Projective-anticipating, projective, and projective-lag synchronization of time-delayed chaotic systems on random networks

We study projective-anticipating, projective, and projective-lag synchronization of time-delayed chaotic systems on random networks. We relax some limitations of previous work, where projective-anticipating and projective-lag synchronization can be achieved only on two coupled chaotic systems. In this paper, we can realize projective-anticipating and projective-lag synchronization on complex dynamical networks composed by a large number of interconnected components. At the same time, although previous work studied projective synchronization on complex dynamical networks, the dynamics of the nodes are coupled partially linear chaotic systems. In this paper, the dynamics of the nodes of the complex networks are time-delayed chaotic systems without the limitation of the partial-linearity. Based on the Lyapunov stability theory, we suggest a generic method to achieve the projective-anticipating, projective, and projective-lag synchronization of time-delayed chaotic systems on random dynamical networks and find both the existence and sufficient stability conditions. The validity of the proposed method is demonstrated and verified by examining specific examples using Ikeda and Mackey-Glass systems on Erdos-Renyi networks.Comment: 14 pages, 6 figure

Active backstepping control of combined projective synchronization among different nonlinear systems

In this article, the authors have studied combination projective synchronization using active backstepping method. The main contribution of this effort is realization of the projective synchronization between two drive systems and one response system. We relax some limitations of previous work, where only combination complete synchronization has been investigated. According to Lyapunov stability theory and active backstepping design method, the corresponding controllers are designed to observe combination projective synchronization among three different classical chaotic systems, i.e. the Lorenz system, Rossler system and € Chen system. The numerical simulation examples verify the effectiveness of the theoretical analysis. Combination projective synchronization has stronger anti-attack ability and antitranslated ability than the normal projective synchronization scheme realized by one drive and one response system in secure communication

The Flare and Warp of the Young Stellar Disk traced with LAMOST DR5 OB-type stars

We present analysis of the spatial density structure for the outer disk from 8$-$14 \,kpc with the LAMOST DR5 13534 OB-type stars and observe similar flaring on north and south sides of the disk implying that the flaring structure is symmetrical about the Galactic plane, for which the scale height at different Galactocentric distance is from 0.14 to 0.5 \,kpc. By using the average slope to characterize the flaring strength we find that the thickness of the OB stellar disk is similar but flaring is slightly stronger compared to the thin disk as traced by red giant branch stars, possibly implying that secular evolution is not the main contributor to the flaring but perturbation scenarios such as interactions with passing dwarf galaxies should be more possible. When comparing the scale height of OB stellar disk of the north and south sides with the gas disk, the former one is slightly thicker than the later one by $\approx$ 33 and 9 \,pc, meaning that one could tentatively use young OB-type stars to trace the gas properties. Meanwhile, we unravel that the radial scale length of the young OB stellar disk is 1.17 $\pm$ 0.05 \,kpc, which is shorter than that of the gas disk, confirming that the gas disk is more extended than stellar disk. What is more, by considering the mid-plane displacements ($Z_{0}$) in our density model we find that almost all of $Z_{0}$ are within 100 \,pc with the increasing trend as Galactocentric distance increases.Comment: 14 pages and 8 figures, Accepted by APJ for publicatio

T cell senescence: a new perspective on immunotherapy in lung cancer

T cell senescence is an indication of T cell dysfunction. The ability of senescent T cells to respond to cognate antigens is reduced and they are in the late stage of differentiation and proliferation; therefore, they cannot recognize and eliminate tumor cells in a timely and effective manner, leading to the formation of the suppressive tumor microenvironment. Establishing methods to reverse T cell senescence is particularly important for immunotherapy. Aging exacerbates profound changes in the immune system, leading to increased susceptibility to chronic, infectious, and autoimmune diseases. Patients with malignant lung tumors have impaired immune function with a high risk of recurrence, metastasis, and mortality. Immunotherapy based on PD-1, PD-L1, CTLA-4, and other immune checkpoints is promising for treating lung malignancies. However, T cell senescence can lead to low efficacy or unsuccessful treatment results in some immunotherapies. Efficiently blocking and reversing T cell senescence is a key goal of the enhancement of tumor immunotherapy. This study discusses the characteristics, mechanism, and expression of T cell senescence in malignant lung tumors and the treatment strategies

Therapeutic effect of Rho kinase inhibitor FSD-C10 in a mouse model of Alzheimer\u27s disease.

Fasudil, a Rho kinase (ROCK) inhibitor, effectively inhibits disease severity in a mouse model of Alzheimer\u27s disease (AD). However, given its significant limitations, including a relatively narrow safety window and poor oral bioavailability, Fasudil is not suitable for long-term use. Thus, screening for ROCK inhibitor(s) that are more efficient, safer, can be used orally and suitable for long-term use in the treatment of neurodegenerative disorders is required. The main purpose of the present study is to explore whether FSD-C10, a novel ROCK inhibitor, has therapeutic potential in amyloid precursor protein/presenilin-1 transgenic (APP/PS1 Tg) mice, and to determine possible mechanisms of its action. The results showed that FSD-C10 effectively improved learning and memory impairment, accompanied by reduced expression of amyloid-β1-42 (Aβ 1-42 ), Tau protein phosphorylation (P-tau) and β-site APP-cleaving enzyme in the hippocampus and cortex area of brain. In addition, FSD-C10 administration boosted the expression of synapse-associated proteins, such as postynaptic density protein 95, synaptophsin, α-amino 3-hydroxy-5-methyl-4-isoxa-zolep-propionate receptor and neurotrophic factors, e,g., brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor. Taken together, our results demonstrate that FSD-C10 has therapeutic potential in the AD mouse model, possibly through inhibiting the formation of Aβ 1-42 and P-tau, and promoting the generation of synapse-associated proteins and neurotrophic factors

FSD-C10: A more promising novel ROCK inhibitor than Fasudil for treatment of CNS autoimmunity.

Rho-Rho kinase (Rho-ROCK) triggers an intracellular signalling cascade that regulates cell survival, death, adhesion, migration, neurite outgrowth and retraction and influences the generation and development of several neurological disorders. Although Fasudil, a ROCK inhibitor, effectively suppressed encephalomyelitis (EAE), certain side effects may limit its clinical use. A novel and efficient ROCK inhibitor, FSD-C10, has been explored. In the present study, we present chemical synthesis and structure of FSD-C10, as well as the relationship between compound concentration and ROCK inhibition. We compared the inhibitory efficiency of ROCKI and ROCK II, the cell cytotoxicity, neurite outgrowth and dendritic formation, neurotrophic factors and vasodilation between Fasudil and FSD-C10. The results demonstrated that FSD-C10, like Fasudil, induced neurite outgrowth of neurons and dendritic formation of BV-2 microglia and enhanced the production of neurotrophic factor brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF) and neurotrophin-3 (NT-3). However, the cell cytotoxicity and vasodilation of FSD-C10 were relatively small compared with Fasudil. Although Fasudil inhibited both ROCK I and ROCK II, FSD-C10 more selectively suppressed ROCK II, but not ROCK I, which may be related to vasodilation insensitivity and animal mortality. Thus, FSD-C10 may be a safer and more promising novel ROCK inhibitor than Fasudil for the treatment of several neurological disorders