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Biomedical subjects

M Julian

Publications and source records attributed to M Julian.

At least 55 records · Page 3Linked to original sources
PubMed1980

[Effect of pyridinol carbamate on long-term lathyrism and experimental atheroma in the rat. Histological and biochemical study].

Three-week-old rats were fed with Beta-aminopropionitrile (BAPN) with a normal or hyperlipidic diet. After a few weeks BAPN induced aortic elastic fibres disruption which as not worsened when the treatment was continued up the seven months. Adding a hyperlipidic diet produced atherosclerotic-like lesions. Pretreatment with Pyridinol Carbamate (PDC) whichever the diet used did not modify serum of aortic cholesterol levels. It decreased the severity of aortic lesions and delayed the onset of less severe atheromatous lesions. It seems that PDC increased the free/esterified aortic cholesterol ratio resulting in a better elimination of the aortic cholesterol.

Aminopropionitrile↗
PubMed1979

Fine structural evidence of increased endothelial permeability in chronic lathyrism.

The endothelium of the thoracic aorta of Wistar rats intoxicated with Beta-Aminopropionitrile (BAPN) for 9 weeks was studied. The animals were sacrificed at intervals, from the first to the 9th week of the treatment and 1, 2 and 3 months after the end of the treatment. Changes in the endothelial cells were studied by electron microscopy after staining with uranyl acetate and lead citrate, after impregnation with lanthanum. BAPN increased endothelial permeability, pinocytosis was more active in treated rats than controls, the intercellular junctions widened and cytoplasmic lesions with cell necrosis occurred. These intimal changes were comparable to those observed in man during ageing and in arteriosclerosis.

Animals↗
PubMed1978

Chronic lathyrism and atheromatosis in the rat. Study of the V.L.D.L. and plasma and arterial wall lipids.

Temporary chronic administration of Beta-amino-propionitrile (B.A.P.N.) produced morphological and biochemical changes of the aortic wall of rat as well as abnormalities of the plasma lipid levels. A hyperlipidic diet resulted in the blood plasma lipid abnormalities as B.A.P.N. intoxication. Nine weeks of B.A.P.N. followed by 42 weeks of a hyperlipidic diet increased the aortic cholesterol level and induced an atheroma. The diet alone produced only an endothelial lipid overload. The structure of arterial wall played the decisive role in atherogenesis.

Aminopropionitrile↗
PubMed1978

Hypothesis on microangiopathy of cutaneous capillaries.

Microangiopathy is a more or less pronounced PAS deposit-located exterior to the endothelial cells of the lymphatics and the basal membrane of the capillaries. This lesion, found in various normal and pathological states, has generated numerous pathogenic hypotheses. The presence of microangiopathy in 5 groups of 50 subjects representing five different clinical conditions, subjects over 60 years old or less than 40, diabetics, latent diabetics or patients with severe coronary heart disease, together with microscopic and/or ultrastructural lesions of the connective tissue (fibroblasts, collagen and elastic fibers, ground substance) has enabled us to propose a pathogenic hypothesis applicable to any microangiopathy. The initial change, hereditary or acquired, would be fibroblastic or interstitial. It would be characterized by the accumulation of glycoproteins, proteoglyacans and soluble collagen in the interstitium. Incomplete drainage of these macromolecules would occur around the blood and lymphatic capillaries and manifest itself by a PAS deposit, the hallmark of the microangiopathy.

Adult↗
PubMed1978

Aortic lathyrism and atheroma in the rat by prolonged hyperlipidic diet.

Constant, deep, extensive aortic atheroma can be induced in rats that are athero-resistant. Two main factors are involved in this experimentation: (1) Parietal alteration following chronic experimentation with beta-aminopropionitrile (BAPN, 8 weeks) and a metabolic factor with hyperlipid diet. Electronmicroscopic examination has shown progressive lesions in the elastic framework and modifications of cells in the media with dedifferentiation into fibromyocytes and also multiply. The changes are responsible for hyperplasia of the intima as well as its thickening and collagenization. They support observations made in man during aortic aging. (2) A metabolic factor with hyperlipidic diet. This diet given at various times during intoxication causes lip deposition in the intima and substantial penetration into the media when the lesions are developing.

Aminopropionitrile↗
PubMed1977

[Chronic lathyrism. Protective effect of pyridinol carbamate on connective tissue lesions in the rat (author's transl)].

