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Biomedical subjects

M Julian

Publications and source records attributed to M Julian.

At least 19 recordsLinked to original sources
PubMed1992

[Non-atherosclerotic aorta in Cynomolgus after a hypercholesterolemic regimen].

The authors present a study on atherosclerotic and non atherosclerotic lesions of aortas of Cynomolgus (Macaca Fascicularis) on high fat diet (HFD) (6-12-24 months), after regression and after resumption. At 6 months 2 aortic responses are seen: an edema, deep and superficial clumps of foam cells, few synthetic smooth muscle cells (SSMC) few collagenic fibers--an edema, few superficial foam cells, many SSMC, secreting collagen and elastin. At 12-24 months, after regression and resumption, two aortic lesions are observed: a pronounced atheroma (47 animals) and no atheroma (14 animals). In this case, in the inner part of the aortic wall there are a fibrosis and an elastogenesis, SSMC and just some superficial lipids deposits. These aortic responses of SSMC are certainly the consequence of the environment (the diet) but also the possible consequence of the genetic determinism of SSMC since some animals only present this early, constant fibro-elastic response during this experimental follow up even though all the animals have been subjected to the same lipidic stress.

Animals↗
PubMed1989

Self-expanding endovascular stent in experimental atherosclerosis. Work in progress.

To investigate the physiologic and histologic responses induced by the self-expanding endovascular prosthesis, rabbits subjected to a combination of high-cholesterol diet and intravascular trauma underwent stent implantation. The results were compared with those obtained with the placement of stents in the healthy aortas of rabbits. Stents in healthy aortic tissue led to stent intimalization, previously reported in canine studies. For stents placed in animals subjected to a high-cholesterol diet but no intimal trauma, it was found that the stent was not the source of atherogenesis. Stents placed in atheromatous plaque were found to radially compress plaque with time and to stimulate for formation of a fibrotic crust. The results suggest that the self-expanding stent protects against progressive encroachment of the vessel lumen by atherosclerotic tissue.

Animals↗
PubMed1989

[Experimental atherogenesis: early wall changes in the cynomolgus monkey].

The early parietal changes in atherogenesis are characterized by: Increase of endothelial permeability with proteoglycans and L.D.L. storage. Lysis of internal elastic lamellae. Penetration into sub-endothelial space of monocytes macrophages and transformation into foam cells. Parietal fibrosis and proliferating smooth muscle cells play a role in the extension of lipid deposit.

Animals↗
PubMed1988

Bicarbonate and fast-twitch muscle: evidence for a major role in pH regulation.

Internal pH (pHi) was analyzed in rat extensor digitorum longus (Edl) muscle at 30 degrees C with single-barrel liquid ion-selective electrodes. Average pHi in 284 cells was 7.197 +/- 0.006. Increases in CO2 from nominally 0 to 5% produced an acidification from which recovery took place. In different groups of cells, recovery from the 5% CO2 acidification was significantly inhibited by 100 microM 4,4' diisothiocyanatostilbene 2,2' disulfonic acid (DIDS), Cl removal, Na removal and 2 mM amiloride. Prepulsing with 20 mM NH4 in the presence of CO2/HCO3 typically reduced pHi to only about neutral, whereas 50 mM reduced pHi to 6.7-6.8. In the nominal absence of CO2/HCO3, 20 mM NH4 reduced pHi to about 6.7 from which recovery took place at about 58% of the rate seen in different cells in the presence of CO2/HCO3. In the presence of CO2/HCO3, cells prepulsed with 50 mM NH4 had fully recovered to an average pHi of 7.22 +/- 0.04 about 90 min after removal of NH4. However, 90 min after removal of 20 mM NH4 in the absence of CO2/HCO3, average pHi was significantly less (7.05 +/- 0.03). Intrinsic buffering capacity (beta i) was obtained during pulses of CO2, acetic acid or after an NH4 pulse. beta i was significantly reduced in the absence of HCO3, Cl or Na and HCO3. The data provide significant support for an important role of HCO3 in the control of pHi in fast-twitch muscle.

Animals↗
PubMed1988

The elastic tissue of the skin. A comparison of spontaneous and actinic (solar) aging.

