Perturbative calculation of the scaled factorial moments in second-order quark-hadron phase transition within the Ginzburg-Landau description

The scaled factorial moments $F_q$ are studied for a second-order quark-hadron phase transition within the Ginzburg-Landau description. The role played by the ground state of the system under low temperature is emphasized. After a local shift of the order parameter the fluctuations are around the ground state, and a perturbative calculation for $F_q$ can be carried out. Power scaling between $F_q$'s is shown, and a universal scaling exponent $\nu\simeq 1.75$ is given for the case with weak correlations and weak self-interactions.Comment: 12 pages in RevTeX, 12 eps figure

Kinetic Roughening in Surfaces of Crystals Growing on Disordered Substrates

Substrate disorder effects on the scaling properties of growing crystalline surfaces in solidification or epitaxial deposition processes are investigated. Within the harmonic approach there is a phase transition into a low-temperature (low-noise) superrough phase with a continuously varying dynamic exponent z>2 and a non-linear response. In the presence of the KPZ nonlinearity the disorder causes the lattice efects to decay on large scales with an intermediate crossover behavior. The mobility of the rough surface hes a complex dependence on the temperature and the other physical parameters.Comment: 13 pages, 2 figures (not included). Submitted to Phys. Rev. Letts. Use Latex twic

Near-Equilibrium Dynamics of Crystalline Interfaces with Long-Range Interactions in 1+1 Dimensional Systems

The dynamics of a one-dimensional crystalline interface model with long-range interactions is investigated. In the absence of randomness, the linear response mobility decreases to zero when the temperature approaches the roughening transition from above, in contrast to a finite jump at the critical point in the Kosterlitz-Thouless (KT) transition. In the presence of substrate disorder, there exists a phase transition into a low-temperature pinning phase with a continuously varying dynamic exponent $z>1$. The expressions for the non-linear response mobility of a crystalline interface in both cases are also derived.Comment: 14 Pages, Revtex3.0, accepted to be published in Phys. Rev. E Rapid Communicatio

Dynamics of Particles Deposition on a Disordered Substrate: II. Far-from Equilibrium Behavior. -

The deposition dynamics of particles (or the growth of a rigid crystal) on a disordered substrate at a finite deposition rate is explored. We begin with an equation of motion which includes, in addition to the disorder, the periodic potential due to the discrete size of the particles (or to the lattice structure of the crystal) as well as the term introduced by Kardar, Parisi, and Zhang (KPZ) to account for the lateral growth at a finite growth rate. A generating functional for the correlation and response functions of this process is derived using the approach of Martin, Sigga, and Rose. A consistent renormalized perturbation expansion to first order in the non-Gaussian couplings requires the calculation of diagrams up to three loops. To this order we show, for the first time for this class of models which violates the the fluctuation-dissipation theorem, that the theory is renormalizable. We find that the effects of the periodic potential and the disorder decay on very large scales and asymptotically the KPZ term dominates the behavior. However, strong non-trivial crossover effects are found for large intermediate scales.Comment: 52 pages & 17 Figs in uucompressed file. UR-CM 94-090

Expression of High-Affinity IgE Receptor on Human Peripheral Blood Dendritic Cells in Children

BACKGROUND: In a mouse model of viral induced atopic disease, expression of FcεRI on dendritic cells is critical. While adult human conventional (cDC) and plasmacytoid (pDC) dendritic cells have been shown to express FcεRI, it is not known if this receptor is expressed in childhood and how its expression is governed by IgE. METHODS: Following informed consent of subjects (n = 27, aged 12-188 months), peripheral blood was stained for surface expression of CD19, ILT7, CD1c, IgE, FcεRI and analyzed by flow cytometry (cDC: CD19(-) ILT7(-) CD1c(+); pDC: CD19(-) ILT7(+) CD1c(-)). Total and specific serum IgE levels to food and inhalant allergens were determined by ImmunoCAP, and the relationship between FcεRI expression on dendritic cells and sensitization, free IgE, cell bound IgE, and age was determined. RESULTS: Independent of sensitization status, FcεRI expression was noted on cDC and pDC as early as 12 months of age. Serum IgE level correlated with expression of FcεRI on cDC, but not pDC. Based on the concentration of IgE, a complex relationship was found between surface bound IgE and expression of FcεRI on cDC. pDC exhibited a linear relationship of FcεRI expression and bound IgE that was consistent through all IgE concentrations. CONCLUSIONS: In children, FcεRI expression on cDC and pDC is modulated differently by serum and cell bound IgE. IgE governance of FcεRI expression on cDC depends upon a complex relationship. Further studies are needed to determine the functional roles of FcεRI on cDC and pDC

Helix movement is coupled to displacement of the second extracellular loop in rhodopsin activation

The second extracellular loop (EL2) of rhodopsin forms a cap over the binding site of its photoreactive 11-cis retinylidene chromophore. A crucial question has been whether EL2 forms a reversible gate that opens upon activation or acts as a rigid barrier. Distance measurements using solid-state 13C NMR spectroscopy between the retinal chromophore and the β4 strand of EL2 show that the loop is displaced from the retinal binding site upon activation, and there is a rearrangement in the hydrogen-bonding networks connecting EL2 with the extracellular ends of transmembrane helices H4, H5 and H6. NMR measurements further reveal that structural changes in EL2 are coupled to the motion of helix H5 and breaking of the ionic lock that regulates activation. These results provide a comprehensive view of how retinal isomerization triggers helix motion and activation in this prototypical G protein-coupled receptor. © 2009 Nature America, Inc. All rights reserved

