Temporal order memories are critical for everyday animal and human functioning. Experiments and our own experience show that the binding or association of various features of an event together and the maintaining of multimodality events in sequential order are the key components of any sequential memories-episodic, semantic, working, etc. We study a robustness of binding sequential dynamics based on our previously introduced model in the form of generalized Lotka-Volterra equations. In the phase space of the model, there exists a multi-dimensional binding heteroclinic network consisting of saddle equilibrium points and heteroclinic trajectories joining them. We prove here the robustness of the binding sequential dynamics, i.e., the feasibility phenomenon for coupled heteroclinic networks: for each collection of successive heteroclinic trajectories inside the unified networks, there is an open set of initial points such that the trajectory going through each of them follows the prescribed collection staying in a small neighborhood of it. We show also that the symbolic complexity function of the system restricted to this neighborhood is a polynomial of degree L - 1, where L is the number of modalities.
Background: Metabolic reprogramming is a hallmark of pulmonary arterial hypertension. Platelet activation has been implicated in pulmonary arterial hypertension (PAH), whereas the role of platelet in the pathogenesis of PAH remains unclear. Methods: First, we explored the platelet function of SU5416/hypoxia mice and monocrotaline-injected rats PAH model. Then we investigated pulmonary arterial smooth muscle cell aerobic glycolysis after being treated with platelet supernatant. TGF (transforming growth factor)-βRI, PKM2, and other antagonists were applied to identify the underlying mechanism. In addition, platelet-specific deletion TGF-β1 mice were exposed to chronic hypoxia and SU5416. Cardiopulmonary hemodynamics, vascular remodeling, and aerobic glycolysis of pulmonary arterial smooth muscle cell were determined. Results: Here, we demonstrate that platelet-released TGF-β1 enhances the aerobic glycolysis of pulmonary arterial smooth muscle cells after platelet activation via increasing PKM2 expression. Mechanistically, platelet-derived TGF-β1 regulates PKM2 expression through mTOR (mammalian target of rapamycin)/c-Myc/PTBP1-hnRNPA1 pathway. Platelet TGF-β1 deficiency mice are significantly protected from SU5416 plus chronic hypoxia–induced PAH, including attenuated increases in right ventricular systolic pressure and less pulmonary vascular remodeling. Also, in Pf4cre + Tgfb1 fl/fl mice, pulmonary arterial smooth muscle cells showed lower glycolysis capacity and their PKM2 expression decreased. Conclusions: Our data demonstrate that TGF-β1 released by platelet contributes to the pathogenesis of PAH and further highlights the role of platelet in PAH.
We study the effects of random perturbations on collective dynamics of a large ensemble of interacting cells in a model of the cell division cycle. We consider a parameter region for which the unperturbed model possesses asymptotically stable two-cluster periodic solutions. Two biologically motivated forms of random perturbations are considered: bounded variations in growth rate and asymmetric division. We compare the effects of these two dispersive mechanisms with additive Gaussian white noise perturbations. We observe three distinct phases of the response to noise in the model. First, for weak noise there is a linear relationship between the applied noise strength and the dispersion of the clusters. Second, for moderate noise strengths the clusters begin to mix, i.e. individual cells move between clusters, yet the population distribution clearly continues to maintain a two-cluster structure. Third, for strong noise the clusters are destroyed and the population is characterized by a uniform distribution. The second and third phases are separated by an order - disorder phase transition that has the characteristics of a Hopf bifurcation. Furthermore, we show that for the cell cycle model studied, the effects of bounded random perturbations are virtually indistinguishable from those induced by additive Gaussian noise, after appropriate scaling of the variance of noise strength. We then use the model to predict the strength of coupling among the cells from experimental data. In particular, we show that coupling must be rather strong to account for the observed clustering of cells given experimentally estimated noise variance.
The solution of how to plan out the cooperative moving trajectory autonomously and control the motion of carrier-based aircraft timely and accurately is the key to helping improve the overall deck operation efficiency. The main problem discussed in this article is coordinated trajectory planning strategy for multicarrier aircraft and cooperative control between tractor and carrier aircraft. First, the kinematic model and three-degree-of-freedom dynamics model of the towbarless traction system are established. Then, a coevolution mechanism for aircraft systems is proposed to ensure coordinated trajectory planning among multiple aircraft and a trajectory adapted to the tractor-aircraft system is generated based on the hybrid RRT∗ algorithm. Next, a double-layer closed-loop controller is designed for the trajectory tracking of the tractor-aircraft system on the deck under the constraints of incomplete constraints and various physical conditions. It includes an outer model predictive controller which effectively controls the cooperative motion between the carrier aircraft and tractor and an inner torque control strategy based on adaptive fuzzy PID control which strictly ensures the stability of the system. Simulation results demonstrate that the controller is more rapid, more accurate, and more robust in tracking line trajectory with initial deviation, sine curve with large curvature, and complex trajectories on decks compared with backstepping control and LQR algorithm.
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