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D Matthews

Publications and source records attributed to D Matthews.

At least 91 records · Page 5Linked to original sources
PubMed1982

Effect of exercise on protein metabolism in humans as explored with stable isotopes.

Exercising for 3.75 h on a treadmill at 50% VO2 max in the fed state induced an increased excretion of 71 mg nitrogen/kg over the 18 h after exercise. However, measurements of the time course of changes in 13CO2 excretion from ingested [1-13C]leucine indicated that all of this increased nitrogen production occurs during the exercise period. Because of the reduced renal clearance and slow turnover of the urea pool, urea excretion lags behind urea production. Measurements of nitrogen flux from the plateau labeling of urinary ammonia achieved by repeated oral doses of 15N-labeled glycine indicated that the nitrogen loss resulted from an increase in protein degradation and a decrease in protein synthesis. Further studies with [1-13C]leucine indicated that a 2-h treadmill exercise induced an increase in the nitrogen loss from 5.4 to 16 mg . kg-1 . h-1 measured with a primed constant infusion of [1-13C]leucine. This resulted from a fall in whole-body protein synthesis. Glucose given at the rate of 0.88 g . kg-1 . h-1 depressed the rate of whole-body protein degradation and appeared to suppress the exercise-induced increase in nitrogen excretion. When leucine oxidation rates were measured at increasing work rates, a linear relationship between percentage of VO2 max and leucine oxidation was observed up to 89% VO2 max when 54% of the flux of leucine was oxidized. These changes may involve nonmuscle as well as muscle tissue. Thus the source of the increased nitrogen losses is probably liver. In muscle, protein degradation is actually decreased judged by methylhistidine excretion, whereas in liver, protein degradation may be increased. Also the fall in whole-body protein synthesis may reflect changes in nonmuscle tissues because in running rats protein synthesis in muscle is maintained. As far as leucine metabolism is concerned, because the increase in leucine oxidation occurs when leucine and its keto acid concentration falls, exercise must specifically activate the 2-oxoacid dehydrogenase.

Amino Acids↗
PubMed1980

Dynamic aspects of whole body glycine metabolism: influence of protein intake in young adult and elderly males.

The influence of adult age and adequacy of dietary protein intake on whole body glycine metabolism was studied in human subjects. Five healthy young adult males (19-25 yr) and six elderly males (64-78 yr) were given an adequate-protein diet (1.5 g protein/kg/day) for 7 days and a low-protein diet (0.4 g protein/kg/day) for 14 days. At the end of each dietary period, whole body glycine flux and rates of glycine synthesis were estimated with the use of a continuous 60 hr oral administration of 15N-glycine and determination of 15N enrichment of plasma glycine by gas chromatography-mass spectrometry with selected ion monitoring. Mean whole body glycine flux and the rate of endogenous glycine synthesis were 458 and 351 micromole/kg body weight/hr, respectively, for young adults receiving the diet adequate in protein; similar values were obtained in the elderly group. Feeding the diet low in protein resulted in an extensive and significant reduction in both parameters in young adults and also in elderly subjects to a similar extent. Measurement of 15N enrichment in plasma serine gave a constant ratio of 15N enrichment in plasma free serine relative to glycine for both age groups and at the two protein intake levels. It is concluded that aging of adults has little impact on the quantitative aspects of whole body glycine metabolism, but that it responds extensively to changes in protein intake. Thus, it appears that glycine synthesis and flux are integrated with the body's total nitrogen metabolism and requirement for dietary nitrogen.

Adult↗
PubMed1980

The use of microvascular free skin-muscle flaps in management of avulsion injuries of the lower leg.

The authors used microvascular free skin-muscle flaps to cover avulsion wounds in the lower leg of ten patients. There were three children and seven adults, ranging in age from 5 to 54 years. Vessels supplying gracilis (four) and tensor fascia lata (six) skin-muscle units were anastomosed to the anterior tibial (nine) and posterior tibial (one) vessels. The tensor fascia lata unit has a more constant anatomy and is preferred. Principles of management include: 1) early adequate, but conservative, debridement; 2) continuous bony stabilization; 3) preoperative arteriography; 4) anticoagulation; 5) recipient vessel identification in healthy uninjured tissue; 6) appropriate timing; 7) delayed bone grafting.

Adolescent↗
PubMed1980

An analysis of hepatic venocclusive disease and centrilobular hepatic degeneration following bone marrow transplantation.

