331 research outputs found
Mott Gap Excitations and Resonant Inelastic X-Ray Scattering in Doped Cuprates
Predictions are made for the momentum- and carrier-dependent degradation of
the Mott gap upon doping in high-Tc cuprates as would be observed in Cu K-edge
resonant inelastic x-ray scattering (RIXS). The two-dimensional Hubbard model
with second- and third-nearest-neighbor hopping terms has been studied by
numerical exact diagonalization. Special emphasis is placed on the
particle-hole asymmetry of the Mott gap excitations. We argue that the Mott gap
excitations observed by RIXS are significantly influenced by the interaction
between charge carriers and antiferromagnetic correlations.Comment: 4 pages, 4 figures, revised version; to be published in Phys. Rev.
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Antiphase Oscillations in the Time-Resolved Spin Structure Factor of a Photoexcited Mott Insulator
Motivated by the recent development of time-resolved resonant-inelastic x-ray
scattering (TRRIXS) in photoexcited antiferromagnetic Mott insulators, we
numerically investigate momentum-dependent transient spin dynamics in a
half-filled Hubbard model on a square lattice. After turning off a pumping
photon pulse, the intensity of a dynamical spin structure factor temporally
oscillates with frequencies determined by the energy of two magnons in the
antiferromagnetic Mott insulator. We find an antiphase behavior in the
oscillations between two orthogonal momentum directions, parallel and
perpendicular to the electric field of a pump pulse. The phase difference comes
from the channel of the two-magnon excitation. Observing the antiphase
oscillations will be a big challenge for TRRIXS experiments when their time
resolution will be improved by more than an order of magnitude.Comment: 5 pages, 4 figure
The TLR4/TRIF-Mediated Activation of NLRP3 Inflammasome Underlies Endotoxin-Induced Liver Injury in Mice
Administration of heat-killed Propionibacterium acnes renders mice highly susceptible to LPS. After LPS challenge P. acnes-primed mice promptly show hypothermia, hypercoagulation (disseminated intravascular coagulation), elevation of serum proinflammatory cytokine levels, and high mortality. The surviving mice develop liver injury. As previously reported, IL-18 plays a pivotal role in the development of this liver injury. Many cell types including macrophages constitutively store IL-18 as biologically inactive precursor (pro) form. Upon appropriate stimulation exemplified by TLR4 engagement, the cells secrete biologically active IL-18 by cleaving pro-IL-18 with caspase-1. Caspase-1 is also constitutively produced as a zymogen in macrophages. Recently, NLRP3, a cytoplasmic pathogen sensor, has been demonstrated to be involved in the activation of caspase-1. Here, we review the molecular mechanisms for the liver injuries, particularly focusing on the TLR4/NLRP3-mediated caspase-1 activation process, with a brief introduction of the mechanism underlying P. acnes-induced sensitization to LPS
Prevention of Hepatocellular Carcinoma Development Associated with Chronic Hepatitis by Anti-Fas Ligand Antibody Therapy
A persistent immune response to hepatitis viruses is a well-recognized risk factor for hepatocellular carcinoma. However, the molecular and cellular basis for the procarcinogenic potential of the immune response is not well defined. Here, using a unique animal model of chronic hepatitis that induces hepatocellular carcinogenesis, we demonstrate that neutralization of the activity of Fas ligand prevented hepatocyte apoptosis, proliferation, liver inflammation, and the eventual development of hepatocellular carcinoma. The results indicate that Fas ligand is involved not only in direct hepatocyte killing but also in the process of inflammation and hepatocellular carcinogenesis in chronic hepatitis. This is the first demonstration that amelioration of chronic inflammation by some treatment actually caused reduction of cancer development
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