264 research outputs found

    Ueber Lungenschwindsuchtentstehung und Tuberkulosebekämpfung

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    Iterative and Iterative-Noniterative Integral Solutions in 3-Loop Massive QCD Calculations

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    Various of the single scale quantities in massless and massive QCD up to 3-loop order can be expressed by iterative integrals over certain classes of alphabets, from the harmonic polylogarithms to root-valued alphabets. Examples are the anomalous dimensions to 3-loop order, the massless Wilson coefficients and also different massive operator matrix elements. Starting at 3-loop order, however, also other letters appear in the case of massive operator matrix elements, the so called iterative non-iterative integrals, which are related to solutions based on complete elliptic integrals or any other special function with an integral representation that is definite but not a Volterra-type integral. After outlining the formalism leading to iterative non-iterative integrals,we present examples for both of these cases with the 3-loop anomalous dimension γqg(2)\gamma_{qg}^{(2)} and the structure of the principle solution in the iterative non-interative case of the 3-loop QCD corrections to the ρ\rho-parameter.Comment: 13 pages LATEX, 2 Figure

    High-Resolution Agent-Based Modeling of COVID-19 Spreading in a Small Town

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    Amid the ongoing COVID-19 pandemic, public health authorities and the general population are striving to achieve a balance between safety and normalcy. Ever changing conditions call for the development of theory and simulation tools to finely describe multiple strata of society while supporting the evaluation of “what-if” scenarios. Particularly important is to assess the effectiveness of potential testing approaches and vaccination strategies. Here, an agent-based modeling platform is proposed to simulate the spreading of COVID-19 in small towns and cities, with a single-individual resolution. The platform is validated on real data from New Rochelle, NY—one of the first outbreaks registered in the United States. Supported by expert knowledge and informed by reported data, the model incorporates detailed elements of the spreading within a statistically realistic population. Along with pertinent functionality such as testing, treatment, and vaccination options, the model accounts for the burden of other illnesses with symptoms similar to COVID-19. Unique to the model is the possibility to explore different testing approaches—in hospitals or drive-through facilities—and vaccination strategies that could prioritize vulnerable groups. Decision-making by public authorities could benefit from the model, for its fine-grain resolution, open-source nature, and wide range of features

    EUV Spectra of the Full Solar Disk: Analysis and Results of the Cosmic Hot Interstellar Plasma Spectrometer (CHIPS)

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    We analyze EUV spectra of the full solar disk from the Cosmic Hot Interstellar Plasma Spectrometer (CHIPS) spanning a period of two years. The observations were obtained via a fortuitous off-axis light path in the 140 -- 270 Angstrom passband. The general appearance of the spectra remained relatively stable over the two-year time period, but did show significant variations of up to 25% between two sets of Fe lines that show peak emission at 1 MK and 2 MK. The variations occur at a measured period of 27.2 days and are caused by regions of hotter and cooler plasma rotating into, and out of, the field of view. The CHIANTI spectral code is employed to determine plasma temperatures, densities, and emission measures. A set of five isothermal plasmas fit the full disk spectra well. A 1 -- 2 MK plasma of Fe contributes 85% of the total emission in the CHIPS passband. The standard Differential Emission Measures (DEMs) supplied with the CHIANTI package do not fit the CHIPS spectra well as they over-predict emission at temperatures below log(T) = 6.0 and above log(T) = 6.3. The results are important for cross-calibrating TIMED, SORCE, SOHO/EIT, and CDS/GIS, as well as the recently launched Solar Dynamics Observatory.Comment: 27 Pages, 13 Figure

    High fat, high sucrose diet causes cardiac mitochondrial dysfunction due in part to oxidative post-translational modification of mitochondrial complex II

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    Abstract not availableAaron L. Sverdlov, Aly Elezaby, Jessica B. Behring, Markus M. Bachschmid, Ivan Luptak, Vivian H. Tu, Deborah A. Siwik, Edward J. Miller, Marc Liesa, Orian S. Shirihai, David R. Pimentel, Richard A. Cohen, Wilson S. Colucc

