M Sakurai

Mie University, Tsu-shi, Mie-ken, Japan

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Publications (349)919.55 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Hydrogen peroxide (H2O2) generation by human polymorphonuclear leukocytes (PMN) incubated with varicella zoster virus (VZV) antigen was studied by cytofluorography. Hydrogen peroxide generation was detected in the presence of VZV-seropositive sera. When seropositive sera were heat-inactivated, H2O2 generation was reduced. When PMN were pre-incubated with Leu-1 1b, a monoclonal antibody to the Fc receptor on PMN, H2O2 generation was also reduced. These results suggest that VZV antigen-antibody-complement complexes induce H2O2 generation by PMN after these complexes attach to Fc receptors on PMN.
    Pediatrics International 01/2011; 36(4):341 - 346. DOI:10.1111/j.1442-200X.1994.tb03198.x · 0.73 Impact Factor
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    ABSTRACT: 2′,5′-oligoadenylate synthetase activity, which is assumed to be induced by interferon, is reported to be one of the useful markers reflecting interferon activity. The enzyme activity of patients with aseptic meningitis and febrile convulsion were compared in order to evaluate interferon activity as one of the local immuno-defense mechanisms of aseptic meningitis. The surface antigen of mononuclear cells in cerebrospinal fluid and peripheral blood of some patients with aseptic meningitis was also measured. The enzyme activity of patients with aseptic meningitis was 191.4 pmol/dL in the cerebrospinal fluid and 395.8 pmol/dL in the serum during the acute phase, while that of patients with febrile convulsion was 45.2 pmol/dL in the cerebrospinal fluid and 326.0 pmol/dL in the serum. The enzyme activity of the former patients significantly decreased during the recovery phase in both the cerebrospinal fluid and serum. CD3 positive cells in the peripheral blood were 56.3% of the total mononuclear cells during the acute phase and 65.2% during the recovery phase, whereas in the cerebrospinal fluid mononuclear cells, they were 87.1 and 85.5%, respectively. During the acute phase, CD4 positive cells were the predominant T lymphocyte subset in the cerebrospinal fluid cells, while CD8 positive cells were predominant during the recovery phase. The relative proportions of CD4 positive and CD8 positive cells during the acute and recovery phase in the cerebrospinal fluid mononuclear cells were quite high compared to the recovery phase, although that ratio of peripheral blood mononuclear cells was not changed throughout the course. It was concluded that T lymphocytes and increased 2′,5′-oligoadenylate synthetase activity in the cerebrospinal fluid may be one of the important components in the local inflammatory process independent of the systemic host defense mechanism in aseptic meningitis.
    Pediatrics International 01/2011; 39(1):48 - 53. DOI:10.1111/j.1442-200X.1997.tb03555.x · 0.73 Impact Factor
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    ABSTRACT: A 2-year-old boy developed acute myositis associated with rotavirus gastroenteritis. He had remarkable swelling and subcutaneous edema, mostly in the legs, 4 days after the onset of gastroenteritis. Marked elevation of creatine kinase was observed while serum albumin, immunoglobulin, and complement were decreased.
    Pediatrics International 10/2007; 40(1):82 - 84. DOI:10.1111/j.1442-200X.1998.tb01409.x · 0.73 Impact Factor
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    ABSTRACT: The endonuclease which causes antibody-induced apoptotic cell death in B cells is not completely understood. We previously established a B-cell line (MBC-1) from a patient with Burkitt's lymphoma at the leukaemic stage which demonstrated the typical morphology and internucleosomal DNA fragmentation of apoptotic cell death when treated with anti-IgM antibody. FK506, an immunosuppressive agent and calcineurin inhibitor, partially rescued the anti-IgM antibody-induced cell death in these MBC-1 cells. DNA SDS-PAGE nuclease activity assay demonstrated that a 17 kD protein exhibited endonuclease activity. Active gel assay showed nuclease activity in the cellular nuclear extract not treated with anti-IgM antibody. This nuclease activity was inhibited by FK506 at concentrations of 10–200 ng/ml in the active gel assay. These results raise the possibility that the 17 kD endonuclease is one of the nuclear members of the immunophilin family, which may function as an endogenous endonuclease in MBC-1 cells.
