Environment-Assisted Error Correction of Single-Qubit Phase Damping

Open quantum system dynamics of random unitary type may in principle be fully undone. Closely following the scheme of environment-assisted error correction proposed by Gregoratti and Werner [M. Gregoratti and R. F. Werner, J. Mod. Opt. 50(6), 915-933 (2003)], we explicitly carry out all steps needed to invert a phase-damping error on a single qubit. Furthermore, we extend the scheme to a mixed-state environment. Surprisingly, we find cases for which the uncorrected state is closer to the desired state than any of the corrected ones

Influence of the detector's temperature on the quantum Zeno effect

In this paper we study the quantum Zeno effect using the irreversible model of the measurement. The detector is modeled as a harmonic oscillator interacting with the environment. The oscillator is subjected to the force, proportional to the energy of the measured system. We use the Lindblad-type master equation to model the interaction with the environment. The influence of the detector's temperature on the quantum Zeno effect is obtained. It is shown that the quantum Zeno effect becomes stronger (the jump probability decreases) when the detector's temperature increases

Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation

Protein phosphatase 1 (PP1) is a key regulator of important cardiac signaling pathways. Dysregulation of PP1 has been heavily implicated in cardiac dysfunctions. Accordingly, pharmacological targeting of PP1 activity is considered for therapeutic intervention in human cardiomyopathies. Recent evidence from animal models implicated previously unrecognized, isoform-specific activities of PP1 in the healthy and diseased heart. Therefore, this study examined the expression of the distinct PP1 isoforms PP1 alpha, beta, and gamma in human heart failure (HF) and atrial fibrillation (AF) and addressed the consequences of beta-adrenoceptor blocker (beta-blocker) therapy for HF patients with reduced ejection fraction on PP1 isoform expression. Using western blot analysis, we found greater abundance of PP1 isoforms alpha and gamma but unaltered PP1 beta levels in left ventricular myocardial tissues from HF patients as compared to non-failing controls. However, expression of all three PP1 isoforms was higher in atrial appendages from patients with AF compared to patients with sinus rhythm. Moreover, we found that in human failing ventricles, beta-blocker therapy was associated with lower PP1 alpha abundance and activity, as indicated by higher phosphorylation of the PP1 alpha-specific substrate eIF2 alpha. Greater eIF2 alpha phosphorylation is a known repressor of protein translation, and accordingly, we found lower levels of the endoplasmic reticulum (ER) stress marker Grp78 in the very same samples. We propose that isoform-specific targeting of PP1 alpha activity may be a novel and innovative therapeutic strategy for the treatment of human cardiac diseases by reducing ER stress conditions