关于Pell方程x~2－2y~2＝1和y~2－Dz~2＝4的公解

本文证明了Ｐｅｌｌ方程ｘ２－２ｙ２＝１和ｙ２－Ｄｚ２＝４，当Ｄ＝２ｐ或２ｐｑ，其中ｐ，ｑ为互异奇素数时有唯一的非平凡解ｘ＝９９，ｙ＝７０，ｚ＝１２（Ｄ＝２ｐ且ｐ＝１７时）。     

Fast wire segmenting algorithm considering layout density and signal integrity

A k-shortest path based algorithm considering layout density and signal integrity for good buffer candidate locations is proposed in this paper. Theoretical results for computing the maximal distance between buffers are derived under the timing, noise and slew rate constraints. By modifying the traditional uniform wire segmenting strategy and considering the impact of tile size on density penalty function, this work proposes k-shortest path algorithm to find the buffer insertion candidate locations. The experiments show that the buffers inserted can significantly optimize the design density, alleviate signal degradation, save the number of buffers inserted and the overall run time.     

CEP41 is mutated in Joubert syndrome and is required for tubulin glutamylation at the cilium

Tubulin glutamylation is a post-translational modification that occurs predominantly in the ciliary axoneme and has been suggested to be important for ciliary function. However, its relationship to disorders of the primary cilium, termed ciliopathies, has not been explored. Here we mapped a new locus for Joubert syndrome (JBTS), which we have designated as JBTS15, and identified causative mutations in CEP41, which encodes a 41-kDa centrosomal protein. We show that CEP41 is localized to the basal body and primary cilia, and regulates ciliary entry of TTLL6, an evolutionarily conserved polyglutamylase enzyme. Depletion of CEP41 causes ciliopathy-related phenotypes in zebrafish and mice and results in glutamylation defects in the ciliary axoneme. Our data identify CEP41 mutations as a cause of JBTS and implicate tubulin post-translational modification in the pathogenesis of human ciliary dysfunction.     

Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism

HIF prolyl hydroxylases (PHD1-3) are oxygen sensors that regulate the stability of the hypoxia-inducible factors (HIFs) in an oxygen-dependent manner. Here, we show that loss of Phd1 lowers oxygen consumption in skeletal muscle by reprogramming glucose metabolism from oxidative to more anaerobic ATP production through activation of a Pparalpha pathway. This metabolic adaptation to oxygen conservation impairs oxidative muscle performance in healthy conditions, but it provides acute protection of myofibers against lethal ischemia. Hypoxia tolerance is not due to HIF-dependent angiogenesis, erythropoiesis or vasodilation, but rather to reduced generation of oxidative stress, which allows Phd1-deficient myofibers to preserve mitochondrial respiration. Hypoxia tolerance relies primarily on Hif-2alpha and was not observed in heterozygous Phd2-deficient or homozygous Phd3-deficient mice. Of medical importance, conditional knockdown of Phd1 also rapidly induces hypoxia tolerance. These findings delineate a new role of Phd1 in hypoxia tolerance and offer new treatment perspectives for disorders characterized by oxidative stress.     

面向集成管理网的TMN-DCN拓扑结构设计

提出了各种网络集成管理的TMN-DCN设计方法,并举出了应用示例.TMN-DCN设备可按各个网络配置.这些设备具有网络管理功能.规模非常大的网络分配多个TMN-DCN设备.下一阶段则利用作为TMN-DCN节点的TMN-DCN设备设计TMN-DCN的布局(物理结构).     

基于移动模糊推理的DoS攻击检测方法

通过对入侵检测中模糊技术应用和移动模糊推理方法的研究,设计并实现了基于移动模糊推理的DoS攻击入侵检测系统.首先,描述了移动模糊推理方法与模糊推理步骤;其次,详细阐述了用时间差与IP地址分布变化的DoS攻击检测方法与基于移动模糊推理的攻击检测系统,创建了用于检测的模糊规则,确定网络攻击.最后,把DoS攻击工具与DARPA 98数据集作为入侵检测数据集,对基于移动模糊推理的方法与现行方法进行测试,验证了所提方法的有效性.     