    British Journal of Haematology 10/2003; 99(4):908 - 913. DOI:10.1046/j.1365-2141.1997.4783287.x · 4.96 Impact Factor
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    ABSTRACT: Several 5-fluorouracil (5-FU) derivatives, 1-hexylcarbamoyl-5-fluorouracil (HCFU), 5'-deoxy-5-fluorouridine (5'-DFUR) and UFT (mixed compound of tegafur and uracil), have been developed and clinically widely used. However, comparative pharmacokinetic studies of the parent compound and other fluorinated drivatives have not been precisely reported. The dosage of the oral clinical use for human cancer of 5-FU, HCFU, 5'-DFUR and UFT as tegafur (FT) is 200-300mg/d, 600mg/d, 800-1,200mg/d and 300-600mg/d respectively. These amounts of the drugs are almost equimolar. Previously, we reported the effect of oral equimolar administration of each four drugs on thymidilate synthase activity, deoxyribonucleotide metabolism and cell cycle progression in L1210 ascites tumor. (1,2) In this study, we examined the antitumor effect and 5-FU concentration in the plasma, intestine and tumor after oral equimolar administrations of each drug using BDF1 mice bearing L1210 ascites tumor. In our study, UFT showed the best life prolongation among these four drugs. The intestine 5-FU level was highest by treatment with 5-FU during the initial 4 h. The plasma 5-FU level was highest by treatment with HCFU for 4 h. But the tumor 5-FU level was highest by treatment with UFT over the 24 h. In spite of the high plasma 5-FU concentration after the treatment with HCFU, the 5-FU concentration in the tumor was below the detectable level until 24 h. These findings suggested that the highest specific accumulation of 5-FU in tumor cells may explain the best therapeutic results of UFT.
    Biological & Pharmaceutical Bulletin 12/2001; 24(11):1329-31. · 1.78 Impact Factor
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    ABSTRACT: Monocytes as antigen-presenting cells play an important role in host defense and transplantation. However, there are little reports on cord blood monocytes, and the role of monocytes in cord blood transplantation is largely unknown. There are several cytokines affecting monocyte function. These include interferon-gamma, interleukin-4, interleukin-10, granulocyte macrophage-colony stimulating factor and hepatocyte growth factor (HGF). We investigated the effect of these cytokines on antigen-presenting capacity (APC) of cord and adult blood monocytes. Using either mononuclear cells or purified CD4+ T cells as responder cells, HGF enhanced APC of adult monocytes most effectively among these cytokines. In contrast, cord blood monocytes failed to respond to HGF. As HLA, costimulatory and adhesion molecules may affect APC function, we examined these antigens of monocytes following HGF stimulation. The HGF upregulated integrin alpha5 subunit (CD49e) and intercellular adhesion molecule-1 (CD54) was expressed in adult blood monocytes, but not in cord blood. In kinetic studies, HGF downregulated c-met protein/HGF receptor expression of adult monocytes in lower concentrations and at shorter incubation time as compared with that of cord blood. The results suggest that impaired response of cord blood monocytes to HGF may be responsible, in large part, for their functional immaturity.
    Pediatrics International 09/2001; 43(4):334-9. DOI:10.1046/j.1442-200X.2001.01420.x · 0.73 Impact Factor
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    ABSTRACT: Monocytes as antigen-presenting cells play an important role in host defence. There are several cytokines affecting monocyte function. We demonstrate that both adult and cord blood monocytes constitutively express hepatocyte growth factor (HGF) receptor, MET. HGF significantly down-regulated MET expression of adult blood monocytes, compared with cord blood monocytes, when cultured either in RPMI-1640 containing 10% FBS or serum-free medium. Surface levels of MET correlated with c-met mRNA levels both in adult and cord blood when cultured. MET expression was down-regulated by treating with actinomycin D or cycloheximide. HGF stimulated DNA synthesis of adult monocytes, but not cord blood. HGF enhanced antigen-presenting capacity of adult blood monocytes but not cord blood monocytes. HGF up-regulated HLA class I expression in adult monocytes but not in cord blood monocytes. The current results suggest that the failure of cord blood monocytes to respond to HGF may be responsible, in large part, for their functional immaturity.
