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A light microscopic and ultrastructural examination of calcified dental tissues of horses: 2. Ultrastructural enamel findings.

Ultrastructural examinations of defined 3 equine enamel types termed equine (Eq.) Types 1, 2 and 3 enamel, according to the transverse appearance of their enamel prisms and the amount and appearance of their interprismatic enamel. Eq. Type 1 enamel contained alternating rows of oval shaped prisms and thick interprismatic enamel plates, and was found adjacent to the amelodentinal junction. Eq. Type 2 enamel consisted of circular, 'keyhole' to 'horseshoe' shaped prisms with little or no interprismatic enamel and was located adjacent to the amelocemental junction. Eq. Type 3 enamel was composed of rounded prisms surrounded by large amounts of interprismatic enamel and was inconsistently present in a thin layer at the amelodentinal and amelocemental junctions. Prism decussation was seen in the thickest peripheral enamel of the upper cheek teeth but was present throughout incisor enamel therefore making incisors highly resistant to cracking. Scanning electron microscopic examination showed enamel crystals to be cylindrical shaped on transverse section; however, on transmission electron microscopic examination these crystals had shapes, ranging from near oval to rectangular and formed small subunits, with crystals diverging from each other at various angles.

Animals↗

Ultrastructure of platelet aggregation in refractory anemia and myelomonocytic leukemia. I. Ultrastructure of aggregation in normal controls and general defects in refractory anemia and myelomonocytic leukemia.

In vitro aggregation of the platelets from four patients with refractory anemia and two patients with acute myelomonocyctic leukemia revealed distinctive abnormalities. In five patients, there was deficient or minimal aggregation with adenosine diphosphate (ADP), epinephrine, or collagen and only one wave of aggregation could be elicited with ADP at any concentration. Ultrastructural studies revealed numerous isolated platelets, small aggregates with few platelet pseudopods, and the presence of a characteristic type of aggregate with heterogeneous platelet composition combining features of both the primary and the secondary waves of aggregation. These "mixed aggregates" were particularly abundant in the four patients who had refractory anemia and may constitute the structural basis of the single wave of aggregation observed.

Adenosine Diphosphate↗

Degeneration and regeneration of some mechanoreceptors. An ultrastructural study. III. Ultrastructure of reinnervated Herbst corpuscles.

The ultrastructure of reinnervated Herbst corpuscles shows that the regenerating nerve branches appear in the inner zone of the receptors at the end of the first month after nerve crush. The nerve branches are accompanied by the Schwann receptor cells. Two periods of regeneration can be established. During the first period the changes reflect mainly the quantitative relations between the regenerating nerve branches and the Schwann receptor cells, whereas during the second period the intracytoplasmic and intraaxoplasmic renewal of the organelles take place. The final regeneration of the receptors finishes at the end of the fifth month after nerve crush and one month later after nerve transection. Also, after transection the number of reinnervated receptors is less encountered.

Animals↗

Degeneration and regeneration of some mechanoreceptors. An ultrastructural study. I. Ultrastructure of denervated Herbst corpusles.

The degenerative changes in the HERBST corpusles have been investigated at ultrastructural level during the 3rd h to 1 year after nerve section. The earliest changes have been established in the nerve ending followed by the remaining nonmyelinated and myelinated portion of the receptor nerve fibre. The changes reflect the retrograde character of the degenerative process. The receptor cell elements pass through the stage of activation followed by their destruction and elimination. The Schwann receptor cells fullfill the pagocytotic role in the elimination of the axonal debris, after that they have been also completely eliminated. Their places are occupied by the activated fibroblasts and developed collagen fibrils. One part of the perineural cells persist a long time after denervation and they preserve the common although modified receptor configuration.

Animals↗

Degeneration and regeneration of some mechanoreceptors. An ultrastructural study. II. Ultrastructure of denervated Grandry corpuscles.

The ultrastructure of denervated Grandry corpuscles reveals the retrograde character of degenerative changes in the receptor nerve fibre. The denervation affects also the specific cell elements: the Schwann receptor cells and specialized cells. The both cell types pass through the phase of activation followed by degeneration and elimination. The process is significantly prolonged by the specialized cells. The Schwann receptor cells appear more dynamic and sensitive elements in the process of degeneration. After the full elimination of the specialized cells the denervated receptors cannot be established.

Animals↗

The classification of ultrastructural topography in the context of an ultrastructural diagnostic service.

Ultrastructural diagnosis relies on the recognition of specific organelles and the identification of various subcellular features and relationships. As E.M. case loads increase, the recall and comparison of particular cases becomes increasingly difficult. A system of classification is proposed, in a format compatible with SNOP and SNOMED, which permits the precise coding of subcellular details. Such a system could assist in the classification of disease, the storage and analysis of data and the retrieval and study of case material on an inter-departmental basis.

Anatomy↗

Ultrastructure of bone marrow megakaryocytes in experimental haemorrhagic shock in rats. I. Correlation between ultrastructure of MK nuclei and DNA ploidy.

The correlation was described between the ultrastructural picture and DNA mass content of MK nuclei in experimental haemorrhagic shock in rats. Significant disproportions were revealed between the morphological pictures and the ploidy of MK nuclei in the successive phases of the shock. Abnormalities of the maturation of marrow MK nuclei were found in the first hours of the shock, being most pronounced in the 24th hour.

Animals↗

Ultrastructure of bone marrow megakaryocytes in experimental haemorrhagic shock in rats. II. Correlation between ultrastructure of MK cytoplasm and thrombopoiesis.

