基于改进OBS的iSCSI SAN

近年来,光突发交换（OBS）作为一种在目前技术条件下承载IP数据的理想光交换方案得到了广泛的关注,同时iSCSI协议的提出则为构筑以IP传输为基础的企业级存储区域网络（SAN）提供了有力的支持。在不同于传统的基于千兆以太网的iSCSI SAN网络体系的基础上,提出了一种基于改进的OBS的iSCSI SAN体系结构,通过对OBS技术进行适应性的改进,充分利用了OBS作为承载IP数据的光交换技术的高数据吞吐量的优点,以及iSCSI协议所提供的SAN与IP网络的紧密结合技术,为构筑企业级高性能IP SAN开辟了     

水泥基复合固化剂对镉和锌混合污染土的固化试验研究

为了研究水泥基复合固化剂对重金属混合污染土的固化稳定效果及其与单一重金属污染土的固化效果差别,探究锌和镉离子之间是否有协同或拮抗作用,采用水泥、石灰、粉煤灰和蒙脱石等作为复合固化剂,通过开展无侧限抗压强度试验、毒性浸出试验、X射线衍射分析（XRD）以及电镜扫描分析（SEM）,研究锌镉混合污染土在不同固化剂掺量下的强度特性与浸出毒性、pH值与浸出毒性间的关系、重金属混合污染土与单一重金属污染土的固化效果差异,并通过XRD和SEM分别对固化产物的成分和形貌进行微观分析,进而分析固化机理。试验结果表明：用生石灰、粉煤灰、海泡石、蒙脱土替代等量水泥可使固化产物的强度提高;Zn²⁺与Cd²⁺之间不存在拮抗作用,Cd²⁺的存在还会有助于Zn²⁺的固定;重金属离子的浸出浓度随浸出液pH值的增大而明显降低;固化效果好的样品相较于固化效果差的样品有更多的针状、网状等较为致密的结构。     

隐私侵犯经历对网络用户自我披露的影响机制

网络用户的自我披露对以用户生成内容为业务基础的互联网企业具有战略意义.然而,隐私侵犯事件层出不穷.如何鼓励有隐私侵犯经历的用户持续披露个人信息对互联网企业至关重要.采用系统性随机分层抽样,结合代理理论和社会契约理论构建模型,研究了隐私侵犯经历对自我披露的作用机制.结果表明,隐私侵犯经历对自我披露意愿具有直接效应和间接效应:隐私侵犯经历与自我披露意愿之间存在强烈负向关系,并通过影响网络用户对隐私政策、隐私保护技术、行业自律和法律执行的有效性感知影响自我披露意愿.本研究阐明了隐私侵犯经历对自我披露的具体作用机制,为互联网企业鼓励有隐私侵犯经历的用户持续披露个人信息提供可操作性建议.     

激光治疗肿瘤的计算研究

根据激光治疗肿瘤的机理建立了激光治疗肿瘤的理论计算模型,并应用有限元计算方法对双光纤照射椭球形肿瘤组织的模型进行了定量计算研究;研究结果表明,对于长轴为2.0 cm、短轴为1.2 cm的实心椭球形肿瘤体,将2个直径为0.4 mm的球状光纤对称放置在主轴上相距0.8~1.0 cm的范围内,可以使光动力学的效果和热疗的效果同时达到最佳值。     

关于Smarandache函数的一个猜想

对于正整数a,设S(a)是Smarandache函数。利用有关Goldbach猜想的结果证明了:对于任何正整数k,方程S(x1) S(x2) … S(xk)=S(x1 x2 … xk)都有无穷多组正整数解(x1,x2,…,xk).     

金丝桃素抑制慢性病毒性心肌炎小鼠心肌细胞凋亡及Fas／FasL蛋白表达

目的观察金丝桃素对慢性病毒性心肌炎（VMC）小鼠心肌细胞凋亡及Fas／FasL蛋白表达的影响。方法Balb／C小鼠多次接种心肌柯萨奇段病毒复制慢性VMC模型,首次感染病毒45天后将存活小鼠分为模型组、金丝桃素组及氯沙坦组,同时设正常对照组．分别给予相应药物干预30天,采用原位末端标记法检测心肌细胞凋亡及免疫组化方法检测Fas／FasL蛋白表达。结果模型组心肌细胞凋亡率较正常组显著增加（P〈0．05）,金丝桃素组和氯沙坦组凋亡率较模型组显著降低（P〈0．05）。模型组Fas／FasL蛋白表达较正常组显著增多（P〈0．01）,金丝桃素组和氯沙坦组较模型组显著降低（P〈0．01）。结论金丝桃素保护心肌细胞与抑制VMC心肌细胞的凋亡．下调Fas／FasL蛋白表达有关。     

