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Biomedical subjects

F A Talley

Publications and source records attributed to F A Talley.

14 recordsLinked to original sources
PubMed1989

Epididymal interstitial (Leydig) cell tumors in B6C3F1 mice.

Six primary interstitial cell tumors of the epididymis were identified from 46,752 male B6C3F1 mice used in chronic toxicity and carcinogenicity studies. Five of the tumors occurred at the end of 2-year studies; none were attributed to treatment. None of the mice with epididymal tumors had a primary testicular tumor. Histologically, tumors were characterized by a nodular or diffuse proliferation of tumor cells in the epididymal interstitium. Most cells were polygonal with highly vacuolated cytoplasm (vacuolated cells) or eosinophilic cytoplasm (eosinophilic cells). Smaller hyperchromatic cells with scant basophilic cytoplasm (basophilic cells) and cells with yellow-brown pigment characteristic of lipofuscin (pigmented cells) were less common. In each tumor two or more cell types were present. Extension of these tumors through the capsule, invasion of the testis, or metastasis did not occur. By electron microscopy both eosinophilic and vacuolated cell types had a large round or oval nucleus with sparse heterochromatin, abundant mitochondria with tubulovesicular cristae, and frequent desmosome structures between cell membranes. Vacuolated cells contained numerous lipid droplets. Morphological features of the epididymal tumors are similar to those of the testicular interstitial (Leydig) cell tumor in mice and rats.

Animals↗
PubMed1988

Classification and morphometric quantitation of insoluble materials from the lungs of patients with alveolar proteinosis.

Insoluble materials isolated by bronchoalveolar lavage from the lungs of four patients with alveolar proteinosis were examined under the electron microscope, categorized according to ultrastructural criteria, and quantitated using morphometric procedures. The major component of the insoluble accumulations was the tubular myelinlike multilamellated structure that accounted for 42.6 +/- 12.4% of the total volume of insoluble material. These structures resembled tubular myelin as found in normal human lungs, consisting of lipid bilayer membranes separated by amorphous proteinaceous material; however, tubular myelinlike multilamellated structures lacked the intersecting membranes of normal tubular myelin. The distance between membranes varied from 150 to 300 A and this was similar to that found in tubular myelin from normal human lungs. Fused-membrane structures that were multilamellated but were without intervening amorphous lamellae accounted for 2.7 +/- 0.6% of the total volume of insoluble material. Crystals, identified by the presence of adhering materials, were present only in small amounts, accounting for only 0.07 +/- 0.03% of the volume of insoluble material. Neither fused-membrane structures nor crystals are present in lavage effluents from the lungs of normal humans. Membranous vesicles and electron-dense bodies, which resembled cell debris, together accounted for 21.2 +/- 10.1% of the total volume of insoluble material. Constituents of the pulmonary extracellular lining of normal human lungs such as secreted lamellar bodies and tubular myelin were minor components, together accounting for only 2.2 +/- 3.2% of the total volume of insoluble material. Amorphous material and miscellaneous structures accounted for 31.4 +/- 5.0% of the volume of insoluble material. Cellular disintegration and extracellular formation of unusual tubular myelinlike multilamellated structures appear to be major processes leading to the accumulation of insoluble materials in the alveoli and distal airways of patients with pulmonary alveolar proteinosis.

Crystallization↗
PubMed1987

Ultrastructural changes in the nasal mucosa of Fischer 344 rats and B6C3F1 mice following an acute exposure to methyl isocyanate.

Male rats and male mice received a single 2-hr exposure to 0 (control), 10, or 30 ppm of methyl isocyanate and were sacrificed after 1, 3, 14, or 90 days to assess the ultrastructural changes in the nasal mucosa by transmission electron microscopy. One day after exposure to methyl isocyanate, there were widespread areas of necrosis and degeneration of the respiratory and olfactory epithelium of rats and mice in the 10 ppm and 30 ppm groups. Qualitatively the ultrastructural findings were similar for both exposure groups and species. Degeneration followed by rapid regeneration was observed for both respiratory and olfactory epithelia but was most striking for olfactory epithelium in the dorsal meatus. Three days after the exposure, the olfactory epithelium was two to three cell layers thick due to a loss of supporting cells, olfactory neurons, and basal cells. By 14 days after exposure, the olfactory epithelium was composed of a heterogeneous cell population three to five cell layers thick. At 90 days following exposure, the epithelium was of normal thickness (eight to ten cell layers), with normal architectural arrangement, and composed of well-differentiated cells that appeared similar to those of controls. There were several findings that suggested the epithelial cells of Bowman's glands were the progenitor for the regenerating supporting cells of the olfactory epithelium. This study demonstrated that the respiratory and olfactory epithelium is capable of complete structural regeneration after an acute destruction by methyl isocyanate.

Animals↗
PubMed1986

Dissolution and reassembly of tubular myelin-like multilamellated structures from the lungs of patients with pulmonary alveolar proteinosis.

