Nobuhiro Narahara

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.

Role of cyclosporin A in remitting nephrotic syndrome in a Japanese patient infected with human immunodeficiency virus type 1

Abstract We report here the case of a 57-year-old Japanese man who developed nephrotic syndrome during the course of human immunodeficiency virus type 1 (HIV-1) infection. Histological examination revealed focal segmental glomerular sclerosis (FSGS), suggesting that HIV-associated nephropathy (HIVAN) was a possible diagnosis. However, he was initially treated with glucocorticoid plus immunosuppressants for primary FSGS, without knowledge that he was seropositive for HIV-1. Of importance, the nephrotic syndrome entered remission after treatment with cyclosporin A (CsA), and there was no recurrence of the nephropathy over the following 4 years. The patient eventually died due to opportunistic infection. This case is the first report of FSGS in a Japanese HIV patient, and also serves to illustrate the potential risks and benefits of CsA for the treatment of nephrotic syndrome associated with HIV-1 infection.

Impairment of Ristocetin-Induced Platelet Aggregation in Patients with Infective Endocarditis

An investigation was carried out on two patients with infective endocarditis associated with reduction of ristocetin-induced aggregation of platelets. The plasma of these patients reduced the aggregability with ristocetin of normal platelets. It is suggested that the patients had certain plasma factors which disturbed platelet aggregation with ristocetin.

顆粒球コロニー刺激因子 (Granulocyte colony-stimulating factor) およびエリスロポエチン (Erythropoietin) の投与により著明な白血球増加を認めた老年者骨髄異形成症候群の1例

A 70-year-old man was admitted to our hospital with pancytopenia. He was diagnosed as having MDS (RA), and therapy with subcutaneous S-CSF (100 micrograms/day) was started. His leukocyte count increased from 800/microliters to 1,400/microliters in two weeks. The dose of G-CSF was raised to 200 micrograms/day in the third week, and leukocytes increased to 2,00/microliters. At the fifth week, intravenous EPO (6,000 U x 3 times/week) was added. His leukocyte count increased to 4,000/microliters. EPO therapy was raised to 12,000 U x 3 times/week at the eighth week, his leukocyte count remained at the same level. G-CSF and EPO was stopped at the eleventh week, and leukocytes decreased to the same level as before administration. Throughout the course, his platelet count and reticulocyte count did not change. G-CSF and EPO are known as the stimulators of granuriod and erythroid progenitor, respectively. However, in this case, combination therapy with G-CSF and EPO induced marked increase of granulocytes only. This was an interesting case in relation to the roles of these cytokines in the hematopoietic system.