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T Shichishima

Publications and source records attributed to T Shichishima.

At least 55 records · Page 3Linked to original sources
PubMed1990

Acetylcholinesterase and lymphocyte function-associated antigen 3 found on decay-accelerating factor-negative erythrocytes from some patients with paroxysmal nocturnal hemoglobinuria are lost during erythrocyte aging.

Erythrocytes from patients with paroxysmal nocturnal hemoglobinuria are deficient in decay-accelerating factor (DAF), a factor called C8-binding protein or homologous restriction factor, acetylcholinesterase (AchE), and lymphocyte function-associated antigen 3 (LFA-3). These proteins share a common feature that glycan-inositolphospholipid anchors the protein to the membrane, suggesting that an abnormality related to this glycolipid causes multiple protein deficiencies. The relationship between the DAF, AchE, and LFA-3 defects was studied by fluorescent flow cytometric analysis. In five patients, DAF-negative erythrocytes were also AchE-negative. In three patients, a fraction of DAF-negative erythrocytes expressed subnormal levels of AchE, indicating that AchE was synthesized in these DAF-negative cells. Erythrocytes from the patients having DAF-negative, AchE-positive cells were separated according to density and analyzed for expression of DAF and AchE. Both proteins decreased with increase of cell density, suggesting that DAF-negative, AchE-positive cells become AchE-negative during erythrocyte maturation by losing AchE. A low level of LFA-3 was found on DAF-negative erythrocytes from one patient and decreased with erythrocyte maturation. These results support an idea that complete deficiency of glycan-inositolphospholipid-anchored proteins on erythrocytes could result from abnormally early termination of surface recruitment of these proteins, and subsequent dilution through cell divisions and loss from the surface.

Acetylcholinesterase↗
PubMed1990

Characterization of the erythropoietic progenitor cells (BFU-E) in paroxysmal nocturnal haemoglobinuria (PNH).

In order to investigate erythropoiesis in paroxysmal nocturnal haemoglobinuria (PNH), the relative proportions of complement-mediated lysed erythroblasts in individual bursts of two cases of PNH were analysed by a modified complement lysis sensitivity test using the trypan blue dye exclusion method. All bursts contained both complement-sensitive and complement-insensitive erythroblasts and the ratio between them varied from burst to burst. The means +/- SD of the haemolytic percentages of individual bursts in cases 1 and 2 were 30.9 +/- 10.8% (n = 20, ranging from 13.2% to 52.8%) and 54.8 +/- 16.4% (n = 31, ranging from 26.4% to 82.5%), respectively. In addition, the cumulative frequency distributions of the proportions of complement-mediated lysed erythroblasts in individual bursts approached normal frequency distributions. These results suggest that two red cell populations with different susceptibilities to complement in PNH are derived from a single population of erythropoietic progenitor cells rather than a dual population of normal and PNH erythropoietic progenitor cells.

Bone Marrow↗
PubMed1989

Complement sensitivity of erythroblasts and erythropoietic precursors in paroxysmal nocturnal haemoglobinuria (PNH).

To clarify the regulation of erythropoiesis of complement (C')-sensitive erythrocytes (E) during erythroid cell maturation and differentiation in paroxysmal nocturnal haemoglobinuria (PNH), the C' sensitivity of (1) erythroblasts from erythropoietic bursts and (2) erythropoietic precursors was examined in seven patients with PNH. For the former, a modified complement lysis sensitivity (CLS) test using the trypan blue dye exclusion method was employed. For the latter, an erythropoietic cell culture following the CLS or sucrose haemolysis (SH) test for mononuclear cells was used. Linear relationships were found between the concentrations of C' and proportions of C'-mediated haemolysed erythroblasts in both PNH and normal erythropoietic bursts. In addition, PNH erythroblasts showed hypersensitivity to C'; in the C' dilution for 50% lysis was 12.5 +/- 8.1 ml in PNH patients and 42.3 +/- 4.5 ml in normal controls. There was also a significant correlation (r = 0.919; P less than 0.01) between the proportions of PNH-III E and haemolysed erythroblasts. Significant hypersensitivity of mature erythroid progenitors (CFU-E) to C' was found in both the SH (P less than 0.01 or P less than 0.05) and CLS (r = -0.712; P less than 0.001) tests in PNH patients. However, no hypersensitivity to C' was observed at the primitive erythroid progenitors (BFU-E) level in either the PNH patients or the normal controls. These findings suggest that in PNH the property of C' sensitivity appears during differentiation and maturation from BFU-E to CFU-E and that the proportions of PNH-III E are already programmed at the level of erythroblasts.

Adult↗
PubMed1989

Signet cell carcinoma of the stomach in a patient with acquired immunodeficiency syndrome: a case report.

