Biomedical subjects
Publications and source records attributed to M E Burt.
The methods of examining nitrogen metabolism in cancer-bearing humans are examined with specific examples. The major nutritional effect of cancer on the host is lean tissue and caloric reserve dissolution, with increased total body water. It seems clear that gluconeogenesis from amino acids can be suppressed by exogenous substrate. With appropriate nutritional repletion, protein catabolism can be suppressed and synthesis stimulated.
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Human sarcoma-bearing limb substrate utilization was characterized by studying 10 otherwise healthy patients with extremity sarcomas (five osteosarcomas, five soft tissue sarcomas). All patients were studied in the postabsorptive state. Extremity blood flow was measured using a non-invasive capacitance plethysmograph. Percutaneous arterial and venous effluent blood samples from the tumor-bearing (TB) and control extremity were obtained and flux was calculated for free fatty acids (FFA), glucose, and amino acids. The control limb showed a release of amino acids similar to that reported previously. There was a dramatic difference in the TB extremity, which consistently released fewer amino acids. Both the TB and control limbs released FFA at the same rate. A significant difference in glucose uptake between TB and control limbs was noted for soft tissue sarcoma patients but not osteogenic sarcoma patients. The amount extracted correlated with excised tumor size and gluconeogenic amino acid release from the contralateral normal limb. This study suggests that the tumor-bearing limb ignores the inherent conservation mechanisms in the postabsorptive state and continues to utilize substrate, apparently at the expense of host tissues.
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Hypercalcemia often complicates the course of patients with malignant neoplasms. Since this metabolic derangement is potentially lethal, knowledge of the expected relative incidence of hypercalcemia in various malignant neoplasms is of importance. The incidence of hypercalcemia and malignant neoplasm at the Clinical Center, National Institutes of Health, Bethesda, Md, was reviewed. Of 17,706 admissions (multiple admissions counted once), the overall incidence of hypercalcemia for all disorders was 5.0%; of these, 38.0% (338 patients) had associated neoplasms (99.4% malignant). Primary hyperparathyroidism represented 19.6% of those admitted with hypercalcemia, and nonneoplastic disorders represented 10.7%. Of the 338 patients with hypercalcemia associated with neoplasia, 44.1% had hematologic and 41.4% had solid neoplasms. The relative incidences of hypercalcemia and neoplasia are reported for each of the solid and hematologic neoplasias evaluated.
A system is described for chronic cannulation of the thoracic aorta and superior vena cava in the rat. This system employs a protective stainless steel coiled spring and water tight swivel and allows chronic infusion of solutions and simultaneous intermittent blood sampling for prolonged periods of time in the undisturbed unanesthetized rat. The rats (200-250 g) lost approximately 25 g in the immediate postoperative period, but then gained weight at a relatively normal rate (cannulated rats, 2.23 g/day; control rats, 2.29 g/day).
The present report describes a viable, isolated, perfused, human, tumor-bearing limb model suitable for the study of human host-tumor metabolism. The model is hemodynamically stable with high flow rates (50 cc/kg/min) and low perfusion pressures (mean, 77.2 mm Hg) which are stable over time. Metabolically, the preparation is viable with initial oxygen and glucose uptake 0.88 cc/kg/min and 0.029 mmole/kg/min, respectively. These parameters and lactate concentrations do not change significantly with time.
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Malignant melanoma occurs in approximately 1.7 per cent of all patients admitted to the Clinical Center, National Institutes of Health, and approximately 1.8 per cent of patients admitted with hypercalcemia and malignant disease. The incidence of hypercalcemia and malignant melanoma is 1.1 per cent. Bone metastases are diagnosed before death in approximately 5.2 per cent of patients with malignant melanoma. The cause of hypercalcemia in our patients appears to be bone metastases in 83.3 per cent and primary hyperparathyroidism in 16.9 per cent.
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The staining method uses alizarin red S and has been adapted for a 4-5 day cycle on a standard tissue processor. It gives consistently well stained bones and clear soft tissues in both rats and mice.
Carbamyl phosphate synthetase (from Escherichia coli) consists of a 7.3S protomeric unit that contains one heavy polypeptide chain (molecular weight about 130,000) and one light chain (molecular weight about 42,000). The heavy and light chains were separated by gel filtration in the presence of 1 M potassium thiocyanate. In contrast to the native enzyme and the reconstituted enzyme (prepared by mixing the separated heavy and light chains), the heavy chain does not catalyze glutamine-dependent carbamyl phosphate synthesis, although it does catalyze the synthesis of carbamyl phosphate from ammonia. The heavy chain also catalyzes two of the partial reactions catalyzed by the intact enzyme; i.e., the bicarbonate-dependent cleavage of ATP and the synthesis of ATP from ADP and carbamyl phosphate. Both positive (ammonia, ornithine, IMP) and negative (UMP) allosteric regulatory sites are located on the heavy chain. The only catalytic activity exhibited by the light chain is the hydrolysis of glutamine. A model is presented according to which glutamine binds to the light chain, which is followed by release of nitrogen from the amide group for use by the heavy chain. The findings suggest that glutamine-dependent carbamyl phosphate synthetase (and perhaps other glutamine amidotransferases) arose in the course of evolution by a combination of a primitive ammonia-dependent synthetic enzyme and a glutaminase; this combination may have been associated with a change from ammonia to glutamine as the principal source of nitrogen.