Human botulism caused by Clostridium botulinum type E: the Birmingham outbreak.
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Biomedical subjects
Publications and source records attributed to R D Watson.
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Antisera to extracts of a variety of bronchogenic carcinoma were raised in rabbits and extensively absorbed with immunoadsorbents prepared with normal lung extracts cyanogen bromide linked to Sepharose 4B, and glutaraldehyde insolubilized normal lung extracts. The antisera were tested by immunodiffusion against a panel of extracts from a variety of bronchogenic carcinoma, foetal lung extracts and pools of normal lung extracts. The results indicate that two distinct antigenic components are associated with bronchogenic carcinoma; one which is present in a high percentage of the tumour extracts tested and appears to have partial identity with a foetal lung component, and one (or more) which is not foetal and appears to have higher cross-reactivity (but not exclusively) with tumours of the same pathological type. Attempts to detect either antibody or antigens relating to these components in the serum of patients with bronchogenic carcinoma by these techniques were unsuccessful. The foetal cross-reacting component was neither carcinoembryonic antigen and alpha1-foetoprotein.
An immunoadsorbent technique is described whereby tumour-specific antibodies may be isolated. Extracts from normal human lung tissue were pooled and bound to cyanogen bromide activated Sepharose 4B. Antisera raised in rabbits to a variety of extracts from human bronchogenic carcinoma were passed through these immunoadsorbent columns to yield antisera specific for tumour-associated antigens as demonstrated by immunodiffusion and immunoelectrophoresis.
Plasma catecholamines were measured before and after treatment with beta-adrenoceptor antagonists in 17 hypertensive patients. Chronic treatment with beta-adrenoceptor antagonists caused substantial reductions in heart rate and intra-arterial blood pressure recorded continuously during ambulation. Before treatment, a quantitative relationship was observed between plasma norepinephrine and blood pressure and heart rate during a variety of activities; a similar relationship was also observed after chronic treatment five of six patients, suggesting that plasma norepinephrine remains an index of sympathetic activity despite the influence of beta-adrenoceptor antagonism. After treatment, plasma norepinephrine tended to be higher at any level of blood pressure, although not significantly so. Chronic treatment caused no significant change in mean resting plasma levels of norepinephrine and epinephrine. During exercise, plasma norepinephrine and epinephrine levels were significantly elevated above control after acute but not after chronic treatment. These observations do not support the hypothesis that beta-adrenoceptor antagonist drugs lower blood pressure in hypertensive man through a sympatholytic mechanism in he central nervous system or at peripheral presynaptic receptors.
The effects of variation in dietary sodium intake on biochemical indices of sympathetic activity were investigated in normal subjects. Sodium restriction for 7 days (mean urinary sodium excretion 21 mmol/day, s.e.m. = 4) increased supine plasma noradrenaline concentration significantly (1.78 nmol/l, s.e.m. = 0.23) compared to levels during medium sodium intake (1.31 nmol/l, s.e.m. = 0.14) and high sodium intake (1.35 nmol/l, s.e.m. = 0.25), when urinary sodium excretion averaged 186 (s.e.m. = 24) and 310 (s.e.m. = 43) mmol/l respectively. Plasma adrenaline concentrations did not vary significantly. During sodium restriction, the apparent release rate of noradrenaline increased significantly; noradrenaline clearance remained unchanged. No changes were observed in the heart rate response after beta-adrenoceptor stimulation with isoprenaline, suggesting that increased sympathetic activity during sodium restriction did not necessarily alter cardiac beta-receptor sensitivity. The responses to cardiac autonomic blockade with propranolol and atropine did not vary with sodium intake. These observations suggest that the sympathetic response to sodium restriction may not be generalized, excluding, in particular, the sympathetic nerves to the heart.
We have investigated the changes in plasma norepinephrine and blood pressure and heart rate during a range of physical activities in eight hypertensive subjects in order to determine whether changes in plasma norepinephrine reflect changes in sympathetic activity. Blood pressure was recorded over 24 hours from an intra-arterial cannula. Plasma norepinephrine, measured by a sensitive radioenzymatic method, increased progressively with increasing levels of physical activity. In each subject a statistically significant linear relationship was observed between the logarithm of plasma norepinephrine and systolic blood pressure. Analysis of variance showed that 66% of the variance of plasma norepinephrine was associated with changes in blood pressure and heart rate. These observations support the hypothesis that plasma norepinephrine reflects short-term changes in sympathetic activity. Use of the quantitative relationship described, in conjunction with measurements of norepinephrine metabolism, may help to determine the significance of increased levels of plasma norepinephrine observed in some hypertensive patients.
