A theta-scheme approximation of basic reproduction number for an age-structured epidemic system in a finite horizon.

This paper focuses on numerical approximation of the basic reproduction number R, which is the threshold defined by the spectral radius of the next-generation operator in epidemiology. Generally speaking, R cannot be explicitly calculated for most age-structured epidemic systems. In this paper, for a deterministic age-structured epidemic system and its stochastic version, we discretize a linear operator produced by the infective population with a theta scheme in a finite horizon, which transforms the abstract problem into the problem of solving the positive dominant eigenvalue of the next-generation matrix.

A model of HBV infection with intervention strategies: dynamics analysis and numerical simulations.

In this paper, we analyze the effect of environment noise on the transmission dynamics of a stochastic hepatitis B virus (HBV) infection model with intervention strategies. By using the Markov semigroups theory, we define the stochastic basic reproduction number and find it can be used to govern disease extinction or persistence. When it is less than one, under a mild extra condition, the stochastic system has a disease-free equilibrium and the disease is predicted to die out with probability one.

Markovian switching for near-optimal control of a stochastic SIV epidemic model.

As it is known that environmental perturbation is a key component of epidemic models, and Markov process reveals how the noise affects epidemic systems. The paper introduces Markov chain into a stochastic susceptible-infected-vaccination(SIV) epidemic model composed of vaccination and saturated treatment to analyze the near-optimal control. Based on Pontryagin stochastic maximum principle, the paper gives adequate and all necessary conditions for near-optimal control.

Value of promoter methylation in colorectal cancer screening and prognosis assessment and its influence on the activity of cancer cells.

Introduction: The aim of the study was to investigate the effect of promoter methylation on the proliferative, invasive and migration potential of colorectal cancer cells, including its potential use for the early detection and prognostic assessment of colorectal cancer.

Material And Methods: Quantitative methylation-specific PCR (qMSP) was used to detect the methylation status of the promoter region in peripheral blood samples drawn from patients with colorectal adenocarcinoma, benign colorectal adenoma, and matched healthy controls. Putative CpG methylation sites were then pyrosequenced.

Inhibition of Nonsmall Cell Lung Cancer Cell Migration by Protein Arginine Methyltransferase 1-small Hairpin RNA Through Inhibiting Epithelial-mesenchymal Transition, Extracellular Matrix Degradation, and Src Phosphorylation In Vitro.

Background: Protein arginine methyltransferases 1 (PRMT1) is over-expressed in a variety of cancers, including lung cancer, and is correlated with a poor prognosis of tumor development. This study aimed to investigate the role of PRMT1 in nonsmall cell lung cancer (NSCLC) migration in vitro.

Methods: In this study, PRMT1 expression in the NSCLC cell line A549 was silenced using lentiviral vector-mediated short hairpin RNAs.

Expansion of NK cells by engineered K562 cells co-expressing 4-1BBL and mMICA, combined with soluble IL-21.

NK cells hold promise for protecting hosts from cancer and pathogen infection through direct killing and expressing immune-regulatory cytokines. In our study, a genetically modified K562 cell line with surface expression of 4-1BBL and MICA was constructed to expand functional NK cells in vitro for further adoptive immunotherapy against cancer. After a long-term up to 21 day co-culture with newly isolated peripheral blood mononuclear cells (PBMCs) in the presence of soluble IL-21 (sIL-21), notable increase in proportion of expanded NK cells was observed, especially the CD56(bright)CD16(+) subset.

Role of unfolded protein response in affecting osteoblast differentiation induced by fluoride.

The objective of this study was to determine the expression of classic bone markers and unfolded protein response (UPR) signaling factors through MC3T3-E1 cells exposed to varying concentrations of fluoride. Excessive fluoride exposure caused the skeletal disease. During this process, osteoblasts played a critical role in the advanced skeletal fluorosis.

Role of endoplasmic reticulum stress in aberrant activation of fluoride-treated osteoblasts.

The aberrant activation of osteoblasts in the early stage is one of the critical steps during the pathogenesis of skeletal fluorosis. The endoplasmic reticulum (ER) stresses and unfolded protein response (UPR) are initiated to alleviate the accumulation of unfolded proteins against cell injury. The previous researches had demonstrated that fluoride induced ER stress in other cells or tissues.

Effect of fluoride on insulin level of rats and insulin receptor expression in the MC3T3-E1 cells.

Studies on the role of insulin and insulin receptor (InsR) in the process of skeletal fluorosis, especially in osteogenic function, are rare. We evaluated the effect of increasing F⁻ doses on the marker of bone formation, serum insulin level and pancreatic secretion changes in vivo and mRNA expression of InsR and osteocalcin (OCN) in vitro. Wistar rats (n = 50) were divided into two groups, i.

Comparative proteomic analysis in left ventricular remodeling following myocardial infarction in rats.

Objective: Left ventricular remodeling (LVR) following myocardial infarction (MI) is a key pathophysiological process in which MI develops into heart failure. The exact mechanism of LVR remains unclear. We performed differential proteomic analysis on the myocardia of rats with LVR after MI, to explore the mechanism of ventricular remodeling after MI.