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Biomedical subjects

E R Walker

Publications and source records attributed to E R Walker.

At least 37 records · Page 2Linked to original sources
PubMed1988

The characterization of normal and scleroderma skin fibroblasts cultured in a collagen gel matrix.

Fibroblasts from normal and progressive systemic sclerosis involved skin more closely resemble in vivo cells when cultured in a collagen gel matrix, than do fibroblasts cultured on plastic. Ultrastructural studies show that the cytoskeleton and secretory organelles from these cells are better developed in the presence of a collagen gel. Fibronectin, glycosaminoglycans and collagen fibrils are produced by the cells and deposited in the preformed matrix. Collagen synthesis is greater in the scleroderma derived fibroblasts for all culture conditions with increased deposition in the matrix. Total collagen production form cells associated with the gel is less than that from those cultured on plastic, suggesting an inhibition of collagen synthesis by the preformed collagen matrix.

Cells, Cultured↗
PubMed1986

Role of phospholipase A inhibition in amiodarone pulmonary toxicity in rats.

Amiodarone is effective in the treatment of ventricular and supraventricular arrhythmias. In man its clinical use is associated with the accumulation of phospholipid-rich multilamellar inclusions in various tissues including lung, liver and others. This report presents evidence showing that amiodarone is a potent inhibitor of lysosomal phospholipase A from rat alveolar macrophages, J-744 macrophages and rat liver. When compared with other cationic amphiphilic agents which are known to produce phospholipidosis, amiodarone is one of the most potent inhibitors yet discovered. The subcellular localization of amiodarone has been determined in lung and its distribution was consistent with a lysosomal localization. It is hypothesized that amiodarone causes cellular phospholipidosis by concentrating in lysosomes and inhibiting phospholipid catabolism.

Amiodarone↗
PubMed1986

Morphological and functional changes in mouse splenic lymphocytes following in vivo and in vitro exposure to chlorphentermine.

With repeated administration to animals, the cationic, amphiphilic drug, chlorphentermine (CP), has been shown by others to induce a phospholipidosis in lymphocytes. In the present study mouse splenic lymphocytes, exposed to CP, either in vivo or in vitro, developed morphological changes consistant with the induction of phospholipidosis. In addition, CP induced functional changes in lymphocytes. Mice, treated with CP in vivo, demonstrated a significantly depressed ability to generate a delayed hypersensitivity response or to produce antibody-secreting cells against de novo antigens. Mouse splenic lymphocytes, exposed to 10(-7) M CP for 3 days in vitro, demonstrated a significantly depressed blastogenic response to the mitogens phytohemagglutinin, concanavalin A and lipopolysaccharide. CP inhibited an event that occurred early during lymphocyte activation, but was subsequent to mitogen/receptor coupling. In addition, CP significantly depressed the increased uptake of choline that occurs in lymphocytes following cellular activation. Since the presence of phospholipidosis is indicative of an impairment in phospholipid metabolism, these results taken together provide evidence for a relationship between this phenomenon and altered immune function.

Animals↗
PubMed1984

Morphological survey of teleost organs important in carcinogenesis with attention to fixation.

Key features of the gross and microscopic anatomy of teleost liver, digestive tract, kidney, and skin were reviewed from the world literature. Illustrations of the above and new findings were obtained from light as well as scanning and transmission electron micrographs of tissues from 7 freshwater fish species: Alosa sapidissima, American shad; Esox lucius, northern pike; Lepomis macrochirus, bluegill sunfish; Pimephales promelas, fathead minnow; Stizostedion vitreum, walleye; Oryzias latipes, Japanese medaka; and Ictalurus nebulosus, brown bullhead catfish. Emphasis was placed on structural features that may influence interpretation of toxic and carcinogenic lesions. A discussion of fixation of small fish for light and electron microscopy and histochemistry is presented.

Animals↗
PubMed1983

Chlorphentermine-induced neonatal and maternal pulmonary phospholipidosis in rats.

Pregnant rats were treated on Days 16-20 of pregnancy with 30 mg/kg chlorphentermine hydrochloride (CP) or an equal volume of 0.9% NaCl. Females delivered on Day 21 and neonates were examined 12 hr postpartum. Electron micrographs showed the CP neonates to have lamellar inclusions, characteristic of drug-induced phospholipidosis in Type I and Type II cells, macrophages, and nonciliated bronchiolar epithelial cells of the lung. These inclusions were either unicentric, multicentric, or consisted of whorls of membranous material. The content of total phospholipids was increased in neonatal lung as a result of CP treatment. A decrease in the percentage of total phospholipid present as phosphatidylinositol plus phosphatidylserine and an increase in the content of disaturated phosphatidylcholine were found in neonatal lung as a result of maternal chlorphentermine treatment. In maternal lung, increases were seen in the content of total phospholipids, total phosphatidylcholine, disaturated phosphatidylcholine, and phosphatidylinositol plus phosphatidylserine. A decrease in the percentage of sphingomyelin was also found. The results of this study indicate that following prepartum maternal administration of CP morphological changes are accompanied by biochemical alterations which are consistent with the induction of phospholipidosis as observed in neonatal lung. These biochemical changes were different than those associated with the induction of this disorder in the maternal lung.

Animals↗
PubMed1982

Neonatal toxicity in rats following in utero exposure to chlorphentermine or phentermine.

