Publications by authors named "Mozere G"

Parasympathetic hyperactivity is found in some infants presenting faint episodes and could be responsible of certain Sudden Infant Death Syndrome cases. Therefore it was interesting to look for a noninvasive biochemical indicator of parasympathetic activity. A parasympaticomimetic syndrome associated with muscarinic receptor stimulation, which has been followed during 48 h, was obtained in the awake rat by reserpine injection (6.

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Bio Breeding (BB) rats develop a genetically determined insulin-dependent diabetes, because of the early destruction of pancreatic beta cells of Langerhans islets, massively infiltrated by inflammatory mononuclear cells. S 5682, registered as Daflon, 500 mg, is a purified micronized flavonoid fraction (90% diosmin, 10% hesperidin), which has been shown to possess antiinflammatory properties, including anti-free radical activity, effects on vascular permeability, venous tone, and perivenous inflammation. We studied the effect of S 5682 on the course of pancreatic insulitis in diabetic BB rats.

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In Diabetes Mellitus, type IV collagen biosynthesis is increased: the alpha 1(IV) procollagen specific mRNA concentration is elevated, particularly in the kidney, and the type IV collagen protein is accumulating is the thickened basement membranes. Aldose reductase inhibitors like sorbinil do prevent basement membrane thickening and type IV collagen overproduction. The latter seems related to intracellular sorbitol accumulation and also to protein kinase C activation.

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Kidney cortex sialic acid level, sialidase and sialyltransferase activities have been measured in spontaneously diabetic BB rats and in streptozotocin-diabetic rats (STZ). In untreated diabetic BB rats, at the onset of the disease, sialidase specific activity was found to be increased by 21% when compared with diabetes-resistant BB controls (P less than 0.05) whereas sialyltransferase activity was not significantly modified and bound sialic acid concentration was diminished (P less than 0.

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Acid-soluble collagen samples were prepared from individual skins of 24 month old rats (n = 8), 2 month old young controls (n = 8) and from 6 month old streptozotocin-diabetic rats (n = 5) and their age-matched controls (n = 10). Less collagen was obtained by acid extraction and salt precipitations from skins of diabetic and aged rats than from those of their respective controls. The collagen preparations from diabetic and aged rats showed an increased ratio of beta/alpha components.

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Because kidney microangiopathy with capillary basement membrane thickening has been reported in spontaneous hypertension, we have studied the activities of three lysosomal glycosidases able to degrade the carbohydrate moieties of basement membrane constituents in the kidney cortex of 12-week-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar Kyoto rats (WKY). These activities were also determined in SHR and WKY treated from 6 to 12 weeks of age with hydralazine (mean dose, 18 mg/kg per day in drinking water). Sialidase specific activity on sialyl-alpha 2-3-[3H]lactitol was markedly decreased in the kidney of untreated SHR, 40% activity remaining relative to that found in untreated age-matched WKY (p less than 0.

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Rat kidney cortex sialidase was studied using alpha-sialyl-(2----3)-[3H]lactitol and alpha-sialyl-(2----6)-[3H]lactitol as substrates. The enzyme was found mainly in the lysosomal fraction. Only 23% of the sialidase activity of this fraction could be solubilized by a combination of freezing-thawing, sonication and Triton X-100 treatment.

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The specificity of the sialidase activity present in rat kidney cortex (12 000 X g pellet) was studied with various tritiated oligosaccharidic substrates: (i) alpha NeuAc2----3 beta Gal1----4Glc-itol[3H], alpha NeuAc2----6 beta Gal1----4Glc-itol[3H]. and alpha NeuAc2----8 alpha NeuAc2----3 beta Gal1----4Glc-itol[3H] from bovine colostrum; (ii) alpha NeuAc2----6 beta Gal1----4 beta GlcNAc-itol[3H], alpha NeuAc2----3 beta Gal1----4 beta GlcNAcl----2 alpha Man1----3 beta Man1----4 GlcNAc-itol[3H] alpha NeuAc2----6 beta Gal1----4 beta GlcNAc1----2 alpha Man1----3(beta Gal 1----4GlcNAc1----2 alpha Man 1----6)beta Man1----4GlcNAc-itol[3H]et alpha NeuAc2----6 beta Gal1----4 beta GlcNAc1----2 alpha Man1----3(alpha NeuAc2----6 beta Gal1----4 beta GlcNAc1----2 alpha Man1----6)beta Man1 4GlNAc-itol[3H] isolated from the urine of a patient with mucolipidosis I. The enzyme cleaves alpha 2----3 and alpha 2----8 linkages at a greater rate than the alpha 2----6 bonds.

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