    Mitochondrial reactive oxygen species mediate cardiac structural, functional, and mitochondrial consequences of diet-induced metabolic heart disease

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    Mitochondrial reactive oxygen species (ROS) are associated with metabolic heart disease (MHD). However, the mechanism by which ROS cause MHD is unknown. We tested the hypothesis that mitochondrial ROS are a key mediator of MHD.Mice fed a high-fat high-sucrose (HFHS) diet develop MHD with cardiac diastolic and mitochondrial dysfunction that is associated with oxidative posttranslational modifications of cardiac mitochondrial proteins. Transgenic mice that express catalase in mitochondria and wild-type mice were fed an HFHS or control diet for 4 months. Cardiac mitochondria from HFHS-fed wild-type mice had a 3-fold greater rate of H2O2 production (P=0.001 versus control diet fed), a 30% decrease in complex II substrate-driven oxygen consumption (P=0.006), 21% to 23% decreases in complex I and II substrate-driven ATP synthesis (P=0.01), and a 62% decrease in complex II activity (P=0.002). In transgenic mice that express catalase in mitochondria, all HFHS diet-induced mitochondrial abnormalities were ameliorated, as were left ventricular hypertrophy and diastolic dysfunction. In HFHS-fed wild-type mice complex II substrate-driven ATP synthesis and activity were restored ex vivo by dithiothreitol (5 mmol/L), suggesting a role for reversible cysteine oxidative posttranslational modifications. In vitro site-directed mutation of complex II subunit B Cys100 or Cys103 to redox-insensitive serines prevented complex II dysfunction induced by ROS or high glucose/high palmitate in the medium.Mitochondrial ROS are pathogenic in MHD and contribute to mitochondrial dysfunction, at least in part, by causing oxidative posttranslational modifications of complex I and II proteins including reversible oxidative posttranslational modifications of complex II subunit B Cys100 and Cys103.Aaron L. Sverdlov, Aly Elezaby, Fuzhong Qin, Jessica B. Behring, Ivan Luptak, Timothy D. Calamaras, Deborah A. Siwik, Edward J. Miller, Marc Liesa, Orian S. Shirihai, David R. Pimentel, Richard A. Cohen, Markus M. Bachschmid, Wilson S. Colucc

    Identifying and Characterizing a Novel Protein Kinase STK35L1 and Deciphering Its Orthologs and Close-Homologs in Vertebrates

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    The human kinome containing 478 eukaryotic protein kinases has over 100 uncharacterized kinases with unknown substrates and biological functions. The Ser/Thr kinase 35 (STK35, Clik1) is a member of the NKF 4 (New Kinase Family 4) in the kinome with unknown substrates and biological functions. Various high throughput studies indicate that STK35 could be involved in various human diseases such as colorectal cancer and malaria. In this study, we found that the previously published coding sequence of the STK35 gene is incomplete. The newly identified sequence of the STK35 gene codes for a protein of 534 amino acids with a N-terminal elongation of 133 amino acids. It has been designated as STK35L (STK35 long). Since it is the first of further homologous kinases we termed it as STK35L1. The STK35L1 protein (58 kDa on SDS-PAGE), but not STK35 (44 kDa), was found to be expressed in all human cells studied (endothelial cells, HeLa, and HEK cells) and was down-regulated after silencing with specific siRNA. EGFP-STK35L1 was localized in the nucleus and the nucleolus. By combining syntenic and gene structure pattern data and homology searches, two further STK35L1 homologs, STK35L2 (previously known as PDIK1L) and STK35L3, were found. All these protein kinase homologs were conserved throughout the vertebrates. The STK35L3 gene was specifically lost during placental mammalian evolution. Using comparative genomics, we have identified orthologous sets of these three protein kinases genes and their possible ancestor gene in two sea squirt genomes. We found the full-length coding sequence of the STK35 gene and termed it as STK35L1. We identified a new third STK35-like gene, STK35L3, in vertebrates and a possible ancestor gene in sea squirt genome. This study will provide a comprehensive platform to explore the role of STK35L kinases in cell functions and human diseases
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