PubMed HealthSearch

Biomedical subjects

V G Lockard

Publications and source records attributed to V G Lockard.

9 recordsLinked to original sources

Soft tissue myofibroblastomas.

Five well-circumscribed solitary soft tissue tumors composed of myofibroblasts are described and termed myofibroblastomas. By light microscopy these lesions are characterized by short, intersecting, or crisscrossing fascicles of spindle cells, sometimes associated with foci of necrosis and/or mitotic activity with less than three mitoses per 10 high power fields. Myofibroblastomas show well-defined myofibroblastic differentiation ultrastructurally with peripheral myofilaments and vimentin, actin, and desmin immunocytochemistry positivity. The five tumors described occurred in patients of various age groups, including one congenital, and in a variety of soft tissue locations. It is important to recognize this benign soft tissue neoplasm to avoid confusion with other soft tissue tumors and to separate this lesion from other myofibromatosis. This study elucidates the spectrum of light microscopic, ultrastructural, and immunocytochemistry findings of soft tissue myofibroblastomas and establishes this soft tissue tumor as a specific clinico-pathologic entity.

Actins

Morphologic features and nuclide composition of infarction-associated cardiac myocyte mineralization in humans.

Low dietary Mg results in Ca loading of cardiac myocytes, which increases the likelihood of myocyte calcification in the event of acute myocardial infarction (AMI), and possibly increases myocyte vulnerability to necrosis. Bloom and Peric-Golia1 previously reported an autopsy study of cases from the Washington, D.C. area (a region with low levels of Mg in the drinking water), demonstrating AMI-associated mineralization in myocytes with histologically normal nuclei and cross striations, as well as in obviously necrotic myocytes. The authors have re-examined mineralized myocytes from the same autopsy material, using electron probe microanalysis, light microscopy, and transmission electron microscopy. Microprobe analysis identified Ca and P as the nuclides composing the inorganic phase of the mineral deposits. Ultrastructurally, all Ca deposits, regardless of size or intracellular location, were composed of aggregates of needlelike hydroxyapatite crystals. The mildest form of intracellular Ca deposition was observed as small Ca deposits limited to some mitochondria of myocytes, which demonstrated intact nuclei and regular sarcomere pattern. More advanced stages of intracellular calcification, in the form of Ca deposits associated with mitochondria, Z-band regions and nuclei, were observed in other myocytes that also retained intact nuclei and sarcomeres. Massive Ca deposits were associated with myocytes which showed morphologic features of advanced necrosis, including loss of nuclei, disruption of sarcomere structure and masses of cellular debris. These observations support the theory originally proposed by Bloom and Peric-Golia1 suggesting that Ca loading of myocytes, possibly related to Mg deficiency in humans, increased vulnerability of the myocytes to subsequent AMI-associated necrosis and dystrophic calcification. In addition, the light microscopic impression of calcification of otherwise normal myocytes is contradicted by the electron microscopic identification of hydroxyapatite crystals free in the sarcoplasm, a condition unlikely to be compatible with viability. Lastly, the fact that all Ca deposits were in the form of hydroxyapatite supports the view that they were formed in a Mg-poor environment, which favors conversion of the more common amorphous form of Ca phosphate into the needlelike crystals of hydroxyapatite.

Calcium

In vivo toxicity and pulmonary effects of promazine and chlorpromazine in rats.

Cationic amphiphilic drugs induce a phospholipid storage disorder known as phospholipidosis. Halogenated analogs of the drugs are more potent inducers of phospholipidosis when compared to nonhalogenated analogs. Two such antipsychotic drugs, promazine and chlorpromazine, are effectively taken up by the lungs and induce lamellar inclusions in vitro. We compared the in vivo toxicity and efficacy of promazine and chlorpromazine to induce phospholipidosis in the lung and in pulmonary alveolar macrophages. Male Sprague-Dawley rats were given promazine or chlorpromazine (25 mg/kg/day, P.O., in water) for 5 weeks. Food intake was decreased in promazine- and chlorpromazine-treated rats, chlorpromazine rats being affected more than promazine rats. To minimize experimental error due to starvation, control rats were pair-fed. The body weight gain was decreased in chlorpromazine rats in comparison to pair-fed controls. Chlorpromazine-treated rats, but not promazine-treated rats, showed increased mortality over the 5-week treatment period. Histopathologic examination of lung revealed loss of alveolar macrophages with no other gross abnormalities in chlorpromazine-treated rats. Quantitative analysis of lung lavage also showed significant reduction in the number of macrophages. This finding is in contrast to other cationic amphiphilic drugs, which induce phospholipidosis as well as accumulation of alveolar macrophages. Phospholipid level increased in alveolar macrophages but not in lavaged lung following chlorpromazine treatment. Acid phosphatase activity in lavaged lung homogenate and macrophages of promazine- and chlorpromazine-treated rats, taken as an index of toxicity to cells, did not differ significantly from control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid Phosphatase

