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H Tate

Publications and source records attributed to H Tate.

23 records · Page 2Linked to original sources

Assessing tumour markers.

This paper explores the factors involved in assessing the value of a medical test in a given clinical situation. It examines the problems involved in designing studies to investigate the role for a tumour marker in differential diagnosis and patient monitoring. An overview is given, including a critical evaluation of the preliminary research, the laboratory assay technique and potential clinical problems. Some examples are given. Specific approaches to the analysis of monitoring data are outlined, including the application of a sequential Bayesian model. This is illustrated using data from patients in the Medical Research Council's series of studies on the tumour marker Carcinoembryonic antigen.

Carcinoembryonic Antigen↗

The effect of enteral glutamine deprivation and supplementation on the structure of rat small-intestine mucosa during a systemic injury response.

BACKGROUND: An aseptic model of tissue injury (the induction of abscesses by subcutaneous injections of turpentine) was used to examine the proposal that changes in glutamine metabolism lead to structural damage in the epithelium of the small intestine during the systemic response to injury and to investigate the role of dietary glutamine in the maintenance of mucosal structure in the small intestine of control and injured rats. METHODS: Glutamine-free and glutamine-rich (3.6% glutamine by weight) diets were fed to rats before and during an acute-phase response to injury. Pair-fed groups of animals enabled an independent assessment to be made of the effects of the associated dietary restriction on the mucosal epithelium. RESULTS: Adaptive increases in villus height and crypt depth were seen in response to 4 days of feeding of the glutamine diet. Pair-feeding (30% dietary restriction) of either diet induced mucosal atrophy (loss of wet weight and nitrogen) without changes in villus height or crypt depth in the proximal tercile of the small intestine. Systemic injury, however, had no effect on the weight or nitrogen content of the mucosa (relative to pair-feeding). Gross histologic appearance, villus height, and crypt depth were also unchanged by the response to injury. CONCLUSIONS: The study provided no evidence to support the proposal that alterations in the availability of dietary glutamine during systemic injury (induced by turpentine injections) lead to structural damage to the epithelium.

Animals↗

The use of a constant infusion of [3H]phenylalanine to measure the effects of glutamine infusions on muscle protein synthesis in rats given turpentine.

Skeletal muscle protein fractional synthetic rate (MPFSR) was measured in rats with a constant infusion of [3H]phenylalanine to study the relationship between the rate of muscle protein synthesis in skeletal muscle and the intracellular glutamine concentration. The values for MPFSR (percentage per day) achieved in this study were in good agreement with those we have already reported with a flooding dose of [3H]phenylalanine to measure MPFSR. This was the case both for control rats and for those that had been injected with turpentine (constant infusion 12.82 +/- 0.43% in saline-injected rats, 6.58 +/- 0.34% in rats injected with turpentine; flooding dose 12.88 +/- 0.73% in saline-injected rats, 7.04 +/- 0.67% in rats injected with turpentine). Therefore, there was no evidence for a stimulating effect of a flooding dose of phenylalanine on MPFSR, an effect that could have invalidated the conclusions drawn in our previous investigation. In this study, turpentine reduced the MPFSR by a mean of 49% (p < 0.001). This reduction in MPFSR was associated with a 39% reduction in the mean intramuscular glutamine concentration (p < 0.001). This reduction in MPFSR was associated with a 39% reduction in the mean intramuscular glutamine concentration (p < 0.001). The reduction in intramuscular glutamine concentration was completely reversed by 5-h intravenous infusions of 0.22 M glutamine solutions, but there was no accompanying increase in the MPFSR. The results of this study therefore provide no evidence to support the proposal that an acute change in intramuscular glutamine concentration is a major factor in controlling the rate of protein synthesis in skeletal muscle.

Animals↗