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J Magre

Publications and source records attributed to J Magre.

At least 19 recordsLinked to original sources

Molecular genetic approaches to the identification of genes involved in the development of nephropathy in insulin-dependent diabetes mellitus.

Genetic factors contribute significantly to the development of diabetic nephropathy in patients with insulin-dependent diabetes mellitus. This report discusses some models of diabetic nephropathy that incorporate genetic susceptibility and presents strategies for identifying the responsible genes. To identify variation at a locus, newly developed methods are discussed that employ denaturing gradient gel electrophoresis to study sequence differences in both polymerase chain reaction-amplified DNA fragments and genomic DNA. These techniques are illustrated with studies of the angiotensinogen gene and the insulin receptor gene. In preliminary data from a comparison between individuals with and without diabetic nephropathy, no DNA sequence difference in that part of the angiotensinogen gene that codes for angiotensin I was found. However, with a probe corresponding to exons 7 and 8 of the insulin receptor gene and denaturing gradient gel electrophoresis of Rsal digestions of genomic DNA, different distributions of a DNA polymorphism were found in patients with fast as compared with slowly progressing nephropathy. The interpretation of this finding and the need for further studies are discussed. In conclusion, the advent of methods of molecular genetics makes possible studies on genetic determinants of diabetic nephropathy. However, more clinical and epidemiologic data are needed to find out how many genes are involved and how they interact with exposure to diabetes. Foremost, DNA from families with two or more siblings with diabetic nephropathy must be collected to permit the necessary genetic studies.

Chromosome Mapping

[Examination of the uterine cervix using the scanning electron microscope].

Scanning by electron microscopy of the cervix of the uterus allows us to study the various aspects, both normal and pathological, as well as the architecture of sections of the organ. All the same, as in all practical examinations carried out using scanning we have to beware of pictures that are but artefacts due to the method of preparation. The views obtained from a normal cervix of from pathological cervices show very different aspects. In the normal cervix the surfaces are more or less smooth and the architecture of the deeper levels shows a thick and regular texture. Infectious lesions of the outer aspect of the cervix show punched-out patterns, like craters, which penetrate more or less deeply into the sub-epithelial plane. While cervical dysplasia shows little except perhaps a more or less bossed-up epithelial surface, cancer of the cervix on the other hand shows a pavement pattern which is irregular. The pavements are formed by buds which are separated by faults which are more or less deep. In section the structures show a degree of disorientation in the texture. After treatment with radium the appearance is rather like ground glass of spiders webs and the architecture of the structures seems to be pock-marked and chaotic.

Cervix Uteri

In vivo and in vitro characterization of insulin resistance in three cases of lipoatrophic diabetes.

Insulin resistance was explored in vivo and in vitro in 3 lipoatrophic diabetic girls (12, 15 and 19 years old = L1, L2 and L3). Patients L1 and L2 were explored with fasting hyperglycaemia (9 mmol/l); patient L3 was normoglycaemic. All had abnormal OGTT with marked hyperinsulinemia. Their basal glucose productions, measured by [6,6(-2)H] glucose constant infusion, were 3.3, 2.6 and 3.4 mg kg-1 min-1, respectively; they did not correlate with fasting plasma glucose. Glucose production in response to a 2 mg kg-1 min- unlabeled glucose infusion, was normally suppressed in L2, but was incompletely suppressed (by 1.5 mg kg-1 min-1) in L1 and L3. The dose-response curve during hyperinsulinemic euglycaemic clamp at 1, 2 and 10 mU kg-1 min-1 insulin infusion was shifted to the right in all three patients. However the maximal glucose disposal rates were close to normal (9 and 9 mg kg-1 min-1) in L1 and L3, while it remained very low (3.6 mg kg-1 min-1 at 10 mU kg-1 min-1 insulin infusion) in L2. The endogenous insulin secretion (plasma C-peptide) was also incompletely suppressed during insulin infusion. Thus, the in vivo insulin resistance of lipoatrophic diabetes concerns not only glucose disposal but also hepatic glucose output and insulin secretion; in addition, the alterations of glucose metabolism were not the same in all subjects. The in vitro studies showed no pre-receptor defect (anti-insulin antibodies, insulin receptor antibodies). Insulin binding to erythrocytes and cultured fibroblasts was normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue

[Celioscopy].

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Female