Adult rhabdomyoma of soft palate.

A case of adult rhabdomyoma of the soft palate in a 60-year-old man studied by methods including electron microscopy, is reported. The patient was free of recurrence 2 years later. The eleven previously documented cases of adult rhabdomyoma involving the oral cavity are reviewed. The concept that rhabdomyoma is a neoplasm rather than a hamartoma is favored. Adequate local excision appears to be curative. The differences between the cardiac and extracardiac forms of rhabdomyoma as well as between adult rhabdomyoma and especially granular-cell myoblastoma and fetal rhabdomyoma are presented.

Cell Membrane

Decreased activity of NADPH oxidase in alveolar macrophages as a result of traumatic shock.

NADPH oxidase activity is significantly decreased in alveolar macrophages isolated from rabbits subjected to traumatic shock. In vitro studies indicate that activity of the enzyme is depressed in subcellular fractions of both resting and phagocytosing macrophages from shocked animals. Phagocytosis stimulates a twofold increase in NADPH oxidation in control alveolar macrophages, whereas NADPH oxidase activity is stimulated to a much lesser degree in macrophages from shocked animals. Results of this study suggest that the decreased activity of NADPH oxidase in alveolar macrophages from shocked animals may be associated with decreased bactericidal ability of the cells which was reported in a previous study (9).

Animals

Alterations in rabbit alveolar macrophages as a result of traumatic shock.

Biochemical and electron microscope studies were conducted to determine the effects of traumatic shock on rabbit alveolar macrophages. Both resting and phagocytosing macrophages from the shocked animals, in comparison to comparable control macrophages, showed increased release of acid phosphatase from the cells into medium upon incubation in vitro, but decreases in the total content of acid phosphatase and beta-glucuronidase. Studies by electron microscopy showed ultrastructural alterations in macrophages from shocked animals consisting of a reduction in the number or a complete absence of lysosomes and, in some cases, increased amounts of rough endoplasmic reticulum and free ribosomes. In vitro incubation of macrophages from shocked animals with Pseudomonas aeruginosa showed that the process of bacterial ingestion was not impaired nor were the numbers of bacteria ingested decreased as compared to control macrophages. However, the ability of macrophages from shocked animals to destroy ingested bacteria appeared to be significantly altered. Extensive degradation of Pseudomonas was observed within phagocytic vacuoles of control macrophages after 15 minutes of incubation. In contrast, the majority of ingested organisms in macrophages from shocked animals showed no evidence of degradative changes.

Acid Phosphatase

Granular-cell myoblastoma of the cercum: report of a case.

A 9-mm granular-cell myoblastoma of the cecum found incidentally during appendectomy in a 17-year-old-girl is reported. Electronmicroscopic findings favor origin of the granular cells from an undifferentiated mesenchymal (fibroblast-like) cell. Review of the small number of previously reported cases revealed three involving the cecum, one each in the ascending and transverse colon and two in the rectum. Four patients were asymptomatic and their lesions were found incidentally. Three lesions simulated maligancy clinically; these patients underwent right hemicolectomy.

Adolescent

A simple technique for postembedding ultrastructural immunogold labeling.

A simple and reproducible method for postembedding ultrastructural immunogold labeling is described. Tissues are fixed in Carson-Millonig phosphate-buffered 4% formaldehyde, and then are embedded in LR White resin. Immunogold labeling of ultrathin sections is accomplished by means of an indirect method that employs a nonconjugated primary antibody and gold particles conjugated to antibody to immunoglobulin G. Technical aspects of fixation, embedding, and immunolabeling that influence the success of this protocol are discussed.

Antibodies