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91.
随机偏好连接图的中心极限定理   总被引:1,自引:0,他引:1       下载免费PDF全文
我们研究了一类具有随机顶点和边的随机连接图模型, 其中顶点的随机性由一个Poisson 点过程所决定, 边的随机性由一个概率连接函数所决定. 我们得到了带偏好的随机连接图模型的关于所有随机边的长度和的一个中心极限定理.  相似文献   
92.
非对称二状态量子密钥分配协议最优参量研究   总被引:5,自引:0,他引:5  
张权  张尔扬 《物理学报》2002,51(8):1684-1689
通过分析各种情况下B92量子密钥分配协议的密钥分配和安全性指标,得出采用非对称信源实现B92协议可以在不损失安全性能的前提下极大提高密钥分配的效率.系统分析了非对称B92协议参量选择与性能之间的约束关系,给出了各种情况下的最优参量,同时比较了不同情况相应的密钥分配效率和安全性指标,获得了一种实现全局最优的非对称B92密钥分配协议关键词:非对称二状态量子密钥分配协议最优参量量子密码术量子信息  相似文献   
93.
用偏压法拉第筒测量强流脉冲离子束   总被引:5,自引:3,他引:5  
 分析了偏压法拉第筒测量强流脉冲离子束的原理和影响测量准确度的主要因素,研制了一种结构简单的偏压离子法拉第筒阵列,利用该装置测量了200kV小型强流脉冲离子束源的束流密度分布,束流中心密度最大值约为170A/cm2。  相似文献   
94.
         下载免费PDF全文
Let G = (V,E) be a graph with m edges. For reals p ∈ [0, 1] and q = 1- p, let mp(G) be the minimum of qe(V1) +pe(V2) over partitions V = V1V2, where e(Vi) denotes the number of edges spanned by Vi. We show that if mp(G) = pqm-δ, then there exists a bipartition V1, V2 of G such that e(V1) ≤ p2m - δ + pm/2 + o(√m) and e(V2) ≤ q2m - δ + qm/2 + o(√m) for δ = o(m2/3). This is sharp for complete graphs up to the error term o(√m). For an integer k ≥ 2, let fk(G) denote the maximum number of edges in a k-partite subgraph of G. We prove that if fk(G) = (1 - 1/k)m + α, then G admits a k-partition such that each vertex class spans at most m/k2 - Ω(m/k7.5) edges for α = Ω(m/k6). Both of the above improve the results of Bollobás and Scott.  相似文献   
95.
A new fluorescent probe for the selective detection of industrially important peracetic acid (PAA) was developed via oxidative cleavage of the phenylselenyl ether derivative of the 4-hydroxynaphthalimide. The probe showed no noticeable changes towards common oxidants and environmentally relevant metal ions and anions. Furthermore, PAA signaling was not influenced by the presence of background ionic species, except for certain redox-active species. Practical application of the probe to the determination of PAA in tap water and atmosphere was successfully executed using a smartphone as a stand-alone signal capturing and processing device.  相似文献   
96.
    
A series of novel synthetic substituted benzo[d]oxazole-based derivatives (5a–5v) exerted neuroprotective effects on β-amyloid (Aβ)-induced PC12 cells as a potential approach for the treatment of Alzheimer’s disease (AD). In vitro studies show that most of the synthesized compounds were potent in reducing the neurotoxicity of Aβ25-35-induced PC12 cells at 5 μg/mL. We found that compound 5c was non-neurotoxic at 30 μg/mL and significantly increased the viability of Aβ25-35-induced PC12 cells at 1.25, 2.5 and 5 μg/mL. Western blot analysis showed that compound 5c promoted the phosphorylation of Akt and glycogen synthase kinase (GSK-3β) and decreased the expression of nuclear factor-κB (NF-κB) in Aβ25-35-induced PC12 cells. In addition, our findings demonstrated that compound 5c protected PC12 cells from Aβ25-35-induced apoptosis and reduced the hyperphosphorylation of tau protein, and decreased the expression of receptor for AGE (RAGE), β-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1), inducible nitric oxide synthase (iNOS) and Bcl-2-associated X protein/B-cell lymphoma 2 (Bax/Bcl-2) via Akt/GSK-3β/NF-κB signaling pathway. In vivo studies suggest that compound 5c shows less toxicity than donepezil in the heart and nervous system of zebrafish.  相似文献   
97.
    
Abundant phosphorylation events control the activity of nuclear proteins involved in gene regulation and DNA repair. These occur mostly on disordered regions of proteins, which often contain multiple phosphosites. Comprehensive and quantitative monitoring of phosphorylation reactions is theoretically achievable at a residue-specific level using 1H-15N NMR spectroscopy, but is often limited by low signal-to-noise at pH>7 and T>293 K. We have developed an improved 13Cα-13CO correlation NMR experiment that works equally at any pH or temperature, that is, also under conditions at which kinases are active. This allows us to obtain atomic-resolution information in physiological conditions down to 25 μm . We demonstrate the potential of this approach by monitoring phosphorylation reactions, in the presence of purified kinases or in cell extracts, on a range of previously problematic targets, namely Mdm2, BRCA2, and Oct4.  相似文献   
98.
    
Cell cycle kinases represent an important component of the cell machinery that controls signal transduction involved in cell proliferation, growth, and differentiation. Nek2 is a mitotic Ser/Thr kinase that localizes predominantly to centrosomes and kinetochores and orchestrates centrosome disjunction and faithful chromosomal segregation. Its activity is tightly regulated during the cell cycle with the help of other kinases and phosphatases and via proteasomal degradation. Increased levels of Nek2 kinase can promote centrosome amplification (CA), mitotic defects, chromosome instability (CIN), tumor growth, and cancer metastasis. While it remains a highly attractive target for the development of anti-cancer therapeutics, several new roles of the Nek2 enzyme have recently emerged: these include drug resistance, bone, ciliopathies, immune and kidney diseases, and parasitic diseases such as malaria. Therefore, Nek2 is at the interface of multiple cellular processes and can influence numerous cellular signaling networks. Herein, we provide a critical overview of Nek2 kinase biology and discuss the signaling roles it plays in both normal and diseased human physiology. While the majority of research efforts over the last two decades have focused on the roles of Nek2 kinase in tumor development and cancer metastasis, the signaling mechanisms involving the key players associated with several other notable human diseases are highlighted here. We summarize the efforts made so far to develop Nek2 inhibitory small molecules, illustrate their action modalities, and provide our opinion on the future of Nek2-targeted therapeutics. It is anticipated that the functional inhibition of Nek2 kinase will be a key strategy going forward in drug development, with applications across multiple human diseases.  相似文献   
99.
    
Pain is an essential modality of sensation in the body. Purinergic signaling plays an important role in nociceptive pain transmission, under both physiological and pathophysiological conditions, and is important for communication between both neuronal and non-neuronal cells. Microglia and astrocytes express a variety of purinergic effectors, and a variety of receptors play critical roles in the pathogenesis of neuropathic pain. In this review, we discuss our current knowledge of purinergic signaling and of the compounds that modulate purinergic transmission, with the aim of highlighting the importance of purinergic pathways as targets for the treatment of persistent pain.  相似文献   
100.
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