基于IDS 80图形系统的液压和气动设备符号库

我们在此给出一个在意大利IDS—80图形计算机系统上实观的符号库。我们扼要地概述了该库的构造和使用方法。这个库是一个遵循机械设计统一标准UNI的标准符号库并且我们的方法(模型扩张)是新的和有价值的。     

Corpus luteum cells grown as monolayers

Zusammenfassung Die Fähigkeit der Corpus-luteum-Zellen als Monolayers zu wachsen wurde untersucht. Die von Schwein und Ratte entnommenen Gelbkörper wurden zerkleinert und mit einer 0,25% igen Trypsinlösung in eine Suspension übergeführt. Die Kulturen wurden bis zum 8. Tag beobachtet. Die wachsenden Luteinzellen zeigen die typische Form und auch die ausgeprägte Aktivität der ⁵-3-OH Steroiddehydrogenase.     

Cadherin 23 is a component of the tip link in hair-cell stereocilia

Mechanoelectrical transduction, the conversion of mechanical force into electrochemical signals, underlies a range of sensory phenomena, including touch, hearing and balance. Hair cells of the vertebrate inner ear are specialized mechanosensors that transduce mechanical forces arising from sound waves and head movement to provide our senses of hearing and balance; however, the mechanotransduction channel of hair cells and the molecules that regulate channel activity have remained elusive. One molecule that might participate in mechanoelectrical transduction is cadherin 23 (CDH23), as mutations in its gene cause deafness and age-related hearing loss. Furthermore, CDH23 is large enough to be the tip link, the extracellular filament proposed to gate the mechanotransduction channel. Here we show that antibodies against CDH23 label the tip link, and that CDH23 has biochemical properties similar to those of the tip link. Moreover, CDH23 forms a complex with myosin-1c, the only known component of the mechanotransduction apparatus, suggesting that CDH23 and myosin-1c cooperate to regulate the activity of mechanically gated ion channels in hair cells.     

Control of phyllotaxy by the cytokinin-inducible response regulator homologue ABPHYL1

Phyllotaxy describes the geometric pattern of leaves and flowers, and has intrigued botanists and mathematicians for centuries. How these patterns are initiated is poorly understood, and this is partly due to the paucity of mutants. Signalling by the plant hormone auxin appears to determine the site of leaf initiation; however, this observation does not explain how distinct patterns of phyllotaxy are initiated. abphyl1 (abph1) mutants of maize initiate leaves in a decussate pattern (that is, paired at 180 degrees), in contrast to the alternating or distichous phyllotaxy observed in wild-type maize and other grasses. Here we show that ABPH1 is homologous to two-component response regulators and is induced by the plant hormone cytokinin. ABPH1 is expressed in the embryonic shoot apical meristem, and its spatial expression pattern changes rapidly with cytokinin treatment. We propose that ABPH1 controls phyllotactic patterning by negatively regulating the cytokinin-induced expansion of the shoot meristem, thereby limiting the space available for primordium initiation at the apex.     

Spectroscopic study of the disulfide bond in oxidized glutathione

Summary Raman and circular dichroism spectra are used for obtaining structural information on the disulfide bridge in oxidized glutathione. Quantitative estimates of dihedral angles and bond angles are proposed.     

Assembling and alerting scents produced by the bedbugCimex lectularius L.

Zusammenfassung Es wird gezeigt, dass die Aggregation der Bettwanzen (Cimex lectularius) durch einen von beiden Geschlechtern abgegebenen Versammlungsduft eingeleitet wird. Letzterer ist in Methylalkohol, aber nicht in Diäthyläther löslich, verdampft bei 32°C und lockt unbegattete sowie begattete Wanzen beider Geschlechter an. Die Lockreaktion ist von der Duftmenge abhängig und bleibt bei antennenlosen Wanzen aus. Die Stinkdrüsen gereizter, respektive verletzter Bettwanzen sondern Hex-2-en-1-al und Oct-2-en-1-al als Alarmduft ab, der die Zerstreuung der Wanzengruppen hervorruft.     

Paxillin binds schwannomin and regulates its density-dependent localization and effect on cell morphology

Neurofibromatosis type 2 is an autosomal dominant disorder characterized by tumors, predominantly schwannomas, in the nervous system. It is caused by mutations in the gene NF2, encoding the growth regulator schwannomin (also known as merlin). Mutations occur throughout the 17-exon gene, with most resulting in protein truncation and undetectable amounts of schwannomin protein. Pathogenic mutations that result in production of defective schwannomin include in-frame deletions of exon 2 and three independent missense mutations within this same exon. Mice with conditional deletion of exon 2 in Schwann cells develop schwannomas, which confirms the crucial nature of exon 2 for growth control. Here we report that the molecular adaptor paxillin binds directly to schwannomin at residues 50-70, which are encoded by exon 2. This interaction mediates the membrane localization of schwannomin to the plasma membrane, where it associates with beta 1 integrin and erbB2. It defines a pathogenic mechanism for the development of NF2 in humans with mutations in exon 2 of NF2.     

Induction of dendritic spines by an extracellular domain of AMPA receptor subunit GluR2

Synaptic transmission from excitatory nerve cells in the mammalian brain is largely mediated by AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid)-type glutamate receptors located at the surface of dendritic spines. The abundance of postsynaptic AMPA receptors correlates with the size of the synapse and the dimensions of the dendritic spine head. Moreover, long-term potentiation is associated with the formation of dendritic spines as well as synaptic delivery of AMPA receptors. The molecular mechanisms that coordinate AMPA receptor delivery and spine morphogenesis are unknown. Here we show that overexpression of the glutamate receptor 2 (GluR2) subunit of AMPA receptors increases spine size and density in hippocampal neurons, and more remarkably, induces spine formation in GABA-releasing interneurons that normally lack spines. The extracellular N-terminal domain (NTD) of GluR2 is responsible for this effect, and heterologous fusion proteins of the NTD of GluR2 inhibit spine morphogenesis. We propose that the NTD of GluR2 functions at the cell surface as part of a receptor-ligand interaction that is important for spine growth and/or stability.