Intra-arterial pressure was recorded continuously in 26 patients with uncomplicated essential hypertension under standardized conditions. Recordings were analyzed beat by beat to obtain mean pressures and variability, expressed as the standard deviation of the frequency histogram. The major factors influencing variability were the level of pressure and the intensity of physical activity; systolic variability increased with progressive impairment of sino-aortic baroreflexes. Diastolic pressure increased with the level of sympathetic activity as reflected by plasma norepinephrine levels. After allowance for the decrease of plasma renin activity (PRA) with age, direct relationships were observed between PRA (log values) and the level of pressure and systolic variability; plasma angiotensin II values did not correlate. Systolic variability increased with the systolic response to cold but was unrelated to the response to dynamic or isometric exercise. Variability also tended to increase with obesity and was unrelated to age, sex, or race.
Sixteen untreated black patients with mild-to-moderate hypertension and no evidence of target organ damage were matched for age, sex, casual blood pressure (BP), and socioeconomic status with 16 white hypertensives. All patients were studied under standardized conditions in the hospital where they underwent continuous intraarterial ambulatory monitoring of BP and assessment of BP control mechanisms. BP characteristics over prolonged periods of recording were similar for both groups, as were sinoaortic baroreflex activity and pressor response to isometric and dynamic exercise and to cold. Fasting cholesterol and triglyceride levels in both groups were similar. Resting plasma renin activity (PRA) was significantly lower in blacks, but no difference was observed in resting plasma norepinephrine levels. Urinary excretion of NA+ and K+ was also similar in both groups. Thus, results showed that casual BPs matched for black and whites, and recorded over a prolonged period, were similar in pattern, variability, and response to pressor stimuli. It appears that, if BP contributes to the different patterns of morbidity in blacks and whites, it is more likely to be the actual level of BP rather than differences in BP characteristics.
The need for routine supplementation of total parenteral nutrition solutions with selenium (Se) has not been clearly defined. Although clinical selenium deficiency in patients on prolonged total parenteral nutrition has been reported, it is rarely observed in the United States. We report a 19-year-old woman with cystic fibrosis who developed muscle pain and weakness after 3 months on total parenteral nutrition which was not supplemented with Se. Coincident with her onset of symptoms, markedly elevated serum creatine kinase values were observed compared to baseline levels. Subsequent evaluations revealed undetectable (less than 0.02 microgram/ml) serum and urine Se levels in this patient. In addition, electromyographic evidence of myositis and nonspecific membrane irritability was documented. Therapy with oral Se rapidly reversed her symptoms and normalized with serum creatine kinase values over a 10-day period. Prolonged treatment with Se was required to achieve normal values of Se in the serum. Patients with severe pancreatic insufficiency, such as cystic fibrosis, may be at risk for clinical Se deficiency if on prolonged total parenteral nutrition without supplementation. Elevated creatine kinase levels should alert physicians to the possibility of Se deficiency in such patients.
Acute and chronic sinusitis are major clinical problems faced by physicians in several disciplines. Although there is a much studied relationship between sinusitis and asthma, as well as a well-known association of sinusitis and Wegener's granulomatosis, there is scant evidence suggesting an association of angioedema with sinusitis. Angioedema can be extremely disfiguring, and is potentially lethal due to compromised airways. It is also a frustrating diagnostic dilemma for patients and physicians. A diagnosis is found in fewer than 25% of chronic urticaria patients and much less for angioedema. In this study, we report the cases of nine patients who were treated for chronic sinusitis, but who were referred for episodes of angioedema. Patients with a known diagnosis, such as the hereditary form, or drug or food allergies, were excluded. Based on clinical suspicion or CT scan results, nine patients were treated for chronic sinusitis. Only three had symptoms suggesting a sinus infection at presentation. After sinusitis treatment, all nine patients had a marked improvement in their angioedema. None had further severe angioedema episodes. Some patients continued to have mild episodes of angioedema, which they related to recurrence of sinusitis symptoms, and which responded to antibiotics. The nine angioedema patients in this series all had strong evidence of sinusitis, albeit, most patients had occult disease identified by CT scan. The dramatic improvement in angioedema with sinusitis treatment corroborates a causal relationship. Such findings encourage the investigation of sinusitis in these otherwise idiopathic patients. Sinusitis evaluation may also be indicated for urticaria.
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