Portable chair for testing isometric muscle strength.
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Biomedical subjects
Publications and source records attributed to W H Taylor.
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Serum profiles of both oestradiol and prolactin were measured during the luteal phase in normal women, in women with cyclical breast pain and in women with recently biopsied benign breast disease. The results suggest that, in women with benign breast disease, the concentration of both hormones may be increased, when compared to the normal controls, during the evening in the latter part of the luteal phase.
Direct-current plasma emission spectrometry determines food calcium and phosphorus, faecal calcium and chromium, and urinary calcium and phosphorus accurately, precisely and rapidly without acid digestion or dry ashing. Food and faeces are homogenised, diluted and aspirated directly into the plasma. The method makes metabolic balances swifter and less labour-intensive; it enables the use of chromium sesquioxide as an inert marker, for perchlorate digestion is avoided. Both plasma emission (-9.9%) and a dry ashing procedure (-13.5%) give lower values for food phosphorus than those derived from food tables.
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1. Arterial plasma histamine concentrations, forced expiratory volume in 1.0 s (FEV1.0) and peak expiratory flow rate were determined in nine patients with exercise-induced asthma and in five control subjects before and after 8 min of cycle-ergometer exercise. 2. In the controls neither FEV1.0 nor peak expiratory flow rate fell by more than 5% in any individual during the 30 min postexercise period. The asthmatic patients all experienced a fall in FEV1.0 or peak expiratory flow rate, or both, of 15% or more in the period 5-20 min after completion of the exercise. 3. There was no difference between the control subjects and the asthmatic patients in the plasma histamine response to exercise. In both groups there was an insignificant rise of about 40% during exercise, although the initial levels were higher in the asthmatic patients. 4. The mean plasma histamine peak of the asthmatic patients preceded the mean maximal fall of FEV1.0 and peak expiratory flow rate by approximately 15 min. However, no positive correlation was found between rise in, or peak, plasma histamine levels and decrease in lung function. 5. Three non-atopic asthmatic patients had a significantly higher mean plasma histamine concentration during exercise than had the atopic subjects. 6. A strong positive correlation in asthmatic patients, and asthmatic and control subjects together was found between age and mean postexercise plasma histamine concentrations. 7. The results do not support a direct role for histamine in the production of exercise-induced asthma.
The serum ionic fluoride concentrations in 497 normal individuals, from areas with non-fluoridated water supplies, ranged from 0.25 to 2.20 micromol F-/1 and were positively correlated with age (r = 0.31, p less than 0.001). Distribution of the data with age, coupled with the distribution of serum calcium with age, suggests a possible change in bone metabolism between 26 and 35 years of age. Serum fluoride levels vary with the time of day with a mean minimum value at 0800 and a mean peak value at 2200. Renal clearance studies gave fluoride ion clearances ranging from 19.5 to 44.0 ml/min and tubular reabsorption of fluoride ion ranging from 61.5 to 86.5%. After oral ingestion of 0.48 mmol sodium fluoride, peak serum levels occurred at 60 to 90 minutes; the peak levels were significantly higher in women than in men.
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A continuous subcutaneous infusion for 24 hr of the gastric secretagogues, pentagastrin (4 micrograms/kg/min) together with carbachol (0.8 micrograms/kg/min) produced a 100% incidence of duodenal ulcers (DU) in male albino Wistar rats. The mean acid output producing these duodenal ulcers was 2.3 mmol/24 hr, with a gastric secretory volume of 25 (+/- 1) ml/24 hr at an acid concentration of 91 (+/- 2) mmol/liter. The pepsin activity in the gastric juice was 185 micrograms/ml. To simulate this acid-pepsin hypersecretion, acid and/or pepsin was infused intragastrically for 24 hr. The intragastric infusion of hydrochloric acid (0.1 M, 0.2 M, 0.5 M) alone and hog purified pepsin (2.5, 5, 10 mg/24 hr) at a constant rate of 1 ml/hr for 24 hr failed to produce duodenal ulcers in rats although gastric lesions in the body of the stomach were produced. The infusion of 0.2 M HCl with 5 mg pepsin over 24 hr produced DU in two of 10 rats. However, pooled secretagogue-stimulated gastric juice, infused intragastrically, produced DUs in 11 of 12 rats. Acid alone does not produce DU experimentally in rats at the rate of infusion used in these experiments. Acid and exogenous procine pepsin (similar to human pepsin 3 on agar gel electrophoresis) rarely produced duodenal ulcers. However, acid and endogenous rat pepsin are needed together for the duodenal ulcerogenesis. This pepsin may be an obligatory ulcerogenic factor in the rat.
