4,067 research outputs found

    Location of Mach Discs and Diamonds Supersonic Air Jets

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/77542/1/AIAA-3788-127.pd

    Faint Infrared Flares from the Microquasar GRS 1915+105

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    We present simultaneous infrared and X-ray observations of the Galactic microquasar GRS 1915+105 using the Palomar 5-m telescope and Rossi X-ray Timing Explorer on July 10, 1998 UT. Over the course of 5 hours, we observed 6 faint infrared (IR) flares with peak amplitudes of ∼0.3−0.6\sim 0.3-0.6 mJy and durations of ∼500−600\sim 500-600 seconds. These flares are associated with X-ray soft-dip/soft-flare cycles, as opposed to the brighter IR flares associated with X-ray hard-dip/soft-flare cycles seen in August 1997 by Eikenberry et al. (1998). Interestingly, the IR flares begin {\it before} the X-ray oscillations, implying an ``outside-in'' origin of the IR/X-ray cycle. We also show that the quasi-steady IR excess in August 1997 is due to the pile-up of similar faint flares. We discuss the implications of this flaring behavior for understanding jet formation in microquasars.Comment: 10 pages, 4 figures Accepted for publication in ApJ Letter

    Characterizing Residue-Bilayer Interactions Using Gramicidin A as a Scaffold and Tryptophan Substitutions as Probes

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    This document is the Accepted Manuscript version of a Published Work that appeared in final form in Journal of Chemical Theory and Computation, copyright © American Chemical Society after peer review and technical editing by the publisher. To access the final edited and published work see http://doi.org/10.1021/acs.jctc.7b00400.Previous experiments have shown that the lifetime of a gramicidin A dimer channel (which forms from two non-conducting monomers) in a lipid bilayer is modulated by mutations of the tryptophan (Trp) residues at the bilayer-water interface. We explore this further using extensive molecular dynamics simulations of various gA dimer and monomer mutants at the Trp positions in phosphatidylcholine bilayers with different tail lengths. gA interactions with the surrounding bilayer are strongly modulated by mutating these Trp residues. There are three principal effects: eliminating residue hydrogen bonding ability (i.e., reducing the channel-monolayer coupling strength) reduces the extent of the bilayer deformation caused by the assembled dimeric channel; a residue’s size and geometry affects its orientation, leading to different hydrogen bonding partners; and increasing a residue’s hydrophobicity increases the depth of gA monomer insertion relative to the bilayer center, thereby increasing the lipid bending frustration

    THEORETICAL INVESTIGATION OF MICROSTRUCTURE EVOLUTION AND DEFORMATION OF ZIRCONIUM UNDER CASCADE DAMAGE CONDITIONS

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    This work is based on our reaction-diffusion model of radiation growth of Zr-based materials proposed recently in [1]. In [1], the equations for the strain rates in unloaded pure crystal under cascade damage conditions of, e.g., neutron or heavy-ion irradiation were derived as functions of dislocation densities, which include contributions from dislocation loops, and spatial distribution of their Burgers vectors. The model takes into account the intra-cascade clustering of self-interstitial atoms and their one-dimensional diffusion; explains the growth stages, including the break-away growth of pre-annealed samples; and accounts for some striking observations, such as of negative strain in prismatic direction, and co-existence of vacancy- and interstitial-type prismatic loops. In this report, the change of dislocation densities due to accumulation of sessile dislocation loops is taken into account explicitly to investigate the dose dependence of radiation growth. The dose dependence of climb rates of dislocations is calculated, which is important for the climb-induced glide model of radiation creep. The results of fitting the model to available experimental data and some numerical calculations of the strain behavior of Zr for different initial dislocation structures are presented and discussed. The computer code RIMD-ZR.V1 (Radiation Induced Microstructure and Deformation of Zr) developed is described and attached to this report

    The Catalytic Machinery of a Key Enzyme in Amino Acid Biosynthesis

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    The aspartate pathway of amino acid biosynthesis is essential for all microbial life but is absent in mammals. Characterizing the enzyme-catalyzed reactions in this pathway can identify new protein targets for the development of antibiotics with unique modes of action. The enzyme aspartate β-semialdehyde dehydrogenase (ASADH) catalyzes an early branch point reaction in the aspartate pathway. Kinetic, mutagenic, and structural studies of ASADH from various microbial species have been used to elucidate mechanistic details and to identify essential amino acids involved in substrate binding, catalysis, and enzyme regulation. Important structural and functional differences have been found between ASADHs isolated from these bacterial and fungal organisms, opening the possibility for developing species-specific antimicrobial agents that target this family of enzymes

    Automated identification of diagnostic labelling errors in medicine

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    Objectives: Identification of diagnostic error is complex and mostly relies on expert ratings, a severely limited procedure. We developed a system that allows to automatically identify diagnostic labelling error from diagnoses coded according to the international classification of diseases (ICD), often available as routine health care data. Methods: The system developed (index test) was validated against rater based classifications taken from three previous studies of diagnostic labeling error (reference standard). The system compares pairs of diagnoses through calculation of their distance within the ICD taxonomy. Calculation is based on four different algorithms. To assess the concordance between index test and reference standard, we calculated the area under the receiver operating characteristics curve (AUROC) and corresponding confidence intervals. Analysis were conducted overall and separately per algorithm and type of available dataset. Results: Diagnoses of 1,127 cases were analyzed. Raters previously classified 24.58% of cases as diagnostic labelling errors (ranging from 12.3 to 87.2% in the three datasets). AUROC ranged between 0.821 and 0.837 overall, depending on the algorithm used to calculate the index test (95% CIs ranging from 0.8 to 0.86). Analyzed per type of dataset separately, the highest AUROC was 0.924 (95% CI 0.887-0.962). Conclusions: The trigger system to automatically identify diagnostic labeling error from routine health care data performs excellent, and is unaffected by the reference standards' limitations. It is however only applicable to cases with pairs of diagnoses, of which one must be more accurate or otherwise superior than the other, reflecting a prevalent definition of a diagnostic labeling error
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