On stochastic models for the spread of infections

Heesterbeek, J.A.P. [Promotor]Meester, R.W.J. [Promotor

Радянські органи державної безпеки у 1939 – червні 1941 р.: документи ГДА СБ України

Рец. на кн.: «Радянські органи державної безпеки у 1939 – червні 1941 р.: документи ГДА СБ України / Упор. Василь Даниленко, Сергій Кокін. – К.: Вид. дім «Києво-Могилянська академія», 2009. – 1311 с.»

Phosporylation of androgen receptor isoforms

Phosphorylation of the human AR (androgen receptor) is directly correlated with the appearance of at least three AR isoforms on an SDS/polyacrylamide gel. However, it is still not clear to what extent phosphorylation is involved in the occurrence of isoforms, which sites are phosphorylated and what are the functions of these phosphosites. The human AR was expressed in COS-1 cells and AR phosphorylation was studied further by mutational analyses and by using reversed-phase HPLC and MS. The reversed-phase HPLC elution pattern of the three isoforms revealed that Ser-650 was phosphorylated constitutively. After de novo synthesis, only Ser-650 was phosphorylated in the smallest isoform of 110 kDa and both Ser-650 and Ser-94 were phosphorylated in the second isoform of 112 kDa. The hormone-induced 114 kDa isoform shows an overall increase in phosphorylation of all the isolated peptides. The activities of the Ser-Ala substitution mutant S650A (Ser-650-->Ala) was found to be identical with wild-type AR activation in four different cell lines and three different functional analyses, e.g. transactivation, N- and C-terminal-domain interaction and co-activation by transcriptional intermediary factor 2. This was also found for mutants S94A and S515A with respect to transactivation. However, the S515A mutation, which should eliminate phosphorylation of the potential mitogen-activated protein kinase site, Ser-515, resulted in an unphosphorylated form of the peptide containing Ser-650. This suggests that Ser-515 can modulate phosphorylation at another site. The present study shows that the AR isoform pattern from AR de novo synthesis is directly linked to differential phosphorylation of a distinct set of sites. After mutagenesis of these sites, no major change in functional activity of the AR was observed

On analytical approaches to epidemics on networks

One way to describe the spread of an infection on a network is by approximating the network by a random graph. However, the usual way of constructing a random graph does not give any control over the number of triangles in the graph, while these triangles will naturally arise in many networks (e.g. in social networks). In this paper, random graphs with a given degree distribution and a given expected number of triangles are constructed. By using these random graphs we analyze the spread of two types of infection on a network: infections with a fixed infectious period and infections for which an infective individual will infect all of its susceptible neighbors or none. These two types of infection can be used to give upper and lower bounds for

Reproduction numbers for epidemics on networks using pair approximation

One way to describe the spread of an infection on a network is by using the method of pair approximation. This method is a deterministic pair-based variant of the usual methods used to describe the progress of an epidemic in randomly mixing populations. However, although the ideas of pair approximation are intuitively clear, it is not straightforward to make all assumptions used explicit. Furthermore, in literature problems arise in defining basic quantities like the basic reproduction number

Estimation in branching processes with restricted observations

We consider an epidemic model where the spread of the epidemic can be described by a discrete-time Galton-Watson branching process. Between times n and n + 1, any infected individual is detected with unknown probability π and the numbers of these detected individuals are the only observations we have. Detected individuals produce a reduced number of offspring in the time interval of detection, and no offspring at all thereafter. If only the generation sizes of a Galton-Watson process are observed, it is known that one can only estimate the first two moments of the offspring distribution consistently on the explosion set of the process (and, apart from some lattice parameters, no parameters that are not determined by those moments). Somewhat surprisingly, in our context, where we observe a binomially distributed subset of each generation, we are able to estimate three functions of the parameters consistently. In concrete situations, this often enables us to estimate π consistently, as well as the mean number of offspring. We apply the estimators to data for a real epidemic of classical swine fever. © Applied Probability Trust 2006

A branching model for the spread of infectious animal diseases in varying environments

This paper is concerned with a stochastic model, describing outbreaks of infectious diseases that have potentially great animal or human health consequences, and which can result in such severe economic losses that immediate sets of measures need to be taken to curb the spread. During an outbreak of such a disease, the environment that the infectious agent experiences is therefore changing due to the subsequent control measures taken. In our model, we introduce a general branching process in a changing (but not random) environment. With this branching process, we estimate the probability of extinction and the expected number of infected individuals for different control measures. We also use this branching process to calculate the generating function of the number of infected individuals at any given moment. The model and methods are designed using important infections of farmed animals, such as classical swine fever, foot-and-mouth disease and avian influenza as motivating examples, but have a wider application, for example to emerging human infections that lead to strict quarantine of cases and suspected cases (e.g. SARS) and contact and movement restrictions