Banach空间中一迭代序列及其耦合不动点

GUO Da-jun教授等在《非线性算子耦合不动点与应用》一文中对某些算子引入了全连续混合单调算子的耦合不动点的概念，得到了极小，极大耦合不动点及其相似，本文建立了一迭代序列，将其结果推广到更广泛的一类映射－半紧1－集映射，并削弱了紧性和全连续的条件，得到了乘积空间中的极小，极大耦合不动点定理。     

关于Submil（3）的一个结论及其半收敛性

证明了Ｌ＾１－有界的独立随机变量序列Ｓｕｂｍｉｌ（１）与Ｓｕｂｍｉｌ（３）的等价性；存在子列其正部为致可积的Ｓｕｂｍｉｌ（３）的半收敛性，并举反例说明了Ｌ＾１－有界的Ｓｕｂｍｉｌ（１）不具有此性质。     

C.Thomassen猜想的证明

证明了若 G是 3连通无爪图 ,且 G的每个同构于 A的导出子图都满足 ( a1,a2 ) ,则 G是泛连通图 (除了 u,v∈ V( G) ,d( u,v) =1时 ,G中可能不存在 ( u,v)—k路外 )。由此立得C.Thomassen猜想 :每个 4连通线图均是 Hamilton图     

取代氧化吡啶气相质子化能的分子轨道法研究

在LCAO-MO-AM1水平上计算了取代氧化吡啶的气相质子化能.发现质子化能大小与取代氧化吡啶中发生质子化的氧原子上净电荷分布有较好的线性关系.△H=1228.73kJmol~(-1),qo/e为-158.98,相关系数为0.995.     

Compensatory caspase activation in MPP+-induced cell death in dopaminergic neurons

Many have hypothesized that cell death in Parkinsons disease is via apoptosis and, specifically, by the mitochondrial-mediated apoptotic pathway. We tested this hypothesis using a mouse dopaminergic cell line of mesencephalic origin, MN9D, challenged with the Parkinsonism-causing neurotoxin MPP⁺ (1-methyl-4-phenylpyridinium ion). Apoptosis was the main mode of cell death when the cells were subjected to MPP⁺ treatment under serum-free conditions for 24 h. Caspase-3 and caspase-9, however, were not activated, thus indicating the existence of alternate or compensatory cell death pathway(s) in dopaminergic neuronal cells. Using caspase inhibitors, we demonstrated that these pathways involve caspase-2, –8, –6 and –7. A time-course study indicated that activation of caspase-2 and –8 occurred upstream of caspase-6 and caspase-7. Upon MPP⁺ challenge, the apoptosis-inducing factor was translocated from the mitochondria into the MN9D cytosol and nucleus. These results suggest the existence of alternative apoptotic pathways in dopaminergic neurons.Received 20 September 2004; received after revision 5 November 2004; accepted 22 November 2004     

土壤和沉积物中1,2,4-三氯苯的超声波提取

以土壤和沉积物中的1,2,4-三氯苯为研究对象,应用超声波提取并以气相色谱进行定量分析。研究结果表明：在一定的超声波处理条件下,1,2,4-三氯苯较为稳定且降解比率很小;最适宜的超声波提取条件为：超声波功率20W、提取温度35℃、提取时间60min、提取剂为石油醚-丙酮混合溶剂(体积比1：1);三种不同提取方法(索氏、振荡和超声波)相比较以超声波提取法最优;该方法的平均回收率为92．18％、变异系数0．82%、检测限0．000μg／g,可满足土壤中微量有机物定量分析要求。     

Emodin inhibits tumor cell migration through suppression of the phosphatidylinositol 3-kinase-Cdc42/Rac1 pathway

Enhanced cell migration is one of the underlying mechanisms in cancer invasion and metastasis. Therefore, inhibition of cell migration is considered to be an effective strategy for prevention of cancer metastasis. We found that emodin (3-methyl-1,6,8-trihydroxyanthraquinone), an active component from the rhizome of Rheum palmatum, significantly inhibited epidermal growth factor (EGF)- induced migration in various human cancer cell lines. In the search for the underlying molecular mechanisms, we demonstrated that phosphatidylinositol 3-kinase (PI3K) serves as the molecular target for emodin. In addition, emodin markedly suppressed EGF-induced activation of Cdc42 and Rac1 and the corresponding cytoskeleton changes. Moreover, emodin, but not LY294002, was able to block cell migration in cells transfected with constitutively active (CA)-Cdc42 and CA-Rac1 by interference with the formation of Cdc42/Rac1 and the p21-activated kinase complex. Taken together, data from this study suggest that emodin inhibits human cancer cell migration by suppressing the PI3K-Cdc42/Rac1 signaling pathway.Received 7 February 2005; received after revision 11 March 2005; accepted 18 March 2005     

A novel pattern of fast calcium oscillations points to calcium and electrical activity cross-talk in rat chromaffin cells

Slow oscillations of cytosolic calcium ion concentration – – typically originate from release by intracellular stores, but in some cell types can be triggered and sustained by Ca²⁺ influx as well. In this study we simultaneously monitored changes in and in the electrical activity of the cell membrane by combining indo-1 and patch-clamp measurements in single rat chromaffin cells. By this approach we observed a novel type of spontaneous oscillations, much faster than those previously described in these cells. These oscillations are triggered and sustained by complex electrical activity (slow action potentials and spike bursts), require Ca²⁺ influx and do not involve release from intracellular stores. The possible physiological implications of this new pathway of intracellular signalling are discussed.Received 30 July 2004; received after revision 14 October 2004; accepted 1 November 2004     

一个带羟基的C_（60）吡咯烷衍生物的合成与表征

氮气流保护下，Ｃ６０与聚甲醇和苏氨酸在干燥的甲苯中反应生成一个带羟基的Ｃ６０。吡咯烷衍生物。标题化合物用ＦＤ－ＭＳ，ＦＴ－ＩＲ，ＵＶ－ＶＩＳ和１Ｈ－ＮＭＲ进行了表征。     

Maternal influences on cardiovascular pathophysiology

Elevated blood pressure (BP) is of special clinical significance because of its association with pathophysiologies such as heart disease, renal failure, and stroke. We described the development of a protocol for use with hypertensive rats in which prepubertal exposure to a high salt (8% NaCl) diet results in a pathophysiological syndrome including rapid increase in BP, failure to maintain normal weight gain, renal damage, cerebrovascular lesions, and early mortality. These phenomena are described for the inbred spontaneously hypertensive rat (SHR), and for reciprocal F₁ hybrids of a cross between SHR and the Dahl salt-sensitive (SS/Jr) inbred strain. The study with reciprocal F₁s revealed striking effects of maternal environment on pathophysiological response to a high salt diet. F₁s nurtured by SHR mothers weighed less at 35 days of age, and after exposure to the high salt diet suffered more rapid BP increases, greater incidence of stroke, body weight loss, and mortality, than F₁s nurtured by SS/Jr dams. These results suggest that maternal mediation of the nutritional status of the animal may play an important role in determining susceptibility to elevated BP and subsequent pathophysiology associated with exposure to a high salt diet. The implication of these findings for human hypertension is briefly discussed.