    Clinical & Experimental Immunology 09/2001; 125(2):222-8. DOI:10.1046/j.1365-2249.2001.01591.x · 3.28 Impact Factor
  • H Hayakawa · Y Komada · M Hirayama · H Hori · M Ito · M Sakurai
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    ABSTRACT: Anthracyclines are effective anticancer drugs for childhood cancer with dose-limiting cardiotoxicity. Children who have received anthracyclines thus need periodical cardiac evaluation. The plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) have been shown to increase in proportion to severity of cardiac dysfunction. We examined whether plasma levels of ANP and BNP, in addition to echocardiographic evaluation, can be used as specific markers for doxorubicin-induced cardiotoxic effects in children. Consecutively, 34 patients (18 boys and 16 girls) who had previously received doxorubicin-containing chemotherapy were enrolled in this study. Plasma ANP and BNP were assayed simultaneously at the time of first cardiac function evaluation by echocardiography. Of the 34 patients, 8 (23.5%) had left ventricular dysfunction as assessed by echocardiography. Both ANP and BNP plasma levels in these patients were significantly elevated in comparison with healthy controls (P < 0.01) or patients with normal cardiac function (P < 0.05). It should be also noted that ANP and BNP levels were correlated significantly with cardiac systolic function, but not with diastolic function. These results suggest that plasma ANP and BNP levels could be markers for doxorubicin-induced cardiotoxicity in children. Measurement of natriuretic peptide levels during treatment may allow earlier-identification of individuals at risk for severe cardiac damage.
    Medical and Pediatric Oncology 07/2001; 37(1):4-9. DOI:10.1002/mpo.1155
  • Y Mitani · M Ueda · R Komatsu · K Maruyama · R Nagai · M Matsumura · M Sakurai
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    ABSTRACT: Primary pulmonary hypertension (PPH) is associated with specific structural alterations, including cellular intimal thickening, intimal fibrosis, and plexiform lesions. To determine the phenotypes of smooth muscle cells (SMCs) in such lesions, the authors conducted an immunohistochemical analysis of lung tissues from two patients with PPH, using two antimuscle actin antibodies, HHF35 and CGA7, and two anti-SMC myosin heavy chain markers, anti-SM1 and anti-SM2 antibodies and related antibodies. Cells that stained positive (+) with HHF35, CGA7, anti-SM1, and anti-SM2 were considered to be SMCs of a mature state. Conversely, those that stained positive with HHF35 and anti-SM1, but weakly positive (+/-) or negative (-) with CGA7 and anti-SM2, were considered to be SMCs exhibiting an immature state. Cellular intimal thickening was composed of SMCs of an immature phenotype (HHF35+, CGA7+/-, SM1+, SM2+/-), accompanied by the expression of fibronectin and the presence of macrophages; intimal fibrosis contained mature SMCs (HHF35+, CGA7+, SM1+, SM2+); and plexiform lesion consisted of proliferative endothelial cells (von Willebrand factor-positive cells, proliferating cell nuclear antigen-positive cells) and underlying immature SMCs (HHF35+, CGA7-, SM1+, SM2-) associated with fibronectin expression and macrophage infiltration. These findings suggest that smooth muscle cells with specific phenotypes may contribute to the development of specific vascular lesions in primary pulmonary hypertension.
    European Respiratory Journal 03/2001; 17(2):316-20. DOI:10.1183/09031936.01.17203160 · 7.13 Impact Factor
  • Biological & Pharmaceutical Bulletin 01/2001; 24(11):1329-1331. DOI:10.1248/bpb.24.1329 · 1.78 Impact Factor
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    ABSTRACT: In the neonate, cellular immunity has generally been hypothesized as being incompetent. Accumulating evidence from several recent studies, together with our present report, contradicts this hypothesis. T-helper cell and T cytotoxic type 1 and 2 (Th1/Th2 and Tc1/Tc2, respectively) cytokine responses to polyclonal T cell receptor (TCR) activation were assessed in medium-term cultures of human cord blood T cells using intracellular cytokine staining, which could measure the frequencies of cytokine-producing cells. In this study, we examined the responses of cord blood CD4(+) and CD8(+) T cells in regard to the production of interferon (IFN)-gamma and interleukin (IL)-4 and compared the responses with those obtained from T cells of healthy adults. We found that the responses in cord blood T cells activated with TCR stimulation were comparable to those of their adult counterparts. Moreover, the Th/Tc cells that developed in cord blood were as competent as adult cells for both IFN-gamma and IL-4 secretion. In addition, IL-12 production, which is critical for both Th1 and Tc1 responses, was equally comparable in the two groups. The production of two major cross-regulatory cytokines, tumor necrosis factor-alpha and IL-10, was similarly comparable and not significantly different between the two groups. Taken together, these results indicate that, though naive, the neonatal T cell is competent to respond to TCR-mediated stimulation and to produce both type 1 and type 2 cytokines.
