Kinanthropometry Study of the Physique of Hong Kong and the Interior of China Correctional Services Recruits

In this paper,the physique of the Hong Kong Correc-tional Services recruits were identified and reported.Kinanthropometry has been applied in the study of Olympic athletes and researchers concluded that specificsports were correlated with a specific type of physique.Athletes involved in the same sports have a similar phys-ique as well as body shape.Gold medal winners could beidentified by their specific type of body shape.And ath-letes in different sport have different and specific bodyshape.Hence,by applying kinanthropometry study,people in different occupations could be identified by their specific body shape and physique.The finalisedbody shape can be used as reference in the vetting stan-dards.The somatotyping and anthropometric input canbe used to improve the uniform sizing system.     

平面图与面的并区域

Ｓａｃｈｓ,Ｋｏｚｙｒｅｖ和Ｇｒｉｎｂｅｒ,指出平面图。有Ｈａｍｌｉｔｏｎ圈的一个必要条件是∑ｓｕｍ　ｆｒｏｍｉ＝３（ｉ－２）φ_ｉ＝∑ｓｕｍｆｒｏｍｉ＝３（ｉ－ ２）φ＇_ｉ＝ｎ－２,其中φ_ｉ和φ＇_ｉ分别为Ｈａｍｉｌｔｏｎ 圈内、外度为ｉ的面数．本文探讨面的度相等的平面图的面数,面并成顶点在边界上的连通区域与 Ｈａｍｉｌｔｏｎ 圈．     

A complex of Shc and Ran-GTPase localises to the cell nucleus

The three isoforms of the adaptor protein Shc play diverse roles in cell signalling. For example, the observation of p46 Shc in the nuclei of hepatocellular carcinoma cells suggests a function quite distinct from the better characterised cytoplasmic role. Ligands responsible for the transport of various Shc isoforms into organelles such as the nucleus have yet to be reported. To identify such ligands a far western approach was used to determine the p52 Shc interactome. The Ran-GTPase nuclear transport protein was identified and found to bind to p52 Shc in vitro with low micromolar affinity. Co-immunoprecipitation, pull down and fluorescence lifetime imaging microscopy experiments in stable cells confirmed cellular interaction and nuclear localisation. The nuclear transport factor protein NTF2, which functions in cohort with Ran, was shown to form a complex with both RAN and Shc, suggesting a mechanism for Shc entry into the nucleus as part of a tertiary complex. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users. Received 20 October 2008; received after revision 04 December 2008; accepted 15 December 2008     

Exome sequencing identifies frequent mutation of ARID1A in molecular subtypes of gastric cancer

Gastric cancer is a heterogeneous disease with multiple environmental etiologies and alternative pathways of carcinogenesis. Beyond mutations in TP53, alterations in other genes or pathways account for only small subsets of the disease. We performed exome sequencing of 22 gastric cancer samples and identified previously unreported mutated genes and pathway alterations; in particular, we found genes involved in chromatin modification to be commonly mutated. A downstream validation study confirmed frequent inactivating mutations or protein deficiency of ARID1A, which encodes a member of the SWI-SNF chromatin remodeling family, in 83% of gastric cancers with microsatellite instability (MSI), 73% of those with Epstein-Barr virus (EBV) infection and 11% of those that were not infected with EBV and microsatellite stable (MSS). The mutation spectrum for ARID1A differs between molecular subtypes of gastric cancer, and mutation prevalence is negatively associated with mutations in TP53. Clinically, ARID1A alterations were associated with better prognosis in a stage-independent manner. These results reveal the genomic landscape, and highlight the importance of chromatin remodeling, in the molecular taxonomy of gastric cancer.     

