Vesnarinone induced agranulocytosis.
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Aged↗
Biomedical subjects
S Furusawa
Publications and source records attributed to S Furusawa.
Effects of granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor on respiratory burst activity of neutrophils in patients with myelodysplastic syndromes.
The superoxide (O2-)-releasing capacity in response to N-formyl-methionyl-leucyl-phenylalanine (FMLP) and the priming effects of recombinant human granulocyte colony-stimulating factor (rhG-CSF) and granulocyte-macrophage colony-stimulating factor (rhGM-CSF) on FMLP-induced O2- release were investigated in neutrophils from 14 patients with myelodysplastic syndromes (MDS). The O2(-)-releasing capacity in MDS neutrophils varied from patient to patient. As compared with normal neutrophils, the O2(-)-releasing capacity in MDS neutrophils was increased in 9/14 patients, normal in three patients and decreased in two patients. There was no close relationship between the O2(-)-releasing capacity and the peripheral blood neutrophil count or the plasma concentration of C-reactive protein. The priming of neutrophils by rhG-CSF was not observed in five patients, whereas rhGM-CSF primed neutrophils from all patients. The priming effect of rhGM-CSF was consistently greater than that of rhG-CSF in each patient. The intravenous administration of rhG-CSF (300 micrograms/body) to two MDS patients showed an increase in the peripheral blood neutrophil count and enhancement of neutrophil O2- release. These findings demonstrate that the neutrophil O2(-)-releasing capacity in MDS varies from patient to patient and is not always impaired, and that rhGM-CSF is able to prime neutrophils which never respond to rhG-CSF.
Adult↗
GM-CSF and eosinophil chemotactic factors in an acute lymphoblastic leukemia patient with eosinophilia.
We describe a patient with common acute lymphoblastic leukemia associated with blood and cerebrospinal fluid (CSF) eosinophilia. Serum obtained at onset and conditioned medium prepared from T cells obtained at remission stimulated with interleukin-2 contained eosinophil colony stimulating activity (Eo-CSA), which was confirmed to be predominantly GM-CSF. Leukemic cell conditioned medium and serum obtained at remission contained no Eo-CSA. The CSF contained increased eosinophil chemotactic activity, however, this factor was not identified.
Adult↗
[Amylase-producing plasma cell dyscrasia. Genomic analysis in a case of intramuscular tumor formation and a review of the literature].
We describe a 53-year-old male patient with multiple myeloma (IgA, kappa) who showed massive intramuscular tumors and hyperamylasemia of the salivary (S) type 10 months after initial diagnosis. Suspension culture of the abnormal plasma cells in the pleural fluid showed the production of S-amylase, which was confirmed by the expression of S-amylase mRNA comigrating with salivary gland mRNA. Cytogenetic analysis of the cells showed common abnormalities 1p+q-and 8q+. They expressed IL-6 mRNA, but not c-myc mRNA. Neither structural abnormality nor amplification was detected in the alleles of S amylase, and c-myc using Southern blot analysis. All of the eight patients with plasma cell dyscrasia with hyperamylasemia reported so far (including the present one) are Japanese, and showed S-type hyperamylasemia and extramedullary tumor formation at initial diagnosis or during the course of the disease. All of the four patients in whom cytogenetic analysis was performed had structural abnormalities of chromosome 1, on which the S-amylase gene is known to be located, although the break point were variable.
Amylases↗
A randomized controlled study of granulocyte colony stimulating factor after intensive induction and consolidation therapy in patients with acute lymphoblastic leukemia. Japan Adult Leukemia Study Group.
To determine the efficacy and optimal daily dose of recombinant human granulocyte colony-stimulating factor (rG-CSF) after intensive chemotherapy, a prospective randomized study was conducted with daily intravenous administration of 2, 5 or 10 micrograms/kg G-CSF after induction therapy, and 0, 2, 5 or 10 micrograms/kg after consolidation therapy, until neutrophil counts recovered to more than 2000/mm3. The subjects were 41 adult patients with newly diagnosed acute lymphoblastic leukemia (ALL). After the induction therapy, neutrophil recovery to more than 1000/mm3 was significantly faster in the 5 (P = 0.047) and 10 micrograms/kg groups (P = 0.011) than in the 2 micrograms/kg group, but did not differ between the 2 former groups. The median days of neutrophil recovery to more than 1000/mm3 were 8.5, 9 and 12 days, respectively. After the consolidation therapy, neutrophil recovery to more than 1000/mm3 was significantly faster in the 2, 5 and 10 micrograms/kg groups than in the no rG-CSF group (P < 0.001, respectively), but did not differ among the 3 former groups. The median days of neutrophil recovery to more than 1000/mm3 were 12, 11, 10, and 23 days, respectively. Febrile neutropenia and incidence of documented infection tended to be less in the 5 and 10 micrograms/kg groups than in 0 and 2 micrograms/kg groups. A dose of 5 micrograms/kg rG-CSF given by a 30 min infusion daily seems to be an effective and optimal daily dose to accelerate neutrophil recovery after intensive remission induction and consolidation chemotherapy in adults with acute lymphoblastic leukemia (ALL).