A case of signet cell carcinoma associated with AIDS is presented. A 50-year old Japanese man with hemophilia A was suffering from human immunodeficiency virus (HIV) infection, the result of multiple injections of clotting factor concentrates. A diagnosis of signet cell carcinoma of the stomach was reached upon endoscopic and histological examinations. Opportunistic infections of esophageal candidiasis and candida septicemia occurred. The patient died of repeated gastrointestinal bleeding and cachexia. Although there is a possibility of the patient having a coincidential carcinoma along with AIDS, the HIV infection, perhaps, had a role in causing signet cell cercinoma.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Acute promyelocytic leukemia with a history of RAEB in transformation and the 15/17 translocation].

A 34-year old female was admitted to our clinic because of fever and general fatigue on March 26, 1987. On admission, peripheral blood (PB) revealed pancytopenia. Bone marrow smears revealed 9. 0% of promyelocytic cells with or without Auer rods. Diagnosis of RAEB in transformation was made. Chromosome study of the bone marrow cells showed t(15; 17) in 3 out of 20 cells analysed. After 3 months, the leukemic cells were observed in PB and increased in number. Then the patient showed bleeding tendency and fibrin degradation products (FDP) increased up to 40 micrograms/ml. And the leukemic cells were over 30% in PB at the end of July, 1987. The diagnosis of APL with DIC was made. To our knowledge, this is the first case of APL with a history of MDS with t(15; 17).

Adult↗
PubMed1989

[Evaluation and quantification of complement-sensitive red cells in PNH and aplastic anemia-PNH syndrome].

In order to clarify the erythropoiesis of complement-sensitive red cells in paroxysmal nocturnal hemoglobinuria (PNH), the proportion of complement-sensitive red cells and compositional classification of examined red cells were investigated by means of complement lysis sensitivity test in 27 patients with initial diagnosis of PNH and 17 patients with aplastic anemia-PNH syndrome, and their bone marrow nucleated cell counts were also compared. The proportion of complement-sensitive erythrocytes was 41.0 +/- 22.0% (n = 26) in PNH and 29. 5 +/- 15.0% (n = 17) in aplastic anemia-PNH syndrome, and no significant difference was recognized between them. The nucleated cell count at the time of PNH diagnosis was 19.1 +/- 12.5 X 10(4)/microliters (n = 21) in PNH and 12.6 +/- 8.8 X 10(4)/microliters (n = 12) in aplastic anemia-PNH syndrome, and no significant difference between them was apparent. These findings suggest that the erythropoiesis of complement-sensitive red cells shows a similarity between PNH at initial occurrence and aplastic anemia-PNH syndrome, once PNH has occurred.

Adult↗
PubMed1989

[Congenital stomatocytosis associated with aplastic anemia].

A seven year-old boy with hereditary stomatocytosis complicated with aplastic anemia was reported. He was admitted to our hospital because of pale and general fatigue. On physical examination, he had severe anemia, petechiae, but no hepatosplenomegaly. Peripheral blood cell count revealed pancytopenia; RBC 103 X 10(4)/microliters, Hb 3.5 g/dl, Ret 21%, WBC 1,200/microliters, Pl 1.3 X 10(4)/microliters, and bone marrow revealed markedly hypocellular marrow. Red cell morphology demonstrated stomatocytosis. Red cell life span (51Cr T1/2) was 12 days, Coombs' test and Ham's test were negative. Indirect bilirubin was 1.1 mg/dl and marked decrease of haptoglobin was found. Family studies showed that his father and sister had stomatocytosis on peripheral blood examination, but no anemia. The patient had severe anemia because of complicated aplastic anemia. Congenital stomatocytosis with aplastic anemia is extremely rare. The authors are interested in a possible relationship between hereditary stomatocytosis and aplastic anemia although the precise mechanism remains to be elucidated.

Anemia, Aplastic↗
PubMed1989

[Bone marrow aplasia without blast crisis in a case of CML of 10-year survival].

A case of chronic myelogenous leukemia (CML) of 10-year survival in described. A 44-year old male was admitted to our hospital because of general malaise, abdominal fullness and fever in February, 1977. On physical examination, giant splenomegaly and hepatomegaly were detected. Peripheral blood examination revealed leukocytosis without hiatus leukemia , normochromic macrocytic anemia and thrombocytosis. NAP rate and score were 16% and 22. Cytogenetic analysis of PB without stimulator revealed 46, XY, Ph1. Then he was diagnosed as having a typical type of Ph1-positive CML. He had been successfully treated over 9 years by intermittent administration of busulfan. However, anemia suddenly progressed in February, 1986 followed by leukopenia and thrombocytopenia. Hemorrhage was not detected by the examination. Though he had been received blood transfusion, the anemia progressed rapidly. He was died of cachexia on 4th of August, 1987. The postmortem examination revealed bone marrow aplasia with no signs of blast crisis nor myelofibrosis. Secondary hemochromatosis was seen in the liver, spleen, pancreas and some other organs.

