Temperature dependence of instantons in QCD

We investigate the temperature dependence of the instanton contents of gluon fields, using unquenched lattice QCD and the cooling method. The instanton size parameter deduced from the correlation function decreases from 0.44fm below the phase-transition temperature $T_c$ ($\approx 150$MeV) to 0.33fm at 1.3 $T_c$. The instanton charge distribution is Poissonian above $T_c$, but it deviates from the convoluted Poisson at low temperature. The topological susceptibility decreases rapidly below $T_c$, showing the apparent restoration of the $U(1)_A$ symmetry already at $T \approx T_c$.Comment: 8 pages TEX, 3 Postscript figures available at http://www.krl.caltech.edu/preprints/MAP.htm

Instantons and <A2><A^2> Condensate

We argue that the $$condensate found in the Landau gauge on lattices, when an Operator Product Expansion of Green functions is performed, might be explained by instantons. We use cooling to estimate the instanton contribution and extrapolate back the result to the thermalised configuration. The resulting$$ is similar to $$.Comment: 6 pages, 1 fig., 1 tab., RevTeX to be use

Protein kinase C is a calcium sensor for presynaptic short-term plasticity

In presynaptic boutons, calcium (Ca2+) triggers both neurotransmitter release and short-term synaptic plasticity. Whereas synaptotagmins are known to mediate vesicle fusion through binding of high local Ca2+ to their C2 domains, the proteins that sense smaller global Ca2+ increases to produce short-term plasticity have remained elusive. Here, we identify a Ca2+ sensor for post-tetanic potentiation (PTP), a form of plasticity thought to underlie short-term memory. We find that at the functionally mature calyx of Held synapse the Ca2+-dependent protein kinase C isoforms α and β are necessary for PTP, and the expression of PKCβ in PKCαβ double knockout mice rescues PTP. Disruption of Ca2+ binding to the PKCβ C2 domain specifically prevents PTP without impairing other PKCβ-dependent forms of synaptic enhancement. We conclude that different C2-domain-containing presynaptic proteins are engaged by different Ca2+ signals, and that Ca2+ increases evoked by tetanic stimulation are sensed by PKCβ to produce PTP. DOI: http://dx.doi.org/10.7554/eLife.03011.00

Relations among neutrino observables in the light of a large theta_13 angle

The recent T2K and MINOS indications for a "large" theta_13 neutrino mixing angle can be accommodated in principle by an infinite number of Yukawa flavour structures in the seesaw model. Without considering any explicit flavour symmetry, there is an instructive exercise one can do: to determine the simplest flavour structures which can account for the data with a minimum number of parameters, simply assuming these parameters to be uncorrelated. This approach points towards a limited number of simple structures which show the minimum complexity a neutrino mass model must generally involve to account for the data. These basic structures essentially lead to only 4 relations between the neutrino observables. We emphasize that 2 of these relations, |sin theta_13|=(tan theta_23/cos delta)*(1-tan theta_12)/(1+tan theta_12) and |sin theta_13| = sin theta_12 R^1/4, with R= Delta m^2_21/Delta m^2_32, have several distinctive properties. First, they hold not only with a minimum number of parameters, but also for complete classes of more general models. Second, any value of theta_13 within the T2K and MINOS ranges can be obtained from these relations by taking into account small perturbations. Third, they turn out to be the pivot relations of models with approximate conservation of lepton number, which allow the seesaw interactions to induce observable flavour violating processes, such as mu -> e gamma and tau -> mu gamma. Finally, in specific cases of this kind, these structures have the rather unique property to allow a full reconstruction of the seesaw Lagrangian from low energy data.Comment: 13 pages, 3 figure

Mesonic Wavefunctions in the three-dimensional Gross-Neveu model

We present results from a numerical study of bound state wavefunctions in the (2+1)-dimensional Gross-Neveu model with staggered lattice fermions at both zero and nonzero temperature. Mesonic channels with varying quantum numbers are identified and analysed. In the strongly coupled chirally broken phase at T=0 the wavefunctions expose effects due to varying the interaction strength more effectively than straightforward spectroscopy. In the weakly coupled chirally restored phase information on fermion - antifermion scattering is recovered. In the hot chirally restored phase we find evidence for a screened interaction. The T=0 chirally symmetric phase is most readily distinguished from the symmetric phase at high T via the fermion dispersion relation.Comment: 18 page

Validation of the disease-specific components of the Kidney Disease Quality of Life-36 (KDQOL-36) in Chinese patients undergoing maintenance dialysis

