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Biomedical subjects

A Ohsaka

Publications and source records attributed to A Ohsaka.

At least 19 recordsLinked to original sources
PubMed2001

Basic fibroblast growth factor up-regulates the surface expression of complement receptors on human monocytes.

OBJECTIVE AND DESIGN: To clarify the possible involvement of basic fibroblast growth factor (b-FGF) in inflammation, we examined the effect of b-FGF on the surface expression of complement receptors (CR) on human monocytes in vitro. MATERIALS AND METHODS: Heparinized venous blood was obtained from healthy adult donors. The surface expression of CR on blood monocytes was determined by two-color immunofluorescent staining using flow cytometry and monoclonal antibodies. A standard whole blood lysis technique was used to avoid any in vitro manipulation that would activate monocytes. RESULTS: b-FGF increased the expression of CR3 on monocytes in a dose- and time-dependent manner. The b-FGF concentrations used were up to 100 ng/ml. The values of mean fluorescence intensity (MFI) of CR3 expression on unstimulated monocytes were 12.6+/-1.3 (n = 3), whereas those on b-FGF-stimulated monocytes were 59.2+/-7.1 (n = 3). b-FGF also up-regulated the expression of CR1 on monocytes in a dose- and time-dependent manner. The MFI values of CR1 expression on unstimulated monocytes were 2.5+/-0.1 (n = 3), whereas those on b-FGF-stimulated monocytes were 11.1+/-0.6 (n=3). The magnitude of CR1 expression by monocytes was significantly smaller than that of CR3 expression. The maximal stimulatory effect of b-FGF on monocytes was observed using greater than 25 ng/ml of b-FGF and 90-120 min incubation period. CONCLUSION: b-FGF may participate in the inflammatory process by modulating the CR expression on blood monocytes.

Adult↗
PubMed2001

Expansion of CD4+CD16+ blood monocytes in patients with chronic renal failure undergoing dialysis: possible involvement of macrophage colony-stimulating factor.

A novel subpopulation of blood monocytes coexpressing CD16 antigen and low levels of CD14 antigen (CD14+CD16+ monocytes) has recently been identified, and expansion of these CD14+CD16+ monocytes has been reported under some pathological conditions. In this study, we examined the immunophenotype of blood monocytes in patients with chronic renal failure (CRF) who were undergoing hemodialysis (HD, n = 52) or continuous ambulatory peritoneal dialysis (CAPD, n = 36) using two-color immunofluorescence flow cytometry. The percentage and absolute number of CD14+CD16+ monocytes were significantly higher (p < 0.001) in both HD and CAPD patients compared with those in healthy control subjects. We also determined the plasma concentrations of hematopoietic growth factors and cytokines using an enzyme-linked immunosorbent immunoassay. The plasma levels of macrophage colony-stimulating factor (M-CSF) were markedly increased in both HD and CAPD patients relative to the normal controls. The plasma M-CSF levels correlated significantly with the number of CD14+CD16+ monocytes in the whole group of subjects. These findings suggest that elevated endogenous M-CSF levels may participate in the expansion of CD14+CD16+ monocytes in CRF patients undergoing dialysis.

Adolescent↗
PubMed2000

Basic fibroblast growth factor modulates the surface expression of effector cell molecules and primes respiratory burst activity in human neutrophils.

Basic fibroblast growth factor (b-FGF) mediates a variety of biological responses such as angiogenesis and hematopoiesis. We examined the effect of b-FGF on human neutrophil functions in vitro. The surface expression of effector cell molecules on neutrophils was determined by flow cytometry and monoclonal antibodies. b-FGF increased the expression of CD11b leukocyte integrin and complement receptor type 1 on neutrophils and decreased the expression of L-selectin on neutrophils in a dose- and time-dependent manner. We also examined the effect of b-FGF on the respiratory burst activity in neutrophils. Although b-FGF alone did not induce intracellular oxidative product formation by neutrophils, it enhanced H(2)O(2) production in neutrophils stimulated by N-formyl-methionyl-leucyl-phenylalanine or phorbol myristate acetate. These findings suggest that b-FGF may participate in the inflammatory process via modulating the surface expression of effector cell molecules and enhancing respiratory burst activity in neutrophils.

Adult↗
PubMed1999

Hereditary thrombocythaemia in a Japanese family is caused by a novel point mutation in the thrombopoietin gene.

