Thesis (M.D.)--University of Hong Kong, 1990. / Also available in print.

Thesis (M.D.)--University of Hong Kong, 1999. / Includes bibliographical references (leaves 157-201) Also available in print.

Blood sugar levels, and tumor size and incidence were determined for alloxanized Wistar rats bearing subcutaneous and intraperitoneal transplants of Novikoff hepatoma and Walker 256 carcinoma, and histological examination of the pancreas was undertaken to determine the extent of the damage to the beta-cells of the islets of Langerhans. Experiments were conducted in which animals were alloxanized 14 days, 7 days, 4 days, and 24 hours prior to, and 24 hours and 4 days after transplanting. The incidence and rate of growth of intraperitoneal tumors was appreciably decreased, and the rate of growth of subcutaneous tumors was slightly decreased in alloxanized animals, as compared with tumor-bearing controls. In tumor-bearing alloxanized animals, the high blood sugar levels characteristic of alloxan-diabetes were reduced to normal in some animals, and considerably ameliorated in others, as compared with alloxan-diabetic controls. Intraperitoneal tumors were more effective than subcutaneous tumors in reducing blood sugar levels, and relief was more pronounced in animals alloxanized just before or after transplanting than in those alloxanized two weeks before transplanting. Histological examination indicated that intraperitoneal tumor tissue invading the pancreas of alloxanized rats exerted a protective or regenerative effect on the beta-cells of the islets of Langerhans, which are selectively destroyed by alloxan. The possible role of sulphydryl groups in the amelioration of alloxan-diabetes in tumor-bearing animals, and in the reduction of tumor size and incidence in alloxan-diabetic animals is discussed. This work was reported in part in Proceedings of the American Association for Cancer Research, 2;20, 1955. / Science, Faculty of / Botany, Department of / Zoology, Department of / Graduate

No description available.

No description available.

Thesis (Ph. D.)--University of Washington, 1988. / Vita. Bibliography: leaves [120]-126.

Thesis (Ph. D.)--Göteborg University, 2006 / Thesis statement inserted. Includes bibliographical references.

Thesis (M.D.)—Boston University

Thesis (Master Diploma (Medical Technology) -- Cape Technikon, Cape Town, 1992 / The steady state in a tumour rapidly changes with its growth and the subsequent deteriorating blood and nutrient supply. This adaptation in the steady state of the tumour is shown in the increased lactate dehydrogenase and acid phosphatase activity in the tumour during it's growth. These alterations in the tumour metabolism places an increased burden on the body to supply nutrient and to discard the waste products of the tumour. This is demonstrated at the macroscopic level by the decreasing body weight and food intake when the tumour burden increases, and also at the metabolic levels by the responses of certain glycolytic and Cori cycle enzymes. Furthermore three distinct stages were observed in the Corl cycle response to the influence of the tumour namely, a silent or preclinical stage, a hypermetabolic stage and a hypometabolic stage. Although the decreasing body weight cannot be directly linked to the process of gluconeogenesis, the onset of anorexia appeared to coincide with the end of the hypermetabolic stage and the beginning of the hypometabolic stage in gluconeogenesis. This clearly shows that the body's steady state is adversely affected by the presence of the tumour and that the conditions at the metabolic level seem to cause the anorexia. Furthermore, it is well known that the success of cancer therapies depends entirely on the effectiveness o{the modality to kill the tumour cell and on the ability . of the host to absorb the damage caused by the modality without being destroyed in the process itself. The second part of this study demonstrates the radioprotective effects of ATP at all levels. It is clear from this work that ATP had a bigger influence in protecting the normal tissue than it had on the tumour tissue. This was demonstrated by the response of acid phosphatase (AP) and glucose-6-phosphate dehydrogenase (G-6-PDH) in the tumour and testis. Furthermore, it would seem that ATP has a multifactorial interaction with the cell, two possible mechanisms of protection are indicated by these results. The fIrst of these interactions is through the receptors of the cell to stimulate enhanced glycolysis, for higher energy production and thus repair. The second possibility is the interaction of ATP with the receptor of the cell to inhibit the production of free radicals and thus damage, as demonstrated by the response of G-6-PDH and AP.

Thesis (BTech (Biomedical Technology))--Cape Technikon, 1992. / The steady state in a tumour rapidly changes with its growth and the subsequent deteriorating blood and nutrient supply. This adaptation in the steady state of the tumour is shown in the increased lactate dehydrogenase and acid phosphatase activity in the tumour during it's growth. These alterations in the tumour metabolism places an increased burden on the body to supply nutrient and to discard the waste products of the tumour. This is demonstrated at the macroscopic level by the decreasing body weight and food intake when the tumour burden increases, and also at the metabolic levels by the responses of certain glycolytic and Cori cycle enzymes. Furthermore three distinct stages were observed in the Cori cycle response to the influence of the tumour namely, a silent or preclinical stage, a hypermetabolic stage and a hypo metabolic stage. Although the decreasing body weight cannot be directly linked to the process of gluconeogenesis, the onset of anorexia appeared to coincide with the end of the hypermetabolic stage and the beginning of the hypometabolic stage in gluconeogenesis. This clearly shows that the body's steady state is adversely affected by the presence of the tumour and that the conditions at the metabolic level seem to cause the anorexia. Furthermore, it is well known that the success of cancer therapies depends entirely on the effectiveness ofthe modality to kill the tumour cell and on the ability' of the host to absorb the damage caused by the modality without being destroyed in the process itself. The second part of this study demonstrates the radioprotective effects of ATP at all levels. It is clear from this work that ATP had a bigger influence in protecting the normal tissue than it had on the tumour tissue. This was demonstrated by the response of acid phosphatase (AP) and glucose-6-phosphate dehydrogenase (G-6-PDH) in the tumour and testis. Furthermore, it would seem that ATP has a multifactorial interaction with the cell, two possible mechanisms of protection are indicated by these results. The first of these interactions is through the receptors of the cell to stimulate enhanced glycolysis, for higher energy production and thus repair. The second possibility is the interaction of ATP with the receptor of the cell to inhibit the production of free radicals and thus damage, as demonstrated by the response of G-6-PDH and AP.