A protocol for quantum secure direct communication with quantum superdense coding is proposed. It combines the ideas of block transmission, the ping-pong quantum secure direct communication protocol, and quantum superdense coding. It has the advantage of being secure and of high source capacity.

We present a way for symmetric multiparty-controlled teleportation of an arbitrary two-particle entangled state based on Bell-basis measurements by using two Greenberger-Horne-Zeilinger states, i.e., a sender transmits an arbitrary two-particle entangled state to a distant receiver, an arbitrary one of the n + 1 agents via the control of the others in a network. It will be shown that the outcomes in the cases that n is odd or it is even are different in principle as the receiver has to perform a controlled-not operation on his particles for reconstructing the original arbitrary entangled state in addition to some local unitary operations in the former. Also we discuss the applications of this controlled teleporation for quantum secret sharing of classical and quantum information. As all the instances can be used to carry useful information, its efficiency for qubits approaches the maximal value.Horne-Zeilinger (GHZ) state |ψ L = 1 √ 2 (|1010 + |0101 ). Recently, Rigolin [17] showed a way to teleport an arbitrary two-qubit entangled state with a four-particle entangled state |ψ R = 1 2 (|0000 + |0101 + |1010 + |1111 ) and four-particle joint measurements.Recently, controlled teleporation for a single-qubit |χ = a| ↑ + b| ↓ [33,34] [35] have been studied. In those teleportation protocols, the qubits can be regenerated by one of the receivers with the help of the others. Those principles can be used to split a quantum secret in QSS [19]. In this paper, we will present a symmetric protocol for multiparty-controlled teleportation of an arbitrary two-particle entangled state with two GHZ states and

Systemic lupus erythematosus (SLE) is an autoimmune/inflammatory disease characterized by autoantibody production and abnormal T cells that infiltrate tissues through not well-known mechanisms. We report that SLE T lymphocytes display increased levels of CD44, ezrin, radixin, and moesin (ERM) phosphorylation, stronger actin polymerization, higher polar cap formation, and enhanced adhesion and chemotactic migration compared with T cells from patients with rheumatoid arthritis and normal individuals. Silencing of CD44 by CD44 small interfering RNA in SLE T cells inhibited significantly their ability to adhere and migrate as did treatment with Rho kinase and actin polymerization inhibitors. Forced expression of T567D-ezrin, a phosphorylation-mimic form, enhanced remarkably the adhesion and migration rate of normal T cells. Anti-CD3/TCR autoantibodies present in SLE sera caused increased ERM phosphorylation, adhesion, and migration in normal T cells. pERM and CD44 are highly expressed in T cells infiltrating in the kidneys of patients with lupus nephritis. These data prove that increased ERM phosphorylation represents a key molecular abnormality that guides T cell adhesion and migration in SLE patients.

Systemic lupus erythematosus (SLE) T cells express high levels of cAMP response element modulator (CREM)that binds to the IL-2 promoter and represses the transcription of the IL-2 gene. This study was designed to identify pathways that lead to increased binding of CREM to the IL-2 promoter in SLE T cells. Ca 2+ /calmodulin-dependent kinase IV (CaMKIV) was found to be increased in the nucleus of SLE T cells and to be involved in the overexpression of CREM and its binding to the IL-2 promoter. Treatment of normal T cells with SLE serum resulted in increased expression of CREM protein, increased binding of CREM to the IL-2 promoter, and decreased IL-2 promoter activity and IL-2 production. This process was abolished when a dominant inactive form of CaMKIV was expressed in normal T cells. The effect of SLE serum resided within the IgG fraction and was specifically attributed to anti-TCR/CD3 autoantibodies. This study identifies CaMKIV as being responsible for the increased expression of CREM and the decreased production of IL-2 in SLE T cells and demonstrates that anti-TCR/CD3 antibodies present in SLE sera can account for the increased expression of CREM and the suppression of IL-2 production.

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