块体纳米材料的研究现状与发展思路

块体纳米材料的制备技术及性能研究 ,是当前纳米材料领域内的一个热点 块体纳米材料具有奇异的结构和特殊性能 ,其在力学、电学、光学和磁学等方面发生了巨大的变化 文中较为详细地介绍了国内外块状纳米材料的制备技术 针对块体纳米材料加工过程中存在热稳定性及致密性等两个主要问题进行了探讨 ,提出了通过加入第二相微粒、强烈塑性加工措施来改善块体纳米材料的热稳定性 ;采用烧结、挤压辅助工艺来提高块体纳米材料的致密性的方案     

同时实现版权保护与内容认证的半易损水印方案

提出一种基于量化的半易损水印方案,能够在不参考原图的情况下对数字图像同时进行版权保护和内容真实性认证.本文算法一方面具有较好的鲁棒性,能够在水印图像遭受攻击以后仍然检测到图像的版权,另一方面具有较好的敏感性,既允许对水印图像进行一般性处理,又能检测并反映出水印图像被篡改的区域.实验结果表明本文算法在同时保护数字图像的版权和内容真实性方面是可行的.     

Altruistic punishment in humans.

Human cooperation is an evolutionary puzzle. Unlike other creatures, people frequently cooperate with genetically unrelated strangers, often in large groups, with people they will never meet again, and when reputation gains are small or absent. These patterns of cooperation cannot be explained by the nepotistic motives associated with the evolutionary theory of kin selection and the selfish motives associated with signalling theory or the theory of reciprocal altruism. Here we show experimentally that the altruistic punishment of defectors is a key motive for the explanation of cooperation. Altruistic punishment means that individuals punish, although the punishment is costly for them and yields no material gain. We show that cooperation flourishes if altruistic punishment is possible, and breaks down if it is ruled out. The evidence indicates that negative emotions towards defectors are the proximate mechanism behind altruistic punishment. These results suggest that future study of the evolution of human cooperation should include a strong focus on explaining altruistic punishment.     

果实成熟与多聚半乳糖醛酸酶基因的研究进展

对与果实成熟相关基因多聚半乳糖醛酸酶 (PG)基因的筛选、鉴定、表达及基因工程的研究进展作一个简要评述     

非线性方程的一种区间迭代算法

把区间算法与正割算法相结合,给出了一种新的区间正割算法．并证明了其收敛性与Newton法相比,具有收敛快,误差小的优点,算例证明了其有效性．     

Ф40自由浮球式疏水阀工况分析

对自由浮球式疏水阀内浮球在开启过程中的受力情况进行了全面的分析,首次提出疏水阀开启疏水的两种不同方式。即滑动开启和滚动开启方式,并分别给出了两种不同开启方式所对应的压差合力和关闭力矩的计算公式。确定了保证此类疏水阀可靠工作的许用最高工作压力。可供此类疏水阀设计和开发参考。     

模拟移动床分离紫杉醇

以东北红豆杉树叶为原料,采用无毒、无污染的乙醇作为提取溶剂．在高分子树脂柱和模拟移动床色谱(SMBC)系统上逐级提纯紫杉醇,除去大量非紫杉烷与紫杉烷类杂质,得到了高纯度的产品、同时,对紫杉醇前处理过程中洗脱液条件,随后的SMBC系统实验中的切换时间等条件进行了优化,并总结出一套优化操作条件,为纯化紫杉醇提供了合理的工艺路线．     

Mutations in the 70K peroxisomal membrane protein gene in Zellweger syndrome.

The peroxisomal membrane protein, with a relative molecular mass of 70,000 (M(r) 70K) (PMP70), is an important component of peroxisomal membranes and an ATP-binding cassette protein. To investigate its possible involvement in Zellweger syndrome (ZS), an inborn error of peroxisome assembly, we cloned and sequenced cDNAs for human PMP70 and mapped the gene to chromosome 1. Amongst 32 probands with ZS or related disorders, we found two mutant PMP70 alleles in single ZS probands from the same complementation group. One allele has a donor splice site mutation and the second a missense mutation. Our results suggest that PMP70 plays an important role in peroxisome biogenesis and that mutations in PMP70 may be responsible for a subset of ZS patients.     

Isolation of a candidate gene for Norrie disease by positional cloning.

The gene for Norrie disease, an X-linked disorder characterized by progressive atrophy of the eyes, mental disturbances and deafness, has been mapped to chromosome Xp11.4 close to DXS7 and the monoamine oxidase (MAO) genes. By subcloning a YAC with a 640 kilobases (kb) insert which spans the DXS7-MAOB interval we have generated a cosmid contig which extends 250 kb beyond the MAOB gene. With one of these cosmids, microdeletions were detected in several patients with Norrie disease. Screening of cDNA libraries has enabled us to isolate and sequence a likely candidate gene for Norrie disease which is expressed in retina, choroid and fetal brain. No homologous sequences were found in DNA and protein databases indicating that this cDNA is part of a gene encoding a 'pioneer' protein.     

Small nuclear ribonucleoprotein polypeptide N (SNRPN), an expressed gene in the Prader-Willi syndrome critical region.

Prader-Willi syndrome (PWS) is associated with paternally derived chromosomal deletions in region 15q11-13 or with maternal disomy for chromosome 15. Therefore, loss of the expressed paternal alleles of maternally imprinted genes must be responsible for the PWS phenotype. We have mapped the gene encoding the small nuclear RNA associated polypeptide SmN (SNRPN) to human chromosome 15q12 and a processed pseudogene SNRPNP1 to chromosome region 6pter-p21. Furthermore, SNRPN was mapped to the minimal deletion interval that is critical for PWS. The fact that the mouse Snrpn gene is maternally imprinted in brain suggests that loss of the paternally derived SNRPN allele may be involved in the PWS phenotype.