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R Armour

Publications and source records attributed to R Armour.

16 recordsLinked to original sources
PubMed2005

Case report: massive postpartum transfusion of Jr(a+) red cells in the presence of anti-Jra.

Jr(a) is a high-prevalence antigen. The rare Jr(a-) individuals can form anti-Jr(a) after exposure to the Jr(a) antigen through transfusion or pregnancy. The clinical significance of anti-Jr(a) is not well established. This study reports a case of a 31-year-old woman with a previously identified anti-Jr(a) who required massive transfusion of RBCs after developing life-threatening postpartum disseminated intravascular coagulopathy. Despite the emergent transfusion of 15 units of Jr(a) untested RBCs, she did not develop laboratory or clinical evidence of acute hemolysis. The patient's anti-Jr(a) had a pretransfusion titer of 4 and a monocyte monolayer assay (MMA) reactivity of 68.5% (reactivity > 5% is considered capable of shortening the survival of incompatible RBCs). The titer increased fourfold to 64 and the MMA reactivity was 72.5% on Day 10 posttransfusion. Review of laboratory data showed evidence of a mild delayed hemolytic transfusion reaction by Day 10 posttransfusion. Despite rare reports of hemolytic transfusion reactions due to anti-Jr(a) in the literature, most cases, including this one, report that this antibody is clinically insignificant or causes only mild delayed hemolysis. Clinicians should be advised to balance the risks of withholding transfusion with the small chance of significant hemolysis after transfusion of Jr(a+) RBCs in the presence of anti-Jr(a).

Adult↗
PubMed2001

Current assessment of thromboembolic disease and pregnancy.

This study was undertaken to assess incidence of deep venous thrombosis and pulmonary emboli in an inner-city pregnant population. Thromboembolic disease is believed to occur in 0.05 to 0.1 per cent of all pregnancies. Historically, postpartum thromboembolic disease was more common; decreased hospital stay may shift the thromboembolic disease to the antepartum period. A 5-year retrospective review of 4910 births assessed for incidence of thromboembolic disease, methods of diagnosis and treatment, and risk factors. A total of 4910 deliveries with 3978 transvaginal resulted in 30 episodes of deep venous thrombosis and five pulmonary emboli. All incidences of deep venous thrombosis but one were left-sided; four of five pulmonary emboli were postpartum. Of the epidsodes of deep venous thrombosis 17 per cent were first trimester, 50 per cent second trimester, 27 per cent third trimester, and 6 per cent postpartum. The diagnosis was confirmed by duplex scan in 24 of 30 patients. Heparin was the standard treatment. Deep venous thrombosis in pregnancy is most common in the second trimester; pulmonary emboli remain most common postpartum.

Adolescent↗
PubMed1988

Amino acid sequence of the BSC-1 cell growth inhibitor (polyergin) deduced from the nucleotide sequence of the cDNA.

The complete amino acid sequence of the BSC-1 cell growth inhibitor, including its precursor polypeptide, is reported. The sequence was deduced from the nucleotide sequence of the cDNA. The N-terminal amino acid sequence of the mature bioactive BSC-1 cell growth inhibitor is identical with the N-terminal sequences of the factors that have been called type beta 2 transforming growth factor and cartilage-inducing factor B, suggesting that these are identical. The complete amino acid sequence of the mature BSC-1 cell growth inhibitor differs from that of human type beta transforming growth factor in 32 of the 112 amino acids. Polyergin is proposed as the name for the BSC-1 cell growth inhibitor.

Amino Acid Sequence↗
PubMed1985

A growth regulatory factor that can both inhibit and stimulate growth.

A growth inhibitor that is produced by BSC-1 cells (African green monkey kidney epithelial cells) has been isolated from conditioned medium. It has been purified by gel chromatography and high performance liquid chromatography. It appears to be a protein with a relative molecular mass (Mr) of 24 000. It is extremely active as a growth inhibitor with some cells, but not with others. Approximately 50% inhibition of thymidine incorporation is observed with CCL64 cells at 0.05 ng/ml and with BSC-1 cells at 1 ng/ml. The growth inhibitor induces BSC-1 cells to synthesize and secrete a glycoprotein of approximately 48 000 Mr. It inhibits Na+ accumulation in BSC-1 cells. Recently, in collaboration with R. F. Tucker, G.D. Shipley and H. L. Moses (Mayo Foundation & Medical School), we have found that the growth inhibitor is very similar to and may be identical with transforming growth factor beta (TGF-beta). Our growth inhibitor stimulates colony formation in soft agar by AKR-2B cells, and it competes with TGF-beta in binding to cell surface receptors. TGF-beta, from human platelets, is extremely active as an inhibitor of thymidine incorporation by BSC-1 cells and CCL64 cells. The growth inhibitor/TGF-beta can, therefore, stimulate or inhibit growth, depending on the cells and the growth conditions.

Animals↗
PubMed1983

Activity of a kidney epithelial cell growth inhibitor on lung and mammary cells.

