diseases in which macrophages are activated. The last decade has witnessed the appearance of a substantial number of studies attempting to unravel its cellular functions, which have yet not been fully defined. A great deal of progress has been made in the study of the physiological roles of ChT. This review is looks at the key areas of investigations addressed to further illuminate whether ChT activation might have different functional meanings in various diseases. Received 7 June 2006; received after revision 24 July 2006; accepted 21 September 2006     

Oncogenic mechanisms in myeloproliferative disorders

Myeloproliferative disorders (MPDs) are clonal haematopoietic malignancies involving the abnormal proliferation of myeloid lineages. The World Health Organisation (WHO) classification of haematopoietic malignancies distinguishes MPDs from myelodysplastic/ myeloproliferative disorders and systemic mastocytosis. These malignancies frequently involve constitutive tyrosine kinase activity, resulting from either oncogenic fusion protein production or from point mutations. Chronic myelogenous leukaemia is the model used for studies of the consequences of such molecular defects. However, the heterogeneity of the clinical course of MPDs should be seen in a more rationale conceptual framework, including the many molecular events associated with these diseases. This review focuses on the various tyrosine kinase-related molecular mechanisms underlying both MPDs and rare diseases with myeloproliferative features. We pay particular attention to the newly identified JAK2 V617F mutation in polycythaemia vera, essential thrombocythaemia and idiopathic myelofibrosis and deal with disease heterogeneity and putative additional molecular mechanisms. Received 9 June 2006; received after revision 28 July 2006; accepted 11 September 2006     

Sleep and sleep disturbances: biological basis and clinical implications

Sleep is a neurochemical process involving sleep promoting and arousal centers in the brain. Sleep performs an essential restorative function and facilitates memory consolidation in humans. The remarkably standardized bouts of consolidated sleep at night and daytime wakefulness reflect an interaction between the homeostatic sleep need that is manifested by increase in sleep propensity after sleep deprivation and decrease during sleep and the circadian pacemaker. Melatonin, the hormone produced nocturnally by the pineal gland, serves as a time cue and sleep-anticipating signal. A close interaction exists between the sleep-wake, melatonin, core temperature, blood pressure, immune and hormonal rhythms leading to optimization of the internal temporal order. With age the robustness of the circadian system decreases and the prevalence of sleep disorders, particularly insomnia, increases. Deviant sleep patterns are associated with increased risks of morbidity, poor quality of life and mortality. Current sleep pharmacotherapies treat insufficient sleep quantity, but fail to improve daytime functioning. New treatment modalities for sleep disorders that will also improve daytime functioning remain a scientific and medical challenge.     

Prion: the chameleon protein

From Creutzfeldt-Jakob disease (CJD) to variant CJD through Gerstmann-Str?ussler-Scheinker syndrome, kuru and fatal familial insomnia, the journey leading to current understanding of the basic aspects of human prion diseases has been full of unexpected, but often dramatic and always fascinating twists. Recent progress in modeling prion diseases and characterization of the various prion protein forms reveal that such a wide spectrum of the diseases is associated with the chameleon-like conformational features of prions.     

求解浅水方程的光滑粒子流体动力学法

文章将光滑粒子流体动力学(SPH)法应用于浅水方程,针对传统SPH法中存在的边界缺陷问题,引入了一种处理边界条件的方法,即虚粒子法,对一维溃坝问题进行模拟,并将所得结果与用有限差分法等数值方法得到的结果相比较,结果表明SPH法能够捕捉到水坝崩溃后的激波现象,并且所得图像较为平滑,在间断处也较为锐利。     

Molybdenum cofactor biosynthesis and deficiency

The molybdenum cofactor (Moco) forms the active site of all molybdenum (Mo) enzymes, except nitrogenase. Mo enzymes catalyze important redox reactions in global metabolic cycles. Moco consists of Mo covalently bound to one or two dithiolates attached to a unique tricyclic pterin moiety commonly referred to as molybdopterin (MPT). Moco is synthesized by an ancient and conserved biosynthetic pathway that can be divided into four steps, according to the biosynthetic intermediates precursor Z (cyclic pyranopterin monophosphate), MPT and adenylated MPT. In a fifth step modifications such as attachment of nucleotides, sulfuration or bond formation between Mo and the protein result in different catalytic Mo centers. A defect in any of the steps of Moco biosynthesis results in the pleiotropic loss of all Mo enzyme activities. Human Moco deficiency is a hereditary metabolic disorder characterized by severe neurodegeneration resulting in early childhood death. Recently, a first substitution therapy was established. Received 17 June 2005; received after revision 18 August 2005; accepted 1 September 2005     

独立集中具有最小特定度和的点的上可嵌入图类(英)

结合边连通度，探讨了独立集中具有最小特定度和的点的上可嵌入图.得到了下列结果. (1)设G,是一个2-边连通简单图且满足条件:对任意一个G的3-独立集I, ∨x_i ,x_j ∈I (i,j = 1,2,3), d(x_i ,x_j)≧3 (1 ≦ i ≠ j ≦ 3) =>∑_{i = 1}³ d(x_i) ≧ v + 1(v = | V(G)|}), 则G是上可嵌入的;(2)设G是一个3-边连通简单图且满足条件:对任意一个G的6-独立集I, ∨x_i ,x_j ∈I (1≦i,j≦6), d(x_i,x_j) ≧3(1 ≦ i ≠ j ≦ 6) => ∑_{i = 1}⁶ d(x_i) ≧ v + 1(v = | V(G)|), 则G是上可嵌入的.