Tubular myelin-like multilamellated structures that accumulate in the alveoli of patients with pulmonary alveolar proteinosis are a characteristic manifestation of the disease. These multilamellated structures appear to be an abnormal form of tubular myelin consisting of phospholipid bilayers separated from each other by amorphous proteinaceous material. Treatment of tubular myelin-like multilamellated structures with 10% N-acetylcysteine in aqueous solution resulted in the dissolution and extraction of the intermembranous amorphous material. Extracts contained three major proteins with molecular weights of 36, 56, and 63 kd under reducing conditions; the 36 kd protein accounted for 76.6% of the total protein extracted. In the presence of N-acetylcysteine the 36 kd protein coexisted with a high molecular weight aggregate form (molecular weight greater than 4 X 10(6) daltons). Liposomes, prepared from lipids extracted from the insoluble phase of lavage effluents from the lungs of patients, were mixed with N-acetylcysteine-extracted proteins and then were dialyzed exhaustively against 0.9% NaCl at 37 degrees C. Examination of the precipitated material by electron microscopy revealed the presence of tubular myelin-like multilamellated structures ultrastructurally indistinguishable from those found in the alveoli of patients with pulmonary alveolar proteinosis. Tubular myelin-like multilamellated structures were also formed in large amounts when protein from the lungs of patients with pulmonary alveolar proteinosis was mixed with liposomes prepared from normal human lung surfactant. Tubular myelin-like multilamellated structures were formed with lipids from rabbit liver microsomes or brain homogenates to only a very small degree. Proteins extracted from pulmonary surfactant from the lungs of normal rabbits together with phospholipids extracted from the same source formed a few tubular myelin-like multilamellated structures in which square tubules were detected. These data demonstrate that specific proteins present in the insoluble accumulations from the lungs of patients with pulmonary alveolar proteinosis can spontaneously form tubular myelin-like multilamellated structures under in vitro conditions and in the presence of appropriate lipids.

Animals↗
PubMed1984

Multilamelled structures from the lungs of patients with pulmonary alveolar proteinosis.

Multilamellated structures (MS), which accumulate in the lungs of patients with pulmonary alveolar proteinosis, were examined under the electron microscope. MS, in general, consisted of alternating light and dark lamellae arranged concentrically about membranous vesicles or electron-dense bodies. The darker osmiophilic lamellae consisted of trilaminar membranes 80 to 100 A thick, and the lighter lamellae, which varied from 150 to 300 A in width, appeared amorphous. MS made up 42.6 +/- 12.4% (n = 4) of the total particulate volume present in the pulmonary lavage effluents. MS resembled tubular myelin structures from the lungs of patients, although these latter structures accounted for only 1.6 +/- 2.3% (n = 4) of the total particulate volume. Abnormalities, such as polygonal tubules, irregular tubule dimensions, and large size potential, indicated that tubular myelin structures in the lungs of patients were variable in structure. MS appear to be a form of tubular myelin structure. MS were treated with a variety of disruptive agents and then examined under the electron microscope. Information was obtained about the composition of the MS and the intermolecular forces involved in their three-dimensional organization. Extraction of the MS with acetone or treatment of the structures with phospholipase c resulted in loss of membranes from the structures without a concomitant loss of the intermembranous amorphous material, indicating that phospholipids were a major membrane component. Analysis of phospholipids in the acetone extracts of the MS revealed that the membranes consisted of 45% phosphatidylcholine and that the major fatty acid of the phosphatidylcholine was palmitate (76%). The amorphous material of the intermembranous spaces consisted primarily of protein, since it was destroyed by the proteases trypsin and pronase without loss of the membranes. Reducing agents such as mercaptoethanol and dithiothreitol were disruptive, indicating the importance of disulfide bridges between the protein constituents in maintaining the integrity of the MS. The significance of hydrophobic interactions between the protein constituents was demonstrated by the disruptive action of chaotropic agents according to the sequence KSCN greater than KI greater than KCl. These data indicate that MS consist of phospholipid membranes organized in a protein matrix maintained by intermolecular disulfide bridges and hydrophobic interactions.

Biological Products↗
PubMed1982

Peritoneal macrophage alterations caused by naturally occurring mouse hepatitis virus.

During routine harvest of murine resident peritoneal cells for macrophage function assays the authors recently noted that mice showed a 3-4-fold spontaneous increase in number of peritoneal cells within 1 week of being placed in one of their animal rooms. While the mice appeared clinically normal, the collected macrophages had highly convoluted membranes, showed enhanced spontaneous tumor cell killing, and showed increased erythrophagocytosis. Histopathologic findings included mild peritonitis and occasional foci of individual hepatocyte necrosis. The results of routine murine serologic studies and bacterial cultures of the peritoneal cavity were negative. Immunosuppressed mice placed in this room showed severe hepatic necrosis within 4 days, and ultrastructural particles characteristic of corona virus could be demonstrated in the necrotic foci. Mouse hepatitis virus (MHV) was isolated from these livers. Untreated mice showed positive MHV titers, as detected by the enzyme-linked immunoabsorbent assay (ELISA) after 21 days in the room. This episode demonstrates that MHV have profound effects on macrophage parameters while causing few clinical signs or histopathologic alterations. Secondly, the complement fixation assay for MHV as included in routine viral screens appears relatively insensitive for detecting outbreaks of MHV.

