Diagnosing quantum phase transition via holographic entanglement entropy at finite temperature

We investigate the behavior of the holographic entanglement entropy (HEE) in proximity to the quantum critical points (QCPs) of the metal-insulator transition (MIT) in the Einstein-Maxwell-dilaton-axions (EMDA) model. Due to the fact that the ground state entropy density of the EMDA model is vanishing for insulating phase, but non-vanishing for the metallic phase, we used to expect that it is the HEE itself that characterizes the QCPs. This expectation is validated for certain case, however, we make a noteworthy observation: for a specific scenario, it is not the HEE itself but rather the second-order derivative of HEE with respect to the lattice wave number that effectively characterizes the quantum phase transition (QPT). This distinction arises due to the influence of thermal effects. These findings present novel insights into the interplay between HEE and QPTs in the context of the MIT, and have significant implications for studying QPT at finite temperatures.Comment: 15 pages, 5 figure

Diagnosing quantum phase transitions via holographic entanglement entropy at finite temperature

We investigate the behavior of the holographic entanglement entropy (HEE) in proximity to the quantum critical points (QCPs) of the metal-insulator transition (MIT) in the Einstein–Maxwell-dilaton-axions (EMDA) model. Since both the metallic phase and the insulating phase are characterized by distinct IR geometries, we used to expect that the HEE itself characterizes the QCPs. This expectation is validated for certain cases, however, we make a noteworthy observation: for a specific scenario where $$-1<\gamma \le -1/3$$, with $$\gamma$$ as a coupling parameter, it is not the HEE itself but rather the second-order derivative of HEE with respect to the lattice wave number that effectively characterizes quantum phase transitions (QPTs). This distinction arises due to the influence of thermal effects. These findings present novel insights into the interplay between HEE and QPTs in the context of the MIT, and have significant implications for studying QPTs at finite temperatures

Synaptotagmin-7 is a key factor for bipolar-like behavioral abnormalities in mice

The pathogenesis of bipolar disorder (BD) has remained enigmatic, largely because genetic animal models based on identified susceptible genes have often failed to show core symptoms of spontaneous mood cycling. However, pedigree and induced pluripotent stem cell (iPSC)-based analyses have implicated that dysfunction in some key signaling cascades might be crucial for the disease pathogenesis in a subpopulation of BD patients. We hypothesized that the behavioral abnormalities of patients and the comorbid metabolic abnormalities might share some identical molecular mechanism. Hence, we investigated the expression of insulin/synapse dually functioning genes in neurons derived from the iPSCs of BD patients and the behavioral phenotype of mice with these genes silenced in the hippocampus. By these means, we identified synaptotagmin-7 (Syt7) as a candidate risk factor for behavioral abnormalities. We then investigated Syt7 knockout (KO) mice and observed nocturnal manic-like and diurnal depressive-like behavioral fluctuations in a majority of these animals, analogous to the mood cycling symptoms of BD. We treated the Syt7 KO mice with clinical BD drugs including olanzapine and lithium, and found that the drug treatments could efficiently regulate the behavioral abnormalities of the Syt7 KO mice. To further verify whether Syt7 deficits existed in BD patients, we investigated the plasma samples of 20 BD patients and found that the Syt7 mRNA level was significantly attenuated in the patient plasma compared to the healthy controls. We therefore concluded that Syt7 is likely a key factor for the bipolar-like behavioral abnormalities.</p