The administration of chlorphentermine (30 mg/kg) to pregnant rats during the last 5 days of gestation resulted in the development of a phospholipidosis in the lungs of the dams. The disorder developed in utero, as the phospholipidosis was evident in the lungs of the neonates when examined at 12 h postpartum. In contrast, a phospholipidosis was not observed in the lungs of the dams or neonates following phentermine treatment (30 mg/kg). Concurrently, neonates of the chlorphentermine-treated dams displayed a significant decrease in body weight in comparison to controls. Between 16 h and 24 h postpartum, 83% of the neonates of chlorphentermine-treated dams died. Cross-fostering and starvation experiments revealed that the lethality was not due to aberrant maternal behavior by the chlorphentermine-treated dams or malnutrition of the neonates. Histological examinations revealed endothelial and septal alterations in the lungs of neonates from chlorphentermine-treated dams. No signs of toxicity, as evidenced by the maintenance of body weight, or lethality were observed in the neonates of the phentermine-treated dams.

Animals↗
PubMed1982

Chlorcyclizine--induced pulmonary phospholipidosis in rats.

Chlorcyclizine (CZ) was administered to rats (100 mg/kg, p.o.) for either 1 or 2 weeks (5 days per week). Controls were pair-fed and received deionized water vehicle for the same periods of time. The level of total phospholipid increased about 50% in the lungs after 1 week of CZ but did not increase further after 2 weeks of treatment. There was a time-dependent increase in the recovery of alveolar macrophages (AMs) from the lungs of the CZ-treated rats as well as in the phospholipid content of the cells. After 2 weeks of CZ, the AMs contained 5.6-fold more phospholipid than controls. The AM fraction showed a greater relative elevation in phospholipid at both time points than did the remainder of the lung tissue. The results illustrated the marked susceptibility of the AM to the disruption of phospholipid metabolism by CZ.

Animals↗
PubMed1981

Morphology of the buccopharyngeal portion of the gill in the fathead minnow Pimephales promelas (Rafinesque).

Buccopharyngeal epithelium covering gill arches and gill rakers of the fathead minnow was studied by light microscopic, scanning, and transmission electron microscopic techniques. Mature mucous cells in goblet pattern and nonmucus containing cells were in the apical one-third of the tissue. The latter cells contributed to a surface microridge system which overlapped apices of goblet cells. The bottom of the epithelium was comprised of a continuous row of darkly stained basal epithelial cells. In this region, two to three epithelial cells of similar staining characteristics were piled up forming apical columns which partially encircled nests of lightly stained cells. A basal lamina and thick basement lamella of about 20 piles of orthogonally arranged collagen supported the epithelium. Numerous taste buds were seen in gill arches and rakers. Taste bud cellular components included marginal cells, light receptor cells, dark receptor cells, and basal cells. These were identical in all taste buds. Taste bud surface morphology differed between gill arch and raker. Pores of the former were depressed, while those of the latter were raised. Thick microvilli of taste pores were apical extensions of light cells, while smaller, more numerous microvilli were projections from dark cells.

Animals↗
PubMed1978

An ultrastructural study of avian synovium infected with an arthrotropic Mycoplasma, Mycoplasma synoviae.

Live Mycoplasma synoviae cells in agar base medium were inoculated intravenously into 10 2-week-old chickens. Joint tissues were collected over a 3-week period for light and transmission electron microscopy. In infected chickens, membrane-bound vacuoles of intact M. synoviae cells were seen in the cytoplasms of adipose cells. Cytoplasmic lipid-containing inclusions had accumulated in enlarged fibroblasts in tendon sheaths and loose connective tissue. Synovial cells had proliferated and contained increased amounts of granular endoplasmic reticulum and lipid inclusions. No abnormalities were seen in control chickens. Infected chickens were positive and control chickens were negative for rheumatoid factor activity by two serological tests: tanned cell hemagglutination and latex agglutination tests.

Animals↗
PubMedDate not supplied

Ultrastructural study of avian synovium infected with an arthrotropic reovirus.

Three-week-old chicks were inoculated via the foot pad with the avian reovirus (strain WVU 2937) that has been proved to be the causative agent in avian viral arthritis. The initial stages of the avian reovirus infection in the synovium of the hock joint were studied by transmission electron microscopy to shed light on the early virus-host relationship of an arthrotropic virus and synovial tissue. At 48 hours postinoculation (PI), coated, partially coated, and uncoated virus particles were seen in a dense lysosome-like inclusion in the cytoplasm of subsynovial fibroblasts. Virus replication was demonstrated in fibroblasts of the subsynovium 4 days PI. Infiltration of leukocytes into the area of the virus replication was noted at the time of virus replication (4 days PI). By the second week of the infection (11 days PI), the subsynovium was heavily infiltrated with lymphocytes and plasma cells, and proliferative changes had occurred in the synovial lining cells.

Animals↗
PubMedDate not supplied

[Synovial membrane and cartilage changes in an arthrosis model. Instability and impact stress model].

UNLABELLED: Surgical instability and repetitive impulsive loading was used to generate degenerative changes in knee joints of rabbits. Light- and electronmicroscopy was carried out at synovial membrane and cartilage samples. The instabilised joints had early synovial inflammation, preceding overall cartilage changes. Synoviocytes were activated and showed more and dilatated cytoplasmatic organells. Invaded round cells--potentially cartilage degenerative--were seen. In the loading model no initial synovial inflammation could be seen. Focal cartilage changes were located at the weight bearing zone. Two different inductive pathways may be involved in cartilage breakdown comparing the two arthrosis models. Mechanical factors seemed to trigger cartilage changes in the loading model, an inflammatory synovial pathway is likely to initiate cartilage breakdown in the instability model. CLINICAL RELEVANCE: The synovial membrane has the key-position for the cartilage degeneration in posttraumatic joint affections. The therapeutic use of antiphlogistic substances is indicated to supreme inflammatory mediators from the synovial membrane. This therapeutic concept seemed not to be useful in primary mechanical induced osteoarthrosis.

Animals↗