Biomedical subjects

N Narahara

Publications and source records attributed to N Narahara.

4 recordsLinked to original sources

PubMed1992

Induction of tissue factor synthesis in human umbilical vein endothelial cells involves protein kinase C.

Incubation of human umbilical vein endothelial cells with one of the following compounds: endotoxin, recombinant interleukin-1 beta, recombinant tumor necrosis factor alpha, allogenic lymphocyte subpopulations or phorbol ester resulted in significant induction of tissue factor synthesis. Diacylglycerol had the same effect and also enhanced synergistically the induction caused by endotoxin and interleukin-1 beta. Two different inhibitors of protein kinase C, H7 and sphingosine, inhibited tissue factor synthesis at concentrations which did not depress protein synthesis in general, suggesting that protein kinase C is involved in the processes leading to tissue factor synthesis. Cells down-regulated for the tissue factor response to TPA responded essentially normally to endotoxin and interleukin-1 with regard to tissue factor synthesis.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1990

One-stage method for assay of tissue factor activity of leukemic cell with special reference to disseminated intravascular coagulation.

Tissue factor activity (TFA) of leukemic cells (1 x 10(8) cells/mL) was measured in 44 patients with acute nonlymphoid leukemia (ANLL) by the one-stage assay using factor-IX deficient plasma (OSA-dIX) and two-stage assay (TSA). According to the preventative heparin dose schedule based on the TFA measured by the TSA, all disseminated intravascular coagulation (DIC) was controlled successfully. The procedure of the TSA was too complicated for clinical use, and its minimal measurable value was 125 units (U)/L of TFA. The OSA-dIX was simpler in its procedure and sensitive enough to measure accurately a TFA quantity as small as 30 U/L with high reproducibility. In 20 ANLL patients with 125 U/L or more of TFA measured by both assays, there was a significant relationship between their logarithms of TFA (r = 0.93, P less than 0.01). These results suggested that DIC complication in ANLL patients would be controlled successfully by the administration of heparin dosage based on the TFA measured by the OSA-dIX.

Adult↗

PubMed1989

Studies on leukemic cell tissue factor.

Apoprotein part of tissue factor of human placenta was purified 871 fold from the starting material with 4.2% yield by concanavalin A-Sepharose affinity chromatography and SDS-PAGE. The molecular weight of purified apoprotein was 45,000 in non-reduced condition and 49,000 in reduced condition. Tissue factor of human leukemia cells (FAB classification:M2 and M3) and cultured leukemia cell lines (HL-60 and Molt-4) was analyzed using specific rabbit anti-tissue factor IgG raised against purified material. Endotoxin stimulated HL-60 and Molt-4 also expressed procoagulant activity which was inhibited by tissue factor immune IgG. By immunostaining of the purified material, the lysate of leukemia cells (M2 and M3) and cultured leukemia cells (HL-60 and MOLT-4) revealed a major band of the same apparent molecular weight. Immuno-electron microscopic study on tissue factor of HL-60 cells produced the following findings: stimulation by endotoxin resulted in the formation of pseudopods of the cell membrane, and immunogold particles accumulated mainly on these pseudopods and cisternal spaces of rough endoplasmic reticulum, indicating exposure of the tissue factor to the surface of perturbed cell membrane with concurrent increase in tissue factor synthesis.

Antibody Formation↗

PubMed1989

Interaction of plasma clotting factors with vascular endothelial cells in hemostasis and thrombosis with special reference to endothelial cell tissue factor.

The interaction of plasma clotting factors with vascular endothelial cells was investigated. Human umbilical cord vein endothelial cells generated tissue factor activity after treatment with various stimulators including IL-1. Cycloheximide inhibited production of the tissue factor in the cells, but did not affect the expression of the tissue factor activity on the surface of endothelial cells. Endotoxin-treated vascular endothelial cells activated Factor X in the presence of Factor VII and calcium ion. Activation of Factor X by endothelial cells with Factor VII was enhanced by the presence of both Factors VIII and IX. Binding study revealed that endotoxin-treated endothelial cells bound Factor IX. These data suggest that perturbed vascular endothelium expresses tissue factor activity on the cell surface, binds factor IX and in the presence of Factor VII, activates not only factor X but also Factor IX.

Blood Coagulation Factors↗