AIM: The aim of this study was to evaluate the validity, reliability and sensitivity of the disease-specific items of the Kidney Disease Quality of Life-36 (KDQOL-36) in Chinese patients undergoing maintenance dialysis. METHODS: The content validity was assessed by content validity index (CVI) in ten subjects. 356 subjects were recruited for pilot psychometric testing. The internal construct validity was assessed by corrected item-subscale total correlation. Confirmatory factor analysis (CFA) was used to confirm the factor structure. The convergent validity was assessed by Pearson's correlation test between the disease specific subscale scores and SF-12 version 2 Health Survey (SF-12 v2) scores. The reliability was assessed by the internal consistency (Cronbach's Alpha coefficient) and 2-week test-retest reliability (intraclass correlation coefficient (ICC)). The sensitivity was determined by performing known group comparisons by independent t-test. RESULTS: The CVI on clarity and relevance was â ¥ 0.9 for all items. Corrected item- total correlation scores were â ¥0.4 for all, except an item related to problems with access site. CFA confirmed the 3-factor structure of the disease-specific component of the KDQOL-36. The correlation coefficients between the disease-specific domain scores and the SF-12 v2 physical and mental component summary scores ranged from 0.328 to 0.492. The reliability was good (Cronbach's alpha coefficients ranged from 0.810 to 0.931, ICC ranged from 0.792 to 0.924). Only the effect subscale was sensitive in detecting differences in HRQOL between haemodialysis and peritoneal dialysis patients, with effect size = 0.68. CONCLUSION: The disease-specific items of the KDQOL-36 are a valid, reliable and sensitive measure to assess the health-related quality of life of Chinese patients on maintenance dialysis.published_or_final_versio

Instantons and Chiral Symmetry on the Lattice

I address the question of how much of QCD in the chiral limit is reproduced by instantons. After reconstructing the instanton content of smoothed Monte Carlo lattice configurations, I compare hadron spectroscopy on this instanton ensemble to the spectroscopy on the original ``physical'' smoothed configurations using a chirally optimised clover fermion action. By studying the zero mode zone in simple instances I find that the optimised action gives a satisfactory description of it. Through the Banks-Casher formula, instantons by themselves are shown to break chiral symmetry but hadron correlators on the instanton backgrounds are strongly influenced by free quark propagation. This results in unnaturally light hadrons and a small splitting between the vector and the pseudoscalar meson channels. Superimposing a perturbative ensemble of zero momentum gauge field fluctuations (torons) on the instantons is found to be enough to eliminate the free quarks and restore the physical hadron correlators. I argue that the torons that are present only in finite volumes, are probably needed to compensate the unnaturally large finite size effects due to the lack of confinement in the instanton ensemble.Comment: 32 pages, LaTeX with 14 eps figure

Paradoxical roles of antioxidant enzymes:Basic mechanisms and health implications

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are generated from aerobic metabolism, as a result of accidental electron leakage as well as regulated enzymatic processes. Because ROS/RNS can induce oxidative injury and act in redox signaling, enzymes metabolizing them will inherently promote either health or disease, depending on the physiological context. It is thus misleading to consider conventionally called antioxidant enzymes to be largely, if not exclusively, health protective. Because such a notion is nonetheless common, we herein attempt to rationalize why this simplistic view should be avoided. First we give an updated summary of physiological phenotypes triggered in mouse models of overexpression or knockout of major antioxidant enzymes. Subsequently, we focus on a series of striking cases that demonstrate “paradoxical” outcomes, i.e., increased fitness upon deletion of antioxidant enzymes or disease triggered by their overexpression. We elaborate mechanisms by which these phenotypes are mediated via chemical, biological, and metabolic interactions of the antioxidant enzymes with their substrates, downstream events, and cellular context. Furthermore, we propose that novel treatments of antioxidant enzyme-related human diseases may be enabled by deliberate targeting of dual roles of the pertaining enzymes. We also discuss the potential of “antioxidant” nutrients and phytochemicals, via regulating the expression or function of antioxidant enzymes, in preventing, treating, or aggravating chronic diseases. We conclude that “paradoxical” roles of antioxidant enzymes in physiology, health, and disease derive from sophisticated molecular mechanisms of redox biology and metabolic homeostasis. Simply viewing antioxidant enzymes as always being beneficial is not only conceptually misleading but also clinically hazardous if such notions underpin medical treatment protocols based on modulation of redox pathways

Hadronic Spectral Functions in Lattice QCD

QCD spectral functions of hadrons in the pseudo-scalar and vector channels are extracted from lattice Monte Carlo data of the imaginary time Green's functions. The maximum entropy method works well for this purpose, and the resonance and continuum structures in the spectra are obtained in addition to the ground state peaks.Comment: 4 pages, 3 eps-figures, revtex (minor modifications in the text and an added reference). To appear in Physical Review D Rapid Communication

Functional role of ICAM-3 polymorphism in genetic susceptibility to SARS infection.

Key Messages 1. Severe acute respiratory syndrome (SARS) patients who are homozygous for intercellular adhesion molecule-3 (ICAM-3) Gly143 showed significant association with higher lactate dehydrogenase levels and lower total white blood cell counts on admission. 2. In vitro functional studies demonstrated low level binding of ICAM-3 to DC-SIGN and a wide variation in T-cell response of the wild-type ICAM-3 genotype.published_or_final_versio