The use of lathyric toxins (BAPN) in low dosage (1 g/kg/day) for a period of 8 weeks caused in the rat simultaneous changes in the skin and aortic connective tissues. In the skin. collagen tissue was dislocated and broken in fragments, the elastic tissue disappeared, the fibroblasts were vacuolized and presented evidence of injury. These lesions were comparable to those observed in human skin during ageing. The addition of pyridinol carbamate (PDC) to BAPN prevents the formation of lesions of the elastic tissue and of fibroblasts. When given after the cessation of the lathyrogen treatment PDC arrested the formation of the lesions and accelerated their regression.

Aminopropionitrile↗
PubMed1976

[Cutaneous cholesterol and phospholipids in atherosclerosis].

Previously, a lesion parallelism between skin and vascular wall was established when aging. Besides, we have pointed out a significant increase of cutaneous sterols rate along with aortic atheromatous stage. This study brings forward a new fact: increase (not significant because wanting much more examples) of cutaneous squalene rate varying with atheroma intensity, but reversely stability of total phospholipids with their various fractions.

Arteriosclerosis↗
PubMed1976

[Incorporation of 32P-orthophosphate in aortic phospholipids in chronic lathyrims in the rat].

Study of 32P orthophosphate incorporation into rat aortic phospholipids after B.A.P.N. treatment, which was followed or not by a lipid-supplemented diet (4.5 p. 100 cholesterol and 37 p. 100 butter). The 32P orthophosphate turnover in the total phospholipid was twice as slow among B.A.P.N.-treated rat than among control-rat. Such a decrease of the 32P orthophosphate turnover could be found as well in phosphatidylethanolamines, phosphatidylcholines and lysophosphatidylcholines. Sphingomyelins showed a very weak metabolic activity among two groups of rats. 32P orthophosphate incorporation into inositolphosphatides was slowed down by B.A.P.N. treatment. Maximal specific activity of inositolphosphatides after injection of 32P orthophosphate was reached within 4 hours in control rats, and 8 hours in B.A.P.N.-treated rats. Three months after the end of B.A.P.N. treatment, no difference in specific activity could be found between control-rats and B.A.P.N.-treated rats. Lipid supplemented diet modified the metabolic activity of phospholipids equally in control rats and B.A.P.N.-treated rats. Specific activity decrease in total phospholipids, phosphatidylcholines, phosphatidylethanolamines, and increase in lysophosphatidylcholines were noted in both groups of animals under a high rat diet. These modifications of the metabolic activity of different phospholipids were most marked fourteen hours after 32P orthophosphate injection. B.A.P.N. treatment only slowed the incorporation of 32P phosphate into phospholipids. Administration of a single lipid supplemented diet or a diet associated with B.A.P.N. treatment induced a slower turnover of phosphatidylcholines and phosphatidylethanolamines, and a faster turnover of lysophosphatidylcholines.

Aminopropionitrile↗
PubMed1976

[Structural and biochemical alterations of human diabetic dermis studied by H-lysine incorporation and microscopy].

The alteration of the structural organization of dermal connective tissue was studied by light and electron microscopy and by biochemical techniques in normal human and in diabetic patients using skin biopsies. Part of the tissue was used for light and electron microscopy, the rest was incubated in the presence of 3H-lysine for four hours. The 3H-lysine labelled biopsies were submitted to a sequential extraction procedure in order to obtain representative macromolecular fractions containing the matrix macromolecules. The extracts were analyzed for their chemical composition and radioactivity. Electron microscopy revealed ultrastructural modifications of the fibroblasts, of the collagen and elastic fibers in the diabetic dermis. Fibroblasts contained an increased amount of electron dense deposits in the cytoplasm and dilated endoplasmic reticulum. The collagen bundles were dissociated. Elastic fibers under the epithelial basal laminae were fragmented or absent. The incorporation pattern of 3H-lysine into these macromolecular fractions was different in the normal and diabetic skin biopsies. The percentage of total radioactivity incorporated increased significantly in the 1M CaCl2 extractable fraction an in the 6M urea extractable fraction and decreased significantly in the collagenase and elastase extracts in diabetic skin biopsy. These results demonstrate the existence of morphological and biochemical alterations in diabetic connective tissue (dermis) reflecting alterations in the relative rates of synthesis and/or degradation of the intercellular matrix macromolecules as well as of their microarchitectural arrangement.

Adolescent↗