Channeling quantum criticality

We analyze the effect of decoherence, modelled by local quantum channels, on quantum critical states and we find universal properties of the resulting mixed state's entanglement, both between system and environment and within the system. Renyi entropies exhibit volume law scaling with a subleading constant governed by a "$g$-function" in conformal field theory (CFT), allowing us to define a notion of renormalization group (RG) flow (or "phase transitions") between quantum channels. We also find that the entropy of a subsystem in the decohered state has a subleading logarithmic scaling with subsystem size, and we relate it to correlation functions of boundary condition changing operators in the CFT. Finally, we find that the subsystem entanglement negativity, a measure of quantum correlations within mixed states, can exhibit log scaling or area law based on the RG flow. When the channel corresponds to a marginal perturbation, the coefficient of the log scaling can change continuously with decoherence strength. We illustrate all these possibilities for the critical ground state of the transverse-field Ising model, in which we identify four RG fixed points of dephasing channels and verify the RG flow numerically. Our results are relevant to quantum critical states realized on noisy quantum simulators, in which our predicted entanglement scaling can be probed via shadow tomography methods.Comment: 7+14 pages, 4+11 figures, published versio

Mixed-state Quantum Phases: Renormalization and Quantum Error Correction

Open system quantum dynamics can generate a variety of long-range entangled mixed states, yet it has been unclear in what sense they constitute phases of matter. To establish that two mixed states are in the same phase, as defined by their two-way connectivity via local quantum channels, we use the renormalization group (RG) and decoders of quantum error correcting codes. We introduce a real-space RG scheme for mixed states based on local channels which ideally preserve correlations with the complementary system, and we prove this is equivalent to the reversibility of the channel's action. As an application, we demonstrate an exact RG flow of finite temperature toric code in two dimensions to infinite temperature, thus proving it is in the trivial phase. In contrast, for toric code subject to local dephasing, we establish a mixed state toric code phase using local channels obtained by truncating an RG-type decoder and the minimum weight perfect matching decoder. We also discover a precise relation between mixed state phase and decodability, by proving that local noise acting on toric code cannot destroy logical information without bringing the state out of the toric code phase

Effect of Physical Exercise on College Students’ Life Satisfaction: Mediating Role of Competence and Relatedness Needs

This study examined the effect of physical exercise on the life satisfaction among college students. On the basis of the Basic Psychological Need Theory, the mediating roles of competence and relatedness needs satisfaction and their differences among college students in physical education (PE) majors and non-PE majors were explored. The sample included 1,012 college students who were selected to participate in an online survey. Major findings were as follows: (1) The total effect of physical exercise commitment on college students’ life satisfaction was marginally significant while that of physical exercise adherence was not significant; (2) The effect of physical exercise commitment was observed exclusively through the mediating role of relatedness need satisfaction, while that of physical exercise adherence was through both competence and relatedness needs satisfaction; (3) In terms of differences caused by major, only one mediation path, that was, physical exercise → competence need satisfaction → college students’s life satisfaction was significant among PE majors. This study thus enriched the empirical research on the benefits of physical exercise to individual mental health, highlighted the particularity of college students majoring in PE, and provided targeted and sensible suggestions for the design of physical exercise intervention programs

Effects of Primary and Secondary Psychopathy on Deontological and Utilitarian Response Tendencies: The Mediator Role of Alexithymia

(1) Background: The purpose of this study is to provide more nuanced insights into the effects of sub-dimensional levels of psychopathy on moral dilemma judgments. To this end, this study examined the effects of primary and secondary psychopathy on utilitarian and deontological response tendencies. Moreover, this study also explored the mediating role of alexithymia as well as the moderating role of gender in these effects. (2) Methods: A total of 1227 participants were recruited through the online questionnaire service wjx.cn. After deleting unfinished questionnaires, the remaining 1170 participants were included in the final data analysis. Each participant completed a demographic information questionnaire, the Levenson Self-Report Psychopathy Scale, the Toronto Alexithymia Scale-20, and six pairs of moral dilemmas. Descriptive and correlational analyses of study variables were conducted in SPSS 22.0. Mediation and gender difference analyses were conducted in AMOS 23.0. (3) Results: Primary psychopathy was negatively correlated with deontological response tendencies and uncorrelated with utilitarian response tendencies. By contrast, secondary psychopathy also correlated negatively with deontological response tendencies, but it correlated positively with utilitarian response tendencies. Mediation analysis revealed that alexithymia only mediated the relationship between secondary psychopathy and deontological response tendencies. Multi-group analysis revealed that there was no difference between females and males in the indirect effect model. (4) Conclusions: People with high primary psychopathy are less likely to reject harm in moral dilemmas. By contrast, people with high secondary psychopathy have high alexithymia, which causes them to be less concerned about avoiding harm, and they are more likely to maximize outcomes in moral dilemmas. These findings shed new light on the moral dilemma judgments of individuals with primary and secondary psychopathy

Parvovirus B19 NS1 protein induces cell cycle arrest at G2-phase by activating the ATR-CDC25C-CDK1 pathway