    Cellular Immunology 12/2000; 205(2):110-9. DOI:10.1006/cimm.2000.1718 · 1.87 Impact Factor
  • Pediatrics International 09/2000; 42(4):383-5. DOI:10.1046/j.1442-200x.2000.01236.x · 0.73 Impact Factor
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    ABSTRACT: During an ongoing immune response, cytokines produced by T helper types 1 (Th1) and 2 (Th2) together with T cytotoxic types 1 (Tc1) and 2 (Tc2) are critical to the effectiveness of that response. Dysregulated expansion of one or the other subset may contribute to the impaired function of the T-cell-mediated immune system in cancer patients. In the present study we have investigated whether such dysregulation might exist in children with acute lymphoblastic leukemia (ALL). We analyzed 61 blood samples from 45 children with B cell precursor ALL and 16 healthy children. Interleukin(IL)-2, IL-4, and interferon gamma (IFN gamma) production of their respective purified CD4+ and CD8+ T cells were assessed at the single-cell level by intracellular-cytokine-staining flow cytometry. At the time of diagnosis, IL-2-producing cell populations in CD4+ and CD8+ T cells were reduced below the normal range in 31 of 44 (70.5%) and 23 of 38 (60.5%) cases respectively. Similarly, IFN gamma-producing cell populations in CD4+ and CD8+ T cells decreased in 17 of 44 (38.6%) and 18 of 38 (47.4%) cases respectively. Conversely cell populations capable of IL-4 production in CD4+ and CD8+ T cell subsets were increased in 13 of 30 (43.3%) and 15 of 30 (50.0%) cases respectively. Therefore, the Th1-to-Th2 and Tc1-to-Tc2 ratios (1.6 +/- 2.2 and 7.7 +/- 6.7 respectively) were significantly lower in peripheral blood T cells of ALL patients (n = 30) than those (6.0 +/- 2.9 and 20.1 +/- 10.3 respectively) in 15 healthy controls (P < 0.0001). Although both CD45RA+/CD4+ and CD45RA+/CD8+ cells significantly increased in 43 ALL patients (P < 0.05), there existed no apparent correlation between CD45 isoform expression and cytokine (IL-2 and IFN gamma) production. Interestingly, the ability to produce both IL-2 and IFN gamma was recovered in 8 cases examined, after complete remission had been achieved. These observations suggest that, in both CD4+ and CD8+ T cells of ALL patients, there is a dysregulation in the functionality of Th1 (Tc1) and Th2 (Tc2) cells with a gross reduction of Th1 (Tc1) cell populations and an expansion in Th2 (Tc2).
    Cancer Immunology and Immunotherapy 07/2000; 49(3):165-72. DOI:10.1007/s002620050616 · 3.94 Impact Factor
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    ABSTRACT: Natriuretic peptides (NPs), such as atrial natriuretic peptide (ANP), C-type natriuretic peptide (CNP), and adrenomedullin (ADM), are endogenous vasodilators acting via specific receptors. This study addressed the question of how pulmonary artery (PA) responses to these peptides and the gene expression of their receptors are modulated in pulmonary hypertension rat models exposed to chronic hypoxia. In this study, isometric tension was measured in PA rings exposed to these NPs and 8-bromoguanosine 3', 5'-cyclic monophosphate (8-bromo-cGMP). It was compared with messenger ribonucleic acid (mRNA) levels of NP-A and -B receptors, which bind to ANP and CNP, respectively, as determined by ribonuclease (RNase) protection assay. Chronic hypoxia increased the maximal relaxation elicited by ANP, but the responses to CNP and 8-bromo-cGMP were unchanged. Chronic hypoxia did not change NP-A and -B receptor mRNA levels. The results showed that pulmonary artery response to atrial natriuretic peptide is selectively enhanced, possibly via a post-transcriptional modulation of its receptor in chronically hypoxia rats. These pharmacological characteristics of atrial natriuretic peptide are consistent with the hypothesis that the atrial natriuretic peptide system is protective against the progression of pulmonary hypertension.
