Optimization of jamming formation of USV offboard active decoy clusters based on an improved PSO algorithm

Offboard active decoys(OADs)can effectively jam monopulse radars.However,for missiles approaching from a particular direction and distance,the OAD should be placed at a specific location,posing high requirements for timing and deployment.To improve the response speed and jamming effect,a cluster of OADs based on an unmanned surface vehicle(USV)is proposed.The formation of the cluster determines the effectiveness of jamming.First,based on the mechanism of OAD jamming,critical conditions are identified,and a method for assessing the jamming effect is proposed.Then,for the optimization of the cluster formation,a mathematical model is built,and a multi-tribe adaptive particle swarm optimization algorithm based on mutation strategy and Metropolis criterion(3M-APSO)is designed.Finally,the formation optimization problem is solved and analyzed using the 3M-APSO algorithm under specific scenarios.The results show that the improved algorithm has a faster convergence rate and superior performance as compared to the standard Adaptive-PSO algorithm.Compared with a single OAD,the optimal formation of USV-OAD cluster effectively fills the blind area and maximizes the use of jamming resources.

Role of Activator Protein-1 in the Transcription of Interleukin-5 Gene Regulated by Protein Kinase C Signal in Asthmatic Human TLymphocytes

Summary: In order to explore the role of activator protein-1 (AP-1) in the transcription of interleukin-5 (IL-5) gene regulated by protein kinase C (PKC) signal in peripheral blood T lymphocytes from asthmatic patient, T lymphocytes were isolated and purified from peripheral blood of each asthmatic patient. The T lymphocytes were randomly divided into 4 groups: group A (blank control), group B (treated with PKC agonist phorbol 12-myristate 13-acetate (PMA)), Group C (treated with PMA and AP-1 cis-element decoy oligodeoxynucleotides (decoy ODNs)), and group D (treated with PMA and AP-1 mutant decoy ODNs). The ODNs were transfected into the T cells of group C and D by cation liposome respectively. Reverse transcription-polymerase chain reaction (RT-PCR) was employed to assess IL-5 mRNA expression, and electrophoretic mobility shift assays (EMSA) for the activation of AP-1. The results showed that the activation of AP-1 (88 003.58±1 626.57) and the expression of IL-5 mRNA (0.8300±0.0294) in T lymphocytes stimulated with PMA were significantly higher than these in blank control (20 888.47±1103.56 and 0.3050±0.0208, respectively, P< 0.01), while the indexes (23 219.83±1 024.86 and 0.3425±0.0171 respectively) of T lymphocytes stimulated with PMA and AP-1 decoy ODNs were significantly inhibited, as compared with group B (P< 0.01). The indexes (87 107.41±1 342.92 and 0.8225±0.0222, respectively) in T lymphocytes stimulated with PMA and AP-1 mutant decoy ODNs did not exhibit significant changes, as compared with group B (P>0.05). The significant positive correlation was found between the activation of AP-1 and the expression of IL-5 mRNA (P< 0.01). It was concluded that AP-1 might participate in the signal transduction of PKC-triggered transcription of IL-5 gene in asthmatic T lymphocytes. This suggests the activation of PKC/AP-1 signal transduction cascade of T lymphocytes may play an important role in the pathogenesis of asthma.

Decoy receptor 3: Its role as biomarker for chronic inflammatory diseases

Members of the tumor-necrosis factor-α(TNF-α) and TNF-α receptor(TNFR) superfamilies of proteins(TNFSF and TNFRSF, respectively) play important roles in the function of the immune system. Decoy receptor 3(Dc R3, TNFRSF6b) is a decoy receptor that binds to three TNFSF ligands, Fas L, LIGHT and TL1 A. Association to these ligands competes with the corresponding functional receptors and blocks downstream signaling, leading to immunomodulatory effects, including the prevention of apoptosis. Dc R3 lacks a transmembrane region and exists only as a secreted protein, which is detectable in biological fluids. Recent studies have shown that Dc R3 is upregulated and may be pathogenetically implicated in several and diverse chronic inflammatory diseases. The strongest associations have been described for rheumatological diseases, mainly systemic lupus erythematosus and rheumatoid arthritis, inflammatory bowel disease, and serious infectious conditions, including systemic inflammatory response syndrome. In the majority of these conditions, Dc R3 m RNA and protein expression is elevated both at the target tissues as well as in the systemic circulation. Dc R3 concentration in the serum is untraceable in the majority of healthy individuals but can be detected in patients with various inflammatory diseases. In mostsuch cases, soluble Dc R3 correlates with disease severity, as patients with severe forms of disease have significantly higher levels than patients with milder or no activity. In addition, effective anti-inflammatory treatment leads to the disappearance of soluble Dc R3 from the circulation. Taken together, current evidence suggests that serum Dc R3 may become a useful biomarker for chronic inflammatory disorders, as it is upregulated in response to inflammatory stimuli, and may serve both as a prognostic marker for disease severity and as a surrogate indicator of response to treatment.

New protocols for non-orthogonal quantum key distribution

Combining the passive decoy-state idea with the active decoy-state idea, a non-orthogonal （SARG04） decoy-state protocol with one vacuum and two weak decoy states is introduced based on a heralded pair coherent state photon source for quantum key distribution. Two special cases of this protocol are deduced, i.e., a one-vacuum-and-one-weak-decoy-state protocol and a one-weak-decoy-state protocol. In these protocols, the sender prepares decoy states actively, which avoids the crude estimation of parameters in the SARG04 passive decoy-state method. With the passive decoy-state idea, the detection events on Bob＇s side that are non-triggered on Alice＇s side are not discarded, but used to estimate the fractions of single-photon and two-photon pulses, which offsets the limitation of the detector＇s low efficiency and overcomes the shortcoming that the performance of the active decoy-state protocol critically depends on the efficiency of detector. The simulation results show that the combination of the active and passive decoy-state ideas increases the key generation rate. With a one-vacuum-and-two-weak-decoy-state protocol, one can achieve a key generation rate that is close to the theoretical limit of an infinite decoy-state protocol. The performance of the other two protocols is a little less than with the former, but the implementation is easier. Under the same condition of implementation, higher key rates can be obtained with our protocols than with existing methods.