Scanning microscopy最新文献

Dental calculus may grow on the denture surface. In order to demonstrate the mechanism of deposition, the interface between calculus and denture resin was investigated using a high resolution electron microscope. Ultrathin sections were also used for electron diffraction of selected areas to reveal any mineral phase. The mineral layers without mineralized bacteria adjacent to the denture surface revealed a marked variation in thickness and crystal shape. Three types of crystal shape were observed at the junction: needle-like, rod-like and plate-like crystals. High resolution electron microscopy (HREM) showed that both rod-like and plate-like crystals were an aggregation of fine crystallites. The lattice fringes of the fine crystallites were observed among the near atomic structures of resin polymer at the interface in all three types of crystals. The electron diffraction patterns of selected areas revealed that needle-like and rod-like crystals were composed of hydroxyapatite (OH-AP), while plate-like crystals were composed of a mixture of OH-AP and whitlockite. These findings indicate that, after saliva penetrates through the acrylic resin, calcium and phosphate ions in the saliva are trapped in the molecular chains of the resin polymer, while the local ion concentration then increases to reach supersaturation, whereas a spontaneous precipitation would occur at the superficial layer of the denture resin. Furthermore, a thin intermediate layer of crystallites might be indispensable for the scaffolding process in the calculus formation on the denture surface.

Healing molar tooth extraction wounds in rats were examined by scanning electron microscopy from 15 minutes to 40 days following tooth removal. The wound epithelium, which was derived mainly from the gingiva but also from the cheek and hard palate, migrated beneath the superficial socket contents. The contents were lost between 5 to 11 days, thus leaving a central epithelial-lined depression. This decreased in width with time as the level of the wound epithelium approached that of the hard palate but was still present at 40 days. Between 5 and 7 days, the wound epithelium became more regular. However, from 11 days on, it became more irregular with increasing numbers of saucer-shaped depressions, circular defects and circular whorls of epithelial cells. The surface structure of the epithelial cells changed as it migrated and matured. The initially plump, then flattened cells mostly had smooth areas along with variable numbers of irregular microridges and microvilli, although cells derived from the cheek had only smooth surfaces. With further maturation, all cells developed a regular honeycomb surface pattern of interconnecting microridges similar to that on the hard palate. Why the wound epithelium became more uneven after 11 days is not known.

The effects of the 26 amino acid, cationic, amphipathic, antibacterial peptide melittin and hecate-1, a 23 amino acid analog of it, on the gram negative bacterium Escherichia coli were investigated using scanning electron microscopy (SEM), transmission electron microscopy (TEM), and freeze-fracture. Both peptides killed virtually all bacteria at the peptide concentration and cell density used. TEM and SEM revealed aggregates of bacteria entangled with material extruded from the bacterial surfaces. SEM revealed irregular bacterial surfaces with bleb-like projections. TEM and freeze-fracture indicate that the bacterial inner and outer membranes, as well as the peptidoglycan layer between, were extensively damaged. The cytoplasmic contents of the cells, however, did not appear radically disturbed, providing little evidence for osmotically induced cytolysis.

The purpose of this study was to examine microvascular regeneration associated with gingival wound healing. A full-thickness piece of gingiva and oral mucosa was excised along the palatal aspect of the right maxillary first and second molars in 20 young Wistar rats. The contralateral side served as unoperated control. After 2, 4, 7, 10 or 20 days of healing, microvascular corrosion casts were produced and examined by scanning electron microscopy. At 2 days, vessels surrounding the wound were dilated and impressions representing sites of leukocyte margination were prominent in the walls of venules. Capillary buds were emerging from venules and capillaries. At 4 days, the vessel buds had lengthened and connected in pairs to produce capillary loops. At 7 days, new vessels extended deeply into the wound space, mainly from the medical side, in a palisade-like pattern. At 10 days, the denuded bone surface was still not completely revascularized and Volkman's canals opening to the wound area were empty. At 20 days, the bone surface was covered by large, irregular vessels which originated mainly from the palatal mucosa. The periodontal ligament was less important in the tissue repair process, while the bony vasculature contributed little or not at all to revascularization of the healing gingiva and palatal mucosa.

The effects of low concentrations (1 pM, 1 nM, 1 microM) of mercuric chloride on ion distribution in cultured myoblasts were analysed by energy dispersive X-ray microanalysis. An increase in intracellular sodium concentration was observed five minutes after addition of HgCl2 to the culture medium. This increase was dose dependent and accompanied by a transient decrease in potassium concentration. Exposure to 1 nM and 1 microM HgCl2 led to a two-fold increase in the cytoplasmic chlorine concentration. The higher HgCl2 concentration (1 microM) induced morphological alterations in the form of cell membrane blebs, perforations and shrinkage or flattening of the myoblasts. It was concluded that even low concentrations of mercuric chloride cause elemental and morphological changes in cultured myoblasts, which may reflect effects of the metal on membrane permeability.

