Fixed scale approach to the equation of state on the lattice

We propose a fixed scale approach to calculate the equation of state (EOS) in lattice QCD. In this approach, the temperature T is varied by Nt at fixed lattice spacings. This enables us to reduce T=0 simulations which are required to provide basic data in finite temperature studies but are quite expensive in the conventional fixed-Nt approach. Since the conventional integral method to obtain the pressure is inapplicable at fixed scale, we introduce a new method, "T-integration method", to calculate pressure non-perturbatively. We test the fixed scale approach armed with the T-integral method in quenched QCD on isotropic and anisotropic lattices. Our method is found to be powerful to obtain reliable results for the equation of state, especially at intermediate and low temperatures. Reduction of the computational cost of T=0 simulations is indispensable to study EOS in QCD with dynamical quarks. The status of our study in Nf=2+1 QCD with improved Wilson quarks is also reported.Comment: 4 pages, 4 figures - To appear in the conference proceedings for Quark Matter 2009, March 30 - April 4, Knoxville, Tennessee. Fonts in the figures magnifie

Innate Immune Sensing of DNA

Discusses efforts to understand how DNA triggers immune responses

Two flavors of dynamical quarks on anisotropic lattices

We report on our study of two-flavor full QCD on anisotropic lattices using $O(a)$-improved Wilson quarks coupled with an RG-improved glue. The bare gauge and quark anisotropies corresponding to the renormalized anisotropy $\xi=a_s/a_t = 2$ are determined as functions of $\beta$ and $\kappa$, which covers the region of spatial lattice spacings $a_s\approx 0.28$--0.16 fm and $m_{PS}/m_V\approx 0.6$--0.9. The calibrations of the bare anisotropies are performed with the Wilson loop and the meson dispersion relation at 4 lattice cutoffs and 5--6 quark masses. Using the calibration results we calculate the meson mass spectrum and the Sommer scale $r_0$. We confirm that the values of $r_0$ calculated for the calibration using pseudo scalar and vector meson energy momentum dispersion relation coincide in the continuum limit within errors. This work serves to lay ground toward studies of heavy quark systems and thermodynamics of QCD including the extraction of the equation of state in the continuum limit using Wilson-type quark actions.Comment: 16 pages, 23 figures, Version accepted for publication in Physical Review

Serotonin and corticosterone rhythms in mice exposed to cigarette smoke and in patients with COPD:implication for COPD-associated neuropathogenesis

The circadian timing system controls daily rhythms of physiology and behavior, and disruption of clock function can trigger stressful life events. Daily exposure to cigarette smoke (CS) can lead to alteration in diverse biological and physiological processes. Smoking is associated with mood disorders, including depression and anxiety. Patients with chronic obstructive pulmonary disease (COPD) have abnormal circadian rhythms, reflected by daily changes in respiratory symptoms and lung function. Corticosterone (CORT) is an adrenal steroid that plays a considerable role in stress and anti-inflammatory responses. Serotonin (5-hydroxytryptamine; 5HT) is a neurohormone, which plays a role in sleep/wake regulation and affective disorders. Secretion of stress hormones (CORT and 5HT) is under the control of the circadian clock in the suprachiasmatic nucleus. Since smoking is a contributing factor in the development of COPD, we hypothesize that CS can affect circadian rhythms of CORT and 5HT secretion leading to sleep and mood disorders in smokers and patients with COPD. We measured the daily rhythms of plasma CORT and 5HT in mice following acute (3 d), sub-chronic (10 d) or chronic (6 mo) CS exposure and in plasma from non-smokers, smokers and patients with COPD. Acute and chronic CS exposure affected both the timing (peak phase) and amplitude of the daily rhythm of plasma CORT and 5HT in mice. Acute CS appeared to have subtle time-dependent effects on CORT levels but more pronounced effects on 5HT. As compared with CORT, plasma 5HT was slightly elevated in smokers but was reduced in patients with COPD. Thus, the effects of CS on plasma 5HT were consistent between mice and patients with COPD. Together, these data reveal a significant impact of CS exposure on rhythms of stress hormone secretion and subsequent detrimental effects on cognitive function, depression-like behavior, mood/anxiety and sleep quality in smokers and patients with COPD

Impaired Cellular Responses to Cytosolic DNA or Infection with Listeria monocytogenes and Vaccinia Virus in the Absence of the Murine LGP2 Protein

Innate immune signaling is crucial for detection of and the initial response to microbial pathogens. Evidence is provided indicating that LGP2, a DEXH box domain protein related to the RNA recognition receptors RIG-I and MDA5, participates in the cellular response to cytosolic double-stranded DNA (dsDNA). Analysis of embryonic fibroblasts and macrophages from mice harboring targeted disruption in the LGP2 gene reveals that LGP2 can act as a positive regulator of type I IFN and anti-microbial gene expression in response to transfected dsDNA. Results indicate that infection of LGP2-deficient mice with an intracellular bacterial pathogen, Listeria monocytogenes, leads to reduced levels of type I IFN and IL12, and allows increased bacterial growth in infected animals, resulting in greater colonization of both spleen and liver. Responses to infection with vaccinia virus, a dsDNA virus, are also suppressed in cells lacking LGP2, reinforcing the ability of LGP2 to act as a positive regulator of antiviral signaling. In vitro mechanistic studies indicate that purified LGP2 protein does not bind DNA but instead mediates these responses indirectly. Data suggest that LGP2 may be acting downstream of the intracellular RNA polymerase III pathway to activate anti-microbial signaling. Together, these findings demonstrate a regulatory role for LGP2 in the response to cytosolic DNA, an intracellular bacterial pathogen, and a DNA virus, and provide a plausible mechanistic hypothesis as the basis for this activity