Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society最新文献

Acid phoshatase (AcP), beta-glucuronidase (GR) and N-acetyl-beta-D-glucosaminidase (NAG) activity in neutrophils obtained from the peritoneal fluid of 50 patients with terminal renal failure treated by intermittent peritoneal dialysis, and of 30 control subjects with normal renal function was semiquantitatively scored using a cytochemical method. This study was repeated in 22 dialyzed patients during the course of bacterial peritonitis. A significant decrease in the AcP score and an increase in the GR score were found in the neutrophils from dialyzed patients. In dialyzed patients with peritonitis, the GR and NAG scores were higher that in those without this complication.

Leukemic cells from 12 patients with lymphoblastic lymphoma (LBL) and T cell acute lymphoblastic leukemia (T-ALL) were studied to determine the inducibility of myeloid antigens in culture in the presence and absence of 12-O-tetradecanoylphorbol-13-acetate (TPA) in association with discrete phenotypic and genotypic analyses on these cells. The investigation revealed that leukemic cells corresponding to common or mature thymocytes were never induced to express any myeloid antigens, and showed rearrangements of T cell antigen receptor (TcR) beta and gamma chain genes. Concomitant examination on leukemic cells from mature T cell malignancies, including adult T cell leukemia (ATL), T cell chronic lymphocytic leukemia (T-CLL) and T cell non-Hodgkin's lymphoma (T-NHL), also failed to express myeloid antigens in culture. By contrast, one of the panmyeloid antigens, CD13 (MCS-2) antigen was induced on leukemic cells corresponding to early thymocytes in 5 out of 7 cases in TPA-added culture and in 3 cases even in TPA-free culture. All of these CD13 antigen inducible cases exhibited the germ line configurations of TcR beta and gamma chain genes except for one case of T-ALL with sole TcR gamma chain gene rearrangement. These findings suggest that primitive T cells, still not undergoing TcR gene rearrangements, retain the characteristics of multipotent progenitor cells to possess different lineage markers and are able to express myeloid antigen not exceptionally. Both phenotypically and genotypically immature thymocytes are considered to be less restricted in the differentiation pathway of hematopoietic cells committed to T cell lineage.

Serum amyloid P component (SAP) has been designated as a female protein in hamsters. To investigate the effects of sex steroids on SAP concentration in rats, SAP was purified from Wistar rats by affinity chromatography. Anti-SAP was raised. Sample sera were obtained from 150 young and old rats, after which, they were injected with either estradiol (E2), testosterone (T), or dehydroepiandrosterone (DHA). Sera were serially obtained from the tail vessels until the 8th day after injection. Serum levels of SAP were measured by micro single radial immuno-diffusion with a standard pooled serum as 100%. As the rats aged, the SAP levels in untreated female rats increase with age from 93% at 11 weeks to 346% at 58 weeks. In 28-week-old rats, the SAP levels in females (135 +/- 40%) were significantly (p less than 0.01) higher than those in males (80 +/- 32%). When old female rats (56 wk) were injected with DHA (3.5 mg), the SAP decreased significantly (p less than 0.01) to 70.8% of the preinjection level on the 8th day after injection. When young male rats (11 wk) were jnjected with E2 (0.5 mg), the SAP levels increased rapidly to 188% of the prelevel on the 5th day. Serum E2 levels reached a peak on the 2nd day. After the injection of T, the SAP levels did not change.

A total of 8,316 barbers were followed up from 1976 to 1987 to examine the relations between hair dye use and deaths from hematopoietic disorders. The follow-up rate was about 95%. Three leukemia deaths and two malignant lymphoma deaths were observed in this cohort. The observed deaths were less than the expected number calculated from age- and sex-specific mortality of the general population in Japan (3.8 and 3.0, respectively). No deaths from aplastic anemia or the other hematopoietic disorders were observed.