The aim of this study was to investigate the localization of ecto-Ca-adenosine-triphosphatase (ecto-Ca-ATPase) in different parenchymal cells of the human pituitary in tissue culture. The distribution of ecto-ATPases on the surface membrane of a particular parenchymal cell varied with the type of cells in contact with this parenchymal cell; the membrane portions immediately exposed to the medium showed low if any ecto-ATPase activity. These results suggest that ecto-Ca-ATPases of the parenchymal cells may be involved in cell adhesion processes and may be of crucial importance in the organization (in vivo) and reorganization (in vitro) of human adenohypophyseal tissue.

In amniote vertebrates, the development of form and structure of the limb bud is accompanied by precise patterns of massive mesodermal cell death with morphological features of apoptosis. These areas of cell death appear to eliminate undifferentiated cells which are required only for a limited time period of limb development. Predictable skeletal and morphological anomalies of the limb occur when the pattern of cell death is modified in mutant species or under experimental conditions. Most evidence points to the occurrence of local triggering mechanisms to account for the establishment of the areas of cell death and the subsequent activation of cell death genes. Modifications of the extracellular matrix and diminution in the contribution of growth factors by neighbouring tissues appear as the most likely potential candidates for triggering the cell death program. Information on the genetical basis of cell death in the developing limb is very scarce. Among the increasing number of cell death genes identified in other cell death systems, such as p-53 and the ced-3/ICE and ced-9/ bcl-2 gene families, only bcl-2 has been studied in detail during limb development and yet, the information obtained is contradictory. Bcl-2 is not expressed in the areas of cell death of the developing limb, but normal limbs develop in mice with disruption of the bcl-2 gene. Obviously, the clarification of the role of the cell death genes constitute a major task in future studies of cell death in the developing limb.

Calcium phosphate (CaP) has been detected in the majority of urinary stones containing predominantly calcium oxalate (CaOx). Therefore, crystal phases of CaP might play an important role with respect to the formation of urinary calcium stones in general. Very often, CaP found in stones or tissue of human kidney occurs in the shape of small spherulites. In this paper, we report on a new flow model of crystallization (FMCG), which has been used to generate spherulites of CaP in a gel matrix of 1% agar-agar at 37 degrees C from a supersaturated, metastable solution continuously flowing over the gel surface. Scanning electron microscopy (SEM), X-ray diffraction and microscopic Fourier transformed infrared spectroscopy (FTIR) revealed that the particles formed (diameter: up to 200 microns) consisted of a poorly crystalline core of carbonatoapatite which was partly surrounded by a well-crystallized shell of octacalcium phosphate (OCP) showing radially oriented sheet-like structures. Subsequently, CaOx was grown on these spherulites from a flow of a correspondingly supersaturated solution conducted over the gel matrix. It could be shown by SEM that growth of calcium oxalate monohydrate (COM) was characteristically induced by the OCP shell. Radial sheet-like forms of OCP were directly continued by COM showing a certain radial orientation. The model of crystallization in gel matrices applied here should be well-suited to simulate the process of urinary stone formation under in vitro conditions.

Enamel prism patterns and enamel deposition rates were compared for specimens representing six mammalian orders. Enamel samples were characterized by either pattern 1 or pattern 3 prisms. Each prism pattern category contained prisms from at least two mammalian orders. Enamel deposition rate was estimated for each sample by measuring prism cross striation repeat intervals. Statistical analysis of cross striation repeat intervals illustrates significant differences in deposition rate between prism patterns 1 and 3. No statistically significant differences were found in deposition rate between the higher-level taxa represented within each prism pattern category. That enamel deposition rate is not taxonspecific reinforces the close association between deposition rate and prism morphology. In accord with previous studies, pattern 1 enamel is deposited more slowly than is pattern 3 enamel. Correlation analyses illustrated a lack of association between enamel deposition rate and body mass, tooth size, and estimated ameloblast size. Evidence that enamel deposition rate is associated with enamel prism morphology, coupled with evidence that deposition rate is not correlated with size parameters, points to developmental homology (i.e., homogeneous deposition rate) within each prism pattern.

Structural analysis of human kidney stones reveals the presence of cellular membranes and other cell fragments. Experimentally, calcium oxalate crystallization is facilitated when an exogenous nephrotoxin is given with ethylene glycol, thus providing cellular degradation products to act as heterogeneous nuclei. In this report, we tested whether oxalate alone could act as a cell toxin capable of producing damaged cells without the presence of an exogenous agent. Cultured LLC-PK1 and MDCK cells, when exposed to 1.0 mmol KOx, a concentration at the limit of metastability for calcium oxalate nucleation, were severely damaged as measured by specific lactate dehydrogenase (LDH) release in the spent media and by trypan blue exclusion. This effect was magnified by the addition of pre-formed calcium oxalate monohydrate crystals; the injury was significantly amplified when compared to exposure to oxalate alone. Scanning electron microscopy studies illustrated attachment of crystals to cells with loss of cell-to-cell and cell-to-substrate contact, as cells were released from the monolayer. In both oxalate and combined crystal-oxalate studies, more cells were released from the monolayer and exhibited considerably more damage when compared to controls. Oxalate, at the limit of metastability for calcium oxalate, is a cell toxin and can produce cellular degradation products. This effect is increased significantly by the addition of calcium oxalate monohydrate crystals.