通用特征函数的性质

从通用特征函数的集合表示出发,运用集合方法论证了通用特征函数的三个重要性质,从而进一步揭示了通用特征函数的本质.     

关于在2—距离空间中集值映射不动点(续)

本文系上篇论文[3]的续篇。在其中,进一步论述了2—距离空间中集值映射不动点的一系列结果。     

HoBa2Cu3Ox的超导电性

通过交流磁化率和X-ray衍射分析，对用固态反应法制备的HoBa2Cu3Ox超导体的超导电性进行了研究．实验结果表明：随淬火温度的升高．由正交相(123相)向介于正交和四方相之间的过渡相变化；超导转变温度Tc(0)(零场下)从90K降到38．5K；交流磁化率虚部峰值温Tp(H)随附加直流磁场的增加而降低，Tp与Hdc之间的关系偏离[1一Tp(H)／丁(0)]∞H^2/3规律．     

Simulation of Weld Depth in A-TIG Welding with Unified Arc-electrode model

Ｉｔｋｎｏｗｎｔｈａｔｓｍａｌｌａｍｏｕｎｔｓｏｆｆｌｕｘｏｎｔｈｅｓｕｒｆａｃｅｏｆｓｔａｉｎｌｅｓｓｓｔｅｅｌｃａｎｉｎｃｒｅａｓｅｔｈｅｄｅｐｔｈｏｆｗｅｌｄｐｅｎｅ ｔｒａｔｉｏｎｉｎＴＩＧｗｅｌｄｉｎｇｂｙａｆａｃｔｏｒｏｆｔｈｒｅｅ[1] .Ｔｈｉｓｐｒｏｃｅｓｓｉｓｒｅｆｅｒｒｅｄｔｏａｓ”ＡＴＩＧ”ｏｒＴＩＧｗｅｌｄｉｎｇａｃｔｉ ｖａｔｅｄｂｙｆｌｕｘ .Ｔｈｅｒｅｈａｖｅｂｅｅｎｔｈｒｅｅｐｕｂｌｉｓｈｅｄｐｈｙｓ ｉｃａｌｍｅｃｈａｎｉｓｍｓｔｈａｔａｒｅｐｏｓｓｉｂｌｅｃｏｎｔｒｉ…     

The gene encoding ganglioside-induced differentiation-associated protein 1 is mutated in axonal Charcot-Marie-Tooth type 4A disease.

We identified three distinct mutations and six mutant alleles in GDAP1 in three families with axonal Charcot-Marie-Tooth (CMT) neuropathy and vocal cord paresis, which were previously linked to the CMT4A locus on chromosome 8q21.1. These results establish the molecular etiology of CMT4A (MIM 214400) and suggest that it may be associated with both axonal and demyelinating phenotypes.     

Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1.

Neurofibromatosis type I (NF1) is one of the most common single-gene disorders that causes learning deficits in humans. Mice carrying a heterozygous null mutation of the Nfl gene (Nfl(+/-) show important features of the learning deficits associated with NF1 (ref. 2). Although neurofibromin has several known properties and functions, including Ras GTPase-activating protein activity, adenylyl cyclase modulation and microtubule binding, it is unclear which of these are essential for learning in mice and humans. Here we show that the learning deficits of Nf1(+/-) mice can be rescued by genetic and pharmacological manipulations that decrease Ras function. We also show that the Nf1(+/-) mice have increased GABA (gamma-amino butyric acid)-mediated inhibition and specific deficits in long-term potentiation, both of which can be reversed by decreasing Ras function. Our results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition. Our findings have implications for the development of treatments for learning deficits associated with NF1.     

The failing heart.

Cardiomyopathies are disorders affecting heart muscle that usually result in inadequate pumping of the heart. They are the most common cause of heart failure and each year kill more than 10,000 people in the United States. In recent years, there have been breakthroughs in understanding the molecular mechanisms involved in this group of conditions, with knowledge of the genetic basis for cardiomyopathies perhaps seeing the largest advance, enabling clinicians to devise improved diagnostic strategies and preparing the stage for new therapies.     

奇特的地转偏向力

地转偏向力是地理教学特别是中学地理教学一大难题。本文就从一个简单的实验入手,分析地转偏向力的产生和实质;并试图利用初等数学(或物理)的方法,求算地转偏向力的大小和方向。最后给出其应用两例。     

Function of DnaJ and DnaK as chaperones in origin-specific DNA binding by RepA

Heat-shock proteins are normal constituents of cells whose synthesis is increased on exposure to various forms of stress. They are interesting because of their ubiquity and high conservation during evolution. Two families of heat-shock proteins, hsp60s and hsp70s, have been implicated in accelerating protein folding and oligomerization and also in maintaining proteins in an unfolded state, thus facilitating membrane transport. The Escherichia coli hsp70 analogue, DnaK, and two other heat-shock proteins, DnaJ and GrpE, are required for cell viability at high temperatures and are involved in DNA replication of phage lambda and plasmids P1 and F. These three proteins are involved in replication in vitro of P1 DNA along with many host replication proteins and the P1 RepA initiator protein. RepA exists in a stable protein complex with DnaJ containing a dimer each of RepA and DnaJ. We report here that DnaK and DnaJ mediate an alteration in the P1 initiator protein, rendering it much more active for oriP1 DNA binding.     

Abnormal pattern detected in fragile-X patients by pulsed-field gel electrophoresis.

The fragile-X syndrome is the most frequent inherited form of mental retardation, with an incidence of 1 in 1,500 males. It is characterized by the presence of a fragile site at Xq27.3 induced in vitro by folate deprivation or by inhibitors of deoxynucleotide synthesis. Its mode of inheritance is unusual for an X-linked trait, with incomplete penetrance in both males and females. Some phenotypically normal males transmit the mutation to all their daughters who rarely express any symptoms, but penetrance is high in sons and daughters of these carrier women. Genetic and physical mapping of the Xq27-q28 region has confirmed that the disease locus is located at or very near the fragile site. Hypotheses proposed to account for the abnormalities in the inheritance of the disease include sequence rearrangements by meiotic recombination or a mutation that affects reactivation of an inactive X chromosome during differentiation of female germ cells. To detect such rearrangements, or methylation changes that may reflect a locally inactive X chromosome, we used pulsed-field gel analysis of DNA from fragile-X patients with probes close to the fragile-X locus. The probe Do33 (DXS465) detected abnormal patterns in fragile-X patients, but not in normal controls or in non-expressing male transmitters.