Biomedical subjects
W L Morrison
Publications and source records attributed to W L Morrison.
Muscle protein synthesis in patients with rheumatoid arthritis: effect of chronic corticosteroid therapy on prostaglandin F2 alpha availability.
Using stable-isotope techniques, we measured rates of quadriceps muscle protein synthesis in twelve women with sero-positive rheumatoid arthritis. The results were compared to those from the normal limb of seven women with unilateral osteoarthritis of the knee. Six patients had never received corticosteroid immuno-suppression, but the other six had taken an average of 8 mg Prednisolone per day for 9 years. Quadriceps atrophy was present in both sets of patients with rheumatoid arthritis (normal legs 444 +/- 182, rheumatoid 190 +/- 40, rheumatoid + steroid 300 +/- 110 micrograms protein/micrograms DNA, means +/- SD, both P less than 0.001). Muscle protein synthesis, calculated by comparing the incorporation of 13C-leucine into biopsy samples taken after an 8 h L-[1-13C] leucine infusion with the time averaged enrichment of blood alpha-ketoisocaproate, was 0.056 +/- 0.005% h-1 in the patients not receiving steroids compared with 0.050 +/- 0.02% h-1 in normals (P greater than 0.05) indicating that muscular atrophy was primarily due to an increase in rate of muscle protein breakdown. Intra-muscular PGE2 concentration was increased in these patients (rheumatoid 0.12 +/- 0.06 ng mg-1 tissue, normals 0.06 +/- 0.03 ng mg-1 tissue, P less than 0.05). Patients taking corticosteroids had a markedly depressed rate of muscle protein synthesis (0.035 +/- 0.008% h-1, P less than 0.05) and reduced intra-muscular PGF 2 alpha concentration (P less than 0.01). We conclude that steroid therapy significantly influences the mechanism of skeletal muscle atrophy in patients with rheumatoid arthritis.
Skeletal muscle and whole-body protein turnover in cirrhosis.
1. We investigated arteriovenous exchanges of tyrosine and 3-methylhistidine across leg tissue in the postabsorptive state as specific indices of net protein balance and myofibrillar protein breakdown, respectively, in eight patients with cirrhosis and in 11 healthy control subjects. Whole-body protein turnover was also measured using L-[1-13C]leucine. 2. Leg efflux of tyrosine was 45% greater in cirrhotic patients than in normal control subjects [-6.5(1.4 to -19.1) vs -4.2(-2.2 to -7.7) mumol min-1 100 mg-1 of leg, median (range), P less than 0.025]. 3-Methylhistidine efflux was not significantly altered. 3. In cirrhosis, whole-body leucine flux was normal but whole-body leucine oxidation was elevated so that whole-body protein synthesis was depressed by 17%. 4. The results indicate the predominant mechanism of muscle wasting in cirrhosis to be a fall in muscle protein synthesis, which is accompanied by an overall fall in whole-body protein turnover.
Mitral annulus calcification.
A 67-year-old woman had aortic and mitral annulus calcification resulting in severe stenosis and incompetence of the valves. Mitral annulus calcification produces specific echocardiographic abnormalities which may forewarn of technical difficulties during surgery.
Effects of therapeutic percutaneous electrical stimulation of atrophic human quadriceps on muscle composition, protein synthesis and contractile properties.
The effects of percutaneous electrical stimulation (70 V, 300 microseconds pulses at 30 Hz) on muscle composition and rate of protein synthesis were studied in seven patients with quadriceps atrophy secondary to unilateral osteoarthritis of the knee (stimulated group). Quadriceps were stimulated on the affected side for 1 h per day. The results were compared to those from seven patients who did not use a muscle stimulator (control group), in whom muscle biopsy at surgery provided evidence of wasting of tissue protein on the side of osteoarthritis (normal leg 608 +/- 266 micrograms protein micrograms-1 DNA, affected leg 256 +/- 100 micrograms protein micrograms-1 DNA, means +/- SD, P less than 0.05; type I fibre diameters: normal 53.2 +/- 6.7 microns, affected 43.8 +/- 4.0 microns, P less than 0.05). In patients who had received stimulation there was no residual difference between the legs in either muscle protein concentration (normal 411 +/- 168 micrograms protein micrograms-1 DNA, affected 373 +/- 112 micrograms protein micrograms-1 DNA) or fibre diameter (type I diameters: normal 56.1 +/- 7.8 microns, affected 58.0 +/- 10.7 microns). Stimulation did not influence the ratios of muscle force elicited by acute stimulation at 20 and 50 Hz (normal 75 +/- 15%, affected 79 +/- 15%), or rates of muscle relaxation (percentage losses of tetanic force 10 ms-1: normal 7.66 +/- 1.2%, affected 8.67 +/- 2.2%).(ABSTRACT TRUNCATED AT 250 WORDS)
Improved whole-body protein turnover after heart-lung transplantation.
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Meningitis after BCG vaccination.
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Muscle wasting in emphysema.
1. We have investigated arteriovenous exchanges of tyrosine and 3-methylhistidine across leg tissue in the postabsorptive state as specific indicators of net protein balance and myofibrillar protein breakdown, respectively, in eight patients with emphysema and in 11 healthy controls. Whole-body protein turnover was measured using L-[1-13C]leucine. 2. Leg efflux of tyrosine was increased by 47% in emphysematous patients compared with normal control subjects, but 3-methylhistidine efflux was not significantly altered. 3. In emphysema, whole-body leucine flux was normal, whole-body leucine oxidation was increased, and whole-body protein synthesis was depressed. 4. These results indicate that the predominant mechanism of muscle wasting in emphysema is a fall in muscle protein synthesis, which is accompanied by an overall fall in whole-body protein turnover.