Adult↗
PubMed1988

Decay-accelerating factor (DAF) on the blood cell membranes in patients with paroxysmal nocturnal haemoglobinuria (PNH): measurement by enzyme-linked immunosorbent assay (ELISA).

We developed a quantitative enzyme-linked immunosorbent assay (ELISA) for decay-accelerating factor (DAF) on blood cell membranes using monoclonal anti-DAF antibodies. DAF is an integral membrane protein of several blood cells. It regulates the C3 and C5 convertase of the classical and alternative pathways of complement activation. It is partially or completely deficient in the membranes of blood cells of patients with paroxysmal nocturnal haemoglobinuria (PNH). The ELISA we developed for DAF measurement indicated a reliable range of measurement from 2.25 to 11.25 ng of DAF. In particular, ELISA proved to be a technically simple method and its sensitivity was enhanced by using avidin-biotin complex. In this study, DAF levels in extracts of erythrocytes from 30 healthy donors and in extracts of PMN and platelets from 15 healthy donors were measured by ELISA. The DAF content of blood cells from eight patients with PNH and erythrocytes from 13 patients with anaemia were also measured. The DAF levels of normal erythrocytes, PMN and platelets were 3110 +/- 960, 28,000 +/- 13,900 and 3100 +/- 1370 (mean +/- SD) molecules/cell, respectively. In general, the DAF content of PNH cells was below the normal range, although it was within the normal range in some cases of PNH. The DAF levels of PNH-I and -II erythrocytes were estimated from the ratio of PNH-I, -II and -III erythrocytes. And, in four cases of PNH, the DAF levels of PNH-I erythrocytes separated by acidified serum lysis were measured by ELISA. In most cases of PNH, DAF was found to be partially deficient in PNH-I and PNH-II erythrocytes.

Adult↗
PubMed1988

Elevated haemoglobin F in juvenile and adult chronic myelogenous leukaemia.

Fetal haemoglobin (Hb F) and its G gamma-globin chain contents were examined in 2 juvenile (JCML) and 9 adult chronic myelogenous leukaemia (ACML) patients. One JCML patient's %Hb F was 28.0% and its %G gamma was 41.8%, while another JCML patient's %Hb F was 58.0% and its %G gamma was 65.6%. Four ACML patients gamma-globin gene arrangements in all cases were normal. The presence of the Xmn I site 5' to the G gamma-globin gene (at-158 base pairs from the G gamma-globin gene cap site) was observed only in 1 typical JCML patient with elevated %G gamma. The subhaplotype 5' to the delta-globin gene in 5 ACML patients was [+----], and the other 4 were suspected to be heterozygotes for [+----] and [-++-+]. The frequency of the A gamma T-globin gene in ACML patients may be higher than in the normal Japanese population.

Adult↗
PubMed1986

Promyelocytic crisis of chronic myelogenous leukemia without t(15;17).

A case of promyelocytic crisis of chronic myelogenous leukemia is reported. The amount of promyelocytoid blasts in peripheral blood and bone marrow were 70% and 58%, respectively, at the onset of the blastic phase. Cytogenetic analyses during the blastic phase did not reveal t(15;17); however, t(3;21) in addition to the t(9;22) in the karyotype of bone marrow or peripheral blood cells was observed.

Adult↗
PubMed1986

Immunocytochemical detection of normal and abnormal megakaryocytes using monoclonal antibody to glycoprotein IIb-IIIa (TP80): the quantitative assay in normal and in leukaemic patients.

We identified bone marrow megakaryocytes by an immunocytochemical technique using a monoclonal antibody (TP80) against platelet glycoprotein IIb-IIIa (GPIIb-IIIa). The immunocytochemical technique using TP80, specific to megakaryocytes, enabled us to observe cellular morphology and immunological reaction under light microscopy, and permitted quantitative assessment of megakaryocytes. In normal marrow, TP80 labelled 22 +/- 5 megakaryocytes/10(4) mononuclear cells (mean +/- 1 SD, n = 14). In addition to typical large megakaryocytes, small immature megakaryocytes (less than or equal to 20 micron) were recognized in 10-15% of total megakaryocytes. 4 out of 18 patients with acute myeloblastic leukaemia and 9 of 10 patients with myelodysplastic syndrome showed increased numbers of megakaryocytes. In these patients, cell size distribution was abnormal, i.e., most of the megakaryocytes consisted of small, atypical megakaryocytes. None of the patients with acute lymphoblastic leukaemia showed increased megakaryocytes. Immunocytochemical identification of megakaryocytes using a specific antibody is useful to quantitate the megakaryocytes and to detect the proliferation of atypical megakaryocytes in several leukaemic conditions.

Acute Disease↗