Animals↗
PubMed1978

Composition of bronchoalveolar lavage effluents from patients with pulmonary alveolar proteinosis.

The lungs of patients with pulmonary alveolar proteinosis were lavaged with saline. The lavage effluents were examined for the presence of unusual components which might be considered characteristic of the disease. Soluble proteins were resolved by electrophoresis on polyacrylamide linear gradient (2.5 to 27 per cent acrylamide) gel slabs and compared with proteins found in the patients' sera and lavage effluents from nondiseased human lungs. Many proteins in lavage effluents from both diseased and nondiseased lungs appeared similar to those found in serum. Several proteins from diseased lungs were not present in serum nor lavage effluents from nondiseased lungs. A number of proteins present in lavage effluents from nondiseased lungs appeared to be absent from lungs with alveolar proteinosis. Particulate components of lavage effluents from diseased and normal lungs were examined and compared using the electron microscope. Many particulate components including degenerate and disintegrating cells, ultrastructurally abnormal alveolar macrophages, and myelin-like structures were present in lavage effluents from diseased lungs but absent from normal lungs. Much of the particulate material resembled cell debris. The insoluble accumulations present in the pulmonary alveoli and airways of patients with alveolar proteinosis do not come from serum leakage nor from hypersecretion of materials normally found in these regions of the lungs. The major insoluble components appear to arise from cellular disintegration and the extracellular formation of myelin-like structures.

Blood Proteins↗
PubMed1977

Intracytoplasmic hyaline globules in the adrenal medulla of laboratory animals.

Intracytoplasmic hyaline globules were found frequently in chromaffin cells of the adrenal medulla from several species of laboratory animals that died from various causes. The globules stained intensely red with PAS, were weakly acid-fast, did not stain with oil-red O and showed bright yellow autofluorescence. Ultrastructurally, they were finely granular, round to oval, intensely osmiophilic and were surrounded by an intimately bound trilaminar membrane. The globules were interpreted as aggregated secretory granules that occur in degenerating cells.

Adrenal Medulla↗
PubMed1976

The fine structure of intracranial neoplasms induced by the inoculation of avian sarcoma virus in neonatal and adult rats.

Groups of F-344 rats were inoculated with the Bratislava-77 strain of avian sarcoma virus (B-77 ASV) within 24 hours of birth, at 9 days of age, or between 97 and 119 days of age. Intracranial tumors developed in each age group. Multiple tumors with mixed histologic patterns developed in rats inoculated at 1 or 9 days of age. Solitary tumors with a uniform histologic pattern developed in rats inoculated as adults. On the basis of light and electron microscopic study, the majority of tumors in each age group were classified as astrocytomas and divided into either poorly differentiated, gemistocytic, pilocytic, or polymorphic varieties. The polymorphic astrocytomas were most common among neonatally inoculated rats, while the pilocytic astrocytomas were most common among rats inoculated as adults. Ultrastructural characteristics of astrocytes, including gap junctions and 7- to 9-nm filaments, were present in the majority of tumors in each age groups. Astrocytomas induced in adult rats were remarkable for the presence of extensive basement membrane alone the astrocytic cell surfaces. Intracytoplasmic virus-like particles (R particles) were common in the tumor cells. These virus-like particles are morphologically distinct from C-type B-77 ASV, and no morphologic evidence of C-type virus replication was observed in any of the tumors.

Animals↗
PubMed1975

Effects of vinyl chloride exposures to rats pretreated with phenobarbital.

Male rats were exposed to 10 consecutive days, 6 hr/day, to vinyl chloride vapors at an average concentration of 13,500 ppm. The exposed rats were divided into three groups of eight rats each: one group was pretreated with 3-methylcholanthrene, one group was pretreated with phenobarbital, and the third group received no treatment. Half the animals in each group were sacrificed 18 hr after the last exposure and half were sacrificed 4 days later. In a second experiment, four rats pretreated with phenobarbital were exposed to vinyl chloride vapors at a concentration of 17,300 ppm for 2 days and sacrificed about 9 A.M. on the third day. In both experiments control animals, also treated with phenobarbital or 3-methylcholanthrene, were exposed to air only. At the time of sacrifice, lungs, kidneys, spleen, heart, and a small piece of liver from each animal were preserved for histological examination. The remainder of the liver was processed for assay of microsomal enzyme activity. The following parameters were investigated: growth rate, organ weights, morphological changes, and both benzphetamine-N-demethylase activity and cytochrome P-450 content of microsomes prepared from the livers. In both experiments the only marked difference noted in any group was a decrease in the growth rate of the animals exposed to vinyl chloride and treated with phenobarbital. This decreased growth rate was particularly apparent on the third day of the vinyl chloride exposures. Occasional morphological changes were also seen in the livers of the animals treated with phenobarbital and exposed to vinyl chloride.

Animals↗