[The value of 99mTc-plasmin scanning in deep venous thrombosis].
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Biomedical subjects
Publications and source records attributed to P Charles.
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We previously reported increased mean serum 1,25-dihydroxyvitamin D (1,25-(OH)2D) and increased trabecular bone remodelling in patients with medullary thyroid carcinoma (MCT) and hypercalcitoninaemia. In the present paper we report that serum 1,25-(OH)2D and trabecular bone remodelling decreased following surgical cure for MCT and hypercalcitoninaemia in 4 patients despite no detectable post-surgical hypoparathyroidism or hypothyroidism. The results obtained in the present small number of patients suggest that the altered vitamin D metabolism and trabecular bone remodelling in patients with MCT is caused by the hypercalcitoninaemia.
Optimization of a four-crystal stretcher geometry whole-body (WB) counter was performed. The measured geometric characteristic did not differ significantly from the theoretically calculated characteristic (p greater than 0.05). The linearity of the WB counter was high in the range 3.7 kBq to 3.7 MBq. Longtime variability of local background was CV = 3.7 per cent. In vivo sensitivity was calculated to 18 cpm/kBq and the detection limit to about 5 kBq. The reproducibility was estimated to 0.7 per cent. The WB counter was used in 47Ca turnover and calcium balance studies of 15 normal individuals. The data were analysed according to a modification of the expanding calcium pool model using an improved Bauer-Carlsson-Lindquist formulation. Variability and method errors of main parameters for calcium metabolism were evaluated.
Calcium and magnesium balance, 47Ca turnover studies, and measurements of vitamin D metabolites were performed before and after 7-10 months of vitamin D2 treatment (36,000 IU/day) in eight patients bypass-operated 3-6 years earlier for gross obesity. All patients had received a daily supplementation of calcium (27 mmol/day) since operation. Before treatment the net calcium absorption and calcium balance were normal compared with that of nine normal controls. Vitamin D metabolites were within normal limits. The endogenous faecal calcium level was increased and the faecal lag time shortened. Bone biopsies revealed osteomalacia in three of the patients. Vitamin D2 treatment induced an increase in calcium absorption and renal excretion of calcium, a reduced bone resorption rate, a more positive calcium balance, and healing of osteomalacia. Moreover, the vitamin D2 treatment induced a prolongation and normalization of faecal lag time, an increase in magnesium absorption, and a more positive magnesium balance. The effect might be mediated through 25-hydroxyvitamin D (25-OHD), which increased, whereas serum levels of 1,25-dihydroxyvitamin D (1,25-(OH)2D) and 24,25-dihydroxyvitamin D (24,25-(OH)2D) were unchanged. The results indicate that in some bypass-operated patients high-dose vitamin D2 has a beneficial effect on calcium and magnesium metabolism.
The effects of varying doses of amphetamine on the permeability of the blood-brain barrier (BBB) to albumin were studied in young and aged Fischer 344 rats. There was no change in the permeability of the BBB associated with aging as revealed by saline-treated control experiments. The changes in the permeability of the BBB did not correlate with the changes in blood pressure produced by corresponding doses of amphetamine in the young or aged animals. In the dose range reported the young and aged rats showed similar pressor responses to amphetamine. The aged rats showed a greater increase in the permeability of the BBB than the young, and this effect was seen with a lower dose of amphetamine in the aged rats. At the highest doses tested the permeability was restored to control levels in both the young and the aged rats. The enhanced vulnerability of the BBB of the aged rats may be related to a deterioration of the noradrenergic control of cerebrovascular permeability.