<div><p>Human parvovirus B19 (B19V) infection of primary human erythroid progenitor cells (EPCs) arrests infected cells at both late S-phase and G2-phase, which contain 4N DNA. B19V infection induces a DNA damage response (DDR) that facilitates viral DNA replication but is dispensable for cell cycle arrest at G2-phase; however, a putative C-terminal transactivation domain (TAD2) within NS1 is responsible for G2-phase arrest. To fully understand the mechanism underlying B19V NS1-induced G2-phase arrest, we established two doxycycline-inducible B19V-permissive UT7/Epo-S1 cell lines that express NS1 or NS1^mTAD2, and examined the function of the TAD2 domain during G2-phase arrest. The results confirm that the NS1 TAD2 domain plays a pivotal role in NS1-induced G2-phase arrest. Mechanistically, NS1 transactivated cellular gene expression through the TAD2 domain, which was itself responsible for ATR (ataxia-telangiectasia mutated and Rad3-related) activation. Activated ATR phosphorylated CDC25C at serine 216, which in turn inactivated the cyclin B/CDK1 complex without affecting nuclear import of the complex. Importantly, we found that the ATR-CHK1-CDC25C-CDK1 pathway was activated during B19V infection of EPCs, and that ATR activation played an important role in B19V infection-induced G2-phase arrest.</p></div

NS1 upregulates expression of cyclin B1, CDK1, and p21, but not expression of ATM and CHK2.

<p>NS1-S1 and NS1^mTAD2-S1 cells were treated with Dox (5 μg/ml) and collected and lysed 72 h later. (A) Cell lysates were analyzed for expression of cyclin B1, phosphorylated CDK1 (CDK1(pY15) and CDK1(pT161), lower band [<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1006266#ppat.1006266.ref042" target="_blank">42</a>]), and total CDK1 by Western blotting. (B) Cell lysates were analyzed for expression of ATM(pS1981), ATM, CHK2, CHK2(pS33/35), and β-actin by Western blotting. (C) Cell lysates were analyzed for expression of p21 by Western blotting with an anti-p21 antibody. β-actin was used as a loading control. Untreated UT7/Epo-S1 (S1) cells, S1 cells treated with nocodazole (Noco), and S1 cells treated with hydroxyurea (HU) were used as controls.</p

NS1 does not block the cyclin B1/CDK1 complex from entering the nucleus but it does inhibit its kinase activity.

<p>(A) Western blot analysis. NS1-S1 and NS1^mTAD2-S1 cells were treated with Dox for 72 h, collected, and lysed, and the nuclei were extracted. Western blot analysis was then performed to detect cyclin B1 and phosphorylated CDK1(pY15), as well as nuclear histone H3 and cytoplasmic GAPDH (Glyceraldehyde-3-Phosphate Dehydrogenase). Nuclear extracts from S1 cells and S1 cells treated with nocodazole (Noco) were loaded as controls. (B&C) <i>In vitro</i> CDK1 kinase assay. Equivalent amounts of proteins derived from whole cell lysate (B) or nuclear extracts (C) from S1 cells, S1 cells treated with Noco, and Dox-induced NS1-S1 and NS1^mTAD2-S1 cells were immunoprecipitated with anti-cyclin B1-crosslinked protein A/G Plus agarose beads for <i>in vitro</i> CDK1 kinase assay. The final products were resolved on a 12% SDS-polyacrylamide gel. The gel was then dried prior to autoradiography, and the phosphorylated histone H1 (pHistone H1) is indicated. (C) Lower panel: Co-Immunoprecipitation (Co-IP) of cyclin B1 and CDK1(pY15) in the nuclear extracts. Nuclear extracts prepared from S1, S1/Noco, NS1-S1/Dox+, and NS1^mTAD2-S1/Dox+ cells were immunoprecipitated with an anti-cyclin B1 antibody. The eluted proteins were analyzed for CDK1(pY15) by Western blotting. Normal mouse IgG (IgG Ctrl) was used as negative control of immunoprecipitation of control S1 cell extracts.</p

Inhibition of ATR activation significantly decreases B19V-induced G2 arrest in infected CD36⁺ EPCs.

<p>(A–C) B19V infection and cell cycle analysis. CD36⁺ EPCs were treated with VE821 for 3 h prior to B19V or mock infection. After 48 h, cells were collected, stained with an anti-capsid antibody, and cell cycle phase was examined by flow cytometry. (A) Total cells were selected for cell cycle analysis. (B) Percentage of B19V capsid-expressing cells were analyzed. (C) Anti-capsid staining-positive were selected for cell cycle analysis. (D–F) Statistical analyses. (D) The percentage of cells treated with DMSO or VE821 that were at G1-, S-, and G2-phase is depicted in color. The numbers shown are the percentages of the cells at G2, and are statistically compared as indicated. (E) The percentage of anti-capsid positive (B19V+) cells is shown the mean ± standard deviation of at least three independent experiments. (F) The percentage of capsid-expressing cells at G1-, S-, and G2-phase is depicted in color. The numbers shown are percentages of the cells at G2. **P<0.01 and *P<0.05. (G) Western blot analysis. CD36⁺ EPCs were either treated with DMSO or VE821 at 3 h prior to B19V infection or mock-infection. After 48 h, cells were collected for Western blotting to detect ATR(pT1989).</p

The NS1 TAD2 domain is responsible for transactivation of various cell cycle related genes.

<p>NS1-S1 and NS1^mTAD2-S1 cells were induced by Dox (5 μg/ml) for 72 h. The cells were then collected, lysed, and immunoblotted with the indicated antibodies in each panel (A-E). S1 cells and S1 cells treated with Noco or HU were loaded as controls. β-actin was used as a loading control.</p