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M Makishima

Publications and source records attributed to M Makishima.

28 records · Page 2Linked to original sources
PubMed1993

[Intensive 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3- nitrosourea hydrochloride (ACNU) and cryopreserved autologous bone marrow transplantation].

High-dose ACNU followed by autologous bone marrow transplantation was administered alone or together with other agents such as cyclophosphamide, dacarbazine, carboquone or/and VP-16. The starting dose of ACNU was 200 mg/m2, with gradual escalation up to 400 mg/m2. Median duration of granulocytes of less than 100/mm3 and platelets of less than 30,000/mm3 was 4.5 days (range; 0-9) and 10.5 days (range; 0-43), respectively. Bacteremia occurred in 4 cases, but no case of pneumonia was encountered. Heart failure possibly due to the cyclophosphamide was noted in one case with arrhythmia. Out of 13 cases with measurable diseases, three patients with Hodgkin's disease, two patients with diffuse lymphoma, and one patient with follicular lymphoma attained a complete response. Partial response was obtained in two patients with non-Hodgkin's lymphoma. Two patients with melanoma and one with acute nonlymphocytic leukemia without measurable disease still remain disease-free.

Adult↗
PubMed1992

Biological activity of a proteoglycan form of macrophage colony-stimulating factor and its binding to type V collagen.

Two different types of macrophage colony-stimulating factors (M-CSF) were found, one with an apparent molecular mass of 85 kDa and the other greater than 200 kDa. The high molecular mass M-CSF was identified as a proteoglycan carrying chondroitin sulfate glycosaminoglycan and was designated as the proteoglycan form of M-CSF (PG-M-CSF). In this study, we compared the biological activity of the 85-kDa M-CSF and PG-M-CSF and examined the binding properties of these two M-CSF to certain extracellular matrix proteins, i.e. types I-V collagen and fibronectin, using a modified enzyme-linked immunosorbent assay. PG-M-CSF was capable of supporting the formation of murine macrophage colonies, and pretreatment of PG-M-CSF with chondroitinase AC, which degrades chondroitin sulfate, did not alter its colony-stimulating activity. The specific activity of PG-M-CSF was similar to that of the 85-kDa M-CSF. The 85-kDa M-CSF had no apparent affinity for the extracellular matrix proteins examined, whereas PG-M-CSF had an appreciable binding capacity to type V collagen, but did not bind to types I, II, III, and IV collagen or to fibronectin. Pretreatment of PG-M-CSF with chondroitinase AC completely abolished the binding of the species to type V collagen. Addition of exogenous chondroitin sulfate inhibited the binding of PG-M-CSF to type V collagen in a dose-dependent manner. These data indicated that the interaction between PG-M-CSF and type V collagen was mediated by the chondroitin sulfate chain of PG-M-CSF. PG-M-CSF bound to type V collagen could stimulate the proliferation of bone marrow macrophages, indicating that the matrix protein-bound PG-M-CSF retained its biological activity. This interaction between PG-M-CSF and type V collagen implies that the role of PG-M-CSF may be distinct from that of 85-kDa M-CSF.

Animals↗
PubMed1992

Effects of novel uracil analogs on proliferation and differentiation of human myeloid leukemia cells.

Twenty-seven novel nucleobases and nucleosides were synthesized by structural modification of uracil, and their effects on growth and differentiation of human myeloid leukemia HL-60 cells were examined. Some of the compounds inhibited the growth of HL-60 effectively. The nitroblue tetrazolium (NBT)-reducing activities of cells treated with the concentrations of these compounds for 50% inhibition of growth were compared. TI-66 (2,4-dibenzyl-6-fluoro-7,7,8,8-tetramethyl-cis-2,4-diazabicyclo-[4.2.0] octane-3,5-dione) was the most effective inducer of NBT-reducing activity and morphological differentiation of HL-60 cells into cells of the myelomonocytic lineage. TI-66 was also effective for induction of differentiation of another human myelogenous leukemia cell line, ML-1 cells, but not for differentiation of human erythroid leukemia K562 or HEL cells, or monocytic U937 cells. The effect of TI-66 in inducing differentiation of HL-60 cells was additive or more than additive in combination with retinoic acid or vitamin D3. Adenine or hypoxanthine alone induced NBT-reducing activity of the cells, and at suboptimal concentrations these compounds enhanced the effect of TI-66, but the enhanced NBT-reducing activities did not exceed the maximal activity induced by TI-66 alone. Simultaneous treatment of HL-60 cells with hypoxanthine reduced the growth inhibition by TI-66 alone. TI-66 was about 150 times more potent on a molar basis than adenine in inducing differentiation of HL-60 cells. These results suggest that nucleobase analogs such as TI-66 should be useful for differentiation therapy of some types of myelogenous leukemia.

Cell Differentiation↗
PubMed1992

[Malignant lymphoma with subdural effusion].

A 64-year-old woman was admitted for treatment of malignant lymphoma involving the pharynx and abdomen. Lymphoma disappeared after chemotherapy and radiotherapy, but she had central nervous system symptoms; euphorism, left facial nerve palsy, right hemiplesia, and disturbance of micturition. Magnetic resonance imaging (MRI) revealed a diffuse dural thickening and a subdural fluid retention. The subdural fluid was determined to be an exudate, and a biopsy of the dura mater revealed a normal dura and a fibrin clot containing lymphoma cells and neutrophils. MRI can be very useful to detect the meningeal involvement of malignant lymphoma.

