No description available.

Many tumour cells are more sensitive to hyperthermia than non-cancerous cells. The nature of this greater thermal sensitivity is not clear. The present study indicates that a likely cause for this increased thermal sensitivity is membrane-associated. Plasma membrane enriched fractions were obtained from two solid rat tumours: D23, a hepatoma, and Mc7, a sarcoma. Lipids from these membranes were extracted, characterized, and compared to equivalent fractions from control tissue (liver). In both cases the tumour membranes had lowered cholesterol: phospholipid ratios. There was little differenceln the phospholipid classes, but there was somecliSigfetice in the fatty acid composition of the individual phospholipids. Fluorescence polarization studies were carried out on whole membranes and indicated that the overall 'order' of the tumour membranes was decreased with respect to the controls. In addition a plasma membrane bound enzyme, the Mg2+ATPase, was found to be considerably more thermolabile in the tumour cells. The addition of the membrane pertubant tetracaine produced a greater degree of disorder in the tumour membranes compared to controls, and enhanced the thermolability of the Mg2+ATPase. These differences are further evidence that the plasma membrane is a likely site for the primary lesion in cell heat injury. Results from in vivo studies support the above mentioned in vitro work. D23 and Mc7 tumours, grown in the foot, were subject to hyperthermia and the simultaneous application of a membrane perturbant, tetracaine. The addition of the tetracaine significantly increased the efficacy of the treatment. When the D23 tumour was grown in ethanol-dependent rats there was no difference in the 'adaptive' response of the tumour, compared to the normal, plasma membranes. There was no difference in the heat sensitivity of foot tumours grown in ethanol-fed rats compared to tumours from pair fed controls.

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Diss. (sammanfattning) Stockholm : Univ., 2005. / Härtill 4 uppsatser.

Considerable evidence has emerged in recent years to suggest that the cell plasma membrane handles univalent and divalent cations abnormally in patients with untreated essential hypertension. Many of the phenomena originally discovered in patients with the established disease have now been found to occur in the genetically hypertension-prone offspring of hypertensive patients when their blood pressure is normal. The studies described in this thesis were designed to investigate the mechanisms which might explain these disturbances of membrane function. The first experiments were performed to investigate whether a circulating blood-borne factor might be present in excess in hypertensive patients and their relatives and by exposing cells from subjects with normal blood pressure and no family history to serum from patients and their offspring, the object was to try and reproduce the findings in hypertension. These studies were negative. Because of many reports of an overactive sympathetic nervous system in hypertension leucocytes were exposed to noradrenaline and this was found to influence sodium transport in cells from control subjects suggesting that at least some of the phenomena described in hypertension might be related to autonomic dysfunction. An alternative hypothesis to explain these abnormalities is that there is a genetically predetermined disturbance of the physicochemical structure of the plasma membrane which alters its function. The abnormality might well lie within the lipid fraction of the cell membrane. Attempts to alter this were undertaken using changes in dietary fat intake. These lowered blood pressure slightly and indeed altered sodium influx. The final series of experiments involved detailed examination of one fraction of plasma membrane phospholipids which is highly metabolically active, namely the phosphoinositides, and indeed using red cells it was possible to demonstrate that these lipids are overactive in the early stages of hypertension. These findings suggest that the plasma membrane is structurally abnormal in hypertension, the abnormality may reside in the phospho- inositide lipids and may possibly be susceptible to dietary manipulation.

No description available.

Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 96-104).

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No description available.

A thesis submitted to the Faculty of Medicine. University of the Witwatersrand. Johannesburg, for the Degree of Doctor of Philosophy / Abnormal cell membrane function and altered cellular cation homeostasis have been implicated in the pathogenesis of essential hypertension. The role of these factors in the aetiology of malignant hypertension is unknown. (Abbreviation abstract) / Andrew Chakane 2019