In order to separate the changes of actinic damage from those of simple aging, we studied the elastic fibers in low and high sun-exposed skins of normal subjects at different ages. Low sun-exposed skin shows chronologic aging lesions only. These begin at age 30 with a disappearance of oxytalan fibers and with some abnormalities in the reticular and deep dermis; at age 40, aging changes are established: no oxytalan fibers, marked abnormalities, and lysis of elaunic and elastic fibers. In high sun-exposed skin, age-related lesions also occur but are associated with more or less precocious elastotic degeneration in reticular and deep dermis. Both types of aging fibers are revealed by the antielastin antibody HB 8, disappear with elastase, but resist collagenase. Actinic elastosis clearly originates from elastin. The two types of change differ in electron microscopic appearance: with spontaneous aging, elastic fibers are disintegrated (loose and porous fibers); in actinic damage, elastotic fibers are thicker and have accentuated microfibril dense masses. The age-associated lesions could be due to the activity of protease of fibroblastic origin whereas the elastotic degeneration is probably due to the actinic stimulation of fibroblasts.

Adult↗
PubMed1988

Fibroblasts in dermal tissue repair. Electron microscopic and immunohistochemical study.

The cellular dynamics of dermal regeneration were studied in nonsutured cutaneous wounds of female pigs and monkeys with electron microscopy and immunohistochemistry to demonstrate the origin and the development of fibroblasts forming granulation tissue. The results indicate that fibroblasts do not originate from histiocytes but from resting fibroblasts in the wound margins. These resting fibroblasts first become undifferentiated mesenchymal cells termed "X" cells. The "X" cells then multiply, migrate, and invade the wound defect in approximately 3 days, transforming into highly active fibroblasts. The active fibroblasts are endowed with the capacity of further transformation to fibroclasts and myofibroblasts. The latter two cell populations then effectively cause remodeling of newly formed tissue and contraction of wound margins.

Animals↗
PubMed1987

[Repair of the connective tissue in a non-sutured skin wound].

During the healing of a second intention wound, granulation tissue is built up during the inflammatory and detersive phase which commences in the wound edges as soon as the loss of substance is created. Granulation tissue becomes scar tissue via connective and vascular proliferation and epidermization takes place concurrently. The origin of the fibroblasts composing the granulation tissue is debated: monocytes or fibroblasts from the wound edges? Ultrastructural and immunohistochemical data from studies of experimental wounds in the pig and the monkey make it possible to determine their origin and follow their progress. These cells originate from the fibroblasts of the wound edges and become undifferentiated cells which multiply and migrate to reach the loss of substance. There they become activated fibroblasts and contribute to repairing the loss of substance by secreting fibronectin and type I and type III collagen. As differentiated fibroblasts and myofibroblasts, they remodel and contract scar tissue.

Acute-Phase Reaction↗
PubMed1986

Coronary atheroma in the cynomolgus monkey: predictive value of serum and cutaneous lipoprotein measurement.

Hyperlipaemia was induced by a high fat diet in 11 cynomolgus monkeys. Morphological study of coronary arteries was carried out in 5 coronary samples from these 11 monkeys. The degree of arterial involvement was compared with the serum and cutaneous lipoprotein levels. These experimental data confirm that cutaneous apoprotein B measurement is the best marker for evaluation of coronary atheroma.

Animals↗
PubMed1986

A kinase able to phosphorylate exogenous protein synthesis initiation factor eIF-2 alpha is present in lysates of mengovirus-infected L cells.

Infection of mouse L929 cells by mengovirus resulted in the expression of a kinase activity that selectively phosphorylated the small, 38,000-molecular-weight subunit of eucaryotic initiation factor 2 and histone H2. This kinase activity was independent of host cell RNA synthesis and was located in the postribosomal supernatant (S-100 fraction) early after infection (up to 3 h). At later times after infection (5 h), kinase activity was also associated with the polysome fraction. The kinase present in the S-100 fraction bound strongly to DEAE-cellulose, its peak activity eluting at 0.5 M KCl. Kinase activity was independent of the presence of exogenous double-stranded RNA, and KCl at concentrations greater than 0.1 M inhibited eucaryotic initiation factor 2 phosphorylation. The 67,000-molecular-weight phosphoprotein activated in interferon-treated cells by double-stranded RNA was not detected by standard phosphorylation assays in lysates from mengovirus-infected cells. Labeling of this protein in vivo during 5 h of infection was also not detected. The DEAE-cellulose-purified mengovirus kinase inhibited protein synthesis in reticulocyte lysates, and the inhibition was not reversible by high concentrations of poly(I).poly(C).

Animals↗
PubMed1986

Staining of elastic tissue by Verhoeff's iron hematoxylin.

The elastic system of normal human skin was studied by light and immunofluorescence. Oxytalan, elaunin et elastic fibers were stained by weigert, orcein, gomori and Verhoeff. By Verhoeff's method all elastic system of dermis is shown, with other three stains, only elaunic and elastic fibers are well visualized. These results are confirmed by immunofluorescence studies.

Adult↗
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↗