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Biomedical subjects

S Fujisawa

Publications and source records attributed to S Fujisawa.

At least 91 records · Page 5Linked to original sources
PubMed1998

The induction of apoptosis and cell cycle arrest by arsenic trioxide in lymphoid neoplasms.

Arsenic trioxide (As2O3) has recently been shown to induce complete remission in acute promyelocytic leukemia (APL). As2O3 reportedly has dose-dependent dual effects on APL cells, triggering apoptosis at relatively high concentrations and inducing differentiation at lower concentrations. However, its effect is still controversial for other AML cells and hematological neoplasms. We studied the in vitro effect of As2O3 on lymphoid lineage cells: lymphoma cell lines, NOL-3, Raji and Daudi, a myeloma cell line, NOP-1, normal peripheral blood lymphocytes (PBL), non-Hodgkin's lymphoma (NHL) cells and chronic lymphocytic leukemia (CLL) cells, and compared it with the effect on APL cell line, NB4, as well as other myeloid cell lines, HL-60 and NKM-1. As2O3 at a concentration of 1 micromol/l markedly inhibited both proliferation and viability of NB4, NOP-1, NOL-3 and NKM-1 cells, but it reduced only viability in normal PBL, CLL cells and NHL cells. As2O3 induced apoptosis and down-regulated bcl-2 expression in NB4, NOP-1 and NKM-1 cells. On the other hand, in HL-60, Raji and Daudi cells, 1 micromol/l As2O3 inhibited only the proliferation weakly, and neither induced apoptosis nor down-regulated bcl-2 expression, but arrested only cell cycle at G1 phase. As2O3 at a low concentration of 0.1 micromol/l had no effect on proliferation and viability of these cells except for NB4. These results showed that As2O3 exerted variable and definite effects on lymphoid cells and indicated that As2O3 might be clinically useful in lymphoid neoplasms such as malignant lymphoma and CLL.

Antineoplastic Agents↗
PubMed1998

Fibronectin in saliva inhibits Porphyromonas gingivalis fimbria-induced expression of inflammatory cytokine gene in mouse macrophages.

The aim of this study was to examine whether fibronectin in saliva plays a regulatory role in Porphyromonas gingivalis fimbria-mediated pathogenesis in adult periodontal disease. Our previous study demonstrated that fibronectin is one of the binding proteins of P. gingivalis fimbrillin. In the present study, we observed that fibronectin in saliva binds specifically to the fimbrillin. The fibronectin content in saliva of adult periodontal patients was significantly lower than that of healthy subject. In addition, the inhibitory action of salivary fibronectin from adult periodontal patients toward P. gingivalis fimbria-induced expression of the neutrophil chemoattractant KC gene in mouse macrophages was clearly weak compared with that of the fibronectin from healthy subjects. These results suggest that fibronectin in saliva plays an important role as a regulator in the pathogenesis of P. gingivalis fimbriae in adult periodontal disease.

Adult↗
PubMed1998

Porphyromonas gingivalis fimbriae use beta2 integrin (CD11/CD18) on mouse peritoneal macrophages as a cellular receptor, and the CD18 beta chain plays a functional role in fimbrial signaling.

In this study, we demonstrate that Porphyromonas gingivalis fimbriae use molecules of beta2 integrin (CD11/CD18) on mouse peritoneal macrophages as cellular receptors and also show that the beta chain (CD18) may play a functional role in signalling for the fimbria-induced expression of interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) genes in the cells. Using a binding assay with 125I-labeled fimbriae, we observed that fimbrial binding to the macrophages was inhibited by treatment with CD11a, CD11b, CD11c, or CD18 antibody but not by that with CD29 antibody. Western blot assays showed that the fimbriae bound to molecules of beta2 integrin (CD11/CD18) on the macrophages. Furthermore, Northern blot analyses showed that the fimbria-induced expression of IL-1beta and TNF-alpha genes in the cells was inhibited strongly by CD18 antibody treatment and slightly by CD11a, CD11b, or CD11c antibody treatment. Interestingly, intracellular adhesion molecule 1 (ICAM-1), a ligand of CD11/CD18, inhibited fimbrial binding to the cells in a dose-dependent manner. In addition, ICAM-1 clearly inhibited the fimbria-induced expression of IL-1beta and TNF-alpha genes in the cells. However, such inhibitory action was not observed with laminin treatment. These results suggest the importance of beta2 integrin (CD11/CD18) as a cellular receptor of P. gingivalis fimbriae in the initiation stage of the pathogenic mechanism of the organism in periodontal disease.