    European Respiratory Journal 03/2000; 15(2):400-6. DOI:10.1034/j.1399-3003.2000.15b29.x · 7.13 Impact Factor
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    ABSTRACT: Fas (Apo-1/CD95) is a cell membrane receptor involved in apoptotic cell death. Soluble variant forms (sFas) lacking the transmembrane domain due to alternative splicing have been identified. Up-regulation of sFas expression is reportedly implicated in prereceptorial blockage of Fas-induced apoptosis in a dose-dependent manner. We examined mRNA expression of Fas and sFas in fresh leukemia cells. All leukemia cells expressed both mRNAs of full-length Fas (FasFull) and sFas with deletion of exon6 (FasDel6). The ratio of FasFull/FasDel6 mRNA expression was not always correlated with Fas-mediated growth inhibition. Interestingly, in a 6-year-old boy with acute myelogenous leukemia, blast cells obtained at onset and at the time of bone marrow relapses expressed distinct amounts of FasDel6 mRNA. Furthermore, the level of FasDel6 expression appeared to be correlated with Fas-resistance in leukemia blasts. In addition, sFas protein levels were elevated in patients' sera at onset with subsequent return to normal levels after complete remission. These results indicated that sFas could be synthesized and released by leukemia blasts and suggested that up-regulation of Fas variant transcript might render leukemia blasts resistant to Fas-mediated growth inhibition in certain cases.
    American Journal of Hematology 12/1999; 62(3):150-8. DOI:10.1002/(SICI)1096-8652(199911)62:33.3.CO;2-P · 3.48 Impact Factor
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    ABSTRACT: Fas (CD95) is a cell surface glycoprotein that mediates apoptotic cell death when cross-linked with agonistic anti-Fas monoclonal antibodies (MAbs) or the endogenous Fas ligand. In this study, we investigated the in vitro biological properties of a panel of anti-human Fas MAbs. We found that five anti-Fas MAbs of IgG1 subclass (B.E28, B.G30, B.L25, DX2, and B.G34) induced marked apoptotic cell death in Fas-expressing leukemia cells, although this killing was delayed when compared to the cytolytic effect mediated by the prototypic anti-Fas MAb of IgM subclass (clone CH-11). On the other hand, four clones (ZB4, B.G27, B.D29, and B.K14) efficiently blocked apoptotic cell death induced by the CH-11 MAb or Fas ligand. The ability of these MAbs to inhibit cell death appeared to correlate with their relative affinity for the Fas molecule. Furthermore, different clones recognized the same epitope and elicited different effects (induction or inhibition of cell killing); conversely, different clones elicited the same effect but recognized different epitopes. These results suggest that the different biological effects of anti-Fas MAbs would not be mediated in an epitope-restricted manner. The relative binding affinity might correlate to some extent with the biological properties of the MAb.
    Hybridoma 11/1999; 18(5):391-8. DOI:10.1089/hyb.1999.18.391
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    ABSTRACT: Many protocol studies have shown that low dose 6-mercaptopurine (6MP) in maintenance chemotherapy for childhood acute lymphoblastic leukemia (ALL) can be utilized to cure the disease. Mitotic or reproductive cell death has been recognized after G2 arrest when cells are treated with antitumor agents. The precise mechanism of mode of action of 6MP still remains unclear. We found delayed cytotoxic effect of 6MP in P388 murine leukemic cells. Morphological study showed that 6MP induced delayed death was characterized by an enlargement of cell size and multinucleated nuclei. Agarose gel electrophoresis of fragmented DNA from cells treated with 6MP showed the typical ladder pattern. These findings were compatible with mitotic death. Our results make us hypothesize that the delayed cytotoxicity of 6MP is one of the drug induced mitotic deaths caused by DNA damage due to incorporation of 6-thioguanine (6TG) into DNA as thioguanine nucleotide (TGN). Mitotic death may be a mechanism for killing the cycling cells from residual leukemic cells in G0 or long G1 phases in the treatment of childhood ALL.
