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C Porter

Publications and source records attributed to C Porter.

70 records · Page 4Linked to original sources
PubMed1987

Isolation and morphologic characterization of human ovarian carcinoma cell clusters present in effusions.

Serous, mucinous, endometrioid and clear cell human ovarian carcinoma cells were isolated as multicellular aggregates from patient effusions by filtration on nylon mesh of defined porosity and examined by light microscopy. The cell clusters ranged from compact to loosely adherent groups of cells to spheroids with a central lumen surrounded by a cell monolayer. There was considerable variation in cluster morphology between effusions from different patients as well as within effusion from the same patient. Apparent budding of clusters was observed as well as different stages of cluster growth and development. This was observed for all histologic types studied. Electron microscopy of serous, mucinous and clear cell types showed that cells forming clusters were attached to each other by desmosomes, demonstrating that cluster formation did not result from a nonspecific stickiness of cells. Irregular microvilli were present on the external periphery of the various carcinoma cells and a prominent glycocalyx was present on the surface of mucinous carcinoma cells. Extensive interdigitation of cytoplasmic extensions and extended villi was present in mucinous and serous clusters which appeared to strengthen cluster cohesiveness. Nuclei were irregular with prominent nucleoli frequently present. The cell clusters usually remained intact and viable in culture but generally did not attach to glass or plastic substrata, whereas mesothelial cells and nonactivated histiocytes rapidly attached. When carcinoma cell clusters did attach, they were resistant to detachment by trypsin-EDTA treatment, in contrast to the nonmalignant cells.

Adenocarcinoma↗
PubMed1986

Anorexia and altered serotonin metabolism in a patient with argininosuccinic aciduria.

We studied serotonin metabolism in a metabolically stable 7-year-old girl with argininosuccinic aciduria who had severe anorexia. The CSF concentration of 5-hydroxyindoleacetic acid (HIAA), the metabolite of serotonin, was markedly elevated at 79 ng/ml (normal 33 +/- 11 ng/ml). Altered serotonin metabolism was also reflected in the sleep EEG, which showed decreased REM sleep. Reducing her intake of tryptophan, the precursor of serotonin, from 35 mg/kg/day to 7 mg/kg/day resulted in a decrease in CSF concentration of HIAA to 20 ng/ml and the onset of spontaneous eating for the first time in 4 1/2 years. REM sleep increased from 3% to 9.5% of total sleep time. Two days after increasing tryptophan intake to 25 mg/kg/day, spontaneous feeding stopped, associated with a rise in CSF HIAA to 45 ng/ml. Caloric/carbohydrate intake was found to affect CSF HIAA levels and food intake in an additive manner with tryptophan intake. These observations suggest that altered serotonin metabolism affected feeding behavior in this child, and that this effect could be modified by changing tryptophan or carbohydrate intake.

Amino Acid Metabolism, Inborn Errors↗
PubMed1986

Long-term outcome of group B streptococcal meningitis.

Group B Streptococcus is a common cause of neonatal sepsis and meningitis. The purpose of this study was to evaluate the neurologic, psychologic, and academic status of children who had group B streptococcal meningitis and to compare these children with their siblings. Seventy-four children who acquired group B streptococcal meningitis between one day and 6 months of life formed the study population. Survivors were 3 to 18 years old at the time of their follow-up evaluations. Twenty children (27%) died, two were institutionalized, one severely affected child died at age 2 years, 15 were assessed by phone interview, and two were lost to follow-up. Thirty-four children and 21 siblings were comprehensively evaluated with physical and neurologic examinations, hearing tests, and tests of intellectual, perceptual-motor, and behavioral-adaptive functions. Of the total population, nine children (12%) had major neurologic sequelae (spastic quadraplegia, profound mental retardation, hemiparesis, deafness, or blindness). Six children had acute hydrocephalus; two were doing well after shunt placement. In general, those children surviving group B streptococcal meningitis without major sequelae appeared to be functioning normally or comparably to their sibling in intellectual, social, and academic matters.

Achievement↗
PubMed1980

Fluorophosphate-sensitive esterases in mammalian liver: the radioautographic localization and measurement of fluorophosphate-reactive sites in adult rat liver.

Fluorophosphate-reactive (FPR) sites in the adult male rat liver, tentatively identified as esterase active centers, were localized and measured using the combined techniques of quantitative electron microscope radioautography and morphometric analysis with the light and electron microscope. The FPR sites were measured in liver which had been prefixed by perfusion with 1.5% glutaraldehyde and reacted with 10(-4) M tritium-labeled diisopropyl fluorophosphate (3H-DFP). Under the experimental conditions 64-67% of the esterase activity in fresh liver was retained for reaction with the 3H-DFP, which is known to bind irreversibly to the active sites of certain esterases. In light and electron microscope radioautographs the developed silver grains were concentrated over the cytoplasm of hepatocytes. A low concentration occurred over erythrocytes. All other areas in the liver had a concentration of grains resembling the background concentration. Quantitative measurements of grain density in the electron microscope radioautographs revealed the highest density, after correcting for radiation spread, in cytoplasmic granules (mainly cytolysomes). The grain densities over the rough and smooth endoplasmic reticulum and associated structures were also equal to or above the average hepatocyte grain density. Due to the large fractional volume of endoplasmic reticulum per hepatocyte (58% of cell volume) and the fraction of the liver occupied by hepatocytes (79% of liver volume) the majority of FPR sites in the liver occurred in the rough and smooth endoplasmic reticulum and associated structures. The average numbers of FPR sites were calculated per micrometer3 of hepatocyte (5.0 x 10(5) sites/micrometer3) and per unit volume of each significantly labeled organelle. In addition, the number of FPR sites per hepatocyte (2.5 X 10(9) sites/cell), per cm3 liver (4.1 X 10(17) sites/cm3) and in the total liver of an average 100 g male rate (2.2 X 10(18) sites/total liver) were also calculated.

Animals↗