Epigenetic identification of receptor tyrosine kinase-like orphan receptor 2 as a functional tumor suppressor inhibiting β-catenin and AKT signaling but frequently methylated in common carcinomas

Through subtraction of tumor-specific CpG methylation, we identified receptor tyrosine kinase-like orphan receptor 2 (ROR2) as a candidate tumor suppressor gene (TSG). ROR2 is a specific receptor or co-receptor for WNT5A, involved in canonical and non-canonical WNT signaling, with its role in tumorigenesis controversial. We characterized its functions and related cell signaling in common carcinomas. ROR2 was frequently silenced by promoter CpG methylation in multiple carcinomas including nasopharyngeal, esophageal, gastric, colorectal, hepatocellular, lung, and breast cancers, while no direct correlation of ROR2 and WNT5A expression was observed. Ectopic expression of ROR2 resulted in tumor suppression independent of WNT5A status, through inhibiting tumor cell growth and inducing cell cycle arrest and apoptosis. ROR2 further suppressed epithelial-mesenchymal transition and tumor cell stemness through repressing β-catenin and AKT signaling, leading to further inhibition of tumor cell migration/invasion and increased chemo-sensitivity. Thus ROR2, as an epigenetically inactivated TSG, antagonizes both β-catenin and AKT signaling in multiple tumorigenesis. Its epigenetic silencing could be a potential tumor biomarker and therapeutic target for carcinomas.     

Influenza infection induces host DNA damage and dynamic DNA damage responses during tissue regeneration

Influenza viruses account for significant morbidity worldwide. Inflammatory responses, including excessive generation of reactive oxygen and nitrogen species (RONS), mediate lung injury in severe influenza infections. However, the molecular basis of inflammation-induced lung damage is not fully understood. Here, we studied influenza H1N1 infected cells in vitro, as well as H1N1 infected mice, and we monitored molecular and cellular responses over the course of 2 weeks in vivo. We show that influenza induces DNA damage to both, when cells are directly exposed to virus in vitro (measured using the comet assay) and also when cells are exposed to virus in vivo (estimated via γH2AX foci). We show that DNA damage, as well as responses to DNA damage persist in vivo until long after virus has been cleared, at times when there are inflammation associated RONS (measured by xanthine oxidase activity and oxidative products). The frequency of lung epithelial and immune cells with increased γH2AX foci is elevated in vivo, especially for dividing cells (Ki-67-positive) exposed to oxidative stress during tissue regeneration. Additionally, we observed a significant increase in apoptotic cells as well as increased levels of DNA double strand break (DSB) repair proteins Ku70, Ku86 and Rad51 during the regenerative phase. In conclusion, results show that influenza induces DNA damage both in vitro and in vivo, and that DNA damage responses are activated, raising the possibility that DNA repair capacity may be a determining factor for tissue recovery and disease outcome.     

基于AlN压电层的薄膜体声波谐振器

以AlN薄膜为压电层,采用体硅微细加工工艺制备背空腔型结构薄膜体声波谐振器.材料测试结果表明,在优化溅射工艺下沉积的AlN薄膜具有(002)择优取向及良好的柱状晶结构.扫描电镜表征结果证实所制得空腔背部平滑且各向异性较好.用网络分析仪测试可知,所制得的谐振器具有较好的频率特性:谐振频率为2.537 GHz,机电耦合系数3.75%,串、并联品质因数分别为101.8、79.7.     

一种改进的iTrace技术的研究

针对现有ICMP反向追踪方法中iTrace信息标记的IP地址或相关信息,导致重构完整攻击路径需要过多的数据包,并且计算量大的问题,提出了在iTrace分组中重新编码的方案。该方案可在较短的时间内推算出主要攻击路径,显著减少路径重构时对数据包的需求量,从而可以使受害者更快捷地追踪到攻击源,为受害者尽快响应攻击、减少攻击带来的损失创造了条件。     

关于Kuratowski十四集定理的一个注记

作者给出了Kuratowski十四集定理的又一个等价形式,并进一步证明了拓扑空间(X,τ)中的任意子集经过取内部和闭包两种运算至多可产生7个不同的集合(包含A本身)。     

Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection

Severe acute respiratory syndrome (SARS) is caused by infection of a previously undescribed coronavirus (CoV). L-SIGN, encoded by CLEC4M (also known as CD209L), is a SARS-CoV binding receptor that has polymorphism in its extracellular neck region encoded by the tandem repeat domain in exon 4. Our genetic risk association study shows that individuals homozygous for CLEC4M tandem repeats are less susceptible to SARS infection. L-SIGN is expressed in both non-SARS and SARS-CoV-infected lung. Compared with cells heterozygous for L-SIGN, cells homozygous for L-SIGN show higher binding capacity for SARS-CoV, higher proteasome-dependent viral degradation and a lower capacity for trans infection. Thus, homozygosity for L-SIGN plays a protective role during SARS infection.