Geometric phase in open systems: beyond the Markov approximation and weak coupling limit

Beyond the quantum Markov approximation and the weak coupling limit, we present a general theory to calculate the geometric phase for open systems with and without conserved energy. As an example, the geometric phase for a two-level system coupling both dephasingly and dissipatively to its environment is calculated. Comparison with the results from quantum trajectory analysis is presented and discussed

The appraisal similarity effect: how social appraisals influence liking

The effects of cognitive appraisals on interpersonal relationships have hardly been studied. Three experiments examined how empathic social appraisal could influence liking. We tested for the appraisal similarity effect in which perceived similarity in appraisals boosts liking. In Experiment 1, perception of appraisal similarity led participants to express liking by disclosing personal contact information. This effect was replicated using a selfreport measure of liking in Experiments 2 and 3. Also, by independently manipulating attitude similarity, the appraisal similarity effect was deactivated under perceived attitude dissimilarity. Likewise, the robust attitude similarity effect was invalidated under perceived appraisal dissimilarity. In Experiment 3, the perception of validated personal beliefs mediated this interactive effect in a moderated mediation scenario, and the appraisal similarity effect

Effective Hamiltonian approach to adiabatic approximation in open systems

The adiabatic approximation in open systems is formulated through the effective Hamiltonian approach. By introducing an ancilla, we embed the open system dynamics into a non-Hermitian quantum dynamics of a composite system, the adiabatic evolution of the open system is then defined as the adiabatic dynamics of the composite system. Validity and invalidity conditions for this approximation are established and discussed. A High-order adiabatic approximation for open systems is introduced. As an example, the adiabatic condition for an open spin-$\frac 1 2$ particle in time-dependent magnetic fields is analyzed.Comment: 6 pages, 2 figure

A Unified Quantum NOT Gate

We study the feasibility of implementing a quantum NOT gate (approximate) when the quantum state lies between two latitudes on the Bloch's sphere and present an analytical formula for the optimized 1-to-$M$ quantum NOT gate. Our result generalizes previous results concerning quantum NOT gate for a quantum state distributed uniformly on the whole Bloch sphere as well as the phase covariant quantum state. We have also shown that such 1-to-$M$ optimized NOT gate can be implemented using a sequential generation scheme via matrix product states (MPS)

On Bures fidelity of displaced squeezed thermal states

Fidelity plays a key role in quantum information and communication theory. Fidelity can be interpreted as the probability that a decoded message possesses the same information content as the message prior to coding and transmission. In this paper, we give a formula of Bures fidelity for displaced squeezed thermal states directly by the displacement and squeezing parameters and birefly discuss how the results can apply to quantum information theory.Comment: 10 pages with RevTex require

Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities

Acute myocardial infarction (AMI) and the heart failure that often follows, are major causes of death and disability worldwide. As such, new therapies are required to limit myocardial infarct (MI) size, prevent adverse left ventricular (LV) remodeling, and reduce the onset of heart failure following AMI. The inflammatory response to AMI, plays a critical role in determining MI size, and a persistent pro-inflammatory reaction can contribute to adverse post-MI LV remodeling, making inflammation an important therapeutic target for improving outcomes following AMI. In this article, we provide an overview of the multiple players (and their dynamic roles) involved in the complex inflammatory response to AMI and subsequent LV remodeling, and highlight future opportunities for targeting inflammation as a therapeutic strategy for limiting MI size, preventing adverse LV remodeling, and reducing heart failure in AMI patients

IL11 (Interleukin-11) causes emphysematous lung disease in a mouse model of marfan syndrome.

BACKGROUND: Marfan Syndrome (MFS) is an inherited connective tissue disorder caused by mutations in the FBN1 (fibrillin-1) gene. Lung abnormalities are common in MFS, but their pathogenesis is poorly understood. IL11 (interleukin-11) causes aortic disease in a mouse model of MFS and was studied here in the lung. METHODS: We examined histological and molecular phenotypes in the lungs of Fbn1C1041G/+ mice (mouse model of Marfan Syndrome [mMFS]), an established mouse model of MFS. To identify IL11-expressing cells, we used immunohistochemistry on lungs of 4- and 16-week-old Fbn1C1041G/+:Il11EGFP/+ reporter mice. We studied the effects of IL11 inhibition by RT-qPCR, immunoblots and histopathology in lungs from genetic or pharmacologic models: (1) 16-week-old IL11 receptor (IL11RA) knockout mMFS mice (Fbn1C1041G/+:Il11ra1-/- mice) and (2) in mMFS mice administered IgG control or interleukin-11 receptor antibodies twice weekly from 4 to 24 weeks of age. RESULTS: mMFS lungs showed progressive loss and enlargement of distal airspaces associated with increased proinflammatory and profibrotic gene expression as well as matrix metalloproteinases 2, 9, and 12. IL11 was increased in mMFS lungs and localized to smooth muscle and endothelial cells in young mMFS mice in the Fbn1C1041G/+:Il11EGFP/+ reporter strain and in fibroblasts, in older mice. In mMFS mice, genetic (Fbn1C1041G/+:Il11ra1-/-) or pharmacologic (anti-interleukin-11 receptor) inhibition of IL11 signaling reduced lung emphysema, fibrosis, and inflammation. This protective effect was associated with reduced pathogenic ERK1/2 signaling and lower metalloproteinase 2, 9, and 12 expression. CONCLUSIONS: IL11 causes lung disease in mMFS. This reveals a shared IL11-driven disease mechanism in lung and aorta in MFS and suggests inhibition of IL11 signaling as a holistic approach for treating multiorgan morbidity in MFS