Ultrastructural evaluation was performed of the MK cytoplasm in the successive phases of experimental haemorrhagic shock in rats. Qualitative abnormalities were revealed in the intracytoplasmic structures of MK. Platelets in the circulating blood were evaluated. A correlation was found between the changes in the intracytoplasmic organelles and the number and biological activity of blood cells. The results obtained indicate significant disturbances in the functioning of the thrombopoietic system in experimental haemorrhagic shock, which are caused by alterations within the intracytoplasmic structures of MK and lead to platelet production from morphologically differentiated but functionally immature MK.

Animals↗

Ultrastructure of cholinergic innervation in the cirrhotic liver in guinea pigs. Neurohistochemical and ultrastructural study.

Hepatic cirrhosis was induced in guinea pigs by ligation of the common bile duct and innervation of the liver was studied by fluorescence histochemistry (glyoxylic acid method), acetylcholinesterase (AChE) neurohistochemistry (modified Karnovsky and Roots method), and transmission electron microscopy. In control animals the adrenergic terminals showed connections with endothelial cells, hepatocytes and fat-storing cells, but no cholinergic terminals were evident. Cirrhosis was present 6 weeks after the bile duct ligation and marked fibrosis, accompanied by bile duct proliferation, was evident in the portal areas. Numerous AChE-positive nerve fibers traversed the collagenous bundles in the fibrotic areas, and cholinergic terminals formed close contacts with fibroblasts. Each axon terminal was found to contain numerous small coreless vesicles and AChE-reaction products were confirmed in the space between a nerve terminal and a fibroblast. In contrast, fluorescence adrenergic nerve fibers and their terminals remained unchanged. This study demonstrates that parasympathetic cholinergic innervation participates in some stages in the development of hepatic cirrhosis.

Acetylcholinesterase↗

Ultrastructural aspects of the small intestinal lead toxicology. Part I: Surface ultrastructure of the small intestine mucosa in rats with lead acetate poisoning.

The effects of low concentration of lead acetate on the apical surface of the jejunal enterocytes were studied. Young male rats were divided into 2 groups which received 0.01% lead acetate solution in drinking water during 30 and 60 d respectively. Blood lead concentrations of poisoned rats were elevated to 30.33 micrograms Pb/100 ml at d 30 of intoxication, then slightly depressed at the end of experiment. Weight gain was impaired only in the 60-d group in comparison with controls. Samples from jejunum were processed for scanning electron microscopy using a critical point drying method and gold evaporation. The fine structure of the surface enterocytes was always determined in the epithelial bands above the levels of crypts nearly half a distance from crypt to villous top. The shape of the jejunal villi in poisoned rats was similar to that in non-poisoned rats. A marked feature of the rats' jejunum exposed to heavy metal for 30 d was a rough appearance of the surface villi, probably associated with distortion of the glycocalyx layer. Extensive areas with degenerative lesions were observed on the surface of the most villi on the 60th d of intoxication. Microvilli of enterocytes distributed within these areas were deformed and sometimes could be completely absent. All enterocytes exhibited various degrees of glycocalyx disturbance. It was concluded that the pronounced toxic effects of lead were related to modification of biochemical properties of the surface coat of enterocytes. This abnormal function of the glycocalyx could result in damage and microvillous malformations.

Animals↗

Schistosoma haematobium: the effect of Astiban on the cell composition and ultrastructure of the vitelline gland and the ultrastructure of the tegument and gastrodermis.

Treatment of Schistosoma haematobium (Nigerian strain) in hamsters with a single dose of 40 mg/kg of Astiban caused a reduction in the number of S1, S2, and S3 vitelline cells and an increase in S4 cells. Following seven daily doses of the drug, a marked reduction in S1 cells and a complete loss of S2 and S3 cells occurred such that 95% of the cells were S4 cells, all of which were structurally abnormal. Coagulation and disintegration of the protein granules of the vitelline droplets occurred with increase in lipid droplets, swelling of the nuclear membrane and an increase in cytosegresomes. Blebbing of the tegument in both sexes occurred following a single treatment and vacuolation of the basal infolds and alterations to the mitochondria also resulted, but severe erosion of the tegument was rare even following repeated drug treatment. Damage to the gastrodermis was severe with the development of autophagic vacuoles containing whorls of myelin and sequestered portions of damaged tissue. The degree of damage increased with the number of drug treatments.

Animals↗

Cartilage ultrastructure after high pressure freezing, freeze substitution, and low temperature embedding. I. Chondrocyte ultrastructure--implications for the theories of mineralization and vascular invasion.

Electron microscopic examination of epiphyseal cartilage tissue processed by high pressure freezing, freeze substitution, and low temperature embedding revealed a substantial improvement in the preservation quality of intracellular organelles by comparison with the results obtained under conventional chemical fixation conditions. Furthermore, all cells throughout the epiphyseal plate, including the terminal chondrocyte adjacent to the region of vascular invasion, were found to be structurally integral. A zone of degenerating cells consistently observed in cartilage tissue processed under conventional chemical fixation conditions was not apparent. Hence, it would appear that cell destruction in this region occurs during chemical processing and is not a feature of cartilage tissue in the native state. Since these cells are situated in a region where tissue calcification is taking place, the implication is that the onset and progression of cartilage calcification are, at least partially, controlled by the chondrocytes themselves. The observation that the terminal cell adjacent to the zone of vascular invasion is viable has important implications in relation to the theory of vascular invasion. This may now require reconceptualization to accommodate the possibility that active cell destruction may be a precondition for vascular invasion.

Animals↗