Exact Pseudofermion Action for Monte Carlo Simulation of Domain-Wall Fermion

We present an exact pseudofermion action for hybrid Monte Carlo simulation (HMC) of one-flavor domain-wall fermion (DWF), with the effective 4-dimensional Dirac operator equal to the optimal rational approximation of the overlap-Dirac operator with kernel $H = c H_w (1 + d \gamma_5 H_w)^{-1}$, where $c$ and $d$ are constants. Using this exact pseudofermion action, we perform HMC of one-flavor QCD, and compare its characteristics with the widely used rational hybrid Monte Carlo algorithm (RHMC). Moreover, to demonstrate the practicality of the exact one-flavor algorithm (EOFA), we perform the first dynamical simulation of the (1+1)-flavors QCD with DWF.Comment: 13 pages, 4 figures, v2: Simulation of (1+1)-flavors QCD with DWF, and references added. To appear in Phys. Lett.

Decay Constants of Pseudoscalar DD-mesons in Lattice QCD with Domain-Wall Fermion

We present the first study of the masses and decay constants of the pseudoscalar $D$ mesons in two flavors lattice QCD with domain-wall fermion. The gauge ensembles are generated on the $24^3 \times 48$ lattice with the extent $N_s = 16$ in the fifth dimension, and the plaquette gauge action at $\beta = 6.10$, for three sea-quark masses with corresponding pion masses in the range $260-475$ MeV. We compute the point-to-point quark propagators, and measure the time-correlation functions of the pseudoscalar and vector mesons. The inverse lattice spacing is determined by the Wilson flow, while the strange and the charm quark masses by the masses of the vector mesons $\phi(1020)$ and $J/\psi(3097)$ respectively. Using heavy meson chiral perturbation theory (HMChPT) to extrapolate to the physical pion mass, we obtain $f_D = 202.3(2.2)(2.6)$ MeV and $f_{D_s} = 258.7(1.1)(2.9)$ MeV.Comment: 15 pages, 3 figures. v2: the statistics of ensemble (A) with m_sea = 0.005 has been increased, more details on the systematic error, to appear in Phys. Lett.

Frameshift PQBP-1 mutants K192Sfs*7 and R153Sfs*41 implicated in X-linked intellectual disability form stable dimers.

Polyglutamine tract-binding protein-1 (PQBP-1) is a nuclear intrinsically disordered protein playing important roles in transcriptional regulation and RNA splicing during embryonic and postembryonic development. In human, its mutations lead to severe cognitive impairment known as the Renpenning syndrome, a form of X-linked intellectual disability (XLID). Here, we report a combined biophysical study of two PQBP-1 frameshift mutants, K192Sfs*7 and R153Sfs*41. Both mutants are dimeric in solution, in contrast to the monomeric wild-type protein. These mutants contain more folded contents and have increased thermal stabilities. Using small-angle X-ray scattering data, we generated three-dimensional envelopes which revealed their overall flat shapes. We also described each mutant using an ensemble model based on a native-like initial pool with a dimeric structural core. PQBP-1 is known to repress transcription by way of interacting with the C-terminal domain of RNA polymerase II, which consists of 52 repeats of a consensus heptapeptide sequence YSPTSPS. We studied the binding of PQBP-1 variants to the labelled peptide which is phosphorylated at positions 2 and 5 (YpSPTpSPS) and found that this interaction is significantly weakened in the two mutants

Role of the Hypoxia-Inducible Factor in Periodontal Inflammation

Human periodontitis is a chronic inflammatory disease induced by opportunistic Gram-negative anaerobic bacteria at the tooth-supporting apparatus. Within the gingivitis-affected sulcus or periodontal pocket, the resident anaerobic bacteria interact with the host inflammatory reactions leading to a lower oxygen or hypoxic environment. A cellular/tissue oxygen-sensing mechanism and its appropriate regulation are needed to assist tissue adaptation to natural/pathology-induced variations in oxygen availability. In this chapter, we reviewed the biological relevance of hypoxia in periodontal/oral cellular development, epithelial barrier function, periodontal inflammation, and immunity. The role of hypoxia-inducible factor-1α in pathogen-host cross talk and alveolar bone homeostasis was also discussed. The naturally occurring pathophysiological process of hypoxia appeared to entail fundamental relevance for periodontal defense and regeneration

Topological susceptibility in finite temperature QCD with physical (u/d,s,c)(u/d, s, c) domain-wall quarks

We perform hybrid Monte-Carlo (HMC) simulation of lattice QCD with $N_f=2+1+1$ domain-wall quarks at the physical point, on the $64^3 \times (64,20,16,12,10,8,6)$ lattices, each with three lattice spacings. The lattice spacings and the bare quark masses are determined on the $64^4$ lattices. The resulting gauge ensembles provide a basis for studying finite temperature QCD with $N_f=2+1+1$ domain-wall quarks at the physical point. In this paper, we determine the topological susceptibility of the QCD vacuum for $T > T_c \sim 150$ MeV. The topological charge of each gauge configuration is measured by the clover charge in the Wilson flow at the same flow time in physical units, and the topological susceptibility $\chi_t(a,T)$ is determined for each ensemble with lattice spacing $a$ and temperature $T$. Using the topological susceptibility $\chi_t(a,T)$ of 15 gauge ensembles with three lattice spacings and different temperatures in the range $T \sim 155-516$ MeV, we extract the topological susceptibility $\chi_t(T)$ in the continuum limit. Moreover, a detailed discussion on the reweighting method for domain-wall fermion is presented.Comment: 36 pages, 5 figure