Homogeneous core/shell ZnO/ZnMgO quantum well heterostructures on vertical ZnO nanowires.

Low-area density ZnO nanowire arrays, growing perpendicularly to the substrate, are synthesized with high-pressure pulsed laser deposition. The introduction of a ZnO buffer layer enables us to fabricate individual nanowires several micrometres apart (area density<0.1 nanowire microm(-2)), suppressing any shadowing effect by neighbouring nanowires during subsequent growth. These low density ZnO nanowires, whose c-axis is perpendicular to the substrate surface, are then used as templates to grow ZnO/ZnMgO core-shell nanowire heterostructures with conventional low-pressure pulsed laser deposition. Cathodoluminescence spectroscopy as well as transmission electron microscopy show that a sharp interface forms between the ZnO core and the ZnMgO shell. Based on these findings, we have grown a series of radial ZnO/ZnMgO quantum wells with different thicknesses that exhibit quantum confinement effects, with thicker quantum wells emitting at lower energies. Spatially resolved cathodoluminescence confirms the homogeneity of the quantum well structure along the full nanowire length of about 3 microm.

Acute hypercalcemia of the heart ("bony heart").

Cardiac abnormalities as a sign of hyperparathyroidism are common. A spectacular pitfall of peracute extended myocardiac hypercalcemia is reported. The history of a 30-year-old woman included symptoms such as insufficiency of the kidneys since childhood, secondary hyperparathyroidism, and hemodialysis for approximately 4 years. After kidney transplantation, the patient died from progressive heart failure. Three days before she died, CT showed a nearly white heart, and myocardial scintigraphy revealed a total infarction. The autopsy revealed a heart of normal size but with a weight of 590 g and with nearly bony texture. The histologic examination showed extended calcifications of the entire myocardium, thus explaining these findings. Laboratory photographs and electron microscopic images will be demonstrated. The metabolic pathogenesis of tertiary hyperparathyroidism and calciphylaxis is discussed. "Malignant" progression after kidney transplantation is stressed.