Animals↗
PubMed1998

Residual leukemic cell counts in the bone marrow at the end point of intensive induction therapy may be a prognostic factor for acute myeloblastic leukemia in adults.

Between January 1990 and May 1994, 59 previously untreated adult patients with acute myeloblastic leukemia (AML) were treated with a combination of behenoyl-cytosine-arabinoside (BHAC), daunorubicin (DNR), 6-mercaptopurine (6-MP) and prednisolone (PSL). Forty one patients (69.5%) achieved complete remission (CR). The Kaplan-Meier analysis revealed an actuarial probability for remaining in remission of 36% in patients who achieved remission and a survival of 29% in all patients at 5 years. A favorable factor relative to achieving CR was performance status (P=0.04). In addition the presence of 300 cells/microl or less of residual leukemic cell counts in the bone marrow at the end point of induction therapy tended to favor remission (P=0.06) using the multivariate analysis with a multiple logistic regression model. In addition the residual leukemic cells counts of less than 300/microl in the bone marrow at the end point of induction therapy was the most significant factor for durable remission (P=0.05) by the Cox's proportional hazard model. We concluded that residual leukemic cells counts in the bone marrow at the end point of intensive induction therapy is a valuable prognostic factor for adults receiving response-oriented individualized induction therapy for AML.

Adolescent↗
PubMed1998

DSC and NMR spectroscopic studies of the interaction between camphorated phenol and phospholipid liposomes.

To clarify the interaction mechanism of biological activities induced by camphorated phenol (CP), the interactions between CP and phospholipid liposomes [dipalmitoyl phosphatidylcholine (DPPC) liposomes, dimyristoyl phosphatidylcholine (DMPC) liposomes and DMPC/dilauloyl phosphatidylethanolamine (DLEA) liposomes] were studies by DSC and NMR spectroscopy. CP exhibited a larger DSC phase transition properties [shift of phase transition temperature to a lower temperature and decrease in Height/Half-Height Width (H/HHW) of DSC peak)] than phenol in the various liposome systems. It was concluded from the NMR studies that CP is highly incorporated into the DPPC bilayer, the 1H and 13C signals of phenol in a complex between phenol and camphor being markedly broadened but shielded in the presence of DPPC liposomes. It was clear that CP is incorporated as a complex into the lipid bilayers.

Anti-Infective Agents, Local↗
PubMed1998

[Chronic myelogenous leukemia with long-term hypoplasia induced by alpha-interferon and hydroxyurea].

A 48-year-old woman was admitted with chronic myelogenous leukemia in November, 1996 and was treated with hydroxyurea (HU), because of marked leukocytosis; WBC 404,000/microliter. On January 29, 1997, administration of HU was stopped, and treatment of alpha-interferon (IFN alpha) was started with 6x 10(6)U, every day. However, the WBC count rose from 19,600/microliter to 56,800/microliter, and the combination of IFN and 2,000 mg of HU was started on February 4. The dose of HU was reduced to 500 mg on February 27, and the IFN administration was reduced to 3 times a week from April 4, because the WBC count was less than 10,000/microliter. Pancytopenia was revealed in May. The bone marrow biopsy specimen demonstrated marked hypoplastic changes, and chromosome analysis of bone marrow cells showed Philadelphia chromosome in all 20 metaphases. Treatment was interrupted for 7 months, but hematologic parameters did not recover. There were 9 cases reported in detail with bone marrow hypoplasia induced by IFN. One patient received IFN alone and 8 patients received anti-cancer drugs before treatment of IFN. We concluded that great care must be taken for IFN treatment of CML.

