ADENOCARCINOMA OF THE BLADDER ASSOCIATED WITH CYSTITIS GLANDULARIS: A CASE REPORT.
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Biomedical subjects
Publications and source records attributed to C MORGAN.
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Ferritin-conjugated antibody has been used to identify by electron microscopy the sites at which nephrotoxic globulins localize in rat kidney during acute experimental glomerulonephritis. Antibody was concentrated in the glomerular basement membrane and in basement membrane-like material contained in distended cisternae of the endoplasmic reticulum. These data confirm and amplify, at the ultrastructural level, the results of studies obtained with the fluorescent antibody technique, and are consistent with the hypothesis that the cisternae and capillary basement membrane possess common proteins.
Sequential stages in the development and release of ECHO 9 virus have been illustrated and described. It is suggested that viral particles differentiate and become oriented in columns upon a fine filamentous lattice at cytoplasmic template sites which are distinct from the endoplasmic reticulum. Subsequently, virus is dispersed in the peripheral cytoplasm and gains egress from the cell through rents in the plasma membrane. Complete cellular disruption with viral release may supervene. The virus consists of a 13 to 15 mmicro dense core and a poorly defined outer membrane, 22 to 24 mmicro in diameter. Incomplete forms, lacking the core, are observed in the cytoplasm but have not been seen in the extracellular space.
Stages in the development and release of Western equine encephalomyelitis virus are illustrated and described. It is suggested that precursor particles 22 mmicro in diameter differentiate at template sites close to membranes bordering cytoplasmic vacuoles and that these particles either pass into the lumen of the vacuole, acquiring in the process a coat and peripheral membrane, or are dispersed in the cytoplasm and extruded through the cellular wall, emerging as viral particles on the surface. Although necrosis and dissolution of the cell with release of contents, including virus, may intervene at any stage of infection, ejection of virus from the vacuoles presumably can occur without rupture of the cell. The virus consists of a 30 mmicro core separated by a zone of lesser density from a sharply defined peripheral membrane 45 to 48 mmicro in diameter. Precursor particles, as well as viral particles, occasionally crystallize, the former in the cytoplasm, the latter in vacuoles and probably on the cellular surface.
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Stages in the nuclear changes consequent to infection with type 5 adenovirus are shown and described. Viral development seems to be confined to the nucleus where characteristic particles are found. The shape of the intracellular virus depends upon the method of preservation employed, appearing spherical after osmium tetroxide or freezing-substitution, occasionally exhibiting angulated faces after formalin and often assuming an hexagonal profile after potassium permanganate. The non-viral crystals are encountered in zones of low density, and it is suggested that crystallization results from the accumulation of protein in these areas. An hypothesis is presented to explain why these crystals, in contrast to the insect polyhedra, contain few viral particles.
The evolution of the intranuclear lesion produced by type 5 adenovirus in HEp-2 and HeLa cells is described as seen in the light microscope and the bodies formed in the course of the infection characterized histochemically. Some 12 hours after infection acidophilic protein bodies, without appreciable nucleic acid, first appear in the nucleus and coalesce into a network. Within or in association with this material, DNA-containing masses (viral aggregates) are formed which rapidly increase in amount and then coalesce. At the same time, a protein is produced, histochemically different from that of the acidophilic or basophilic structures mentioned, within the infected nucleus, which constitutes a matrix within which regular cytstals of a protein, (presumably non-viral) materialize. These structural and histochemical features are correlated with details which have been observed in parallel studies with the electron microscope.
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Study of the J.M. strain of herpes simplex virus in human amnionic and HeLa cell tissue cultures revealed the presence of intranuclear crystals composed of viral particles with a single membrane enclosing a central body. Randomly dispersed virus with double coats was seen in the nuclear matrix and between multiple membranes at the nuclear periphery. The majority of intracytoplasmic viral particles were within walled vacuoles. It is suggested that this strain of virus differentiates and frequently crystallizes at template sites which are characterized by aggregates of granules near the nuclear margin; that particles, either singly or occasionally in small groups, become enclosed by a second peripheral membrane while still within the nucleus; that the virus can pass into the cytoplasm through reduplications of the nuclear membrane which are deposited behind the virus in such a manner as to prevent rupture of the nucleus; that most of the intracytoplasmic virus is contained within sacks formed by nuclear membranes; and that rupture of these sacks at the cell surface results in extrusion of virus without disruption of the cell. No evidence was obtained to support the hypothesis that virus develops in the cytoplasm. Examination of the H.R. and C.G. strains of herpes simplex virus in identical cell lines grown under similar conditions failed to show viral crystals, but reduplication of the nuclear membranes was evident. Study of the J.M. strain in cells of chicken embryo chorioallantoic membranes indicated that the basic mechanisms of viral development and release did not differ from those operating in HeLa and human amnionic cells.
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