一定条件下PA序列部分和的完全收敛性

根据PA序列的一些基本性质和定理,比照独立随机变量下的结论,对PA序列的完全收敛性作了初步的推导和论证,从而完善了相关结果.     

关于随机序列的若干强大数定律

设{,ξ1ξ,…,nξ,n≥1}是一随机序列,且{nξ,n≥1}<.ξ利用鞅差序列几乎处处收敛定理,给出受控随机序列的若干强大数定律.     

探讨积分的极限

证明了若可积函数列{fn}在[a,b]上一致收敛,则nl→im∞∫abfn(x)dx中极限运算与积分运算可交换,从而揭示了"积分的极限"解法的内在本质,并且对于limn→∞∫01xnF(x)dx及nl→im∞∫ab[f(x)]ndx两种类型给出了更为具体有效的一般性解法.     

Adams谱序列中的非平凡积(γ)s+3g0

利用Adams谱序列,May谱序列和上纤维序列等工具,并以某些相对低维的Ext群的结果为基础,具体地计算了Ext群中的某些元的第一阶数与第二阶数,并由此得出在Adams谱序列中乘积(γ)s 3g0∈Exts 5,(s 3)p2q (s 3)pq (s 3)q s-A(Zp,Zp)非平凡,并且收敛到π*S中的非平凡的P阶元素,其中p≥7的奇数,O≤s相似文献   

求周期序列线性复杂度的快速算法

基于有限域GF(q)上的分圆多项式理论,提出和证明了求周期为qnpm的GF(q)上序列的线性复杂度和极小多项式的一个快速算法,这里p与q均为素数,且q是模p2的本原根.该算法既推广了求周期为pm的GF(q)上周期序列的线性复杂度的一个快速算法,也推广了求周期为2npm的二元周期序列的线性复杂度的一个快速算法.     

基于灰色理论的主观信任计算方法

通过讨论传统信任模型和信任计算,提出了以灰色系统理论为基础的灰序白化评估算法.方法的基本原理是:以主体的网上交易额为参考序列,由客体对主体的关键属性评分构成计算序列,得出主体的信任水平序列,根据灰关联分析计算灰关联信任空间,求出序化点列,作序化点列图,得出白度序列,最后按照灰序白化分析得出主体的关键属性对主体的信任水平的影响次序.该算法克服了传统分析中将主体的关键属性对主体信任水平的影响大小视为相等的做法,具有评价可靠,可操作性强,适合软件自动处理等特点,在开放式环境中具有广阔的应用前景.     

一类低相关序列

给出一类d型函数,用该函数构造出了一类低相关序列集.这类序列集的周期为2n-1,集合中序列的条数为2n,其中n=4m 2.证明了其非平凡相关值只取以下4个值{-1,±2n/2-1,2n/2 1-1}.     

Taming theory with thought experiments: Understanding and scientific progress

I claim that one way thought experiments contribute to scientific progress is by increasing scientific understanding. Understanding does not have a currently accepted characterization in the philosophical literature, but I argue that we already have ways to test for it. For instance, current pedagogical practice often requires that students demonstrate being in either or both of the following two states: 1) Having grasped the meaning of some relevant theory, concept, law or model, 2) Being able to apply that theory, concept, law or model fruitfully to new instances. Three thought experiments are presented which have been important historically in helping us pass these tests, and two others that cause us to fail. Then I use this operationalization of understanding to clarify the relationships between scientific thought experiments, the understanding they produce, and the progress they enable. I conclude that while no specific instance of understanding (thus conceived) is necessary for scientific progress, understanding in general is.     

Structural characterization of two papaya chitinases, a family GH19 of glycosyl hydrolases

Two chitinases, able to use tetra-N-acetylglucosamine, chitin and chitosan as substrates, were characterized after purification from Carica papaya latex. The complete amino acid sequence of the major form and about 40% of the minor one were determined through proteolytic digestions and mass spectroscopy analysis. Sequencing demonstrated that both papaya chitinases are members of the family 19 of glycosyl hydrolases (GH19). Based on the known 3-D structures of other members of family GH19, it was expected that papaya chitinases would adopt all-alpha structures. However, circular dichroism and infrared spectroscopy indicated, for the papaya chitinases, a content of 15–20% of extended structures besides the expected 40% of alpha helices. Since the fully sequenced papaya chitinase contains a large number of proline residues the possibility that papaya chitinase contains polyproline II stretches was examined in the context of their resistance against proteolytic degradation. Received 11 July 2006; received after revision 13 October 2006; accepted 25 October 2006     

Glycogen synthase kinase 3β and Alzheimer’s disease: pathophysiological and therapeutic significance

Alzheimer’s disease (AD) is a neurodegenerative disorder associated with cognitive and behavioral dysfunction and is the leading cause of dementia in the elderly. Several studies have implicated molecular and cellular signaling cascades involving the serine-threonine kinase, glycogen synthase kinase β(GSK-3β) in the pathogenesis of AD. GSK-3β may play an important role in the formation of neurofibrillary tangles and senile plaques, the two classical pathological hallmarks of AD. In this review, we discuss the interaction between GSK-3β and several key molecules involved in AD, including the presenilins, amyloid precursor protein, tau, and β-amyloid. We identify the signal transduction pathways involved in the pathogenesis of AD, including Wnt, Notch, and the PI3 kinase/Akt pathway. These may be potential therapeutic targets in AD. Received 19 December 2005; received after revision 24 January 2006; accepted 6 February 2006