    Journal of experimental & clinical cancer research: CR 10/1999; 18(3):417-24. · 4.23 Impact Factor
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    ABSTRACT: Histone H3 (H3) phosphorylation at Ser(10) occurs during mitosis in eukaryotes and was recently shown to play an important role in chromosome condensation in Tetrahymena. When producing monoclonal antibodies that recognize glial fibrillary acidic protein phosphorylation at Thr(7), we obtained some monoclonal antibodies that cross-reacted with early mitotic chromosomes. They reacted with 15-kDa phosphoprotein specifically in mitotic cell lysate. With microsequencing, this phosphoprotein was proved to be H3. Mutational analysis revealed that they recognized H3 Ser(28) phosphorylation. Then we produced a monoclonal antibody, HTA28, using a phosphopeptide corresponding to phosphorylated H3 Ser(28). This antibody specifically recognized the phosphorylation of H3 Ser(28) but not that of glial fibrillary acidic protein Thr(7). Immunocytochemical studies with HTA28 revealed that Ser(28) phosphorylation occurred in chromosomes predominantly during early mitosis and coincided with the initiation of mitotic chromosome condensation. Biochemical analyses using (32)P-labeled mitotic cells also confirmed that H3 is phosphorylated at Ser(28) during early mitosis. In addition, we found that H3 is phosphorylated at Ser(28) as well as Ser(10) when premature chromosome condensation was induced in tsBN2 cells. These observations suggest that H3 phosphorylation at Ser(28), together with Ser(10), is a conserved event and is likely to be involved in mitotic chromosome condensation.
    Journal of Biological Chemistry 10/1999; 274(36):25543-9. DOI:10.1074/jbc.274.36.25543 · 4.57 Impact Factor
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    ABSTRACT: Granisetron has been used widely for the prevention and treatment of nausea and vomiting associated with anticancer drugs in adult patients with cancer. This multi-center open study was conducted to study the efficacy, safety and usefulness of granisetron in children with cancer. Among 166 evaluable patients, the efficacy rate (percentage of "remarkably effective" or "effective") was 84.9% and the usefulness rate (percentage of "extremely useful" or "useful") was 87.3%. No serious adverse effects were observed. As granisetron 40 micrograms/kg had an excellent antiemetic effect and a high degree of safety against nausea and vomiting associated with anticancer drugs, it was shown to be useful for children with cancer.
    Gan to kagaku ryoho. Cancer & chemotherapy 09/1999; 26(9):1295-304.
  • Y Komada · T Matsuyama · A Takao · T Hongo · Y Nishimura · K Horibe · M Sakurai
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    ABSTRACT: This randomised study was performed to assess the anti-emetic efficacy and tolerability of two-dose regimens of granisetron in children with leukaemia. 49 children with leukaemia were treated with three consecutive courses of high-dose methotrexate or cytarabine regimen. During the first course, patients were evaluated regarding the emetogenicity of each regimen. They were randomised in a crossover manner to receive 20 or 40 micrograms/kg of granisetron before the second and third course of chemotherapy. Neither emesis nor severe appetite loss were observed in over 80% of patients within the first 24 h in all treatment groups. There was no significant difference in the anti-emetic efficacy between the two-dose regimens of granisetron. However, complete protection was achieved less frequently on days 2 and 3. Older children and girls appeared to be less well protected. No adverse events attributable to granisetron were observed. Granisetron dose regimens of 20 and 40 micrograms/kg are, comparably, well tolerated and effective in controlling chemotherapy-induced emesis in the first 24 h, though this protection fails thereafter, particularly in older patients and girls.
    European Journal of Cancer 08/1999; 35(7):1095-101. DOI:10.1016/S0959-8049(99)00071-4 · 4.82 Impact Factor

Publication Stats

4k Citations
919.55 Total Impact Points


  • 1986–2011
    • Mie University
      • • Department of Pediatrics
      • • School of Medicine
      Tsu-shi, Mie-ken, Japan
    • St. Jude Children's Research Hospital
      • Department of Pathology
      Memphis, Tennessee, United States
    • University of Texas Southwestern Medical Center
      Dallas, Texas, United States
  • 2001
    • Mie-chuo Medical Center
      Matsusaka, Mie, Japan
  • 1990–2001
    • Social Insurance Chukyo Hospital
      Nagoya, Aichi, Japan
  • 1986–1999
    • Saitama Cancer Center
      • Saitama Cancer Center Hospital
      Saitama, Saitama, Japan
  • 1997
    • Gifu University
      • Department of Pediatrics
      Gihu, Gifu, Japan
  • 1995
    • Tokyo Medical and Dental University
      • Medical Research Institute
      Tokyo, Tokyo-to, Japan
  • 1991–1995
    • Noguchi Memorial Institute for Medical Research
      Akra, Greater Accra, Ghana
    • Kyoto Prefectural University of Medicine
      • Department of Pediatrics
      Kyoto, Kyoto-fu, Japan
  • 1989
    • Tokyo Dental College
      • Department of Dental Anesthesiology
      Tiba, Chiba, Japan