Antineoplastic Agents↗
PubMed1998

[The effect of continuous and intravenous application of carteolol chloride on tissue blood flow in the rabbit optic nerve head].

The effect of systemic application of carteolol, which induces almost the same plasma carteolol level as obtained by a long-term instillation on rabbit eyes, on the tissue blood flow in the optic nerve head (ONH) was investigated in rabbits. The plasma carteolol levels in 27 rabbits which received 3-week instillation, intravenous injection (10, 20, 30 micrograms/kg), or continuous intravenous injection (2.5, 5, 20, 40, 80 micrograms/kg/hr) were measured by gas chromatography-negative-ion chemical ionization mass spectrometry. The plasma level with 3-week instillation was determined as 5.55 ng/ml and a continuous intravenous injection (5 micrograms/kg/hr) caused nearly the same plasma level. The intravenous injection of this dose significantly increased the ONH blood flow which was determined by the hydrogen clearance method, compared with controls from 30 minutes to 2 hours after the injection (n = 10). The vascular resistance in ONH was thought to be reduced because mean blood pressure and intraocular pressure (n = 6) were not significantly changed. The results suggest that the plasma carteolol level in rabbits after a long-term instillation can increase ONH blood flow due to a decreased vascular resistance.

Adrenergic beta-Antagonists↗
PubMed1997

Action of eugenol as a retarder against polymerization of methyl methacrylate by benzoyl peroxide.

This study was undertaken to examine an effect of eugenol on polymerization of methyl methacrylate (MMA) by benzoyl peroxide (BPO) and 2,2'-azobisisobutyronitrile (AIBN) in the presence of eugenol. The induction period and initial rate of polymerization (IRP) were determined from polymerization curves of MMA using differential scanning calorimetry (DSC). The induction period increased with increasing concentration of eugenol in both BPO and AIBN systems. The IRP decreased as the concentration of eugenol in both BPO and AIBN systems. The IRP decreased as the concentration of eugenol increased. Its decreasing rate in the BPO system was higher than that in the AIBN system. In the BPO system, the IRP was reduced to zero at 0.5 mol% of eugenol. Eugenol in the BPO system was an efficient retarder, although the decrease in IRP was relatively small, below 0.05 mol%. Eugenol was an inhibitor even at high concentration in the AIBN system. The suppressible effect of eugenol appears to be due to the interaction between free radicals from BPO and eugenol.

Benzoyl Peroxide↗
PubMed1997

[4-year clinico-statistical observation of outpatients].

Clinico-statistical observations were made on the outpatients visiting the Department of Initial Diagnosis and Emergency, Faculty of Dentistry Hospital, Tokyo Medical and Dental University in 1986, 1987, 1989 and 1990. The following findings were obtained according to sex, age group, and chief complaints of new outpatients. Approximately 60% of the outpatients were female during the year examined. The number of outpatients tended to increase in March and to decrease during the winter. The largest number of new outpatients visiting the hospital was in the 20-24-year-old group in both males and females. In the female patients, the 50-54-year-old group had a relatively higher peak. The greatest chief complaint was tooth pain. Further, the chief complaint involving oral soft tissues was due to inflammation. The main disease diagnosed due to chief complaints was caries in the 20-29-year-old group, marginal periodontitis in the 50-59, pericoronitis of wisdom tooth in the 20-29, temporomandibular joint problem in the < or = 19 and masticatory disturbance in the 60 < or = -year-old groups.

Adult↗
PubMed1997

Influence of blood substrate levels on myocardial kinetics of iodine-123-BMIPP.

