The utilization of ethyl acetate vapor byDrosophila buzzatii adults

Cellular and Molecular Life Sciences - Ethyl acetate is utilizdd byDrosophila buzzatii adults under some physiological conditions, reducing mortality rate and body weight loss. Ethanol has similar...     

Study on Injection Moulding of High Precision Aspheric Plastic Lens

With the rapid development of information and multi me dia technologies, the demand for the optical plastic aspheric elements used in o pto-electronic devices, camera, optical disc and projector lens etc. has been i ncreased rapidly in the recent years. The key technologies of fabrication of asp heric plastic lens are the design and manufacturing moulds, selection of proper injection moulding equipment, and optimization of injection moulding parameters etc. In this paper, the effect of injection pressure,...     

Research on Nanofabrication Technology of Micro-/Nano-Stereo Rapid Prototyping of PCVD

At present, the most common micro/nano-scale fabri ca tion processes include the plane silicon process based on IC technology, stereo silicon process, LIGA, quasi-LIGA based on near ultra violet deep lithography, MEMS, energy beam etching and micro/nano-machining, etc. A common problem for t hese processes is the difficulty to fabricate arbitrary form for 3-dimensional micro/nano-parts, devices or mechanisms. To develop advanced MEMS manufacturin g technology, and to achieve fabrication of true 3-dimen...     

四元数矩阵方程AX=B的反问题

研究了四元数矩阵AX=B的反问题,得到了AX=B的反问题具有亚正定阵解的充要条件,以及此解存在的一般形式.     

基于DEA法的虚拟企业合作伙伴效益评价应用研究

虚拟企业合作伙伴选择是虚拟企业组建过程中的重要问题，也是一个复杂的问题。从虚拟企业合作伙伴效益评价的角度出发，在AHP(层次分析)法的基础上，给出了DEA(数据包络分析)法的C^2R模型，并结合具体企业进行了实例验证，从而证明了DEA法对于虚拟企业合作伙伴选择的科学性和有效性。     

A functional switch from lung cancer resistance to susceptibility at the Pas1 locus in Kras2LA2 mice

Pulmonary adenoma susceptibility 1 (Pas1) is the major mouse lung cancer susceptibility locus on chromosome 6 (ref. 1). Kras2 is a common target of somatic mutation in chemically induced mouse lung tumors and is a candidate Pas1 gene. M. spretus mice (SPRET/Ei) carry a Pas1 resistance haplotype for chemically induced lung tumors. We demonstrate that the SPRET/Ei Pas1 allele is switched from resistance to susceptibility by fixation of the parental origin of the mutant Kras2 allele. This switch correlates with low expression of endogenous Kras2 in SPRET/Ei. We propose that the Pas1 modifier effect is due to Kras2, and that a sensitive balance between the expression levels of wild-type and mutant alleles determines lung tumor susceptibility. These data demonstrate that cancer predisposition should also be considered in the context of somatic events and could have major implications for the design of human association studies to identify cancer susceptibility genes.     

Flow signaling and atherosclerosis

Atherosclerosis rarely develops in the region of arteries exposed to undisturbed flow (u-flow, unidirectional flow). Instead, atherogenesis occurs in the area exposed to disturbed flow (d-flow, multidirectional flow). Based on these general pathohistological observations, u-flow is considered to be athero-protective, while d-flow is atherogenic. The fact that u-flow and d-flow induce such clearly different biological responses in the wall of large arteries indicates that these two types of flow activate each distinct intracellular signaling cascade in vascular endothelial cells (ECs), which are directly exposed to blood flow. The ability of ECs to differentially respond to the two types of flow provides an opportunity to identify molecular events that lead to endothelial dysfunction and atherosclerosis. In this review, we will focus on various molecular events, which are differentially regulated by these two flow types. We will discuss how various kinases, ER stress, inflammasome, SUMOylation, and DNA methylation play roles in the differential flow response, endothelial dysfunction, and atherosclerosis. We will also discuss the interplay among the molecular events and how they coordinately regulate flow-dependent signaling and cellular responses. It is hoped that clear understanding of the way how the two flow types beget each unique phenotype in ECs will lead us to possible points of intervention against endothelial dysfunction and cardiovascular diseases.     

A regulatory mutation in IGF2 causes a major QTL effect on muscle growth in the pig

Most traits and disorders have a multifactorial background indicating that they are controlled by environmental factors as well as an unknown number of quantitative trait loci (QTLs). The identification of mutations underlying QTLs is a challenge because each locus explains only a fraction of the phenotypic variation. A paternally expressed QTL affecting muscle growth, fat deposition and size of the heart in pigs maps to the IGF2 (insulin-like growth factor 2) region. Here we show that this QTL is caused by a nucleotide substitution in intron 3 of IGF2. The mutation occurs in an evolutionarily conserved CpG island that is hypomethylated in skeletal muscle. The mutation abrogates in vitro interaction with a nuclear factor, probably a repressor, and pigs inheriting the mutation from their sire have a threefold increase in IGF2 messenger RNA expression in postnatal muscle. Our study establishes a causal relationship between a single-base-pair substitution in a non-coding region and a QTL effect. The result supports the long-held view that regulatory mutations are important for controlling phenotypic variation.     

TPX2: of spindle assembly,DNA damage response,and cancer

For more than 15 years, TPX2 has been studied as a factor critical for mitosis and spindle assembly. These functions of TPX2 are attributed to its Ran-regulated microtubule-associated protein properties and to its control of the Aurora A kinase. Overexpressed in cancers, TPX2 is being established as marker for the diagnosis and prognosis of malignancies. During interphase, TPX2 resides preferentially in the nucleus where its function had remained elusive until recently. The latest finding that TPX2 plays a role in amplification of the DNA damage response, combined with the characterization of TPX2 knockout mice, open new perspectives to understand the biology of this protein. This review provides an historic overview of the discovery of TPX2 and summarizes its cytoskeletal and signaling roles with relevance to cancer therapies. Finally, the review aims to reconcile discrepancies between the experimental and pathological effects of TPX2 overexpression and advances new roles for compartmentalized TPX2.