In patients with peptic ulceration, both vagal stimulation by insulin hypoglycaemia and stimulation by pentagastrin cause pepsin 1 to be secreted into gastric juice. There is a secretory threshold for pepsin 1, below which only pepsins 3 and 5 are secreted. Pepsin 1 accounts for an increasing proportion of the total peptic activity/ml of gastric juice as the total activity increases. Higher concentrations of pepsin 1 in the basal gastric secretion occurred significantly more frequently in patients with duodenal ulcer than with gastric ulcer. In these patients there may be an increased 'background' secretory drive.
Gastric juice was collected from 27 children for 9 to 21 hr following cardiac surgery, from 4 further children during and following cardiac surgery, and from 3 children who had not undergone surgery. Each sample was analyzed for hydrogen ion and pepsin content. The pH of the postoperative secretions from 26 patients was 1.25 to 5.30, and the mean hydrogen ion concentration was 60.1 mmol/liter (range, 21.5 to 119.3 mmol/liter). The mean peptic activity (83.0 units/ml; range, 42.4 to 158.4 units/ml) was not age related and was significantly higher than that of the basal and pentagastrin-stimulated secretion and similar to that of vagally stimulated secretion of adults with peptic ulcer. The pepsin:hydrogen ion and pepsin 1:total pepsin ratios also resembled those of vagally stimulated secretion. During the first 90 min of cardiac surgery, the pH of aspirated gastric juice was 1.40 to 4.90, the hydrogen ion concentration was 15.8 to 72.3 mmol/liter, peptic activity was 39.2 to 164.0 units/ml (mean, 97.2 units/ml). Pepsin 1 was present in all samples. Aspirates from 3 unoperated children had low total peptic activity and only trace amounts of pepsin 1. Children from the age of 5.5 months thus have the capacity to secrete all the major pepsins, including pepsin 1. The findings suggest that vagal stimulation of gastric secretion was occurring during the postoperative period.
Carbenoxolone may bind to enzymes, inhibiting or activating them. Enzymes inhibited are human pepsins 1, 3 and 5, human pepsinogens 1, 3 and 5, swine pepsin, bovine trypsin, bovine chymotrypsin, porcine elastase, human gastric proteinase 2, human gastric prostaglandin 15-OH dehydrogenase and delta-5 reductase, and pronase. Enzymes activated are papain, bovine carboxypeptidase and gastric microsomal glycosyl transferase. Enzymes unaffected are human pancreatic amylase and porcine pancreatic lipase. Binding occurs away from the active site; inhibition thus occurs when binding impedes access of substrate to, or products from, the active site, and activation when access is facilitated. Carbenoxolone causes increased secretion of mucus; this action can be explained by activation of the gastric glycosyl transferases. Carbenoxolone also causes intraluminal loss of peptic activity and diminished secretion of pepsins; these actions are explained respectively by intraluminal inhibition of the pepsins and intramucosal inactivation of the pepsinogens, particularly of the peptic ulcer-associated enzyme, pepsin 1. The healing effect of carbenoxolone in peptic ulcer involves these actions together with a reduced turnover of gastric mucosal cells. Pepsins 1 and 3 have collagenolytic activity, causing release of alpha-chains from native collagens. Pepsin 1 is five-fold the more active. Carbenoxolone inhibits peptic collagenolysis.
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