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Biomedical subjects

J M Jamison

Publications and source records attributed to J M Jamison.

32 records · Page 2Linked to original sources
PubMed1993

Subcellular localization and antiviral activity of carminic acid/poly r(A-U) combinations.

Carminic acid (CAR) enhances the antiviral activity of poly r(A-U) twelve-fold without increasing interferon induction, inactivating the vesicular stomatitis virus or inducing host cell cytotoxicity. Phase contrast photomicrographs of human foreskin fibroblasts (HSF) incubated with CAR alone, poly r(A-U) alone or with a CAR/poly r(A-U) combination illustrate that the CAR/poly r(A-U) combinations display altered subcellular distribution with the CAR being localized in the nucleoli and chromatin. Phase contrast and fluorescence photomicrographs of adriamycin (ADR)-treated and ADR/poly r(A-U)-treated HSF cells corroborate these findings. These results suggest that modulation of one or more nucleolar processes may be responsible for the enhanced antiviral activity.

Antiviral Agents↗
PubMed1993

Effect of ethidium on the morphology, antiviral activity and subcellular distribution of poly r(A-U).

When ethidium bromide (EB) is combined with poly r(A-U) at an EB/ribonucleotide ratio of 1/4, the antiviral activity of the EB increases 22-fold. The increased antiviral activity is not due to increased interferon induction, direct viral inactivation or host cell cytotoxicity. Phase contrast, confocal and fluorescence microscopic observations reveal an increase in the nucleolar accumulation of the EB and/or the poly r(A-U) in the EB/poly r(A-U)-treated fibroblasts. Ultrastructure of negatively stained and replica preparations demonstrated that EB-induced condensation of poly r(A-U). These results suggest the elevated antiviral activity may be related to the altered uptake and subcellular distribution of the EB/poly r(A-U) complex.

Antiviral Agents↗
PubMed1992

Enhanced antiviral activity and altered subcellular distribution of magnesium/poly r(A-U) combinations.

When Mg2+ or ethidium bromide (EB) were combined with poly r(A-U) at a ligand/ribonucleotide ratio of 1/4, the antiviral activity of the Mg2+ and EB increased 136-fold and 154-fold. Eriochrome Blue SE was employed to visualize the subcellular distribution of Mg2+ following co-incubation of Human Foreskin Fibroblasts (HSF) with Mg2+ alone or with the Mg2+/poly r(A-U) combination. Phase contrast micrographs of these Mg(2+)-treated HSF cells as well as phase contrast and fluorescence micrographs of EB-treated or EB/poly r(A-U)-treated HSF cells illustrated that the Mg2+ (or EB)/poly r(A-U) combinations display altered subcellular distribution with the Mg2+ and EB being localized in the nucleoli and chromatin of the HSF cells. These results suggest that modulation of nuclear processes may be responsible for the enhanced antiviral activity.

Antiviral Agents↗
PubMed1990

Enhancement of the antiviral activity of poly r(A-U) by ametantrone and mitoxantrone.

The role of ametantrone (HAQ) and mitoxantrone (DHAQ) in modulating the antiviral and interferon-inducing activities of poly r(A-U) was examined using the human foreskin fibroblast-vesicular stomatitis virus (HSF-VSV) bioassay system in which the concentration of poly r(A-U) was fixed at 0.05 mM or 0.2 mM while the HAQ or DHAQ concentration was varied to produce variable HAQ (or DHAQ)/ribonucleotide ratios ranging from 1:16 to 2:1. HAQ, DHAQ and poly r(A-U) tested individually were not efficacious antiviral agents. When poly r(A-U) was combined with the ametantrone or mitoxantrone the antiviral activity was potentiated 10-fold at HAQ (or DHAQ)/ribonucleotide ratios in the region of 1/4 to 1/6. The interferon-inducing activity of the HAQ (or DHAQ)/poly r(A-U) combinations were equal to the sum of the interferon-inducing activity of the poly r(A-U) and the HAQ (or DHAQ). These results indicate that the HAQ and DHAQ potentiate the antiviral activity of the poly r(A-U) without the superinduction of interferon. The direct viral inactivation study demonstrated that HAQ, DHAQ, poly r(A-U) and the HAQ (or DHAQ)/poly r(A-U) combinations did not inactivate the VSV at concentrations near the viral 50% inhibitory dose.

Biological Assay↗
PubMed1990

Potentiation of the antiviral activity of poly r(A-U) by xanthene dyes.

Ten xanthene dyes (XAN) are evaluated for their ability to potentiate the antiviral activity of poly r(A-U) using a human foreskin fibroblast-vesicular stomatitis virus bioassay in which the XAN is combined with 0.2 mM poly r(A-U) to produce a XAN/ribonucleotide ratio of 1/4. Four of the ten XANs tested in this study, rhodamine 123, rhodamine B, rhodamine 6G and sulforhodamine B, enhance the antiviral activity of poly r(A-U) 8- to 15-fold. The interferon-inducing activity of the four active XAN/poly r(A-U) combinations is equal to the sum of the activities of their constituents. These four XANs appear to potentiate the antiviral activity of the poly r(A-U) without superinduction of interferon. The direct viral inactivation study demonstrates that the XANs, poly r(A-U) and the XAN/poly r(A-U) combinations do not inactivate the VSV at concentrations near the 50% effective dose.

Antiviral Agents↗
PubMed1990

Polyribonucleotide-anthraquinone interactions: in vitro antiviral activity studies.