Crystal Structure of the PIM2 Kinase in Complex with an Organoruthenium Inhibitor

BACKGROUND: The serine/threonine kinase PIM2 is highly expressed in human leukemia and lymphomas and has been shown to positively regulate survival and proliferation of tumor cells. Its diverse ATP site makes PIM2 a promising target for the development of anticancer agents. To date our knowledge of catalytic domain structures of the PIM kinase family is limited to PIM1 which has been extensively studied and which shares about 50% sequence identity with PIM2. PRINCIPAL FINDINGS: Here we determined the crystal structure of PIM2 in complex with an organoruthenium complex (inhibition in sub-nanomolar level). Due to its extraordinary shape complementarity this stable organometallic compound is a highly potent inhibitor of PIM kinases. SIGNIFICANCE: The structure of PIM2 revealed several differences to PIM1 which may be explored further to generate isoform selective inhibitors. It has also demonstrated how an organometallic inhibitor can be adapted to the binding site of protein kinases to generate highly potent inhibitors. ENHANCED VERSION: This article can also be viewed as an enhanced version in which the text of the article is integrated with interactive 3D representations and animated transitions. Please note that a web plugin is required to access this enhanced functionality. Instructions for the installation and use of the web plugin are available in Text S1

Investigation of cracks in GaN films grown by combined hydride and metal organic vapor-phase epitaxial method

Cracks appeared in GaN epitaxial layers which were grown by a novel method combining metal organic vapor-phase epitaxy (MOCVD) and hydride vapor-phase epitaxy (HVPE) in one chamber. The origin of cracks in a 22-μm thick GaN film was fully investigated by high-resolution X-ray diffraction (XRD), micro-Raman spectra, and scanning electron microscopy (SEM). Many cracks under the surface were first observed by SEM after etching for 10 min. By investigating the cross section of the sample with high-resolution micro-Raman spectra, the distribution of the stress along the depth was determined. From the interface of the film/substrate to the top surface of the film, several turnings were found. A large compressive stress existed at the interface. The stress went down as the detecting area was moved up from the interface to the overlayer, and it was maintained at a large value for a long depth area. Then it went down again, and it finally increased near the top surface. The cross-section of the film was observed after cleaving and etching for 2 min. It was found that the crystal quality of the healed part was nearly the same as the uncracked region. This indicated that cracking occurred in the growth, when the tensile stress accumulated and reached the critical value. Moreover, the cracks would heal because of high lateral growth rate

Ischemia-Reperfusion Injury Leads to Distinct Temporal Cardiac Remodeling in Normal versus Diabetic Mice

Diabetes is associated with higher incidence of myocardial infarction (MI) and increased propensity for subsequent events post-MI. Here we conducted a temporal analysis of the influence of diabetes on cardiac dysfunction and remodeling after ischemia reperfusion (IR) injury in mice. Diabetes was induced using streptozotocin and IR performed by ligating the left anterior descending coronary artery for 30 min followed by reperfusion for up to 42 days. We first evaluated changes in cardiac function using echocardiography after 24 hours reperfusion and observed IR injury significantly decreased the systolic function, such as ejection fraction, fractional shortening and end systolic left ventricular volume (LVESV) in both control and diabetic mice. The longitudinal systolic and diastolic strain rate were altered after IR, but there were no significant differences between diabetic mice and controls. However, a reduced ability to metabolize glucose was observed in the diabetic animals as determined by PET-CT scanning using 2-deoxy-2-(18F)fluoro-D-glucose. Interestingly, after 24 hours reperfusion diabetic mice showed a reduced infarct size and less apoptosis indicated by TUNEL analysis in heart sections. This may be explained by increased levels of autophagy detected in diabetic mice hearts. Similar increases in IR-induced macrophage infiltration detected by CD68 staining indicated no change in inflammation between control and diabetic mice. Over time, control mice subjected to IR developed mild left ventricular dilation whereas diabetic mice exhibited a decrease in both end diastolic left ventricular volume and LVESV with a decreased intraventricular space and thicker left ventricular wall, indicating concentric hypertrophy. This was associated with marked increases in fibrosis, indicted by Masson trichrome staining, of heart sections in diabetic IR group. In summary, we demonstrate that diabetes principally influences distinct IR-induced chronic changes in cardiac function and remodeling, while a smaller infarct size and elevated levels of autophagy with similar cardiac function are observed in acute phase

Proteins on the catwalk: modelling the structural domains of the CCN family of proteins

The CCN family of proteins (CCN1, CCN2, CCN3, CCN4, CCN5 and CCN6) are multifunctional mosaic proteins that play keys roles in crucial areas of physiology such as angiogenesis, skeletal development tumourigenesis, cell proliferation, adhesion and survival. This expansive repertoire of functions comes through a modular structure of 4 discrete domains that act both independently and in concert. How these interactions with ligands and with neighbouring domains lead to the biological effects is still to be explored but the molecular structure of the domains is likely to play an important role in this. In this review we have highlighted some of the key features of the individual domains of CCN family of proteins based on their biological effects using a homology modelling approach