Erythrocyte distribution in arterial blood flow: II. The hypothesis of minimal energy dissipation

In a previous paper (Bull. Math. Biophysics,29, 549–563, 1967) the author derived equations to represent the flow of blood in an artery. It was pointed out that these did not completely characterize the system and that an additional hypothesis was required. The hypothesis of minimal energy dissipation had been thought to imply a central tendency on the part of suspended particles (erythrocytes). It is here shown that if the fluid is non-Newtonian this may not be so.     

Erythrocyte distribution in arterial blood flow: I. Basic equations and anisotropic effects

Equations are derived for the flow of an anisotropic fluid in a tube. It is argued that these provide a model for arterial blood flow. Particular attention is paid to the effect of radial differences in hematocrit. Sequels to this paper (Bull. Math. Biophysics,29, 565–574; forthcoming, 1967) will respectively demonstrate possible wall-directed forces on the erythrocyte and enlarge on the physiological consequence of hematocrit variations. The present article develops the basic equations and explores the possible role of anisotropic effects in blood flow.     

The extension of two-dimensional cable theory to arteries and arterioles

Electrical polarization of an artery or an arteriole may be modeled by the use of equations developed for two-dimensional cable theory. Two special cases have previously been solved: those corresponding to the case in which the radius is either zero (one-dimensional cable theory) or infinite. This paper presents the general solution.     

Asymptotic analysis of the Michaelis-Menten reaction equations

The irreversible Michaelis-Menten reaction is studied by the use of the method of multiple scales. Three stages of the reaction are identified, one of which is studied in detail. The results are compared with those of two earlier analyses.     

Proposed follow up programme after curative resection for lower third oesophageal cancer

Cyclins are indispensable elements of the cell cycle and derangement of their function can lead to cancer formation. Recent studies have also revealed more mechanisms through which cyclins can express their oncogenic potential. This review focuses on the aberrant expression of G1/S cyclins and especially cyclin D and cyclin E; the pathways through which they lead to tumour formation and their involvement in different types of cancer. These elements indicate the mechanisms that could act as targets for cancer therapy.