Macrophage response to Mycobacterium tuberculosis infection.

The immune response to Mycobacterium tuberculosis (Mtb) infection is the formation of multicellular lesions, or granolomas, in the lung of the individual. However, the structure of the granulomas and the spatial distribution of the immune cells within is not well understood. In this paper we develop a mathematical model investigating the early and initial immune response to Mtb. The model consists of coupled reaction-diffusion-advection partial differential equations governing the dynamics of the relevant macrophage and bacteria populations and a bacteria-produced chemokine. Our novel application of mathematical concepts of internal states and internal velocity allows us to begin to study this unique immunological structure. Volume changes resulting from proliferation and death terms generate a velocity field by which all cells are transported within the forming granuloma. We present numerical results for two distinct infection outcomes: controlled and uncontrolled granuloma growth. Using a simplified model we are able to analytically determine conditions under which the bacteria population decreases, representing early clearance of infection, or grows, representing the initial stages of granuloma formation.

Estimating the selective advantage of mutant p53 tumour cells to repeated rounds of hypoxia.

The tumour suppressor gene, p53, plays an important role in tumour development. Under low levels of oxygen (hypoxia), cells expressing wild-type p53 undergo programmed cell death (apoptosis), whereas cells expressing mutations in the p53 gene may survive and express angiogenic growth factors that stimulate tumour vascularization. Given that cells expressing mutations in the p53 gene have been observed in many forms of human tumour, it is important to understand how both wild-type and mutant cells react to hypoxic conditions. In this paper a mathematical model is presented to investigate the effects of alternating periods of hypoxia and normoxia (normal oxygen levels) on a population of wild-type and mutant p53 tumour cells. The model consists of three coupled ordinary differential equations that describe the densities of the two cell types and the oxygen concentration and, as such, may describe the growth of avascular tumours in vitro and/or in vivo. Numerical and analytical techniques are used to determine how changes in the system parameters influence the time at which mutant cells become dominant within the population. A feedback mechanism, which switches off the oxygen supply when the total cell density exceeds a threshold value, is introduced into the model to investigate the impact that vessel collapse (and the associated hypoxia) has on the time at which the mutant cells become dominant within vascular tumours growing in vivo. Using the model we can predict the time it takes for a subpopulation of mutant p53 tumour cells to become the dominant population within either an avascular tumour or a localized region of a vascular tumour. Based on independent experimental results, our model suggests that the mutant population becomes dominant more quickly in vivo than in vitro (12 days vs 17 days).

An investigation into the potential hazard to animal health of effluent sludge from dairy factories.

Sixty-three samples of the more solid material (sludge) separated from the effluent plants of dairy factories were examined for the presence of salmonellas and brucellas. Salmonellas were isolated from two samples (S. heidelberg. [1]; S. indiana [1]. No brucellas were isolated. None of the samples supported the growth of S. dublin. Salmonellas added to effluent sludge at a concentration of 10(6) organisms/ml. survived less than 70 days. The sludge from dairy factory effluent plants does not appear to be a source for the spread of salmonellosis or brucellosis.

Adenosine 5'-triphosphate-arginine phosphotransferase from lobster muscle. Molecular weight.

1. The molecular weight of arginine kinase from lobster muscle has been determined by three procedures: ultracentrifuge analysis, gel filtration and density-gradient centrifugation. 2. The three methods give similar results and the best estimate of the molecular weight is 37000. 3. The enzyme does not readily show association-dissociation phenomena. 4. The usefulness of density-gradient centrifugation for determinations of molecular weight is briefly discussed.