Seventy-seven calcium balance and 47Ca turnover studies were performed in normal volunteers (n = 15) and in patients with osteoporosis (n = 12), primary hyperparathyroidism (n = 8), osteogenesis imperfecta (n = 5), medullary carcinoma of the thyroid (n = 4), thyrotoxicosis (n = 2) and intestinal bypass for obesity (n = 11). After intravenous injection of 20 microCi of 47Ca two retention curves of 47Ca were obtained: R1(t) directly measured on a whole-body counter and R2(t) calculated from the cumulated daily excretions of 47Ca in urine and faeces. The data were fitted to a modification of the continuously expanding exchangeable calcium pool model. Dermal calcium loss was estimated from the serum 47Ca specific radioactivity curve and the constantly increasing difference between the two retention curves. The median dermal calcium loss in 77 studies was 1.50 mmol 24 h-1 1.73 m-2 (range 0.13-4.60). The dermal calcium loss might be overestimated by redistribution of tracer or by eventual insufficient collection of urine and faeces. The possible influences of these errors have been evaluated. Patients with primary hyperparathyroidism had a greater (P less than 0.02) dermal calcium loss (2.64 mmol; range 0.80-4.50) than a control group (1.38 mmol; range 1.25-2.34).
Sixty-two calcium balance and 47Ca-turnover studies were performed in 51 individuals to evaluate the accuracy and the sensitivity of the methods. The data were analysed according to a modification of the expanding calcium pool model using an improved Bauer-Carlsson-Lindquist (BCL) formulation and an iterative computer procedure. A 7-day whole body retention curve (R1) combined with a retention curve constructed from excretion data alone (R2) was used to estimate dermal calcium loss (d) and to demonstrate the significance of individual corrections for delay in faecal excretion (faecal lag time = delta t). The mean d was 1.58 mmol Ca/day. The introduction of delta t improved the goodness of fit of the data to the model. delta t based on 47Ca-kinetics was superior to a fixed delta t of zero (P less than 0.01) or 2 days (P less than 0.05). The model derived renal calcium excretion rate was highly correlated (r = 0.98, P less than 0.001) to the chemical measured excretion rate. A similar highly significant correlation [RS = 0.78 (Spearman), P less than 0.001] was found between the model derived delta t and the carmine red delta t. These results indicate a high accuracy of the model. The directly measured parameters showed an excellent reproducibility with a coefficient of variation (CV) less than 4%. The reproducibility of the derived parameters was acceptable (CV = 10-20%) except for the balance (CV = 72%).
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The tissue/medium distribution of the nonmetabolized glucose analog [14C]-3-O-methyl-D-glucose was measured in pigeon erythrocytes and related to changes in 45Ca uptake and efflux, total calcium content and ATP levels. Sugar transport was not affected by changes in external Ca2+. However, both sugar and 45Ca influx were increased by the Ca-ionophore A23187. In the absence of external Ca2+, the ionophore caused a delayed increase in sugar transport and net loss of calcium, probably through releasing Ca2+ from internal storage sites into the cytoplasm. Increasing internal Na+ through Na+ pump inhibition or using the sodium ionophore monensin did not alter influx of sugar or 45Ca, indicating Na+-Ca2+ exchange was absent in these cells. The results are consistent with A23187 causing increased Ca2+ influx or release from mitochondrial storage and the resulting rise in cytoplasmic Ca2+ stimulating hexose transport. Experiments with low Mg++ and high K+ media and measurements of ATP levels exclude alternative explanations for the action of A23187. We conclude that sugar transport regulation in avian erythrocytes is Ca2+-dependent and resembles that in muscle in its basic mechanism. It differs in the response to some modulating agents, largely because of a different pattern of Ca2+ fluxes in these cells.
A family with MEN IIa (medullary thyroid carcinoma (MCT), pheochromocytoma and hyperparathyroidism) was identified. Three relatives had been treated for MCT earlier. Eleven asymptomatic family members had elevated pentagastrin (PG)-stimulated serum immunoreactive calcitonin (i-CT) concentrations, including one who earlier had a pheochromocytoma removed. Nine of these subjects underwent thyroidectomy, and histological examination revealed multifocal MCT in all. Although surgery was judged complete in all, elevated PG-stimulated serum i-CT levels postoperatively indicated residual disease in 5. The natural history of MCTs in the present family varied, with most cases behaving benignly. Occasionally, however, the disease pursued an aggressive course. As MCT often metastasizes before being clinically evident, high cure rates can only be obtained by early diagnosis and treatment, possibly in the pre-metastasizing phase of C-cell hyperplasia, detectable only by elevated PG-stimulated serum i-CT levels.
