This paper focuses on the better performance between the garment simulation result and the simulation speed. For simplicity and clarity, a notation “PART” is defined to indicate the areas between the garment and the human body satisfying some constraints. The discrete mechanical model can be achieved by the two-stage process. In the first stage, the garment can be divided into several PARTs constrained by the distance. In the second stage, the mechanical model of each PART is formulated with a mathematical expression. Thus, the mechanical model of the garment can be obtained. Through changing the constrained distance, the simulation result and the simulation speed can be observed. From the variable distance, a desired value can be chosen for an optimal value. The results of simulations and experiments demonstrate that the better performance can be achieved at a higher speed by saving runtime with the acceptable simulation results and the efficiency of the proposed scheme can be verified as well.
Porcine epidemic diarrhoea virus (PEDV) infection causes watery diarrhoea, vomiting, anorexia, and weight loss, especially among neonatal piglets, inflicting on them morbidity and mortality potentially reaching 90%–100%. Despite it being known that certain mammalian cell phases are arrested by PEDV, the mechanisms have not been elucidated, and PEDV pathogenesis is poorly understood. This study determined the effect of an epidemic PEDV strain on cell cycle progression.
Material and Methods
We observed the effect of the PEDV SHpd/2012 strain on an infected Vero cell cycle through flow cytometry and Western blot, investigating the interrelationships of cell-cycle arrest, the DNA damage–signalling pathway caused by PEDV and the phosphorylation levels of the key molecules Chk.2 and H2A.X involved upstream and downstream in this pathway.
PEDV induced Vero cell-cycle arrest at the G1/G0 phase. The phosphorylation levels of Chk.2 and H2A.X increased with the prolongation of PEDV infection, and no significant cell-cycle arrest was observed after treatment with ATM or Chk.2 inhibitors. The proliferation of PEDV was also inhibited by treatment with ATM or Chk.2 inhibitors.
PEDV-induced cell-cycle arrest is associated with activation of DNA damage–signalling pathways. Our findings elucidate the molecular basis of PEDV replication and provide evidence to support further evaluation of PEDV pathogenesis.