Gill remodelling during terrestrial acclimation in the amphibious fish Polypterus senegalus

Fishes are effectively weightless in water due to the buoyant support of the environment, but amphibious fishes must cope with increased effective weight when on land. Delicate structures such as gills are especially vulnerable to collapse and loss of surface area out of water. We tested the ‘structural support’ hypothesis that amphibious Polypterus senegalus solve this problem using phenotypically plastic changes that provide mechanical support and increase stiffness at the level of the gill lamellae, the filaments, and the whole arches. After 7 d in terrestrial conditions, enlargement of an inter-lamellar cell mass filled the water channels between gill lamellae, possibly to provide structural support and/or reduce evaporative water loss. Similar gill remodelling has been described in several other actinopterygian fishes, suggesting this may be an ancestral trait. There was no change in the mechanical properties or collagen composition of filaments or arches after 7 days out of water, but 8 months of terrestrial acclimation caused a reduction in gill arch length and mineralized bone volume. Thus, rather than increasing the size and stiffness of the gill skeleton, P. senegalus may instead reduce investment in supportive gill tissue while on land. These results are strikingly similar to the evolutionary trend of gill loss that occurred during the tetrapod invasion of land, raising the possibility that genetic assimilation of gill plasticity was an underlying mechanism.     

Tumour-stromal interactions in acid-mediated invasion: A mathematical model

It is well established that the tumour microenvironment can both promote and suppress tumour growth and invasion, however, most mathematical models of invasion view the normal tissue as inhibiting tumour progression via immune modulation or spatial constraint. In particular, the production of acid by tumour cells and the subsequent creation of a low extracellular pH environment has been explored in several ‘acid-mediated tumour invasion’ models where the acidic environment facilitates normal cell death and permits tumour invasion. In this paper, we extend the acid-invasion model developed by Gatenby and Gawlinski (1996) to include both the competitive and cooperative interactions between tumour and normal cells, by incorporating the influence of extracellular matrix and protease production at the tumour-stroma interface. Our model predicts an optimal level of tumour acidity which produces both cell death and matrix degradation. Additionally, very aggressive tumours prevent protease production and matrix degradation by excessive normal cell destruction, leading to an acellular (but matrix filled) gap between the tumour and normal tissue, a feature seen in encapsulated tumours. These results sugest, counterintuitively, that increasing tumour acidity may, in some cases, prevent tumour invasion.     

On the spatial spread of the grey squirrel in Britain

We present a diffusion-competition model to describe the interaction between the externally introduced grey squirrel and the indigenous red squirrel in Britain. We estimate the model parameters from field data. Solution of the model predicts waves of grey squirrel invasion with speed of invasion typical of that observed in the field. Numerical solution of the model on a two-dimensional domain gives population distributions qualitatively similar to those observed. We suggest that competition alone could account for the observed displacement of the red squirrel by the grey in large regions of Britain. The solutions are qualitatively similar to those for a single species spreading in the absence of competition. The quantitative difference is because competition slows down the speed of advance of the invading species.     

Bradycardiac Angina: Haemodynamic Aspects and Treatment

A patient with a sinus bradycardia and angina is described who was unable to increase his heart rate on vigorous exercise by more than a few beats. His severe angina was attributed to the bradycardia. Atrial pacing of his heart abolished his angina and increased his exercise tolerance. Circulatory changes at rest, on exertion, and with atrial pacing are described. The cause of angina in this patient is discussed.