10,805 research outputs found

    The L-amino acid oxidase of Neurospora

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    In 1944 one of us described a D-amino acid oxidase in extracts of Neurospora crassa (1). Except for slight activity against L-glutamate, no oxidation of L-amino acids was observed. Recently a means for inducing the formation of a soluble L-amino acid oxidase by the mold was reported by Bender, Krebs, and Horowitz (2). This is accomplished by reducing the biotin content of the basal medium (3) from the 5 γ per liter usually employed to 0.25 γ per liter. When cultured in such a medium, Neurospora produces an active L-amino acid oxidase which can be demonstrated both in extracts and in the medium. Reduction of the biotin level produces no effect on the D-amino acid oxidase, which is still found in extracts but not in the culture medium. The activity of the L-oxidase toward thirty-eight amino acids has been investigated by Bender and Krebs (4). The initial purpose of the present investigation was to explore certain possibilities for a genetic study of the enzyme. Of special interest was the fact, cited by Bender et al. (a), that the oxidase could not be detected in all of the wild type strains tested. The question arose as to whether this is due to the genetic inability of certain strains to form the enzyme. In connection with the investigation of this problem a general survey of the properties of the enzyme was carried out, together with a preliminary study of the mechanism of the biotin effect and of the adaptive formation of the enzyme. The results of these studies are reported below. Simultaneously with our investigation and independently of it, Dr. K. Burton (5), working in Professor Krebs’ laboratory, has carried out a study of the Neurospora L-amino acid oxidase. Where our respective studies overlap mutual confirmation was obtained in most essential points. We wish to thank Dr. Burton for permission to read his manuscript before publication

    The Crystallography of Aluminum and its Alloys

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    This chapter begins with pure aluminium and a discussion of the form of the crystal structure and different unit cells that can be used to describe the crystal structure. Measurements of the face-centred cubic lattice parameter and thermal expansion coefficient in pure aluminium are reviewed and parametrisations given that allow the reader to evaluate them across the full range of temperatures where aluminium is a solid. A new concept called the vacancy triangle is introduced and demonstrated as an effective means for determining vacancy concentrations near the melting point of aluminium. The Debye-Waller factor, quantifying the thermal vibration of aluminium atoms in pure aluminium, is reviewed and parametrised over the full range of temperatures where aluminium is a solid. The nature of interatomic bonding and the history of its characterisation in pure aluminium is reviewed with the unequivocal conclusion that it is purely tetrahedral in nature. The crystallography of aluminium alloys is then discussed in terms of all of the concepts covered for pure aluminium, using prominent alloy examples. The electron density domain theory of solid-state nucleation and precipitate growth is introduced and discussed as a new means of rationalising phase transformations in alloys from a crystallographic point of view.Comment: 93 pages, 21 figures, 4 tables and 4 tabular appendices, 465 reference

    Ground state energy of a dilute two-dimensional Bose gas from the Bogoliubov free energy functional

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    We extend the analysis of the Bogoliubov free energy functional to two dimensions at very low temperatures. For sufficiently weak interactions, we prove two term asymptotics for the ground state energy.Comment: revised versio

    A Self-Consistent Marginally Stable State for Parallel Ion Cyclotron Waves

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    We derive an equation whose solutions describe self-consistent states of marginal stability for a proton-electron plasma interacting with parallel-propagating ion cyclotron waves. Ion cyclotron waves propagating through this marginally stable plasma will neither grow nor damp. The dispersion relation of these waves, {\omega} (k), smoothly rises from the usual MHD behavior at small |k| to reach {\omega} = {\Omega}p as k \rightarrow \pm\infty. The proton distribution function has constant phase-space density along the characteristic resonant surfaces defined by this dispersion relation. Our equation contains a free function describing the variation of the proton phase-space density across these surfaces. Taking this free function to be a simple "box function", we obtain specific solutions of the marginally stable state for a range of proton parallel betas. The phase speeds of these waves are larger than those given by the cold plasma dispersion relation, and the characteristic surfaces are more sharply peaked in the v\bot direction. The threshold anisotropy for generation of ion cyclotron waves is also larger than that given by estimates which assume bi-Maxwellian proton distributions.Comment: in press in Physics of Plasma

    The stellar mass-accretion rate relation in T Tauri stars and brown dwarfs

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    Recent observations show a strong correlation between stellar mass and accretion rate in young stellar and sub-stellar objects, with the scaling M˙accM2\dot{M}_{acc} \propto M_*^2 holding over more than four orders of magnitude in accretion rate. We explore the consequences of this correlation in the context of disk evolution models. We note that such a correlation is not expected to arise from variations in disk angular momentum transport efficiency with stellar mass, and suggest that it may reflect a systematic trend in disk initial conditions. In this case we find that brown dwarf disks initially have rather larger radii than those around more massive objects. By considering disk evolution, and invoking a simple parametrization for a shut-off in accretion at the end of the disk lifetime, we show that such models predict that the scatter in the stellar mass-accretion rate relationship should increase with increasing stellar mass, in rough agreement with current observations.Comment: 4 pages, 2 figures. Accepted for publication in ApJ Letter

    Immune-Mediated Inflammation May Contribute to the Pathogenesis of Cardiovascular Disease in Mucopolysaccharidosis Type I.

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    BackgroundCardiovascular disease, a progressive manifestation of α-L-iduronidase deficiency or mucopolysaccharidosis type I, continues in patients both untreated and treated with hematopoietic stem cell transplantation or intravenous enzyme replacement. Few studies have examined the effects of α-L-iduronidase deficiency and subsequent glycosaminoglycan storage upon arterial gene expression to understand the pathogenesis of cardiovascular disease.MethodsGene expression in carotid artery, ascending, and descending aortas from four non-tolerized, non-enzyme treated 19 month-old mucopolysaccharidosis type I dogs was compared with expression in corresponding vascular segments from three normal, age-matched dogs. Data were analyzed using R and whole genome network correlation analysis, a bias-free method of categorizing expression level and significance into discrete modules. Genes were further categorized based on module-trait relationships. Expression of clusterin, a protein implicated in other etiologies of cardiovascular disease, was assessed in canine and murine mucopolysaccharidosis type I aortas via Western blot and in situ immunohistochemistry.ResultsGene families with more than two-fold, significant increased expression involved lysosomal function, proteasome function, and immune regulation. Significantly downregulated genes were related to cellular adhesion, cytoskeletal elements, and calcium regulation. Clusterin gene overexpression (9-fold) and protein overexpression (1.3 to 1.62-fold) was confirmed and located specifically in arterial plaques of mucopolysaccharidosis-affected dogs and mice.ConclusionsOverexpression of lysosomal and proteasomal-related genes are expected responses to cellular stress induced by lysosomal storage in mucopolysaccharidosis type I. Upregulation of immunity-related genes implicates the potential involvement of glycosaminoglycan-induced inflammation in the pathogenesis of mucopolysaccharidosis-related arterial disease, for which clusterin represents a potential biomarker
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