Biomedical subjects
Publications and source records attributed to A Chauvel.
The differential diagnosis of a midfacial mass in a child includes a great variety of tumours. Odontogenic myxoma is a benign tumour arising from the mesenchymal portion of the odontogenic apparatus that is usually seen in adolescents and adults.
Explore the source record for details and available documents.
INTRODUCTION: Microvenular hemangioma belongs to the group of acquired vascular tumors. It is important to differentiate such lesions because of their prognostic and nosologic consequences. We report a case of microvenular hemangioma. CASE REPORT: A 31 year-old man presented with a 3 cm erythematous and asymptomatic nodule of the abdomen, which had grown for 2 months. Histopathology showed the irregular dermal proliferation of small vessels, composed of capillaries and venules, without atypia. No relapse was noted 6 months after complete exeresis. DISCUSSION: Microvenular hemangioma is a recently described vascular tumor. The first three cases were reported in 1989, with the denomination of "microcapillar hemangioma". Twenty-one further cases have been reported since 1991. We discuss the typical clinical and histological characteristics of this lesion and present criteria permitting the differential diagnosis with other vascular neoplasms. Dermatologists should be aware of this lesion, notably for the differential diagnosis with early onset Kaposi's disease.
We report a case of arrhythmogenic right ventricular cardiomyopathy revealed by sudden death during exercise in a 13-year-old patient. Postmortem diagnosis was made on multiple tissue samples taken from right ventricular free wall, showing light adipous infiltration of the myocardium at gross examination. Arrhythmogenic right ventricular cardiomyopathy is histologically characterized by fibro-fatty replacement of right ventricular myocardium. Left ventricular involvement may be observed. Diagnosis at an early stage is often difficult. Etiology remains unknown. Since familial occurrence has been documented, postmortem identification is useful for the other members of the family.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Food intake depends on the palatability of the diet and on the energy delivered to the body. It is not known, however, whether the palatability of a diet is able to modulate the inhibitory effect of energy input on food intake. To address this question, we have measured intake during sham feeding for diets of different palatabilities in rats receiving varying levels of duodenal energy load. Rats were offered sucrose solutions (6, 10, or 30%) or mixed liquid diets without or with physiological duodenal energy loads using a mixed liquid diet. Compared with that seen during real feeding, meal size during sham feeding was increased for palatable diets but not for less palatable diets. Intraduodenal infusion of the mixed liquid diet inhibited the intake of all diets given by sham feeding. This inhibition was dependent on the level of duodenal energy load and was significantly greater for more palatable diets than for less palatable ones. We conclude that the inhibitory effects of intestinal nutrient load on intake are significant for all diets but have a more pronounced effect on the intake of highly palatable diets.
Cell surface tyrosine kinase receptors are subject to a rapid activation by their ligand, which is followed by secondary regulatory processes. The IHE2 cell line is a unique model system to study the regulation of EGF binding to EGF receptors after activation of the EGF receptor kinase. IHE2 cells express both a chimeric insulin-EGF receptor kinase (IER) and a kinase-deficient EGF receptor (HER K721A). We have previously reported that IER is an insulin-responsive EGF receptor tyrosine kinase that activates one or several serine/threonine kinases, which in turn phosphorylate(s) the unoccupied HER K721A. In this article we show that insulin through IER activation induces a decrease in 125I-EGF binding to IHE2 cells. Scatchard analysis indicates that, as for TPA, the effect of insulin can be accounted for by a loss of the high affinity binding of EGF to HER K721A. Since this receptor transmodulation persists in protein kinase C downregulated IHE2 cells, it is likely to be due to a mechanism independent of protein kinase C activation. Using an in vitro system of 125I-EGF binding to transmodulated IHE2 membranes, we illustrate that the inhibition of EGF binding induced by IER activation is related to the phosphorylation state of HER K721A. Further, studies with phosphatase 2A, or at a temperature (4 degrees C) where only IER is functional, strongly suggest that the loss of high affinity EGF binding is related to the serine/threonine phosphorylation of HER K721A after IER activation. Our results provide evidence for a "homologous desensitization" of EGF receptor binding after activation of the EGF receptor kinase of the IER receptor.
In the present report we further approach the mechanism by which insulin and phenylarsine oxide (PAO), a trivalent arsenical compound, regulate glucose transport in mouse fibroblasts (NIH3T3). First, we show that PAO is a powerful stimulatory agent on glucose transport. Second, at least three series of observations indicate that this action of PAO is not mediated through the insulin receptor: (i) the same effect of PAO is observed in NIH3T3 and in transfected cells expressing 6 x 10(6) insulin receptors, while the effect of insulin is markedly increased in the transfected cells; (ii) PAO does not affect the tyrosine phosphorylation of the insulin receptor; (iii) the tyrosine kinase activity of the insulin receptor toward exogenous substrates is not increased by PAO. Since PAO appears to act on glucose transport by a different mechanism than insulin, we have compared the effect of PAO and insulin on tyrosine phosphorylation of cellular proteins. Using Western blot analysis we did not detect common substrates in PAO- and insulin-treated cells. However, we found in cell extracts from both PAO- and insulin-treated cells a 50-kDa protein that is immunoprecipitated by antiphosphotyrosine antibody. In addition, PAO activates a cytosolic tyrosine kinase capable of poly(Glu/Tyr) phosphorylation. As a whole, our data suggest that the 50-kDa protein found in cells incubated with PAO and insulin could be the convergence point of the insulin and PAO signaling pathways.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.