Hereditary thrombocythaemia (HT) with clinical features very similar to essential thrombocythaemia (ET) has been found to be transmitted as an autosomal dominant trait in several families. Here we studied the pathogenesis of HT in a previously described Japanese kindred. We found markedly elevated thrombopoietin (TPO) serum levels in all affected individuals and identified a novel point mutation in the TPO gene, a G --> T transversion at position 516 of the TPO mRNA (G516T) that co-segregated with the HT phenotype in all affected family members. This mutation is located in the 5'-untranslated region (5'-UTR) of the TPO mRNA and when assayed in reticulocyte lysates, improved translational efficiency of in vitro transcribed TPO mRNA. Cell lines transfected with the mutant TPO cDNA secreted up to 8-fold more TPO protein than cells transfected with the normal cDNA. We provide a molecular model of how the mutation partially disables the physiologic repression of TPO translation and thereby causes thrombocytosis. This is the third family in which HT has been caused by the loss of translational inhibition of TPO mRNA.

Female↗
PubMed1999

Bone marrow aplasia with prominent atypical plasmacytic proliferation preceding acute lymphoblastic leukemia.

A two-year-old boy presented with pancytopenia. Bone marrow examination revealed an aplastic marrow with prominent immature plasma cell proliferation, which mimicked plasma cell leukemia. Immunohistochemistry, however, revealed a polyclonal population consistent with a reactive process, excluding plasma cell neoplasia. Administration of granulocyte-colony stimulating factor resulted in recovery of normal hematopoiesis with resolution of plasmacytosis. Seven months later, the patient had an elevated white blood cell count and bone marrow findings diagnostic of acute lymphoblastic leukemia. To the best of our knowledge this is the first reported case of bone marrow aplasia with prominent polyclonal plasmacytosis presenting as a prodrome of acute lymphoblastic leukemia in childhood.

Anemia, Aplastic↗
PubMed1998

Granulocyte colony-stimulating factor administration increases serum concentrations of soluble selectins.

In order to explore the possible role of granulocyte colony-stimulating factor (G-CSF) in the inflammatory process, we examined the serum concentrations of soluble selectins (sL-selectin, sE-selectin and sP-selectin) following in vivo administration of G-CSF to five healthy volunteers and 12 neutropenic patients with haematological malignancies. The serum concentrations of both sL-selectin and sE-selectin were slightly but significantly increased after G-CSF administration in the healthy volunteers. The serum concentrations of all three selectins were significantly increased after G-CSF administration in the neutropenic patients concomitant with an increase in their neutrophil counts. These findings suggest that G-CSF may participate in the leucocyte-endothelial cell interactions in vivo.

Adult↗
PubMed1998

In vivo administration of granulocyte colony-stimulating factor increases the surface expression of sialyl-Lewis(x) on neutrophils in healthy volunteers.

We examined the in vivo effect of granulocyte colony-stimulating factor (G-CSF) on the surface expression of putative counterligands for endothelial selectins on neutrophils in healthy volunteers. G-CSF (50 microg/m2/day) was administered subcutaneously to 5 healthy volunteers for 4 days. The expression of surface antigens on neutrophils was determined by flow cytometry and monoclonal antibodies. G-CSF administration increased the number of leukocytes, mainly of neutrophils, which was associated with an increase in the expression of the high-affinity Fc receptor for IgG (FcRI, CD64) and CD14 on neutrophils. G-CSF administration decreased the surface expression of L-selectin on neutrophils, whereas it increased the expression of sialyl-Lewisx but not Lewisx on neutrophils. These findings suggest that G-CSF participates in the neutrophil-endothelial cell interactions in vivo by modulating the expression of adhesion molecules and ligands for endothelial selectins on neutrophils.

Gangliosides↗
PubMed1998

Pyoderma gangrenosum following cytosine arabinoside, aclarubicin and granulocyte colony-stimulating factor combination therapy in myelodysplastic syndrome.

Pyoderma gangrenosum (PG) is a neutrophilic dermatosis, which may be associated with systemic conditions such as hematologic disorders. We present a patient who had been diagnosed as having myelodysplastic syndrome associated with PG at onset, in whom a febrile ulcerative skin lesion developed following cytosine arabinoside, aclarubicin and granulocyte colony-stimulating factor (G-CSF) combination chemotherapy in the course of the disease. Skin biopsy revealed dense neutrophilic infiltrate in the dermis with central epidermal ulceration, consistent with the diagnosis of PG. Oral prednisolone was effective for the skin lesion. In this case, G-CSF application may participate in the recurrence of PG.

Aclarubicin↗
PubMed1998

Phenotypic conversion from t(8;21) acute myeloid leukemia to MLL gene rearrangement-positive acute lymphoblastic leukemia.

