The 3-Loop Non-Singlet Heavy Flavor Contributions and Anomalous Dimensions for the Structure Function F2(x,Q2)F_2(x,Q^2) and Transversity

We calculate the massive flavor non-singlet Wilson coefficient for the heavy flavor contributions to the structure function $F_2(x,Q^2)$ in the asymptotic region $Q^2 \gg m^2$ and the associated operator matrix element $A_{qq,Q}^{(3), \rm NS}(N)$ to 3-loop order in Quantum Chromodynamics at general values of the Mellin variable $N$. This matrix element is associated to the vector current and axial vector current for the even and the odd moments $N$, respectively. We also calculate the corresponding operator matrix elements for transversity, compute the contributions to the 3-loop anomalous dimensions to $O(N_F)$ and compare to results in the literature. The 3-loop matching of the flavor non-singlet distribution in the variable flavor number scheme is derived. All results can be expressed in terms of nested harmonic sums in $N$ space and harmonic polylogarithms in $x$-space. Numerical results are presented for the non-singlet charm quark contribution to $F_2(x,Q^2)$.Comment: 82 pages, 3 style files, 33 Figure

New Results on Massive 3-Loop Wilson Coefficients in Deep-Inelastic Scattering

We present recent results on newly calculated 2- and 3-loop contributions to the heavy quark parts of the structure functions in deep-inelastic scattering due to charm and bottom.Comment: Contribution to the Proc. of Loops and Legs 2016, PoS, in prin

Recent progress on the calculation of three-loop heavy flavor Wilson coefficients in deep-inelastic scattering

We report on our latest results in the calculation of the three-loop heavy flavor contributions to the Wilson coefficients in deep-inelastic scattering in the asymptotic region $Q^2 \gg m^2$. We discuss the different methods used to compute the required operator matrix elements and the corresponding Feynman integrals. These methods very recently allowed us to obtain a series of new operator matrix elements and Wilson coefficients like the flavor non-singlet and pure singlet Wilson coefficients.Comment: 11 pages Latex, 2 Figures, Proc. of Loops and Legs in Quantum Field Theory, April 2014, Weimar, German

3-loop heavy flavor Wilson coefficients in deep-inelastic scattering

We present our most recent results on the calculation of the heavy flavor contributions to deep-inelastic scattering at 3-loop order in the large $Q^2$ limit, where the heavy flavor Wilson coefficients are known to factorize into light flavor Wilson coefficients and massive operator matrix elements. We describe the different techniques employed for the calculation and show the results in the case of the heavy flavor non-singlet and pure singlet contributions to the structure function $F_2(x,Q^2)$.Comment: 4 pages Latex, 2 style files, 4 Figures, Contribution to the Proceedings of QCD '14, Montpellier, Jult 201

3-Loop Corrections to the Heavy Flavor Wilson Coefficients in Deep-Inelastic Scattering

A survey is given on the status of 3-loop heavy flavor corrections to deep-inelastic structure functions at large enough virtualities $Q^2$.Comment: 13 pages Latex, 8 Figures, Contribution to the Proceedings of EPS 2015 Wie

Emission lines of Fe XI in the 257--407 A wavelength region observed in solar spectra from EIS/Hinode and SERTS

Theoretical emission-line ratios involving Fe XI transitions in the 257-407 A wavelength range are derived using fully relativistic calculations of radiative rates and electron impact excitation cross sections. These are subsequently compared with both long wavelength channel Extreme-Ultraviolet Imaging Spectrometer (EIS) spectra from the Hinode satellite (covering 245-291 A), and first-order observations (235-449 A) obtained by the Solar Extreme-ultraviolet Research Telescope and Spectrograph (SERTS). The 266.39, 266.60 and 276.36 A lines of Fe XI are detected in two EIS spectra, confirming earlier identifications of these features, and 276.36 A is found to provide an electron density diagnostic when ratioed against the 257.55 A transition. Agreement between theory and observation is found to be generally good for the SERTS data sets, with discrepancies normally being due to known line blends, while the 257.55 A feature is detected for the first time in SERTS spectra. The most useful Fe XI electron density diagnostic is found to be the 308.54/352.67 intensity ratio, which varies by a factor of 8.4 between N_e = 10^8 and 10^11 cm^-3, while showing little temperature sensitivity. However, the 349.04/352.67 ratio potentially provides a superior diagnostic, as it involves lines which are closer in wavelength, and varies by a factor of 14.7 between N_e = 10^8 and 10^11 cm^-3. Unfortunately, the 349.04 A line is relatively weak, and also blended with the second-order Fe X 174.52 A feature, unless the first-order instrument response is enhanced.Comment: 9 pages, 5 figures, 13 tables; MNRAS in pres

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

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

Overexpression of catalase diminishes oxidative cysteine modifications of cardiac proteins

Reactive protein cysteine thiolates are instrumental in redox regulation. Oxidants, such as hydrogen peroxide (H2O2), react with thiolates to form oxidative post-translational modifications, enabling physiological redox signaling. Cardiac disease and aging are associated with oxidative stress which can impair redox signaling by altering essential cysteine thiolates. We previously found that cardiac-specific overexpression of catalase (Cat), an enzyme that detoxifies excess H2O2, protected from oxidative stress and delayed cardiac aging in mice. Using redox proteomics and systems biology, we sought to identify the cysteines that could play a key role in cardiac disease and aging. With a 'Tandem Mass Tag' (TMT) labeling strategy and mass spectrometry, we investigated differential reversible cysteine oxidation in the cardiac proteome of wild type and Cat transgenic (Tg) mice. Reversible cysteine oxidation was measured as thiol occupancy, the ratio of total available versus reversibly oxidized cysteine thiols. Catalase overexpression globally decreased thiol occupancy by ≥1.3 fold in 82 proteins, including numerous mitochondrial and contractile proteins. Systems biology analysis assigned the majority of proteins with differentially modified thiols in Cat Tg mice to pathways of aging and cardiac disease, including cellular stress response, proteostasis, and apoptosis. In addition, Cat Tg mice exhibited diminished protein glutathione adducts and decreased H2O2 production from mitochondrial complex I and II, suggesting improved function of cardiac mitochondria. In conclusion, our data suggest that catalase may alleviate cardiac disease and aging by moderating global protein cysteine thiol oxidation.Chunxiang Yao, Jessica B. Behring, Di Shao, Aaron L. Sverdlov, Stephen A. Whelan, Aly Elezaby, Xiaoyan Yin, Deborah A. Siwik, Francesca Seta, Catherine E. Costello, Richard A. Cohen, Reiko Matsui, Wilson S. Colucci, Mark E. McComb, Markus M. Bachschmi

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

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