Recapitulation of premature ageing with iPSCs from Hutchinson-Gilford progeria syndrome

Hutchinson-Gilford progeria syndrome (HGPS) is a rare and fatal human premature ageing disease, characterized by premature arteriosclerosis and degeneration of vascular smooth muscle cells (SMCs). HGPS is caused by a single point mutation in the lamin A (LMNA) gene, resulting in the generation of progerin, a truncated splicing mutant of lamin A. Accumulation of progerin leads to various ageing-associated nuclear defects including disorganization of nuclear lamina and loss of heterochromatin. Here we report the generation of induced pluripotent stem cells (iPSCs) from fibroblasts obtained from patients with HGPS. HGPS-iPSCs show absence of progerin, and more importantly, lack the nuclear envelope and epigenetic alterations normally associated with premature ageing. Upon differentiation of HGPS-iPSCs, progerin and its ageing-associated phenotypic consequences are restored. Specifically, directed differentiation of HGPS-iPSCs to SMCs leads to the appearance of premature senescence phenotypes associated with vascular ageing. Additionally, our studies identify DNA-dependent protein kinase catalytic subunit (DNAPKcs, also known as PRKDC) as a downstream target of progerin. The absence of nuclear DNAPK holoenzyme correlates with premature as well as physiological ageing. Because progerin also accumulates during physiological ageing, our results provide an in vitro iPSC-based model to study the pathogenesis of human premature and physiological vascular ageing.     

《庚辛玉册》：中国炼丹术在历史上的最后一部巨著

《庚辛玉册》是朱权（１３７８－１４４８年）的一部有关炼丹术的著作。西方学者琼克尔（Ｄ．Ｒ．Ｊｏｎｋｅｒ）认为这部书已经失佚。明代李时珍在《本划纲目》中多次引述此书。另外,有一些片段也散载在某些类书中。文章英译了多年来所辑得的引自此书的条文,并试从这点蛛丝马迹中探讨这部书。自从１９５８年和李约瑟博士合作研究中国炼丹术史以来,他们两人就一直注意这部书。作者数十年来访问海外学术机构多处,顺便查访此书,但还没有发现整本的《庚辛玉册》。１９９０年访问北京期间,薄树人陪作者和中山茂到北京图书馆查询此书,也无收获。今竟然读到１９９３年姚品文著《朱权研究》中有“北京图书馆有藏本”一句话。希望将来学者们能够对这部典籍做更全面的研究。     

低糖型金耳饮料口感调配研究初探

以金耳发酵液为主要原料，用木糖醇和低聚异麦芽糖作甜味剂，柠檬酸为酸味剂制成低糖型金耳饮料并进行口感调配。经正交试验，当添加木糖醇5．0％、低聚异麦芽糖3．5％、柠檬酸0．10％时产品口感较佳。且还原糖含量仅为0．52％。     

Reversing EphB2 depletion rescues cognitive functions in Alzheimer model

Amyloid-β oligomers may cause cognitive deficits in Alzheimer's disease by impairing neuronal NMDA-type glutamate receptors, whose function is regulated by the receptor tyrosine kinase EphB2. Here we show that amyloid-β oligomers bind to the fibronectin repeats domain of EphB2 and trigger EphB2 degradation in the proteasome. To determine the pathogenic importance of EphB2 depletions in Alzheimer's disease and related models, we used lentiviral constructs to reduce or increase neuronal expression of EphB2 in memory centres of the mouse brain. In nontransgenic mice, knockdown of EphB2 mediated by short hairpin RNA reduced NMDA receptor currents and impaired long-term potentiation in the dentate gyrus, which are important for memory formation. Increasing EphB2 expression in the dentate gyrus of human amyloid precursor protein transgenic mice reversed deficits in NMDA receptor-dependent long-term potentiation and memory impairments. Thus, depletion of EphB2 is critical in amyloid-β-induced neuronal dysfunction. Increasing EphB2 levels or function could be beneficial in Alzheimer's disease.