Theory of regular arrays of defects: The void lattice
Defects in crystals may form a regular array, rather than a random distribution. The lattice of voids produced in irradiated molybdenum is a remarkable example of this. We give a general method of calculating the energy per defect in the array which exploits the periodicity of the defect lattice. The existence of the void lattice depends on the elastic interaction between voids. The present approach can treat both arbitrarily anisotropic elastic continua and discrete lattices, and is readily extended to discuss the stability of the defect lattice. The results predict that a void lattice should occur in molybdenum, and compare a number of models for the void. Stability against shear of the void lattice is not discussed in the present paper. The ratio of the void lattice spacing to void radius predicted is 2.2 to 4.5 and is smaller than the value of about 10 observed. The results are in general agreement with the more approximate Malen-Bullough treatment.
Point defects in face-centred cubic lattice-II X-ray scattering effects
Abstract The method developed in Part I is applied for calculating the X-ray scattering effects due to defects. It is found that all of the X-ray effects can be expressed in terms of the normal co-ordinates used in Part I. Several examples are treated in the case of a face-centred cubic lattice. It is found that there are two groups of defects as far as the distribution of diffuse scattering intensity is concerned. One shows a lemniscate type similar to H uang 's previous predictions and the other shows an ellipsoid type which is observed in the experiments on irradiated crystals. Both isolated vacancies and isolated interstitial atoms in possibly favoured positions show the lemniscate type, but pairs of these defects show the ellipsoid type.
Protective effect of ginsenoside Re on acute gastric mucosal lesion induced by compound 48/80
The protective effect of ginsenoside Re, isolated from ginseng berry, against acute gastric mucosal lesions was examined in rats with a single intraperitoneal injection of compound 48/80 (C48/80). Ginsenoside Re (20 mg/kg or 100 mg/kg) was orally administered 0.5 h prior to C48/80 treatment. Ginsenoside Re dose-dependently prevented gastric mucosal lesion development 3 h after C48/80 treatment. Increases in the activities of myeloperoxidase (MPO; an index of neutrophil infiltration) and xanthine oxidase (XO) and the content of thiobarbituric acid reactive substances (TBARS; an index of lipid peroxidation) and decreases in the contents of hexosamine (a marker of gastric mucus) and adherent mucus, which occurred in gastric mucosal tissues after C48/80 treatment, were significantly attenuated by ginsenoside Re. The elevation of Bax expression and the decrease in Bcl2 expression after C48/80 treatment were also attenuated by ginsenoside Re. Ginsenoside Re significantly attenuated all these changes 3 h after C48/80 treatment. These results indicate that orally administered ginsenoside Re protects against C48/80-induced acute gastric mucosal lesions in rats, possibly through its stimulatory action on gastric mucus synthesis and secretion, its inhibitory action on neutrophil infiltration, and enhanced lipid peroxidation in the gastric mucosal tissue.