Phenotypic conversion from acute myeloid leukemia (AML) to acute lymphoblastic leukemia (ALL) is rare. A 38-year-old man was initially diagnosed as having AML (FAB-M2) associated with the t(8;21)(q22;q22) chromosomal abnormality. The blasts showed myeloperoxidase (MPO) activity and CD13 antigen expression. He showed complete remission after standard chemotherapy for AML. However, the patient relapsed with blasts showing ALL morphology (FAB-L1), MPO negativity, and CD19 antigen expression 33 months after cessation of AML therapy. Cytogenetic analysis at relapse was unsuccessful. Molecular analysis of ALL blasts revealed immunoglobulin heavy-chain gene and MLL gene rearrangements but no AML1 gene. MLL gene rearrangement or the 11q23 chromosomal abnormality has been associated with therapy-related leukemia. The subsequent ALL in our patient may have been induced by the chemotherapy including daunorubicin, known as a topoisomerase II inhibitor.

Adult↗
PubMed1997

Interstitial pneumonia in patients receiving granulocyte colony-stimulating factor during chemotherapy: survey in Japan 1991-96.

Twenty cases of interstitial pneumonia secondary to treatment with granulocyte colony-stimulating factor (G-CSF) were reviewed. Their interstitial pneumonia had the following features: (a) it occurred predominantly in patients aged 60 years or older; (b) it was prevalent among patients with haematological malignancies, particularly non-Hodgkin's lymphoma; (c) in all patients G-CSF was given after anti-cancer agents with potential to affect the lungs; (d) at the onset, many patients had symptoms such as dyspnoea and fever; and (e) the leucocyte (neutrophil) count as well as lactate dehydrogenase (LDH) and C-reactive protein (CRP) levels were usually higher than normal at the onset. These findings indicate that, when G-CSF is used in combination with pneumotoxic anti-cancer agents, respiratory function should be monitored before and during treatment. If the leucocyte (or neutrophil) count and/or LDH and CRP increase suddenly in association with dyspnoea and fever during administration of G-CSF, interstitial pneumonia should be suspected. Accordingly, a chest radiograph and pulmonary functional tests should be performed promptly. If a diagnosis of interstitial pneumonia is made, steroid pulse therapy should be commenced immediately.

Adult↗
PubMed1997

Altered surface expression of effector cell molecules on neutrophils in myelodysplastic syndromes.

The surface expression of effector cell molecules on neutrophils was examined in 18 patients with myelodysplastic syndromes (MDS) and 20 healthy control subjects. The MDS patients were further classified as low clinical risk (L-MDS, n=7) and high clinical risk (H-MDS, n=11). The expression of Fc receptors for IgG (FcR), complement receptors (CR) and cellular adhesion molecules on neutrophils was determined by flow cytometry and monoclonal antibodies. The effect of granulocyte colony-stimulating factor (G-CSF) and tumour necrosis factor-alpha (TNF) on L-selectin shedding and CR up-regulation on neutrophils was also examined. The percentage of FcRI-positive neutrophils and CD11b/CR3 expression on neutrophils were significantly increased in the H-MDS patients when compared to the controls. In contrast, the expression of FcRII, FcRIII, L-selectin, LFA-1 and CD18 on neutrophils was significantly reduced in the H-MDS patients compared with the controls. The L-MDS neutrophils exhibited lower expressions of CR1, L-selectin, LFA-1 and CD18 than those of the controls. Neutrophils from some H-MDS patients showed impaired L-selectin shedding and CR up-regulation after stimulation with G-CSF or TNF, although these were not significantly different when assessed in the whole H-MDS group. These findings suggest that an altered surface expression of effector cell molecules and an impaired modulation of cellular adhesion molecules on neutrophils may contribute to the increased susceptibility to bacterial infections in MDS patients.

Aged↗
PubMed1996

Multiple gastric involvement by myeloid antigen CD13-positive non-secretory plasma cell leukaemia.

Gastrointestinal tract involvement is a rare complication of plasma cell neoplasia. We present a case of non-secretory type primary plasma cell leukaemia (PCL) with multiple gastric involvement. Dual surface antigen analysis of bone marrow cells revealed that atypical plasma cells coexpressed CD38 and myeloid antigen CD13. Upper gastrointestinal endoscopy disclosed multiple submucosal masses in the body of the stomach. Endoscopic biopsy specimens showed marked infiltration of atypical plasma cells consistent with a diagnosis of gastric involvement by PCL. Since CD13 antigen is identical to aminopeptidase N, a membrane-bound glycoprotein thought to be involved in the process of tumour invasion, CD13 expression on neoplastic plasma cells may be related to the gastric involvement in this patient.

ADP-ribosyl Cyclase↗
PubMed1996

Sustained trilineage recovery and disappearance of abnormal chromosome clone in a patient with myelodysplastic syndrome following combination therapy with cytokines (granulocyte colony-stimulating factor and erythropoietin) and high-dose methylprednisolone.