Twelve anthraquinones (AQ) were evaluated for their ability to potentiate the antiviral activity of poly r(A-U) using a human foreskin fibroblast-vesicular stomatitis virus bioassay in which the AQ was combined with 0.2 mM poly r(A-U) to produce an AQ/ribonucleotide ratio of 1/4. Poly r(A-U) and the AQ alone were not effective antiviral agents. Five of the twelve AQs tested, mitoxantrone, adriamycin, ametantrone, carminic acid and daunomycin, enhanced the antiviral activity of poly r(A-U) 9- to 13-fold. The interferon-inducing activity of the five active AQ/poly r(A-U) combinations was equal to the sum of the interferon-inducing activities of their constituents. These five AQs appear to potentiate the antiviral activity of poly r(A-U) without superinduction of interferon.

Anthraquinones↗
PubMed1989

Potentiation of the antiviral activity of poly r(A-U) by riboflavin, FAD and FMN.

The role of riboflavin (RFN), FAD or FMN in modulating the antiviral activity of poly r(A-U) was examined by the human foreskin fibroblast-vesicular stomatitis virus bioassay in which the concentrations of poly r(A-U) was fixed at 0.1 mM or 0.2 mM while the riboflavin, FAD or FMN concentration was varied to produce variable RFN (or FAD or FMN)/ribonucleotide ratios ranging from 1/16 to 2/1. Riboflavin, FAD and FMN tested individually did not exhibit any antiviral activity, while poly r(A-U) alone exhibited antiviral activity. When poly r(A-U) was combined with riboflavin, FAD or FMN, the antiviral activity was potentiated seven- to twelve-fold at RFN (or FAD or FMN)/ribonucleotide ratios in the region of 1/4.

Cytopathogenic Effect, Viral↗
PubMed1988

Enhancement of the antiviral and interferon-inducing activities of poly r(A-U) by carminic acid.

Experiments have been designed to systematically examine the effects of carminic acid (CAR) on the antiviral/interferon-inducing activity of poly r(A-U), using the human foreskin fibroblast-vesicular stomatitis virus bioassay system. Modulation of the antiviral/interferon-inducing activity of poly r(A-U) by carminic acid was examined at fixed poly r(A-U) concentrations of 0.05 mM or 0.2 mM while varying the carminic acid concentrations to produce variable CAR/ribonucleotide ratios ranging from 1:16 to 2:1. Carminic acid and poly r(A-U) were tested individually at the concentrations employed in the CAR/poly r(A-U) combinations. Neither the carminic acid alone nor poly r(A-U) alone were effective antiviral agents/interferon inducers. The antiviral/interferon-inducing activity of poly r(A-U) was potentiated twelve-fold at CAR/ribonucleotide ratios in the region of 1/6 to 1/4. These results suggest a synergism between the poly r(A-U) and the carminic acid at the concentrations employed in this study.

Anthraquinones↗
PubMedDate not supplied

Autoschizis of human ovarian carcinoma cells: scanning electron and light microscopy of a new cell death induced by sodium ascorbate: menadione treatment.

Human ovarian carcinoma (MDAH 2774) cells were treated with sodium ascorbate (VC), menadione (VK3), or a combination of both in a ratio 100:1 for 1h and then examined with scanning electron microscopy (SEM) and light microscopy (LM). Light microscopy data corroborated SEM observations, which demonstrated that death of VC+VK3-treated tumor cells occurred primarily by autoschizis. This type of cell death is characterized by a decrease in cell size, cytoplasmic self-excisions, and nuclear and nucleolar morphologic degradations without the formation of apoptotic bodies. Ultimately, cell death results from karyorrhexis and karyolysis. This study illustrates that plasma membrane damage (branching filopodia, blisters, blebs) results from VC treatment; cytoskeletal damage and self-morsellation are caused by VC, VK3 and VC+VK, treatments. The VC treatment results in a 23% decrease in cell diameter while VK3-treated cells decrease cell diameter by 66%. After 1h of VC+VK3 treatment, a heterogenous cell population is found. This population can be resolved into one population whose diameters are 23% smaller than those of sham-treated cells, and a second population whose diameters are approximately twice those of sham-treated cells. This second population is indicative of doublet formation in which the cells appear to be dividing (an early stage of autoschizic cell death). One half of the doublet contains the cell nucleus while the other half consists of cytoplasm and membrane only. The enucleate portion of this doublet will then be excised. When the types of cell death are enumerated following VC+VK3 treatment, 43% of the cells die by autoschizis, 3% by apoptosis, and 1.9% by oncosis. These results confirm that autoschizis is the principal form of cell death that results from the in vitro treatment of human ovarian carcinoma cells with the vitamin combination.

Adenocarcinoma↗
PubMedDate not supplied

Ultrastructural aspects of autoschizis: a new cancer cell death induced by the synergistic action of ascorbate/menadione on human bladder carcinoma cells.

Scanning and transmission electron microscopy were employed to further characterize the cytotoxic effects of a ascorbic acid/menadione (or vitamin C/vitamin K3) combination on a human bladder carcinoma T24 cell line. Following 1-h treatment T24 cells display membrane and mitochondrial defects as well as excision of cytoplasmic fragments that contain no organelles. These continuous self-excisions reduce the cell size. Concomitant, nuclear changes, chromatin disassembly, nucleolar condensation and fragmentation, and decreased nuclear volume lead to cell death via a process similar to karyorrhexis and karyolysis. Because this cell death is achieved through a progressive loss of cytoplasm due to self-morsellation, the authors named this mode of cell death autoschizis (from the Greek autos, self, and schizein, to split, as defined in Scanning. 1998; 20: 564-575). This morphological characterization of autoschizic cell death confirms and extends the authors previous reports and demonstrates that this cell death is distinct from apoptosis.

Ascorbic Acid↗