High concentrations of ionomycin induced arachidonic acid metabolism, while its magnitude appeared to be poorly correlated with the increase in intracellular Ca++ induced by ionomycin. Intracellular pH elevation had no direct effect on arachidonic acid release. On the other hand, the elevation in intracellular pH potentiated arachidonic acid release induced by low concentrations of ionomycin, and appeared to increase the sensitivity to Ca++ of the arachidonic acid releasing mechanism. pHi fixed at low values suppressed the formation of the product of the cyclooxygenase pathway more severely than that of 12-lipoxygenase in platelet activation induced by receptor-mediated agonists. Inhibition of the Na+/H+ exchanger, which participates in intracellular pH elevation, reduced the production of arachidonic acid metabolites, with a more profound effect on the product of the cyclooxygenase pathway. The findings suggest that intracellular Ca++ and pH act synergistically to activate the arachidonic acid releasing mechanism in platelets, and that pH also regulates the activity of the cyclooxygenase pathway.

Adhesion of platelets to the subendothelium is an essential step in hemostasis and thrombosis. Several receptors for adhesive macromolecules have been identified on platelets and are included in the integrin family. To clarify the role of platelet membrane glycoproteins in the interaction of platelets with the subendothelium, 51Cr-labeled platelet adhesion assay and antibody-blocking experiments were performed by using in vitro cultured subendothelium under the static condition. The platelet adhesion in this assay was inhibited by anti-GPIa (VLA-2), GPIc (VLA-5) and -GPIc'-(VLA-6) antibodies, while anti-GPIb and -GPIIb/IIIa antibodies had no effect. Platelets from the patients with Glanzmann's thrombasthenia could also attach to the subendothelium, whereas those from a patient whose platelets lacked GPIa failed to attach to the extracellular matrix (ECM). The monoclonal antibodies against fibronectin and laminin which recognized the cell binding domain of these molecules inhibited the platelet adhesion when they were pre-treated with ECM. Furthermore, antibody-blocking experiments revealed that the percent inhibition by the combination of anti-GPIa, -GPIc and -GPIc' antibodies used herein was approximately 75%. They did not completely inhibit the attachment. These results suggest that the interactions of collagen, fibronectin and laminin with their receptors on platelets are involved in the mechanism of platelet adhesion to subendothelium.

In 3 studies for adult acute myelogenous leukemia (AML) treated with BHAC-DMP, BHAC-DMP(II) and M-85 from 1979 to 1987, intensive induction resulted in a higher cure rate, since reduction of the blasts in bone marrow at 2 weeks after the initiation of therapy to less than 20% was the most significant prognostic factor to predict the long complete remission (CR), followed by initial WBC counts (less than 60,000/cmm) and achievement of CR within 50 days or by one course of induction therapy. However, it seemed impractical to give very intensive chemotherapy during the induction because of the high frequency of complications due to prolonged myelosuppression. Consolidation should be as intensive as possible. Non-cross resistant drugs will theoretically produce better results. In M-85 protocol, 71% of 41 adult AML achieved CR. The predicted 3.5-year survival and CR length of CR cases are 74 and 56%; respectively. The preliminary results of JALSG-AML87 and -ALL87 were also reviewed.

We investigated abnormalities in calcium ion influx in platelets of patients with myeloproliferative disorders (MPD). 45Ca2+ influx into the cytosol of MPD platelets was lower than that of normal controls. To determine whether the low Ca2+ influx is caused by a functional abnormality of membrane glycoprotein (GP) IIb-IIIa complex for Ca2+ channel or not, we investigated the Ca2+ influx through GP IIb-IIIa complex, which was reconstituted into liposomes. The purified GP IIb-IIIa complex from platelets of 5 patients was reconstituted into phospholipid liposomes. Ca2+ influx into the liposomes measured by fluorescence of intravesicular Fura-2 was lower in 2 of these patients. These findings corresponded with the results of intracellular calcium concentration after stimulation in these platelets. We concluded that functional abnormalities of GP IIb-IIIa is involved in the mechanism of impaired Ca2+ influx in MPD platelets.