coli is not a small-world network. (C) 2010 Elsevier Ltd. All rights reserved.”
“Airway epithelium has been shown to elicit fluid secretion after a rise in intracellular calcium. This rise in intracellular calcium has been shown to display complex oscillations in many species after the binding of particular agonists to extracellular receptors.

Fluid secreted by the airway epithelium is used to maintain the depth of the periciliary CA-4948 liquid (PCL) above the apical membrane of the epithelial cells lining the bronchial airways. Previous mathematical models have been published which separately consider the electrophysiology involved in regulating periciliary liquid depth, and the

transmission of intracellular calcium waves in airway epithelial tissue. In this paper we present a mathematical model that combines these previous models and allows the effect of oscillations in intracellular calcium on fluid secretion by airway epithelial cells to be investigated. We show that an oscillatory calcium response produces different fluid secretion properties to that elicited by a tonic rise in intracellular calcium. These differences are shown to be due to saturation of the Ca(2+) activated ion channels. (C) 2010 Elsevier Ltd. All rights reserved.”
“A general assumption of quasispecies models of replicons

ATM inhibitor dynamics is that the fitness of a genotype is entirely determined by its sequence. However, a more biologically plausible situation is that fitness depends on the proteins that catalyze metabolic reactions, including replication. In a stirred population of replicons, such as viruses replicating and accumulating within the same cell, the association between a given genome and

the proteins it encodes is not tight as it can be replicated by proteins translated from other genomes. We have investigated how this complementation phenomenon affects the error threshold in simple quasispecies mean field models. We first Protein kinase N1 studied a model in which the master and the mutant genomes code for wild-type and mutant replicases, respectively. We assume that the mutant replicase has a reduced activity and that the wild-type replicase does not have increased affinity for the master genome. The whole pool of replicases can bind and replicate both genomes. We then analyze a different model considering a more extreme case of mutant genomes, the defective interfering particles (DIPs) described in many cases of viral infection. DIPs, with a higher replication rate owed to their shorter genomes, do not code for replicase, but they are able of using the replicase translated from the master genome. Our models allow to study how the probability of interaction between the genomes and the whole pool of replicases affects the error threshold.