Skeletal muscle and whole body protein turnover in thyroid disease.
The effects of disturbances of thyroid hormone secretion on leg and whole body amino acid and protein metabolism have been investigated in seven patients with untreated thyrotoxicosis and eight patients with untreated hypothyroidism; the results were compared to those obtained in 11 normal control subjects. After treatment, the patients were restudied. Arterio-venous exchanges of tyrosine and 3-methylhistidine across leg tissue in the post-absorptive state were used as indices of net protein balance and myofibrillar protein breakdown, respectively. Whole body protein turnover was measured using stable isotope labelling techniques with 1-[1-13C] leucine. Efflux of tyrosine from leg tissues was six-fold greater in patients with untreated thyrotoxicosis than in normal control subjects (-19.39 +/- 2.21 vs. -4.20 +/- 0.31 nmol 100 g-1 leg tissue min-1, P less than 0.005, mean +/- SEM), but 3-methyl-histidine efflux was not significantly different (-0.11 +/- 0.03 nmol 100 g-1 leg tissue min-1 vs. 0.14 +/- 0.02 nmol 100 g-1 leg tissue min-1). After treatment, when the thyrotoxic patients became euthyroid, tyrosine efflux was normalized (at -4.94 +/- 0.84 nmol 100 g-1 leg tissue min-1) and 3-methylhistidine efflux was unchanged. In hypothyroid patients, neither tyrosine nor 3-methylhistidine effluxes were significantly different from those in normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Skeletal muscle and whole body protein turnover in cardiac cachexia: influence of branched-chain amino acid administration.
Muscle protein wasting commonly accompanies severe heart failure. The mechanism of this so-called cardiac cachexia has been investigated in eight patients with an average body weight decrement of 19%, whose results have been compared with those from 11 healthy control subjects. Exchanges of tyrosine and 3-methylhistidine across leg tissue were used as specific indicators of net protein balance and myofibrillar protein breakdown, respectively. Whole body protein turnover was measured using a stable isotope labelling technique with L-[1-13C]leucine as tracer. In patients with cardiac cachexia there were greater values, relative to those values in normal control subjects, of leg efflux of tyrosine (-8.1 +/- 0.6 nmol 100 ml leg tissue-1 min-1 vs. -4.2 +/- 0.3 nmol 100 ml-1 min-1 (P less than 0.01) and of 3-methylhistidine (-0.8 +/- 0.1 nmol 100 ml leg tissue-1 min-1 vs. -0.1 +/- 0.02 nmol 100 ml-1 min-1 (P less than 0.005), mean +/- SEM). The results suggest that in patients with cardiac cachexia the state of net negative protein balance across leg tissue is associated with an increased rate of myofibrillar protein breakdown. In cardiac cachexia, neither efflux of tyrosine (-8.4 +/- 0.7 nmol 100 ml leg tissue-1 min-1) nor of 3-methylhistidine (-1.0 +/- 0.2 nmol 100 ml leg tissue-1 min-1) were significantly altered by branched-chain amino acid (BCAA) infusion to plasma concentrations of 1300 +/- 14 mumol ml-1, i.e., four times normal plasma values (282 +/- 11 mumol ml-1).(ABSTRACT TRUNCATED AT 250 WORDS)
Heart block and paragonimiasis.
Intracardiac granulomas can cause complete heart block. A case of complete heart block is reported in a patient who had had paragonimiasis 30 years before and who had radiographic evidence of calcified granulomas in the heart and lungs.
Decrease in human quadriceps muscle protein turnover consequent upon leg immobilization.
Quadriceps muscle protein turnover was assessed in the post-absorptive state in six men immediately after the end of unilateral leg immobilization (37 +/- 4 days) in a plaster cast after tibial fracture. A primed-constant intravenous infusion of L-[1-13C]leucine was administered over 7 h. Quadriceps needle biopsies, taken bilaterally at the end of the infusion, were analysed for muscle protein leucine enrichment with 13C. Quadriceps muscle protein synthetic rate, calculated from the fractional incorporation of [13C]leucine into protein compared with the average enrichment of blood alpha-ketoisocaproate, was 0.046 +/- 0.012%/h in the uninjured leg, but was only 0.034 +/- 0.007%/h in the quadriceps of the previously fractured leg (P less than 0.05, means +/- SD). Muscle RNA activity (i.e. protein synthetic rate per RNA) fell from 0.27 +/- 0.08 microgram of protein synthesized h-1 microgram-1 of RNA in the control leg to 0.14 +/- 0.03 microgram of protein synthesized h-1 microgram-1 of RNA in the immobilized leg (P less than 0.02). Immobilization was associated with a significant atrophy of type I muscle fibres (mean diameter 69.5 +/- 21 microns immobilized, 81.1 +/- 18 microns control, P less than 0.05), but no significant change occurred in type II fibre diameter. Mean quadriceps fibre volume calculated from the values for fibre diameter and percentage of each fibre type, was smaller in the injured leg by 10.6%; this value was near to the calculated difference in muscle thigh volume (calculated from thigh circumference and skin-fold thickness) which was less by 8.3%.(ABSTRACT TRUNCATED AT 250 WORDS)