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Membrane transport of sugar and Ca2+ was studied in pigeon erythrocytes by measuring the cell to medium distribution of 3-O-[14C]methyl-D-glucose and 45Ca. We have found that stimulation of sugar transport by anoxia, adrenaline, or ascorbic acid was not dependent on external Ca2+, nor was it additive to the stimulatory effect of the calcium ionophore A23187. Stimulation by ascorbic acid was dependent on concentration and time. The slow basal 45Ca efflux was greatly accelerated by A23187, and this was further increased by adrenaline. A metabolic substrate mixture consisting of adenine, inosine, and fumarate (AIF) did not alter 45Ca efflux, except for antagonizing the effect of adrenaline in the presence of A23187. Sugar transport, whether basal or stimulated by adrenaline or ascorbic acid, was significantly decreased by AIF, independently of external Ca2+. Stimulation by A23187 in the absence of external Ca2+ was also antagonized by AIF. In cells depleted of Ca2+ by treatment with A23187 and EGTA, transport stimulation by adrenaline was abolished. These results suggest that release of Ca2+ from intracellular storage into the cytoplasm plays a role in the stimulation of sugar transport by adrenaline and anoxia and also by A23187 in the absence of external Ca2+. The data provide further indirect support for a calcium-dependent mechanism of sugar transport regulation in nucleated erythrocytes.
Postabsorptive plasma concentrations of citrate, glucose, lactate, free fatty acids (FFA), ketone bodies and free insulin were measured once weekly for 5 weeks in 18 male juvenile diabetics. The circadian rhythms of the same substances were followed in 12 male diabetics. In 8 of them, daily rhythms were measured twice, before and after plasma glucose was lowered by increasing insulin doses. In the postabsorptive state, the mean plasma citrate concentration of the diabetics, 117 mumol/l (range 65--160), did not differ from that of non-diabetics despite two- to threefold higher levels of plasma glucose, FFA and ketone bodies in diabetics. Daily plasma citrate profile in diabetics showed peak concentrations in the morning and late afternoon. Citrate level throughout the day fell after increased insulin administration, whereas the diurnal pattern remained unchanged. Both the week-to-week coefficient of variation (mean 10%) and the diurnal coefficient of variation (mean 17%) of plasma citrate were below those of any other substances measured (p less than 0.001). Postabsorptive citrate concentration correlated negatively to the diurnal variation of plasma glucose whether diabetic control was apparently good or poor. The results support the idea that plasma citrate level reflects intracellular citrate regulation of glucose utilization. In spite of an interindividual range of 100%, individual citrate level was remarkably constant. Postabsorptive plasma citrate concentration is proposed as a control marker of lability of circulating glucose in insulin-treated diabetics.
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The REG technique permitting an estimation of the grey matter flow was applied in conjunction with the simultaneous recording of the EEG analysed by the SULG manual method with 21 normal adult subjects. A relationship was established between the REG index and the EEG frequency index in a resting situation with eyes closed. An increase of the REG index was observed when the eyes were open, for looking at a picture and during a test of visual attention. At opening of the eyes a delay is observed between the desynchronisation of the EEG and the increase of the REG.
Bone mineral content (BMC) and bone mineral concentration (BMC') of the forearm were determined by photon absorptiometry in 20 untreated hyperthyroid patients and in 33 patients previously treated for hyperthyroidism. In untreated hyperthyroidism a significant decrease was found in both BMC and BMC'. In treated hyperthyroidism BMC and BMC' were normalized. The findings suggest that a previous hyperthyroid state is not a risk factor for development of spontaneous fractures providing the hyperthyroid state is effectively treated.
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