Basal autophagy is involved in the degradation of the ERAD component EDEM1

Little is known about the fate of machinery proteins of the protein quality control and endoplasmic reticulum(ER)-associated degradation (ERAD). We investigated the degradation of the ERAD component EDEM1, which directs overexpressed misfolded glycoproteins to degradation. Endogenous EDEM1 was studied since EDEM1 overexpression not only resulted in inappropriate occurrence throughout the ER but also caused cytotoxic effects. Proteasome inhibitors had no effect on the clearance of endogenous EDEM1 in non-starved cells. However, EDEM1 could be detected by immunocytochemistry in autophagosomes and biochemically in LC3 immuno-purified autophagosomes. Furthermore, influencing the lysosome-autophagy pathway by vinblastine or pepstatin A/E64d and inhibiting autophagosome formation by 3-methyladenine or ATGs short interfering RNA knockdown stabilized EDEM1. Autophagic degradation involved removal of cytosolic Triton X-100-insoluble deglycosylated EDEM1, but not of EDEM1-containing ER cisternae. Our studies demonstrate that endogenous EDEM1 in cells not stressed by the expression of a transgenic misfolded protein reaches the cytosol and is degraded by basal autophagy. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users. Received 15 January 2009; received after revision 16 February 2009; accepted 17 February 2009 V. Le Fourn, K. Gaplovska-Kysela: These authors equally contributed to this work.     

The Documentary Real: Thinking Documentary Aesthetics

In this article we consider the growing interest in recent years in the use of documentary strategies in the wold of contemporary art, film and performing arts and explore some of the central epistemological assumptions underpinning the persistent idea that the documentary should be equated with ‘non-fiction’. Following Stella Bruzzi we argue that if documentary theory maintains objectivity as the primary measure of value, it will inevitably and continuously arrive at the conclusion that the documentary genre is fundamentally flawed. Instead, we propose to move beyond the ‘realist epistemology’ of documentary theory and focus on the ‘documentary real’, i.e. the specific performativity of the reality constructed in and by the documentary genre. In the last paragraphs, we introduce the various articles that address the “documentary real” in this special issue.     

Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis

Atopic disease, including atopic dermatitis (eczema), allergy and asthma, has increased in frequency in recent decades and now affects approximately 20% of the population in the developed world. Twin and family studies have shown that predisposition to atopic disease is highly heritable. Although most genetic studies have focused on immunological mechanisms, a primary epithelial barrier defect has been anticipated. Filaggrin is a key protein that facilitates terminal differentiation of the epidermis and formation of the skin barrier. Here we show that two independent loss-of-function genetic variants (R510X and 2282del4) in the gene encoding filaggrin (FLG) are very strong predisposing factors for atopic dermatitis. These variants are carried by approximately 9% of people of European origin. These variants also show highly significant association with asthma occurring in the context of atopic dermatitis. This work establishes a key role for impaired skin barrier function in the development of atopic disease.     

Irf6 is a key determinant of the keratinocyte proliferation-differentiation switch

The epidermis is a highly organized structure, the integrity of which is central to the protection of an organism. Development and subsequent maintenance of this tissue depends critically on the intricate balance between proliferation and differentiation of a resident stem cell population; however, the signals controlling the proliferation-differentiation switch in vivo remain elusive. Here, we show that mice carrying a homozygous missense mutation in interferon regulatory factor 6 (Irf6), the homolog of the gene mutated in the human congenital disorders Van der Woude syndrome and popliteal pterygium syndrome, have a hyperproliferative epidermis that fails to undergo terminal differentiation, resulting in soft tissue fusions. We further demonstrate that mice that are compound heterozygotes for mutations in Irf6 and the gene encoding the cell cycle regulator protein stratifin (Sfn; also known as 14-3-3sigma) show similar defects of keratinizing epithelia. Our results indicate that Irf6 is a key determinant of the keratinocyte proliferation-differentiation switch and that Irf6 and Sfn interact genetically in this process.