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

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

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

Relações contratuais e perfil dos cirurgiões-dentistas em centros de especialidades odontológicas de baixo e alto desempenho no Brasil

Introdução: No Brasil, a partir da década de 1990, quando foram implementadas novas modalidades contratuais flexíveis na administração pública, tem se destacado o debate sobre as relações de trabalho. Esse movimento de mudanças tem repercutido no sistema público de saúde pela tendência à instabilidade dos vínculos laborais e à desproteção social. Objetivo: Investigar o perfil profissional de cirurgiões-dentistas dos centros de especialidades odontológicas e analisar a natureza das relações de trabalho em vigor nos contratos firmados entre esses profissionais e os municípios. Metodologia:O estudo, de natureza exploratória, foi realizado a partir de entrevistas semiestruturadas com 289 profissionais alocados em 59 centros de especialidades odontológicas das 5 macrorregiões do país, selecionados entre os 10% com melhor e pior desempenho na produção de procedimentos. Resultados:Entre os profissionais investigados, a maioria era do sexo feminino (55,0%). Quanto à qualificação profissional, 72,7% do total dos entrevistados afirmaram ter cursado ou estar cursando pós-graduação no momento da entrevista. A presença de vínculos precários e a instabilidade laboral sobressaem nas entrevistas, o que evidencia algumas distinções entre as macrorregiões do país. Conclusões:Ao ressaltar o debate sobre o conceito de trabalho precário, os autores reafirmam que essa condição se faz presente no espaço da Política Nacional de Saúde Bucal implementada por estados e municípios

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

A Cellular Potts Model simulating cell migration on and in matrix environments

Cell migration on and through extracellular matrix plays a critical role in a wide variety of physiological and pathological phenomena, and in scaffold-based tissue engineering. Migration is regulated by a number of extracellular matrix- or cell-derived biophysical parameters, such as matrix fiber orientation, gap size, and elasticity, or cell deformation, proteolysis, and adhesion. We here present an extended Cellular Potts Model (CPM) able to qualitatively and quantitatively describe cell migratory phenotype on both two-dimensional substrates and within three-dimensional environments, in a close comparison with experimental evidence. As distinct features of our approach, the cells are represented by compartmentalized discrete objects, differentiated in the nucleus and in the cytosolic region, while the extracellular matrix is composed of a fibrous mesh and of a homogeneous fluid. Our model provides a strong correlation of the directionality of migration with the topological ECM distribution and, further, a biphasic dependence of migration on the matrix density, and in part adhesion, in both two-dimensional and three-dimensional settings. Moreover, we demonstrate that the directional component of cell movement is strongly correlated with the topological distribution of the ECM fibrous network. In the three-dimensional networks, we also investigate the effects of the matrix mechanical microstructure, observing that, at a given distribution of fibers, cell motility has a subtle bimodal relation with the elasticity of the scaffold. Finally, cell locomotion requires deformation of the cell's nucleus and/or cell-derived proteolysis of steric fibrillar obstacles within rather rigid matrices characterized by small pores, not, however, for sufficiently large pores. In conclusion, we here propose a mathematical modeling approach that serves to characterize cell migration as a biological phenomen in health, disease and tissue engineering applications. The research that led to the present paper was partially supported by a grant of the group GNFM of INdA

Squark Flavor Implications from B --> K(*) l+ l-

Recent experimental and theoretical progress regarding B --> K(*) l+ l- decays led to improved bounds on the Wilson coefficients C_9 and C_10 of four-fermion operators of the |Delta B|=|Delta S|=1 effective Hamiltonian. We analyze the resulting implications on squark flavor violation in the MSSM and obtain new constraints on flavor-changing left-right mixing in the up-squark-sector. We find the dimensionless flavor mixing parameter (delta^u_23)_LR, depending on the flavor-diagonal MSSM masses and couplings, to be as low as \lesssim 0.1. This has implications for models based on radiative flavor violation and leads to BR(B_s --> mu+ mu-) \gtrsim 1 x 10^-9. Rare top decays t --> c gamma, t --> c g, t --> c Z have branching ratios predicted to be below \lesssim few times 10^-8, 10^-6 and 10^-7, respectively.Comment: v2: 21 pages, 5 figures; Eq (A.2) and chirality-flipping mass insertion results clarified, references added, conclusions unchange

STK35L1 Associates with Nuclear Actin and Regulates Cell Cycle and Migration of Endothelial Cells

BACKGROUND: Migration and proliferation of vascular endothelial cells are essential for repair of injured endothelium and angiogenesis. Cyclins, cyclin-dependent kinases (CDKs), and cyclin-dependent kinase inhibitors play an important role in vascular tissue injury and wound healing. Previous studies suggest a link between the cell cycle and cell migration: cells present in the G(1) phase have the highest potential to migrate. The molecular mechanism linking these two processes is not understood. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we explored the function of STK35L1, a novel Ser/Thr kinase, localized in the nucleus and nucleolus of endothelial cells. Molecular biological analysis identified a bipartite nuclear localization signal, and nucleolar localization sequences in the N-terminal part of STK35L1. Nuclear actin was identified as a novel binding partner of STK35L1. A class III PDZ binding domains motif was identified in STK35L1 that mediated its interaction with actin. Depletion of STK35L1 by siRNA lead to an accelerated G(1) to S phase transition after serum-stimulation of endothelial cells indicating an inhibitory role of the kinase in G(1) to S phase progression. Cell cycle specific genes array analysis revealed that one gene was prominently downregulated (8.8 fold) in STK35L1 silenced cells: CDKN2A alpha transcript, which codes for p16(INK4a) leading to G(1) arrest by inhibition of CDK4/6. Moreover in endothelial cells seeded on Matrigel, STK35L1 expression was rapidly upregulated, and silencing of STK35L1 drastically inhibited endothelial sprouting that is required for angiogenesis. Furthermore, STK35L1 depletion profoundly impaired endothelial cell migration in two wound healing assays. CONCLUSION/SIGNIFICANCE: The results indicate that by regulating CDKN2A and inhibiting G1- to S-phase transition STK35L1 may act as a central kinase linking the cell cycle and migration of endothelial cells. The interaction of STK35L1 with nuclear actin might be critical in the regulation of these fundamental endothelial functions