[Measure of pulmonary capillary output in relation to the mechanical environment].
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Biomedical subjects
Publications and source records attributed to C Jacquemin.
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Although cholera toxin induces a marked stimulation of adenylate cyclase activity in rat adipocyte plasma membranes, the holotoxin induces only a slight increase of cyclic AMP accumulation in intact cells. A similar apparent anomaly is seen with pertussis toxin, which has been shown to inhibit the Gi subunit of adenylate cyclase, and has a greater effect on cAMP accumulation and lipolysis than the activation by cholera toxin of the Gs subunit. To understand better the way in which these bacterial toxins are modifying the adipocyte cells, we prepared adipocyte plasma membranes and submitted them to ADP-ribosylation by cholera and pertussis toxins. During the incubation of control cells, we found endogenous ADP-ribosylation of Gs as a result of sustained stimulation of Gi by adenosine. Our results point to a possible homoeostatic system in which the autonomous adjustment of the basal activity of Gs as a function of that of Gi, under the control of feedback inhibitory ligands, ensures a steady production of cAMP within the cell.
Epidemiological studies have indicated that hypertension enhances the development of atherosclerosis in patients with lipid disorders. However, it was still unclear whether this promoting effect resulted only from hemodynamic changes or whether part of it was mediated by humoral or neurogenic factors independent of blood pressure alteration. The aim of this study was to determine whether mineralocorticoids, which are known to be involved in the pathogenesis of hypertension, could be implicated in the atherosclerotic process independent of pressure changes. For this purpose, the effect of deoxycorticosterone (DOCA, 200 mg/kg s.c.) on aortic atherosclerosis was studied in Watanabe heritable hyperlipidemic (WHHL) rabbits in comparison with New Zealand rabbits. After 4 weeks of treatment, DOCA significantly increased the size of atherosclerotic lesions in the arch and thoracic aorta (+115%) in parallel with the aortic cholesterol ester content (+83%). The vascular free cholesterol and triglyceride content remained unchanged on DOCA treatment, as were arterial pressure and plasma cholesterol levels. None of these effects was observed in New Zealand rabbits. DOCA did not accentuate the alteration of endothelial function usually found in WHHL rabbits. The sensitivity to serotonin was not altered, but the maximal contraction to this agonist was decreased in both strains by mineralocorticoid treatment.
PURPOSE: To report two infants with tuberous sclerosis who initially were considered to have retinoblastoma. PATIENTS AND METHODS: An 8-day-old infant was referred with small tumors in the posterior poles of both eyes. A left microphthalmos with ciliochoroidal coloboma was present. Computed tomographic (CT) scanning of the brain showed scattered high-density subependymal foci in the lateral ventricle thought to be consistent with calcification resulting from intrauterine viral infection. Argon laser photocoagulation was applied to lesions in the right eye. Because one tumor was situated on the retina straddling the coloboma in the left eye, external beam radiotherapy was administered. A 5-month-old girl presented with a large mass in a left microphthalmic eye. Calcification was present on B-scan ultrasonography and CT scanning. Vitreous seeding was noted to originate from the tumor. The contralateral eye manifested four small gray translucent retinal tumors in the posterior pole. CT scan and magnetic resonance imaging (MRI) revealed multiple periventricular subependymal lesions, including one at the foramen of Monro. RESULTS: Repeated examinations in the younger child under anesthesia revealed small new retinal lesions that appeared to enlarge gradually. She developed intractable seizures and her electroencephalogram revealed a modified hypsarrhythmia recording. A careful review of available CT scans and MRI displays suggested the diagnosis of tuberous sclerosis. The child's most recent examination under anesthesia revealed multiple newly developed hamartomas. In the older child, prompt diagnosis was made on the basis of the intracranial radiologic findings. CONCLUSION: Retinal hamartoma presentation may vary in infancy. Small, initially fleck-like gliotic lesions appear to enlarge gradually and eventually may form gray, translucent tumors. Large astrocytic hamartomas of the retina associated with tuberous sclerosis may resemble retinoblastoma, particularly if the mass is large, calcified, and associated with vitreous seeding. Although ophthalmic presentation was reminiscent of retinoblastoma in both patients, radiologic evidence of subependymal hamartomas pathognomic for tuberous sclerosis helped establish the correct diagnosis. We stress the importance of intracranial radiologic findings in this regard.
Lipolysis in rat fat pads was studied by determination of free fatty acid and glycerol production in various experimental conditions (absence or presence of glucose, adrenaline and insulin). These results were compared to the accumulation of endogenous prostaglandins E2 and F2 alpha during lipolysis. In the absence of glucose the prostaglandin production followed the adrenaline-ininduced fluctuations in released free fatty acids both in the presence or absence of insulin. In the presence of glucose and insulin, a drop in prostaglandin accumulation was observed whereas free fatty acid production was strongly stimulated. These results suggest either that free fatty acid composition is modified influencing the acitvity of prostaglandin synthetase, or that there exists a specific mechanism controlling prostaglandin synthesis.
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