We report a case of hypoplastic myelodyplastic syndrome (MDS) (refractory anemia (RA)) in which sustained trilineage haematological response and persistent disappearance of an abnormal chromosome clone were achieved after treatment with combination therapy of cytokines (granulocyte colony-stimulating factor (G-CSF) and erythropoietin (Epo)) and methylprednisolone (mPSL) pulse dose. The patient's haematological recovery was rapid and maintained even after cessation of the therapy. In addition, the predominant chromosome clone 13q- in bone marrow cells disappeared in the fourth week. The patient's improved bone marrow haemopoiesis and disappearance of the abnormal chromosome has continued to the present, 13 months after treatment. The occurrence of both trilineage response and abnormal chromosome disappearance in MDS patients treated with cytokine(s) or steroids is rare. Combination therapy might therefore be advantageous in MDS.

Anti-Inflammatory Agents↗
PubMed1996

Clonal involvement of eosinophils in therapy-related myelodysplastic syndrome with eosinophilia, translocation t(1;7) and lung cancer.

We report a therapy-related MDS (RAEB) patient with eosinophilia, unbalanced translocation der(7)t(1;7) (q12;q22) and lung cancer. We observed no increase in cytokine levels in serum or in the conditioned medium (CM) of peripheral T cells cultured with or without IL-2. When bone marrow (BM) cells were cultured with GM-CSF, IL-3 and SCF in a semisolid system, the colonies were exclusively eosinophilic. Cytogenetic analysis of the colony cells identified the same chromosome abnormality in all metaphases to that of BM cells. Suspension and clonogenic colony assay of BM cells cultured with various cytokines showed predominant eosinophilic growth and differentiation with GM-CSF, but not with the other cytokines examined. These findings, together with mild morphological abnormalities of eosinophils, indicate clonal involvement of eosinophils in the myelodysplastic syndrome (MDS) clone, and that the eosinophilia was derived from the neoplastic clone with the translocation and was not associated with the patient's lung cancer.

Aged↗
PubMed1996

[Retrospective analysis on 21 patients with follicular lymphoma].

We retrospectively analyzed the clinical data of the 21 patients with follicular lymphoma admitted to our institution from 1977 to 1994. The frequency of follicular lymphoma was 9.1% in the 231 patients with non-Hodgkin's lymphoma. Overall survival rates at 1 year, 3 years, and 5 years were 90.2%, 78.2%, and 52.1%, respectively. The median follow-up of surviving patients and time to treatment failure (TTF) was 43 months and 30 months, respectively. The median time from disease progression to death was 171 days. In univariate analysis, factors associated with poor survival were stage IV (Ann Arbor staging system), anemia (hemoglobin level less than 10g/dl), bone marrow involvement, two or more extranodal sites, and failure in induction of complete remission (CR) in the entire course. Factors associated with short TTF were anemia, bone marrow involvement, and failure in induction of CR. In multivariate analysis, induction of CR affected survival and TTF independently.

Adult↗
PubMed1996

Increased expression of the high-affinity receptor for IgG (FcRI, CD64) on neutrophils in multiple myeloma.

The surface expression of effector cell molecules on neutrophils was examined in 19 patients with multiple myeloma (MM), 6 patients with monoclonal gammopathy of undetermined significance (MGUS) and 22 healthy control subjects. The expression of Fc receptors for IgG (FcR), complement receptors (CR), and cellular adhesion molecules on neutrophils was determined by flow cytometry and monoclonal antibodies. MM neutrophils exhibited higher expression of FcRI, CR3, and CR4 and lower expression of FcRII and L-selectin than that in MGUS and controls. Granulocyte colony-stimulating factor (G-CSF, 50 micrograms/m2/d) was administered subcutaneously to 8 patients with MM and to 4 healthy volunteers. G-CSF administration increased the expression of FcRI, FcRII, and CR1 on neutrophils and decreased the expression of FcRIII on neutrophils in both groups. The application of G-CSF also resulted in increase of CR3 and CR4 expression and in decrease of L-selectin expression on neutrophils in healthy volunteers but not in MM patients. These findings suggest that MM neutrophils may be activate in vivo and that effector cell molecular expression on MM neutrophils is further modulated by G-CSF application.

Adult↗
PubMed1995

Alterations of effector cell molecule expression on neutrophils in granulocyte colony-stimulating factor-producing tumour.

A 68-year-old man was diagnosed as having a granulocyte colony-stimulating factor (G-CSF)-producing mediastinal tumour. Mediastinotomy was performed, and thereafter the elevated leucocyte count and serum G-CSF concentration returned to the normal range. The surface expression of effector cell molecules on neutrophils was serially examined. Before operation, the expression of FcRI and CR1 was increased but the expression of FcRIII and L-selectin was reduced in the patient. The altered expression of these molecules returned to the normal levels after operation. These findings suggest that G-CSF produced by the tumour modulated neutrophil effector cell molecule expression in the patient.

Aged↗