Periodic paralysis in quarter horses: a sodium channel mutation disseminated by selective breeding.

We recently reported on a linkage study within a Quarter Horse lineage segregating hyperkalaemic periodic paralysis (HYPP), an autosomal dominant condition showing potassium-induced attacks of skeletal muscle paralysis. HYPP co-segregated with the equine adult skeletal muscle sodium channel alpha subunit gene, the same gene that causes human HYPP. We now describe the Phe to Leu mutation in transmembrane domain IVS3 which courses the horse disease. This represents the first application of molecular genetics to an important horse disease, and the data will provide an opportunity for control or eradication of this condition.     

Prediction of the structure of a receptor-protein complex using a binary docking method.

To validate procedures of rational drug design, it is important to develop computational methods that predict binding sites between a protein and a ligand molecule. Many small molecules have been tested using such programs, but examination of protein-protein and peptide-protein interactions has been sparse. We were able to test such applications once the structures of both the maltose-binding protein (MBP) and the ligand-binding domain of the aspartate receptor, which binds MBP, became available. Here we predict the binding site of MBP to its receptor using a 'binary docking' technique in which two MBP octapeptide sequences containing mutations that eliminate maltose chemotaxis are independently docked to the receptor. The peptides in the docked solutions superimpose on their original positions in the structure of MBP and allow the formation of an MBP-receptor complex. The consistency of the computational and biological results supports this approach for predicting protein-protein and peptide-protein interactions.     

Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.     

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.     

用测量模态阻尼和振型的方法对复合材料薄平板进行无损质量检测

复合材料薄平板经热压制成后,都需要进行质量检测。本文探索用测量模态阻尼和振型的方法,对复合材料薄平板的制作质量进行无损检测,作为对其它昂贵的无损检测方法的补充。略述用振动方法进行无损检测的原理,测量薄平板阻尼的方法以及提高测量精度的措施。还讨论在测量薄平板阻尼时可能遇到的一些特殊问题(如非线性刚度、拍、模态密集等问题);以云母基复合材料薄平板作为例子,从测量其阻尼和振型的结果,对这种板的制作质量进行讨论。     

Host cell reactivation of ozone-treated T3 bacteriophage by different strains ofEscherichia coli

Summary Host cell reactivation capacity for ozone T3 phage was determined for differentE. coli strains deficient in one or more of the DNA repair mechanisms. The results indicate that DNA polymerase I appears to play a key role in the repair of damage produced on the DNA by ozone while thelexA gene product seems to play a minor one.This research was sponsored by the National Sciences and Engineering Council of Canada. One of us (PLH) acknowledges a scholarship from the NSERCof Canada.     

Leaning Towards Agile in 21~(st) Century

Background: During the last fifteen years there ha s been an increased drive for organisations to reduce costs. From a production po int, this has often centred on lean manufacturing and JIT waste elimination proc esses. However, in 1991, the Iaccocca Institute Bethlehem P.A commissioned a re port specifically to analyse the changing nature of the marketplace. As a result , in the following year, the Agile Manufacturing Forum was initiated and the ter m ‘agile or responsive manufacturing‘ was first intr...     

无格式设计观

当 Kjell Ekhorn 还在学校学习图形设计,Jon Forss 已在这个行业里工作了不少年头。1989年 Jon Forss 于1LeicesterPolytechnic 毕业后就在 Bath 为一家广告代理商工作,四年之后他移居伦敦为 namara 设计公司设计图书封面。五年以后,他遇到从伦敦 Centrl St.Martins 学校毕业不过两年,正以自由职业者身份从事图书封面设计、图片制作和摄影工作的 Kjell Ekhorn。两人惊讶于互相对图书封面设计的看法,一时相见恨晚,然后自然而然的开始了两人合作的NON-FORMAT 时代。