UNLABELLED: To evaluate the influence of blood substrate levels on myocardial uptake of 123I-labeled beta-methyl-iodophenyl-pentadecanoic acid (BMIPP), we examined the correlation between myocardial BMIPP uptake and blood levels of free fatty acid (FFA), glucose, insulin, triglyceride and total cholesterol. METHODS: In 180 patients, venous blood samples were obtained, and the early and late myocardial uptakes (MU15 and MU150) were determined on planar images at 15 and 150 min after injection at rest, respectively, and the clearance rate of BMIPP from the myocardium was calculated. Dynamic SPECT with BMIPP, PET with [18F]fluoro-deoxyglucose and determination of myocardial carnitine contents were performed in 15, 1 and 3 patients, respectively. RESULTS: In the 180 patients, MU15 correlated with blood insulin (r = 0.22, p = 0.005) and FFA (r = -0.19, p = 0.02) levels, whereas MU150 did not correlate with blood levels of any variables that were measured (p > 0.05). The clearance rate correlated with blood insulin (r = 0.28, p < 0.001), glucose (r = 0.17, p = 0.03) and FFA (r = -0.40; p < 0.001) levels. The correlations were, however, weak, and five patients (2.8%) with no myocardial BMIPP uptake, all of whom had anterior myocardial infaction, had no characteristics regarding the blood substrate levels. Although dynamic SPECT demonstrated rapid myocardial extraction of BMIPP in 13 patients with myocardial BMIPP uptake, it demonstrated no myocardial BMIPP extraction in two patients with no myocardial BMIPP uptake. One of the five patients with no myocardial BMIPP uptake showed increased myocardial [18F]fluorodeoxyglucose uptake and decreased myocardial carnitine content. CONCLUSION: The influence of blood substrate levels on myocardial BMIPP uptake is not very significant, although high serum FFA levels may be associated with slow clearance of BMIPP from the myocardium. The complete absence of myocardial BMIPP uptake is not rare and may not be associated with changes in blood substrate levels or early back diffusion of BMIPP.

Adolescent↗
PubMed1996

Pure red cell aplasia after major ABO-incompatible bone marrow transplantation: two case reports of treatment with recombinant human erythropoietin.

A 34-year-old man with acute myelocytic leukemia (AML: MO) and a 32-year-old woman with AML: M2 developed pure red cell aplasia (PRCA) after receiving a major ABO incompatible bone marrow transplant (BMT). The first patient responded to recombinant human erythropoietin (rhEPO) therapy, while the second did not. The second patient also received methylprednisolone (m-PSL) but developed reticulocytosis and hemolysis after the administration of m-PSL. Plasmapheresis was then performed and the patient promptly recovered from hemolysis and PRCA. We conclude that close attention must be paid when treating PRCA following major ABO-incompatible BMT with rhEPO and m-PSL, as there is always the potential for massive hemolysis.

ABO Blood-Group System↗
PubMed1996

DNA topoisomerase II inhibitors enhance random integration of transfected vectors into human chromosomes.

To study the involvement of DNA topoisomerase (topo) II on nonhomologous (illegitimate) recombination, we examined the effect of topo II inhibitors on random integration of exogenous vectors into human chromosomes. We transfected human cell lines PA1, HeLa and EJ-1 with linearized plasmid pSV2neo by electroporation, treated with topo II inhibitors and determined the frequency of Geneticin-resistant (G418r) colonies. We found that three topo II inhibitors, etoposide (VP-16), ICRF-193 and amsacrine (m-AMSA), greatly enhanced the frequency of G418r colonies. These effects were maximally expressed by as little as 12 hrs treatment with the drugs. Similar enhancements were found with different vectors (closed-circular and linear), different cell types, or by different transfection methods (calcium precipitation and lipofection). In contrast, the inhibitor treatments did not affect the transient expression of chloramphenicol acetyltransferase and beta-galactosidase activity following transfection with pSV2CAT and pCH110, respectively. Southern blot analysis revealed that the integration pattern of transfected pSV2neo into PA1 chromosomes was random and not characteristic for each inhibitor. These results suggest that topo II inhibitors directly act at a nonhomologous recombination reaction, promoting the integration process of transfected vectors into human chromosomes. We discuss the enhancement mechanism with a special emphasis on DNA strand breaks induced by the inhibitors.

Amsacrine↗