Chiral Central Charge from a Single Bulk Wave Function.

A (2+1)-dimensional gapped quantum many-body system can have a topologically protected energy current at its edge. The magnitude of this current is determined entirely by the temperature and the chiral central charge, a quantity associated with the effective field theory of the edge. We derive a formula for the chiral central charge that, akin to the topological entanglement entropy, is completely determined by the many-body ground state wave function in the bulk. According to our formula, nonzero chiral central charge gives rise to a topological obstruction that prevents the ground state wave function from being real valued in any local product basis.

Clustering of Conditional Mutual Information for Quantum Gibbs States above a Threshold Temperature.

We prove that the quantum Gibbs states of spin systems above a certain threshold temperature are approximate quantum Markov networks, meaning that the conditional mutual information decays rapidly with distance. We demonstrate the exponential decay for short-ranged interacting systems and power-law decay for long-ranged interacting systems. Consequently, we establish the efficiency of quantum Gibbs sampling algorithms, a strong version of the area law, the quasilocality of effective Hamiltonians on subsystems, a clustering theorem for mutual information, and a polynomial-time algorithm for classical Gibbs state simulations.

Macroscopic Thermodynamic Reversibility in Quantum Many-Body Systems.

The resource theory of thermal operations, an established model for small-scale thermodynamics, provides an extension of equilibrium thermodynamics to nonequilibrium situations. On a lattice of any dimension with any translation-invariant local Hamiltonian, we identify a large set of translation-invariant states that can be reversibly converted to and from the thermal state with thermal operations and a small amount of coherence. These are the spatially ergodic states, i.e., states that have sharp statistics for any translation-invariant observable, and mixtures of such states with the same thermodynamic potential. As an intermediate result, we show for a general state that if the gap between the min- and the max-relative entropies to the thermal state is small, then the state can be approximately reversibly converted to and from the thermal state with thermal operations and a small source of coherence. Our proof provides a quantum version of the Shannon-McMillan-Breiman theorem for the relative entropy and a quantum Stein's lemma for ergodic states and local Gibbs states. Our results provide a strong link between the abstract resource theory of thermodynamics and more realistic physical systems as we achieve a robust and operational characterization of the emergence of a thermodynamic potential in translation-invariant lattice systems.

Proton concentrations can be a major contributor to the modification of osteoclast and osteoblast differentiation, working independently of extracellular bicarbonate ions.

We established a system to separately analyze the role of protons and bicarbonate ions in vitro in which the pH of the medium was controlled by HEPES at various concentrations of sodium bicarbonate (NaHCO3) in the absence of carbon dioxide (CO2). Using this system, we demonstrated that acidosis promoted osteoclast formation independently of extracellular NaHCO3 in a short-term culture. Protons and bicarbonate ions acted on osteoclast differentiation with opposite effects, the former positively and the latter negatively. The HEPES-based system maintained pH in the absence of extracellular NaHCO3 without CO2. Therefore, we could demonstrate that osteoblast differentiation was promoted at higher pH in a long-term culture system without NaHCO3 in which ALP activity and nodule mineralization were enhanced. This finding indicates that protons negatively control osteoblast differentiation independently of extracellular bicarbonate ions. However, the difference in the concentration of NaHCO3 did not have any influence on nodule mineralization. The opposite effects of protons, the promotion of osteoclast formation and the inhibition of osteoblast differentiation, were suppressed in the presence of 5 mM N-acetyl cysteine, a reagent activating the scavenging of reactive oxygen species (ROS), implying that ROS act on both systems, the promotion of large osteoclast formation and the deterioration of osteoblast formation under acidosis.

NMDA receptor stimulation in the absence of extracellular Ca2+ potentiates Ca2+ influx-dependent cell death system.

The meaning of Ca2+ influx in the time course of glutamate stimulation of neuronal cells was addressed. We demonstrated that Ca2+ influx did not work straightforward in the determination of the fate of neuronal cells. There appears to be a critical period for Ca2+ influx to work efficiently in glutamate-induced neuronal cell death. When Ca2+ influx for 5 min from the beginning of glutamate stimulation was allowed in the whole stimulation period for 15 min, potent neuronal cell death could not be attained. On the other hand, when neuronal cells had been pre-treated with glutamate or NMDA for 5-10 min in the absence of extracellular Ca2+ following Ca2+ influx for 5 min fully induced neuronal cell death. APV inhibited this pre-treatment effect. It appears that the pre-treatment of neuronal cells with glutamate or NMDA in the absence of extracellular Ca2+ promotes the Ca2+ influx-dependent process executing cell death. The pre-treatment itself did not change the pattern of intracellular Ca2+ elevation by the activation of NMDA receptors. These results imply that glutamate activation of NMDA receptors consists of two different categories of pathways relating to neuronal cell death, i.e., Ca2+ influx independent and dependent, and that the former facilitates the latter to drive neuronal cells to death. This study clarified a mechanism by which glutamate quickly determines cell fate.

Promotion of osteoclast differentiation and activation in spite of impeded osteoblast-lineage differentiation under acidosis: effects of acidosis on bone metabolism.

The acidosis that accompanies many diseases and pathological conditions can promote osteoclast formation and activation. Acidosis mainly acts on the last phase of osteoclast formation to generate large osteoclasts and promote bone resorption. There are several acid-sensing mechanisms, among which transient receptor potential (TRP) channels and G protein-related receptors have been focused on. TRPV4 channels appear to be, at least partly, implicated in acidosis-promoted large osteoclast formation. Other TRP channels including TRPV1 and TRPV2 might be components of the acid-sensing machinery. Several reports suggest the involvement of ovarian cancer G protein-coupled receptor 1 (OGR1), a G-protein-related acid sensor, in receptor activator of nuclear factor kappa-B ligand (RANKL) expression via cyclooxygenase-2 (COX-2). On the other hand, acidosis impairs osteoblast differentiation, which is further impeded in the presence of inflammatory cytokines.

Acidosis environment promotes osteoclast formation by acting on the last phase of preosteoclast differentiation: a study to elucidate the action points of acidosis and search for putative target molecules.

Acidosis promoted tartaric acid-resistant acid phosphatase-positive multinuclear cell (TRAP+MNC) or osteoclast formation. Large osteoclast or TRAP+LMNC formation was observed far more in an acidosis environment than in a physiologically neutral environment. One of the major action points of acidosis was determined to be located in the last phase of preosteoclast differentiation using a co-culture system and a soluble RANKL-dependent bone marrow cell culture system. On-going osteoclast formation in an acidosis environment markedly deteriorated when the medium was replaced with physiologically neutral medium within the first 6h; however, bone marrow cells previously stimulated in an acidosis environment for 9h differentiated into TRAP+LMNC in pH 7.4 medium. Messenger RNA (mRNA) expression levels of DC-STAMP, a key molecule in cell fusion, and NFATc1 did not increase in the acidosis environment compared with those under physiologically neutral conditions. Ruthenium red, a general TRP antagonist, deteriorated acidosis-promoted TRAP+LMNC formation. 4-Alpha-PDD, a TRPV4-specific agonist, added in the last 21 h of preosteoclast differentiation, potentiated TRAP+LMNC formation in a mild acidosis environment, showing synergism between TRPV4 activation and acidosis. RN1734, a TRPV4-specific antagonist, partly inhibited acidosis-promoted TRAP+LMNC formation. We thus narrowed down the major action points of acidosis in osteoclast formation and elucidated the characteristics of this system in detail. Our results show that acidosis effectively uses TRPV4 to drive large-scale cell fusion and also utilizes systems independently of TRPV4.