Microstructures in high-Tc Bi(Pb)-family 2212 superconductors as revealed by scanning and transmission electron microscopy.

Microstructures of Bi(Pb)-family 2212 superconductors, which were prepared by a sol-gel method with three different compositions, were examined mainly by scanning and transmission electron microscopy. The magnetization of the specimens strongly depends on the ratio between Bi and Pb content, while Tc is almost constant. In specimen 1, prepared with the nominal composition of Bi/Pb = 9/1, small grains of 2212 phase are formed with a minor fraction of some impurity phases. In specimen 2, with Bi/Pb = 17/3, which is optimum from the viewpoint of magnetization, large grains of the 2212 phase are formed during heating at 800 degrees C, also with the impurity phases. In specimen 3, with Bi/Pb = 8/2, the 2212 grains are divided by layers of (Bi0.86, Pb0.14) (Ca0.7, Sr0.3)Ox. Moreover, plate-like 2212 crystals are severely bent so that small cracks appear often with an inclusion of amorphous substance being rich in Ca and Pb. These layers and cracks must degrade the magnetization. A modulated structure of Bi-type is formed in the 2212 grains of specimens 1 and 2, while not only Bi-type but also Pb-type are formed in specimen 3. The wavelength of Bi-type is different for each specimen.

Morphometric studies of pancreatic acinar granule formation in NCTR-Balb/c mice.

NCTR-Balb/c mice are afflicted with a cholesterol lysosomal storage disorder stemming from a defect in intracellular cholesterol processing. The clinical and biochemical abnormalities expressed in the mice resemble Niemann-Pick type C and D disorders in humans. One of the proposed mechanisms to explain the pathophysiology of the disorder implies a defect in the process of membrane transport that normally takes place in the vesicular movement of cholesterol to specific target sites in the cell. Secretory granule formation in pancreatic acinar cells is one of the biological processes known to involve massive membrane flow. Thus, we have undertaken a morphometric study of the regranulation mechanism in the pancreatic acinar cells of the mutant mice, as a way of studying cellular membrane movement. Electron micrographs of pancreatic acinar cells from mutant and normal mice were taken at several time points after extensive degranulation induced by pilocarpine injection. Two hours after stimulation the pancreatic cells demonstrated a complete loss of granules, and at later time points newly formed granules appeared. Identical unit granule volumes were observed in both groups, indicating that the progranules were of normal size. However, the rate of granule formation and maturation was reduced in the mutant mice, which might be the result of a defect in membrane function.