Dynamic modeling and aperiodically intermittent strategy for adaptive finite-time synchronization control of the multi-weighted complex transportation networks with multiple delays

The idea of network splitting according to time delay and weight is introduced.Based on the cyber physical systems(CPS),a class of multi-weighted complex transportation networks with multiple delays is modeled.The finite-time synchronization of the proposed complex transportation networks model is studied systematically.On the basis of the theory of stability,the technique of adaptive control,aperiodically intermittent control and finite-time control,the aperiodically intermittent adaptive finite-time synchronization controller is designed.The controller designed in this paper is beneficial for understanding the synchronization in multi-weighted complex transportation networks with multiple delays.In addition,the conditions for the existence of finite time synchronization have been discussed in detail.And the specific value of the settling finite time for synchronization is obtained.Moreover,the outer coupling configuration matrices are not required to be irreducible or symmetric.Finally,simulation results of the finite-time synchronization problem are given to illustrate the correctness of the results obtained.

Self-Organized Optimization of Transport on Complex Networks

We propose a self-organized optimization mechanism to improve the transport capacity of complex gradient networks. We find that, regardless of network topology, the congestion pressure can be strongly reduced by the self-organized optimization mechanism. Furthermore, the random scale-free topology is more efficient to reduce congestion compared with the random Poisson topology under the optimization mechanism. The reason is that the optimization mechanism introduces the correlations between the gradient field and the local topology of the substrate network. Due to the correlations, the cutoff degree of the gradient network is strongly reduced and the number of the nodes exerting their maximal transport capacity consumedly increases. Our work presents evidence supporting the idea that scale-free networks can efficiently improve their transport capacity by self- organized mechanism under gradient-driven transport mode.

Control mechanisms in mitochondrial oxidative phosphorylation

Distribution and activity of mitochondda are key factors in neuronal development, synaptic plasticity and axogenesis. The majority of energy sources, necessary for cellular functions, originate from oxidative phosphorylation located in the inner mitochondrial membrane. The adenosine-5＇- triphosphate production is regulated by many control mechanism-firstly by oxygen, substrate level, adenosine-5＇-diphosphate level, mitochondrial membrane potential, and rate of coupling and proton leak. Recently, these mechanisms have been implemented by ＂second control mechanisms,＂ such as reversible phosphorylation of the tricarboxylic acid cycle enzymes and electron transport chain complexes, aUosteric inhibition of cytochrome c oxidase, thyroid hormones, effects of fatty acids and uncoupling proteins. Impaired function of mitochondria is implicated in many diseases ranging from mitochondrial myopathies to bipolar disorder and schizophrenia. Mitochondrial dysfunctions are usually related to the ability of mitochondria to generate adenosine-5＇-triphosphate in response to energy demands. Large amounts of reactive oxygen species are released by defective mitochondria similarly, decline of antioxidative enzyme activities （e.g. in the elderly） enhances reactive oxygen species production. We reviewed data concerning neuroplasticity, physiology, and control of mitochondrial oxidative phosphorylation and reactive oxygen species production.

Spastin is required for human immunodeficiency virus-1 efficient replication through cooperation with the endosomal sorting complex required for transport(ESCRT)protein

Human immunodeficiency virus-1(HIV-1)encodes simply 15 proteins and thus depends on multiple host cellular factors for virus reproduction.Spastin,a microtubule severing protein,is an identified HIV-1 dependency factor,but the mechanism regulating HIV-1 is unclear.Here,the study showed that knockdown of spastin inhibited the production of the intracellular HIV-1 Gag protein and new virions through enhancing Gag lysosomal degradation.Further investigation showed that increased sodium tolerance 1(IST1),the subunit of endosomal sorting complex required for transport(ESCRT),could interact with the MIT domain of spastin to regulate the intracellular Gag production.In summary,spastin is required for HIV-1 replication,while spastin-IST1 interaction facilitates virus production by regulating HIV-1 Gag intracellular trafficking and degradation.Spastin may serve as new target for HIV-1 prophylactic and therapy.