A kidney epithelial cell growth inhibitor, isolated from BSC-1 cell-conditioned medium, has been found to be active on certain lung and mammary gland cell lines in culture. The most responsive cell observed thus far is the CCL64 mink lung cell line. With CCL64 cells, 60% inhibition of [3H]thymidine incorporation is observed at a 0.1 nanogram/ml concentration of the growth inhibitor, and approximately 95% inhibition at 1 nanogram/ml. A human mammary tumor cell line, Hs578T, shows 75% inhibition of [3H]thymidine incorporation, in cell culture. Preliminary studies indicate that injection of the kidney epithelial cell growth inhibitor in vivo into human mammary carcinomas growing in nude mice inhibits [3H]thymidine incorporation in the tumors.

Animals↗
PubMed1980

Purification of kidney epithelial cell growth inhibitors.

Two high molecular weight growth inhibitors have been isolated from the culture medium of BSC-1 cells, epithelial cells of African green monkey kidney. The purified kidney epithelial cell growth inhibitors, at ng/ml concentrations, reversibly arrest the growth of BSC-1 cells in the G1 phase of the cell cycle. Their action is selective; they are most active on BSC-1 cells, are less active as inhibitors of the growth of rat lung and human breast epithelial cells, and do not inhibit the growth of 3T3 mouse embryo fibroblasts ad human skin fibroblasts in culture. Their growth inhibitory action on BSC-1 cell cultures is counteracted by epidermal growth factor or calf serum.

Animals↗
PubMed1978

Density-dependent regulation of growth of BSC-1 cells in cell culture: control of growth by low molecular weight nutrients.

BSC-1 cells, epithelial cells of African green monkey kidney origin, show pronounced density-dependent regulation of growth in cell culture. Growth of the cells is rapid to a density of approximately 1.5 x 10(5) cells/per cm(2) in Dulbecco-modified Eagle's medium supplemented with 10% calf serum. Above this "saturation density," growth is much slower. It has been found that the glucose concentration in the culture medium is important in determining the "saturation density." If the glucose concentration is increased 4-fold, the "saturation density" increases approximately 50%. Reduction of the "saturation density" of BSC-1 cells is also possible by decreasing the concentrations of low molecular weight nutrients in the culture medium. In medium supplemented with 0.1% calf serum, decreasing the concentrations of all of the organic constituents of the medium, from the high levels present in Dulbecco-modified Eagle's medium to concentrations near physiological levels, decreases the "saturation density" by approximately half. The decreased "saturation density" is not the result of lowering the concentration of any single nutrient but rather results from reduction of the concentrations of several nutrients. When the growth of BSC-1 cells is limited by low concentrations of all of the nutrients, some stimulation of growth results from increasing, separately, the concentrations of individual groups of nutrients, but the best growth stimulation is obtained by increasing the concentrations of all of the nutrients. The "wound healing" phenomenon, one manifestation of density-dependent regulation of growth in cell culture, is abolished by lowering the concentration of glutamine in the medium. Density-dependent regulation of growth of BSC-1 cells in cell culture thus appears to be a complex phenomenon that involves an interaction of nutrient concentrations with other regulatory factors.

Biological Transport↗
PubMed1978

Density-dependent regulation of growth of BSC-1 cells in cell culture: growth inhibitors formed by the cells.

Inhibitors formed by a monkey epithelial cell line, BSC-1, play an important role in limiting growth at high cell densities. At least three inhibitors are formed: lactic acid, ammonia, and an unidentified inhibitor that may be an unstable protein. The unidentified inhibitor is destroyed by shaking the conditioned medium, by bubbling gas through the medium, or by heating or storing the medium in the absence of cells. The concentrations of lactic acid and ammonia that accumulate in conditioned medium inhibit growth when added to fresh medium. These results, together with earlier studies, indicate that density-dependent regulation of growth of BSC-1 cells results from the combined effects of (a) inhibitors formed by the cells, (b) decreased availability of receptor sites for serum growth factors as the cells become crowded, and (c) limiting concentrations of low molecular weight nutrients in the medium. In contrast, density-dependent regulation of growth in 3T3 mouse embryo fibroblasts results almost entirely from inactivation of serum factors.

Ammonia↗
PubMed1977

Density-dependent regulation of growth of BSC-1 cells in cell culture: control of growth by serum factors.

BSC-1 cells grow slowly, to high cell density, in medium with 0.1% calf serum. An increase in the serum concentration increases both the growth rate of the cells and the final cell density. The serum can be replaced to some extent by epidermal growth factor (EGF). Initiation of DNA synthesis in BSC-1 cells that have spread into a "wound" in a crowded cell layer requires the addition of a trace of serum or EGF, if the cells have previously been deprived of serum. The binding of 125I-labeled EGF to low-density and high-density BSC-1 cells has been studied. Binding is faster to low-density cells. Cells at low cell density also bind much more EGF per cell than cells at high cell density. The fraction of bound 125I-labeled EGF that is present on the cell surface as intact EGF is larger at low than at high cell density. The results indicate that the number of available EGF receptors per cell decreases drastically as the cell density increases. It is suggested that a decrease in the number of available EGF receptor sites per cell, and the accompanying decrease in sensitivity of the cells to EGF, contributes to density-dependent regulation of growth of these cells.

Binding Sites↗