Female↗
PubMed1992

[Hereditary angioneurotic edema associated with DIC and treated effectively by nafamostat mesilate].

A 36-year-old woman with disseminated intravascular coagulation syndrome (DIC) was admitted to the Third Department of Internal Medicine of the National Defense Medical College Hospital. Even after she recovered from DIC, she had a low level of C1-inactivator. Her past history, family history and family study revealed that she and her family showed hereditary angioneurotic edema (HANE). There have been no reports of HANE associated with DIC. She had two HANE attacks after discharge. We used nafamostat mesilate, a strong inhibitor of activated first complement component, to treat the attacks. She obtained subjective relief and her serological data were improved. Nafamostat mesilate was considered effective for HANE attack.

Adult↗
PubMed1991

Induction of differentiation of human myeloid leukemia HL-60 cells by novel pyrimidine nucleoside analogs.

New pyrimidine nucleoside analogs (18 compounds) were synthesized and their growth-inhibiting and differentiation-inducing activities on human myeloid leukemia HL-60 cells were examined. Some of the analogs were found to induce nitroblue tetrazolium (NBT) reducing activity in the HL-60 cells. The inducing activities of these compounds were compared at their concentrations for 50% inhibition of cell growth. TI-79 (3-benzyl-5-methyl-3-(beta-D-ribofuranosyl)pyrido[2,3-d]pyrimidine- 2,4(1H,3H)-dione) was a very effective inducer of NBT-reduction and of differentiation of the cells into mature granulocytes. The induction of NBT-reducing activity by TI-79 was inhibited by high concentrations of the natural nucleoside, adenosine. Other differentiation inducers, such as retinoic acid, 1 alpha,25-dihydroxyvitamin D-3 and staurosporin markedly enhanced the induction of differentiation of HL-60 cells by TI-79. Nucleoside analogs such as TI-79 should be useful for differentiation therapy of some types of myelogenous leukemia.

Adenosine↗
PubMed1991

Induction of differentiation of human leukemia cells by inhibitors of myosin light chain kinase.

Inhibitors of myosin light chain kinase, 1-(5-chloronaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine hydrochloride (ML-9) and 1-(5-iodonaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine hydrochloride (ML-7), induced Nitroblue tetrazolium reducing activity, lysozyme activity and morphological maturation of human monoblastic U937, THP-1 and promyelocytic HL-60 cells, but not of erythroblastic K562 cells. However, three analogs of ML-9, which are an inhibitor and an activator of protein kinase C, and a calmodulin antagonist, respectively, did not induce differentiation of the cells.

Azepines↗
PubMed1991

Effects of inhibitors of protein tyrosine kinase activity and/or phosphatidylinositol turnover on differentiation of some human myelomonocytic leukemia cells.

The activities of protein tyrosine kinase and phosphatidylinositol turnover have been found to be associated with cell growth and differentiation. We examined the effects of some inhibitors for these biochemical activities in human myelogenous leukemia cells. Genistein, which is known to inhibit the activities of protein tyrosine kinase, phosphatidylinositol turnover and topoisomerase II, induced nitroblue tetrazolium (NBT) reduction and lysozyme activity in ML-1, HL-60 and U937 cells. Morphological studies showed that genistein-induced differentiation of myeloblastic ML-1 cells into promyelocytes and of promyelocytic HL-60 cells into mature granulocytes. The differentiation-inducing effect of genistein was augmented by addition of 1 alpha,25-dihydroxyvitamin D3 (VD3) or retinoic acid, VD3 being more effective than retinoic acid. Methyl 2,5-dihydroxycinamate, a protein tyrosine kinase inhibitor, had only a weak effect in inducing differentiation of ML-1 cells. On the other hand, psi-tectorigenin was more effective than genistein in inducing the differentiations of ML-1 and HL-60 cells. Psi-tectorigenin is reported to inhibit phosphatidylinositol turnover without inhibiting protein tyrosine kinase. Thus modulation of phosphatidylinositol turnover might be more important than that of protein tyrosine kinase activity for differentiation of some myelogenous leukemia cells.

Cell Differentiation↗
PubMed1990

[Myelofibrosis associated with immunological abnormalities].

A 74-year-old man was admitted to the National Defense Medical College Hospital because of purpura on the extremities. The blood hemoglobin level was 11.5 g/dl, the white blood cell count 7. 3 x 10(9)/l with 3% blastic cells, and the platelet count 4.0 x 10(9)/l. There was leukoerythroblastosis with only mild teardrop appearance of erythrocytes. The blastic cells consisted of two types, megakaryoblast-like cells and myeloblast-like cells. There was a very mild hepatosplenomegaly, but no lymphadenopathies. The bone marrow aspirations yielded dry taps. The marrow biopsy specimen revealed myelofibrosis associated with trilineage hyperplasia, but no apparent infiltration of leukemic cells. Platelet-associated IgG (PAIgG) had a high titer and the response to platelet transfusions was poor. On prednisolone and colchicine, the blastic cells in the peripheral blood disappeared and the platelet count increased. He died of pneumonia. The autopsy showed myelofibrosis with hyperplasia of myeloid and erythroid lineage in the bone marrow. Megakaryocytes were relatively few and there was no infiltration of leukemic cells.

Aged↗