Aerospace medicine and biology: A continuing bibliography with indexes, supplement 183

This bibliography lists 273 reports, articles, and other documents introduced into the NASA scientific and technical information system in July 1978

A multiscale model for collagen alignment in wound healing

It is thought that collagen alignment plays a significant part in scar tissue formation during dermal wound healing. We present a multiscale model for collagen deposition and alignment during this process. We consider fibroblasts as discrete units moving within an extracellular matrix of collagen and fibrin modelled as continua. Our model includes flux induced alignment of collagen by fibroblasts, and contact guidance of fibroblasts by collagen fibres. We can use the model to predict the effects of certain manipulations, such as varying fibroblast speed, or placing an aligned piece of tissue in the wound. We also simulate experiments which alter the TGF-β concentrations in a healing dermal wound and use the model to offer an explanation of the observed influence of this growth factor on scarring

Cancer modelling: Getting to the heart of the problem

Paradoxically, improvements in healthcare that have enhanced the life expectancy of humans in the Western world have, indirectly, increased the prevalence of certain types of cancer such as prostate and breast. It remains unclear whether this phenomenon should be attributed to the ageing process itself or the cumulative effect of prolonged exposure to harmful environmental stimuli such as ultraviolet light, radiation and carcinogens (Franks and Teich, 1988). Equally, there is also compelling evidence that certain genetic abnormalities can predispose individuals to specific cancers (Ilyas et al., 1999). The variety of factors that have been implicated in the development of solid tumours stems, to a large extent, from the fact that ‘cancer’ is a generic term, often used to characterize a series of disorders that share common features. At this generic level of description, cancer may be viewed as a cellular disease in which controls that usually regulate growth and maintain homeostasis are disrupted. Cancer is typically initiated by genetic mutations that lead to enhanced mitosis of a cell lineage and the formation of an avascular tumour. Since it receives nutrients by diffusion from the surrounding tissue, the size of an avascular tumour is limited to several millimeters in diameter. Further growth relies on the tumour acquiring the ability to stimulate the ingrowth of a new, circulating blood supply from the host vasculature via a process termed angiogenesis (Folkman, 1974). Once vascularised, the tumour has access to a vast nutrient source and rapid growth ensues. Further, tumour fragments that break away from the primary tumour, on entering the vasculature, may be transported to other organs in which they may establish secondary tumours or metastases that further compromise the host. Invasion is another key feature of solid tumours whereby contact with the tissue stimulates the production of enzymes that digest the tissue, liberating space into which the tumour cells migrate. Thus, cancer is a complex, multiscale process. The spatial scales of interest range from the subcellular level, to the cellular and macroscopic (or tissue) levels while the timescales may vary from seconds (or less) for signal transduction pathways to months for tumour doubling times The variety of phenomena involved, the range of spatial and temporal scales over which they act and the complex way in which they are inter-related mean that the development of realistic theoretical models of solid tumour growth is extremely challenging. While there is now a large literature focused on modelling solid tumour growth (for a review, see, for example, Preziosi, 2003), existing models typically focus on a single spatial scale and, as a result, are unable to address the fundamental problem of how phenomena at different scales are coupled or to combine, in a systematic manner, data from the various scales. In this article, a theoretical framework will be presented that is capable of integrating a hierarchy of processes occurring at different scales into a detailed model of solid tumour growth (Alarcon et al., 2004). The model is formulated as a hybrid cellular automaton and contains interlinked elements that describe processes at each spatial scale: progress through the cell cycle and the production of proteins that stimulate angiogenesis are accounted for at the subcellular level; cell-cell interactions are treated at the cellular level; and, at the tissue scale, attention focuses on the vascular network whose structure adapts in response to blood flow and angiogenic factors produced at the subcellular level. Further coupling between the different spatial scales arises from the transport of blood-borne oxygen into the tissue and its uptake at the cellular level. Model simulations will be presented to illustrate the effect that spatial heterogeneity induced by blood flow through the vascular network has on the tumour’s growth dynamics and explain how the model may be used to compare the efficacy of different anti-cancer treatment protocols

Aerospace Medicine and Biology. A continuing bibliography with indexes (supplement 225)

This bibliography lists 140 reports, articles, and other documents introduced into the NASA scientific and technical information system in October 1981

Aerospace medicine and biology: A continuing bibliography with indexes, supplement 130, July 1974

This special bibliography lists 291 reports, articles, and other documents introduced into the NASA scientific and technical information system in June 1974

Aerospace medicine and biology: A continuing bibliography with indexes, supplement 125

This special bibliography lists 323 reports, articles, and other documents introduced into the NASA scientific and technical information system in January 1974

Southwest Research Institute assistance to NASA in biomedical areas of the technology utilization program Final report, 1 Feb. 1969 - 24 Aug. 1970

Research progress in technology transfer by NASA Biomedical Application Tea

Mathematical model for ionic exchanges in renal tubules: the role of epithelium.

This thesis deals with a mathematical model for a particular component of the kidney, the loop of Henle. We focus our attention on the ionic exchanges that take place in the tubules of the nephron, the functional unit of this organ. The model explicitly takes into account the epithelial layer at the interface between the tubular lumen and the surrounding environment (interstitium) where the tubules are immersed. The main purpose of this work is to understand the impact of the epithelium (cell membrane) on the mathematical model, how its role influences it and whether it provides more information on the concentration gradient, an essential determinant of the urinary concentrating capacity. In the first part of this transcript, we describe a simplified model for sodium exchanges in the loop of Henle, and we show the well-posedness of problem proving the existence, uniqueness and positivity of the solution. This model is an hyperbolic system 5x5 with constant speeds, a 'source' term and specific boundary conditions. We present a rigorous passage to the limit for this system 5x5 to a system of equations 3x3, representing the model without epithelial layers, in order to clarify the link between them. In the second part, thanks to the analysis of asymptotic behaviour, we show that our dynamic model converges towards the stationary system with an exponential rate for large time. In order to prove rigorously this global asymptotic stability result, we study eigen-elements of an auxiliary linear operator and its dual. We also perform numerical simulations on the stationary system solution to understand the physiological behaviour of ions concentrations