RESUMO
Unlike the electroweak sector of the standard model of particle physics, quantum chromodynamics (QCD) is surprisingly symmetric under time reversal. As there is no obvious reason for QCD being so symmetric, this phenomenon poses a theoretical problem, often referred to as the strong CP problem. The most attractive solution for this requires the existence of a new particle, the axion-a promising dark-matter candidate. Here we determine the axion mass using lattice QCD, assuming that these particles are the dominant component of dark matter. The key quantities of the calculation are the equation of state of the Universe and the temperature dependence of the topological susceptibility of QCD, a quantity that is notoriously difficult to calculate, especially in the most relevant high-temperature region (up to several gigaelectronvolts). But by splitting the vacuum into different sectors and re-defining the fermionic determinants, its controlled calculation becomes feasible. Thus, our twofold prediction helps most cosmological calculations to describe the evolution of the early Universe by using the equation of state, and may be decisive for guiding experiments looking for dark-matter axions. In the next couple of years, it should be possible to confirm or rule out post-inflation axions experimentally, depending on whether the axion mass is found to be as predicted here. Alternatively, in a pre-inflation scenario, our calculation determines the universal axionic angle that corresponds to the initial condition of our Universe.
RESUMO
We compute the leading, strong-interaction contribution to the anomalous magnetic moment of the electron, muon, and tau using lattice quantum chromodynamics (QCD) simulations. Calculations include the effects of u, d, s, and c quarks and are performed directly at the physical values of the quark masses and in volumes of linear extent larger than 6 fm. All connected and disconnected Wick contractions are calculated. Continuum limits are carried out using six lattice spacings. We obtain a_{e}^{LO-HVP}=189.3(2.6)(5.6)×10^{-14}, a_{µ}^{LO-HVP}=711.1(7.5)(17.4)×10^{-10} and a_{τ}^{LO-HVP}=341.0(0.8)(3.2)×10^{-8}, where the first error is statistical and the second is systematic.
RESUMO
Expression of the CCK-A receptor gene in the pancreas and pancreatic exocrine function was examined in diabetic model rats (OLETF) at 5 wks of age. Little or no CCK-A receptor was detected in the pancreas of OLETF rats. Pancreatic exocrine function in response to exogenous CCK and to bile-pancreatic juice diversion (endogenous CCK) was impaired in conscious OLETF rats. The pancreatic insulin and protein contents of OLETF (Otsuka Long-Evans Tokushima Fatty) and control LETO (Long-Evans Tokushima Otsuka) rats were not significantly different. No histological abnormalities or expression of pancreatitis associated protein (PAP) mRNA was detected in the pancreas in either group. These results suggest that OLETF rats are a new experimental model for congenital deficiency of CCK-A receptor in the pancreas.