个人计算机的发展趋势是用记录针代替键盘

合众国际社9月30日报道,第一台用记录针代替键盘的个人计算机在一年前首次在美国推出,但美国计算机业都关心这个发展趋势。这种计算机是用笔一般的记录针(sty-lus)代替标准的键盘。使用者只需用这种笔在计算机屏板上书写指令即可使计算机工作。美国几家大计算机公司都在研制这种计算机,日本的索尼和佳能公司也在研制,索尼已经在日本推出原型产品。美国研制这种计算机的软件公司博兰国际公司的总经理菲利普·卡恩说,现在美国国内经常使用个人计算机的有500万到1000万人,如果个人计算机使用法简化为用记录笔书写指令,使用者会增加到3000万至     

个人电脑的未来之路

随着PC相关软硬件技术的不断发展和通讯技术与计算机技术一体化趋势的日益明晰,PC的功能将在越来越广泛的领域向着纵深方向延伸,PC的未来之路将朝着智能化、网络化和个性化方向继续发展。更“聪明”的PC(智能之路):目前的PC正在数以亿计普通用户的案头充任着     

宁波磁性材料行业发展的若干思考和对策

随着世界高新技术产业的迅速发展，磁性材料特别是以钕铁硼为代表的永磁材料无疑是新材料行业中前景看好、增长速度最快的佼佼者。宁波作为中国钕铁硼稀土永磁材料产业化生产的发源地和国内目前最大的生产基地和销售集散地，业已形成独具区域特色和优势的产业集群，是宁波高新技术产业中为数不多、特色突出、国内竞争优势明显的支柱行业之一。中国已经加入世界贸易组织（WTO），这意味着我们许多行业和企业要与世界行业巨头强手同场竞技、一比高低，挑战的严峻性和竞争的严酷性不言自明。面对挑战和竞争，也并不意味着我们将毫无作为、坐…     

在醋酸介质中合成二氯乙二胺合铂（Ⅱ）

按文献[1]合成cis-PtenCl_2的操作条件很难控制,因产品中含有紫色的[Pt(en)_2][PtCl_4]等副产物,必须在液氨中分离提纯,产率仅68.1%。本文提出了一种在醋酸介质中合成cis—PtenCl_2的新方法。工艺简单,操作方便,产品质量高,产率可达90.4%。这项研究对促进铂系化合物的合成具有积极意义。     

β—环糊精与邻,对氨基苯甲酸包结物诱导圆二色性的情况

探讨了β—环糊精与氨基苯甲酸包结物的诱导圆二色性。β—CD_x主体分子不对称场诱导了非手性客体分子,使其产生了ICD谱。若客体分子被极化的电子跃迁方向沿客体分子长轴时得到正的ICD信号;否则得到负的ICD信号。其包结物的旋转强度可用Kirkwood—Tinoco方程近似求得。     

浅析建筑工程保修金、保修费用、保修义务的管理

本文介绍了建筑工程保修金、保修费用、保修义务的管理。     

Lymphatic reprogramming of blood vascular endothelium by Kaposi sarcoma-associated herpesvirus

Kaposi sarcoma is considered a neoplasm of lymphatic endothelium infected with Kaposi sarcoma-associated herpesvirus. It is characterized by the expression of lymphatic lineage-specific genes by Kaposi sarcoma tumor cells. Here we show that infection of differentiated blood vascular endothelial cells with Kaposi sarcoma-associated herpesvirus leads to their lymphatic reprogramming; induction of approximately 70% of the main lymphatic lineage-specific genes, including PROX1, a master regulator of lymphatic development; and downregulation of blood vascular genes.     

The knockout mouse project

Mouse knockout technology provides a powerful means of elucidating gene function in vivo, and a publicly available genome-wide collection of mouse knockouts would be significantly enabling for biomedical discovery. To date, published knockouts exist for only about 10% of mouse genes. Furthermore, many of these are limited in utility because they have not been made or phenotyped in standardized ways, and many are not freely available to researchers. It is time to harness new technologies and efficiencies of production to mount a high-throughput international effort to produce and phenotype knockouts for all mouse genes, and place these resources into the public domain.     

A critical role for the protein tyrosine phosphatase receptor type Z in functional recovery from demyelinating lesions

Several lines of evidence suggest that tyrosine phosphorylation is a key element in myelin formation, differentiation of oligodendrocytes and Schwann cells, and recovery from demyelinating lesions. Multiple sclerosis is a demyelinating disease of the human central nervous system, and studies of experimental demyelination indicate that remyelination in vivo requires the local generation, migration or maturation of new oligodendrocytes, or some combination of these. Failure of remyelination in multiple sclerosis could result from the failure of any of these processes or from the death of oligodendrocytes. Ptprz encodes protein tyrosine phosphatase receptor type Z (Ptpz, also designated Rptpbeta), which is expressed primarily in the nervous system but also in oligodendrocytes, astrocytes and neurons. Here we examine the susceptibility of mice deficient in Ptprz to experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. We observe that mice deficient in Ptprz show impaired recovery from EAE induced by myelin oligodendrocyte glycoprotein (MOG) peptide. This sustained paralysis is associated with increased apoptosis of mature oligodendrocytes in the spinal cords of mutant mice at the peak of inflammation. We further demonstrate that expression of PTPRZ1, the human homolog of Ptprz, is induced in multiple sclerosis lesions and that the gene is specifically expressed in remyelinating oligodendrocytes in these lesions. These results support a role for Ptprz in oligodendrocyte survival and in recovery from demyelinating disease.