12 research outputs found

    Transport Simulasion in a Burning Tokamak Plasma

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    A one-dimensional tokamak transport code (TASK/TR) has been developed to analyze the evolution of a burning plasma accompanied with fusion reaction. This code deals with the electrons, deuterons, tritons, thermalized α particles, fast α particles and beam ions, separately, in order to describe the dependence of the reaction rate on the ion mixture ratio. As an energy transport model, the drift wave turbulence mode is employed. The heating and current drive by the neutral beam injection as well as the pellet injection for fuelling are also included. This code is applied to a reactor-grade plasma aimed at in the ITER project. The cases of an ignited plasma and a current-driven plasma are examined. The required power for full current drive is estimated. The effect of pellet injection, both fuel and impurity ions, is also studied

    One-Electron State of a Partially Ionized High-Z Ion

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    An effective potential of an isolated partially ionized high-Z ion, calculated within the framework of the statistical models of atoms, is injected into the one-electron Schrödinger equation, in view of evaluating the electron density and comparing it with the results of statistical models. Starting from this initial value, a self-consistent electron density is obtained on the basis of the density functional theory, where quantum natures of electrons are fully taken into account

    Quantum-corrected Hybrid Bohm and Classical Diffusion in a Laser-driven Plasma

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    Within the framework of the hydrodynamic guidingcenter approximation, we have investigated such quantum effects as the diffraction correction and the symmetry effect on the classical version of the particle diffusion coefficient D(1) across a dc magnetic field through the temperature-dependent pseudo-potentials. Analytic results are explicitly given with recourse to the order-of-magnitude estimate of a set of parameters pertaining to a laser-driven plasma

    Enhancement of protein production via the strong DIT1 terminator and two RNA-binding proteins in Saccharomyces cerevisiae

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    Post-transcriptional upregulation is an effective way to increase the expression of transgenes and thus maximize the yields of target chemicals from metabolically engineered organisms. Refractory elements in the 3′ untranslated region (UTR) that increase mRNA half-life might be available. In Saccharomyces cerevisiae, several terminator regions have shown activity in increasing the production of proteins by upstream coding genes; among these terminators the DIT1 terminator has the highest activity. Here, we found in Saccharomyces cerevisiae that two resident trans-acting RNA-binding proteins (Nab6p and Pap1p) enhance the activity of the DIT1 terminator through the cis element GUUCG/U within the 3′-UTR. These two RNA-binding proteins could upregulate a battery of cell-wall–related genes. Mutagenesis of the DIT1 terminator improved its activity by a maximum of 500% of that of the standard PGK1 terminator. Further understanding and improvement of this system will facilitate inexpensive and stable production of complicated organism-derived drugs worldwide

    Effect of Major Diseases on Productivity of a Large Dairy Farm in a Temperate Zone in Japan

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    The objective of the present study was to investigate the associations between major diseases (clinical mastitis, peracute mastitis, metabolic disorders, peripartum disorders) and four parameters related to productivity (305-day milk yield, number of days open, culling rate, death rate) on a large dairy farm in a temperate zone with approximately 2500 Holstein cows. Data were collected from 2014 to 2018 and involved 9663 calving records for 4256 cows. We found negative effects of clinical mastitis, peracute mastitis, metabolic disorders, and peripartum disorders on the productivity of cows. Clinical-mastitis-suffered cows with multiple diseases had more days open compared with those with clinical mastitis alone and the healthy group, and they had a higher death rate than the healthy group, whereas there was no difference in death rate between the clinical mastitis only and healthy groups. Cows suffering from peracute mastitis, metabolic disorders, and peripartum disorders with either single or multiple diseases exhibited reduced productivity compared with the healthy group. Our findings clearly show that major diseases of cows in a temperate zone have severely negative effects on their productivity

    Noonan syndrome‐associated biallelic LZTR1 mutations cause cardiac hypertrophy and vascular malformations in zebrafish

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    Abstract Background Variants in the LZTR1 (leucine‐zipper‐like transcription regulator 1) gene (OMIM #600574) have been reported in recessive Noonan syndrome patients. In vivo evidence from animal models to support its causative role is lacking. Methods By CRISPR‐Cas9 genome editing, we generated lztr1‐mutated zebrafish (Danio rerio). Analyses of histopathology and downstream signaling were performed to investigate the pathogenesis of cardiac and extracardiac abnormalities in Noonan syndrome. Results A frameshift deletion allele was created in the zebrafish lztr1. Crosses of heterozygotes obtained homozygous lztr1 null mutants that modeled LZTR1 loss‐of‐function. Histological analyses of the model revealed ventricular hypertrophy, the deleterious signature of Noonan syndrome‐associated cardiomyopathy. Further, assessment for extracardiac abnormalities documented multiple vascular malformations, resembling human vascular pathology caused by RAS/MAPK activation. Due to spatiotemporal regulation of LZTR1, its downstream function was not fully elucidated from western blots of adult tissue. Conclusion Our novel zebrafish model phenocopied human recessive Noonan syndrome and supported the loss‐of‐function mechanism of disease‐causing LZTR1 variants. The discovery of vascular malformations in mutants calls for the clinical follow‐up of patients to monitor for its emergence. The model will serve as a novel platform for investigating the pathophysiology linking RAS/MAPK signaling to cardiac and vascular pathology
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