In order to assess the prevalence of venocclusive disease in autopsied recipients of bone marrow transplantation, we reviewed coded liver histology from 204 consecutive autopsied recipients transplanted for leukemia (142), other malignancies (5), or aplastic anemia (57). Twenty-seven patients with leukemia, 2 with carcinoma, and 3 with aplasia had venocclusive disease and survived 2-86 days post-transplant. Early lesions showed subintimal edema and hemorrhage within small central venules and centrilobular congestion with hepatocyte degeneration. Later lesions showed subtotal to complete fibrous obliteration of the central venule lumina and centrilobular sinusoidal fibrosis. Thirteen patients had a subclinical course, and 19 were symptomatic. Venocclusive disease was life-threatening or lethal in 13. Typical symptoms developed 1-3 wk post-transplant and consisted of sudden weight gain, hepatic enlargement, ascites, high bilirubin, and encephalopathy. Statistical analyses showed a significantly higher prevalence of venocclusive disease associated with transplantation for leukemia (P = 0.014), pretransplant conditioning with more rigorous chemoradiotherapy regimens (P < 0.001) and three- to fourfold increase of venocclusive disease in patients whose conditioning included dimethyl busulfan (P < 0.005). Abnormal liver tests before transplant were also more prevalent among patients with venocclusive disease. No factors predicted the clinical outcome of established venocclusive disease. Venocclusive disease showed no association with hepatic graft-versus-host disease even among prolonged cases with severe periportal hepatitis and cholestasis. Other centrilobular lesions (hepatocyte degeneration, sinusoidal fibrosis, and phlebosclerosis) were identified in 23 patients. These non-specific changes may occur with viral hepatitis, graft-versus-host disease or chemoradiotherapy effects.

Anemia, Aplastic↗
PubMed1980

Inpatient medical rehabilitation: 1979 survey of hospitals and units.

This survey by questionnaire was conducted by the Hospital Data Center of the American Hospital Association. The survey universe consisted of 516 hospitals; of these, 416 (80.6%) completed the questionnaire. The responding hospitals are classified into 4 categories: 1) independent rehabilitation hospitals, 2) self-contained rehabilitation hospitals within larger medical centers, 3) defined rehabilitation units of institutions, and 4) no formalized units. The survey yielded information concerning: 1) utilization, and predicted future trends in utilization; 2) referral sources of admissions; 3) the areas to which patients are discharged (their homes, nursing homes, etc); 4) the classes of fulltime equivalent personnel and their relative proportions, and those types of personnel that hospitals would most like to hire if it were possible to do so; 5) the sources of payment for inpatient claims, and problems with reimbursement; and 6) other findings including the use of beds designated for rehabilitation for other types of patients, and the number of fulltime administrators and of fulltime medical directors.

Humans↗
PubMed1979

Insulin deficiency and insulin resistance interaction in diabetes: estimation of their relative contribution by feedback analysis from basal plasma insulin and glucose concentrations.

The liver and beta cells function in a negative feedback loop, which appears to have a predominant role in regulating both the basal plasma glucose and insulin concentrations. The degree of basal hyperglycemia in diabetes probably provides a bioassay of both the effect of a reduction in insulin secretory capacity and the degree of insulin resistance. A mathematic model of the interaction of insulin deficiency and insulin resistance has been constructed, based on the known response characteristics of the beta cells to glucose, and of plasma glucose and insulin control of hepatic and peripherpal glucose flux. The degree to which beta cell deficiency increases basal plasma glucose reflects the hyperbolic shape of the normal insulin secretory response to different glucose concentrations. The height of basal plasma insulin is a function of the degree of insulin resistance. From the basal plasma insulin and glucose concentrations, the model provides an estimate of the degree to which both beta cell deficiency and insulin resistance contribute to diabetes. The predictions arising from the model are in accord with experimental data in man and in animals. In normal-weight diabetics who do not have increased insulin resistance, the model predicts that more than 85% of beta cell function has to be lost for the basal plasma glucose to rise to 6 mmol/liter, but a further 5%--10% loss increases the basal plasma glucose to over 10 mmol/liter. In a third of a consecutive series of 65 newly presenting, uncomplicated diabetics, both normal weight and obese, the analysis from the model suggested that insulin resistance, rather than beta cell deficit, was the predominant feature.

Blood Glucose↗
PubMed1979

Arterial wall renin and renal venous renin in the hypertensive rat.

1. Infusion of sufficient renin to raise the blood pressure of normal rats to hypertensive levels resulted in increased renin in the arterial wall. 2. Arterial wall renin and renal venous renin were normal in younger spontaneously hypertensive rats, but in older spontaneously hypertensive rats arterial wall renin was significantly increased and renal venous renin was significantly decreased. 3. Arterial wall renin in rats with either acute or chronic two-kidney Goldblatt renal hypertension was significantly increased, whereas circulatory renin was elevated in the former, but depressed in the latter. 4. Arterial wall renin may play a role in the maintenance of acute and chronic renal hypertension and also perhaps of spontaneous hypertension of long duration in older rats.

Angiotensin I↗