Surface instabilities of epitaxial films on a substrate

The energy variation of an epitaxial film on a substrate is calculated when sinusoidal roughness appears at the surface, using the method of the surface dislocation model. The energy variation is negative beyond a critical value of wavelength which depends on the thickness of the film and on the ratio of the shear moduli of substrate and film. The kinetic of roughness development during film growing are discussed.La méthode des dislocations de surface est utilisée pour calculer la variation d'énergie d'un film mince en épitaxie sur un substrat lorsqu'une rugosité de forme sinusoïdale apparaît à sa surface. On détermine une longueur d'onde critique dépendant du rapport des coefficients d'élasticité du substrat et du film et aussi de l'épaisseur du film, au-delà de laquelle la variation d'énergie est négative. On discute également de la cinétique du développement de la rugosité

Magnetic Fe60Al40 thin films

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Localized surface instability of a non-homogeneously stressed solid

A wavelet-shaped deformation has been introduced onto the free surface of a homogeneously stressed solid submitted to an additional non-homogeneous stress due to a surface or near-surface defect. An energy variation calculation determines when the development of this instability is energetically favorable

Morphological instabilities of stressed solids

When a solid is submitted to constant and homogeneous applied stresses, sinusoidal instabilities are supposed to develop by diffusion on its surface. When sources of non-homogeneous stresses like defects are present in its bulk, localized instabilities seem to be more adapted to describe its surface evolution

Model for instabilities during plastic deformation at constant cross-head velocity

We consider the case of mobile dislocations; with a finite velocity there is then a phase displacement between the time of loop nucleation and the time at which the strain is recorded With this hypothesis applied in an equation analogous to the Mecking and Lücke relation, we can explain the appearance of instabilities on the strain-stress curves, the influence of stiffness of the loading system, the formation processes of dislocation loops, and the phase displacement which appear in the criterion of stability are studied.On attribue aux dislocations mobiles une vitesse finie; par conséquent, un déphasage a lieu entre le temps où les boucles sont créées et le temps où la déformation est réalisée. Cette hypothèse appliquée à la relation de Mecking et Lücke permet d'expliquer l'apparition d'instabilités sur les courbes effort-deformation. Le rôle de la dureté de la machine, les processus de formation des boucles, le déphasage apparaissent dans le critère de stabilité

Sugar-specific endocytosis of glycoproteins by Lewis lung carcinoma cells

International audienceLewis lung carcinoma cells from tumors, metastasis nodules, or from culture bind fluorescent derivatives of neoglycoproteins containing alpha-D-glucose residues: This binding is competitively inhibited by neoglycoproteins containing alpha-D-glucose, by mannan, and by several other neoglycoproteins. Cell binding and uptake of the fluorescent derivatives of the neoglycoproteins was quantified by lysing the cells with an alkylpolyol (MAC 19 or MAC 18) and measuring the fluorescence intensity of the supernatant. The amount of cell-associated neoglycoprotein was higher at 37 degrees C than at 4 degrees C with LLC from tumor. The binding and uptake were inhibited by glycoconjugates containing alpha-D-glucose. These results suggest the presence of sugar specific receptors in Lewis lung carcinoma cells which are involved in a sugar-specific binding and endocytosis phenomenon. The implication of the existence of a carbohydrate-binding protein on the surface of Lewis lung carcinoma cells are discussed with regard to the in vivo behaviour of these cells, especially in relation to their metastatic properties and to the possibility of using neoglycoproteins as specific carriers of cytotoxic drugs. Hybrid molecules of gelonin and neoglycoprotein containing alpha-D-glucose were used as targetted toxin: The targetted toxin was found to bind to and to enter the intact cells and was 100 times more toxic than free drug