Showdown for health vigilantes.
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Biomedical subjects
Publications and source records attributed to C Potter.
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Benign osteoblastoma is an uncommon tumor in the skull and particularly rare in the temporal bone. This article presents the clinical, radiologic, and pathologic findings of the fifth case known to involve the temporal bone, and only th second case limited to the temporal bone itself. Subtotal removal was performed following embolization of the tumor. The patient currently has no evidence of disease eighteen months following therapy. Benign osteoblastoma is rarely synchronously or metachronously associated with its malignant counterpart, osteosarcoma. Treatment should be conservative. Subtotal curettage is acceptable and often results in long-term resolution. Radiotherapy is not recommended unless the removal is incomplete and the consequences of local recurrence are serious, as in vertebral lesions. This lesion may be highly vascular, and preoperative embolization should be considered to minimize blood loss at surgery.
Fifty-nine patients with primary gout were treated with either a combination of colchicine and allopurinol or colchicine alone. Assessments of renal function over 2 years revealed a statistically significant fall of glomerular filtration rate an urine concentrating ability in those receiving only colchicine. The renal function of patients given allopurinol did not change. Treatment with allopurinol resulted ina significant reduction of ammonium excretion, a phenomenon which could not be readily explained. Urate clearance also declined during allopurinol treatment, and the impaired urate clearance associated with gout became more evident. The most important observation was that allopurinol retarded an apparent decline of renal function. Presumably this was achieved through its hypouricaemic effect and implies that the hyperuricaemia of gouty patients is deleterious to the kidneys.
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A study of renal function of 51 patients with gout and an equal number of normouricaemic controls revealed significant differences. A relative impairment of the glomerular filtration rate and urine concentrating ability in the gouty subjects could not be wholly explained on the basis of aging or hypertension. Renal dysfunction was generally mild and was not associated with specific clinical characteristics higher levels of uric acid excretion, or hypertriglyceridaemia. Gout patients excreted urine with a significantly lower pH. This was associated with a relatively high excretion of titratable acid and a deficit of ammonium excretion, which was accentuated by ingestion of an acid load. Urate clearance was significantly reduced in gout, even when expressed as a fraction of the glomerular filtration rate.
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The terminals of the fast axon on extensor tibiae muscle fibres of Locusta were examined in untreated nerve-muscle preparations and in preparations stimulated electrically at frequencies varying from 0.5 to 100 Hz. The ultrastructure of the terminals in preparations stimulated at the lower range of these frequencies, which induce twitch contractions of the muscles, is similar to that of the controls. Stimulation at the higher frequencies induced tetanic muscle responses and rapid fatigue of the muscles after which they would not respond again to high frequency stimulation for about 1 h. This loss and recovery of the responses of the muscles is correlated with changes in the ultrastructural appearance of the terminals, in particular in the number and shape of the synaptic vesicles. The ultrastructure of these "recovering" axon terminals closely resembles that of the controls.
The distribution and size of synaptic vesicles in excitatory terminals of the extensor tibiae muscle were determined after stimulation at frequencies varying from 0.5 to 100 Hz and after subsequent rest. Only in preparations stimulated at the higher frequencies do these parameters differ from those in the controls. The synaptic vesicles in the nonsynaptic areas of these terminals are depleted in number, and the remaining vesicles are reduced in size. These effects are reversed after a 1 h rest.
The distribution of radioactivity at branches and terminals of the fast axon in extensor tibiae muscle incubated in the radiolabelled putative neurotransmitter L-glutamate was determined by electron microscopic autoradiography. Quantitative analysis of the distribution of silver grains at the axon branches and terminals in preparations stimulated at a low frequency shows that most of the radioactivity is present in the glial cells. In preparations stimulated to the point of fatigue substantial radioactivity is present in both the glial cells and the axoplasm of the terminals. It is suggested that the uptake of L-glutamate into the axoplasm of the terminals is correlated with the depletion and recovery of vesicle numbers after stimulation.
1 The pharmacokinetics of cytosine arabinoside were studied after a single i.v. bolus of 2 mg/kg ara-C in patients with newly diagnosed untreated AML, using a bioassay and GC-MS method to measure the plasma concentrations. 2 Most patients showed a bi- or tri-phasic decline in plasma concentrations with time. Plasma clearance was 3.9 to 18.1 l/min as measured by the GC-MS method, and terminal half-lives varied from 7--107 min. 3 There was poor correlation of the GC-MS assay with the bioassay, probably because the latter was interfered with by the release of endogenous nucleosides from blasts after after ara-C. 4 Plasma concentrations were measured by GC-MS during continuous infusions in 14 patients. Plasma clearances were much lower than after a bolus, 0.39 to 5.25 l/min. 5 There was no correlation of response (remission or fall in peripheral blast count) with exposure to ara-C calculated from infusion dose, clearance and duration of infusion. 6 This study shows that ara-C pharmacokinetics varies markedly from patient to patient and that there is a wide range in the plasma concentrations associated with therapeutic response.
We studied the clinical and biochemical manifestations of complete adenine phosphoribosyltransferase deficiency in the kindred of a male homozygous child excreting stones of 2,8-dihydroxyade-nine. Abnormal amounts of adenine, 8-hydroxyade-nine and 2,8-dihydroxyadenine (25 per cent of total purine metabolites) appeared in the urine of the propositus and his clinically normal brother, but not in heterozygotes or a control. Adenine phosphoribosyl-transferase activity in erythrocytes was less than 1 per cent of normal in both homozygotes and varied from 20 to 57 per cent of normal in six heterozygotes. Heterozygotes exhibited neither hyperuricemia nor gout. Treatment of the propositus with allopurinol and a low purine diet stopped stone formation. In addition, excretion of 2,8-dihydroxyadenine decreased. An autosomal recessive mode of inheritance with variable expression in the phenotype is indicated. Homozygotes may be detected by their raised urinary adenine levels or absence of detectable erythrocyte adenine phosphoribosyltransferase activity (or both).
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Sensitization to human myelin basic protein or encephalitogenic factor (EF), and antigen thought to be analogous to different human tumours, can be measured by the macrophage migration inhibition test (MMI). The MMI test was done on one occasion in 51 women with dysplasia and carcinoma in situ of the cervix; 20 women with non-malignant gynaecological conditions served as controls. Sensitization to EF was found in 71 per cent of women with carcinoma in situ and 42 per cent of women with dysplasia. None of the controls showed sensitization. Sensitization could not be related to histological evidence for cellular infiltration within the cervix.
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