1,865 research outputs found
Charge Qubit Storage and Its Engineered Decoherence via Microwave Cavity
We study the entanglement of the superconducting charge qubit with the
quantized electromagnetic field in a microwave cavity. It can be controlled
dynamically by a classical external field threading the SQUID within the charge
qubit. Utilizing the controllable quantum entanglement, we can demonstrate the
dynamic process of the quantum storage of information carried by charge qubit.
On the other hand, based on this engineered quantum entanglement, we can also
demonstrate a progressive decoherence of charge qubit with quantum jump due to
the coupling with the cavity field in quasi-classical state.Comment: 6 pages, 4 figure
Decay process of quantum open system at finite-temperature
Starting from the formal solution to the Heisenberg equation, we revisit an
universal model for a quantum open system with a harmonic oscillator linearly
coupled to a boson bath. The analysis of the decay process for a Fock state and
a coherent state demonstrate that this method is very useful in dealing with
the problems in decay process of the open system. For finite temperature, the
calculations of the reduced density matrix and the mean excitation number for
the open system show that an initial coherent state will evolve into a
temperature-dependant coherent state after tracing over the bath variables.
Also in short-time limit, a temperature-dependant effective Hamiltonian for the
open system characterizes the decay process of the open system
Simultaneous eigenstates of the number-difference operator and a bilinear interaction Hamiltonian derived by solving a complex differential equation
As a continuum work of Bhaumik et al who derived the common eigenvector of
the number-difference operator Q and pair-annihilation operator ab (J. Phys. A9
(1976) 1507) we search for the simultaneous eigenvector of Q and
(ab-a^{+}b^{+}) by setting up a complex differential equation in the bipartite
entangled state representation. The differential equation is then solved in
terms of the two-variable Hermite polynomials and the formal hypergeometric
functions. The work is also an addendum to Mod. Phys. Lett. A 9 (1994) 1291 by
Fan and Klauder, in which the common eigenkets of Q and pair creators are
discussed
Association of the Resistin Gene Promoter Region Polymorphism with Kawasaki Disease in Chinese Children
Objectives. The −420 C > G polymorphism located in the resistin gene (RETN) promoter has recently been suggested to play a potential role in proinflammatory conditions and cardiovascular disease. This study investigated the association of the RETN promoter polymorphism with Kawasaki disease (KD) and its clinical parameters in Chinese children. Methods. We compared patients with complete KD to incomplete KD children. Genotyping of the RETN promoter polymorphism was performed using MassARRAY system, and serum resistin levels were estimated using the sandwich enzyme immunoassay method. Results. There was no significant difference in RETN (−420 C > G) genotypes between KD and control groups. However, the frequency of the G allele was higher in iKD patients than in cKD children due to a significantly increased frequency of the GG genotypes. Serum levels of resistin were significantly higher in KD patients than in controls regardless of the presence of coronary artery lesions (CALs). Conclusion. The present findings suggest that while resistin may play a role in the pathogenesis of KD, there is no apparent association between CAL and the RETN (−420 C > G) gene polymorphism in KD children. However, the diagnosis of iKD is challenging but can be supported by the presence of the G allele and the GG genotypes
Theaflavin-3, 3\u27-digallate induces apoptosis and G2 cell cycle arrest through the Akt/MDM2/p53 pathway in cisplatin-resistant ovarian cancer A2780/CP70 cells
Ovarian cancer is the most lethal gynecological cancer among women worldwide. Adverse side effects and acquired resistance to conventional platinum based chemotherapy are major impediments in ovarian cancer treatment, and drive the development of more selective anticancer drugs that target cancer-specific defects. In this study, theaflavin-3, 3\u27-digallate (TF3), the major theaflavin monomer in black tea, exhibited a potent growth inhibitory effect on the cisplatinresistant ovarian cancer A2780/CP70 cells (IC50, 23.81 μM), and was less cytotoxic to a normal ovarian IOSE‑364 cells (IC50, 59.58 μM) than to the cancer cells. Flow cytometry analysis indicated that TF3 induced preferential apoptosis and G2 cell cycle arrest in A2780/CP70 cells with respect to IOSE‑364 cells. TF3 induced apoptosis through both the intrinsic and extrinsic apoptotic pathways, and caused G2 cell cycle arrest via cyclin B1 in A2780/CP70 cells. The p53 protein played an important role in TF3-induced apoptosis and G2 cell cycle arrest. TF3 might upregulate the p53 expression via the Akt/MDM2 pathway. Our findings help elucidate the mechanisms by which TF3 may contribute to the prevention and treatment of platinum-resistant ovarian cancer
Theaflavin-3, 3\u27-digallate induces apoptosis and G2 cell cycle arrest through the Akt/MDM2/p53 pathway in cisplatin-resistant ovarian cancer A2780/CP70 cells
Ovarian cancer is the most lethal gynecological cancer among women worldwide. Adverse side effects and acquired resistance to conventional platinum based chemotherapy are major impediments in ovarian cancer treatment, and drive the development of more selective anticancer drugs that target cancer-specific defects. In this study, theaflavin-3, 3\u27-digallate (TF3), the major theaflavin monomer in black tea, exhibited a potent growth inhibitory effect on the cisplatinresistant ovarian cancer A2780/CP70 cells (IC50, 23.81 μM), and was less cytotoxic to a normal ovarian IOSE‑364 cells (IC50, 59.58 μM) than to the cancer cells. Flow cytometry analysis indicated that TF3 induced preferential apoptosis and G2 cell cycle arrest in A2780/CP70 cells with respect to IOSE‑364 cells. TF3 induced apoptosis through both the intrinsic and extrinsic apoptotic pathways, and caused G2 cell cycle arrest via cyclin B1 in A2780/CP70 cells. The p53 protein played an important role in TF3-induced apoptosis and G2 cell cycle arrest. TF3 might upregulate the p53 expression via the Akt/MDM2 pathway. Our findings help elucidate the mechanisms by which TF3 may contribute to the prevention and treatment of platinum-resistant ovarian cancer
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