Adolescent↗
Antitumor activity of acemetacin in mice bearing colon 26 carcinoma: a preliminary report.
The antitumor activity of acemetacin (ACM) was examined in mice bearing colon 26 carcinoma and its effect was compared with indomethacin (IND). The addition of ACM (0.001-0.003%) to drinking water prolonged the survival time of mice bearing colon 26. On the other hand, prostaglandin E2 (PGE2) reduced the effect of ACM. The results suggest that the antitumor activity of ACM may be associated with the reduction of PGE2 levels.
Animals↗
[Idiopathic bilateral sensorineural hearing loss: clinical study of cases with rapidly progressed deafness].
In a series of 127 patients with idiopathic bilateral sensorineural hearing loss (IBSH) at the Hearing Clinic in the Department of Otolaryngology, Kitasato University Hospital, 20 cases showed rapid progression of hearing impairment. These patients had been treated with the same therapeutic regimen used in sudden deafness (S.D.). Improvement of hearing loss after treatment was generally less effective in the cases with rapidly progressed IBSH than in the cases with S.D. However, hearing improvement was achieved in some cases with rapidly progressed IBSH when the treatment had started in the early stages after the onset of rapidly progressive hearing loss. The mode of fluctuating hearing loss in the cases with rapidly progressed deafness was assumed to be similar to that in the group of all cases with IBSH.
Adolescent↗
[Assay of flow cytometry for the effect of cepharanthine on resistance to doxorubicin].
The biochemical activity of cepharanthine and the possible mechanism by which it reverses the resistance to doxorubicin in P388 leukemia cells were examined in vitro. The microfluorometric analysis of the cellular level of doxorubicin in drug-resistant cells showed that cepharanthine markedly enhanced the sensitivity of doxorubicin against resistant cells in the cellular level. Cepharanthine also enhanced the inhibitory effect of doxorubicin on the incorporation of thymidine into DNA in resistant cells. The analysis of DNA histogram obtained by flow cytometry showed that doxorubicin exerted its growth-inhibitory effect by blocking the cell cycle at the G2 phase in P388 cells. At higher concentrations, doxorubicin prolonged the S phase and inhibited cell cycle progression to the G2/M phase in cells. The treatment with cepharanthine potentiated these blocking effects induced by doxorubicin in cells. It seems that the modifications of the biological effect of doxorubicin by cepharanthine are due to the change of their ability to induce DNA damage in cells.
Alkaloids↗
[The effect of aging on observation in hearing in the same individuals over a 5 year period].
The purpose of this study was to investigate the process of changes in hearing of pure tones with aging. Among individuals who had undergone thorough medical examination for the purpose of annual health-checks, 293 males (586 ears) whose hearing level had been examined for five years or more were enrolled in this study. Cases having conductive deafness or known sensori-neural deafness were excluded. Since the most typical change with aging is observed at 8 kHz, the investigation was carried out only on hearing at 8 kHz. Hearing level increasingly declined with advancing age. Hearing distribution for young subjects showed a peak in the normal hearing level range. This peak decreased with aging, and another peak appeared at 50 dB. Investigation of differences in hearing in the individuals over the five years showed that most subjects had a hearing level difference of 0 dB up to 54 years of age. From 55 years old onward, however, the difference was 5 dB. This indicates that gradual deterioration of hearing level with aging occurs most frequently. On the other hand, in some subjects, deafness progressed faster. Thirty-four and a half percent of the subjects had deteriorations of 20 dB or more in a single year during the entire observation period. A deterioration of 20 dB or more was noted in 4% of the young and 8% of the elderly. Such rapid progression of deafness was believed to be involved in formation of the 50 dB peak in the hearing distribution.
Adult↗
Comparative effects of G-CSF, GM-CSF and IL-3 on cytosine arabinoside- and daunorubicin-mediated cytotoxicity of acute myeloid leukemia cells and normal myeloid progenitors.
We carried out an in vitro study on the combined effects of three CSF (G-CSF, GM-CSF and IL-3) plus the cycle-specific chemotherapeutic drugs [cytosine arabinoside (Ara-C) and daunorubicin (DNR)] on the proliferation and cytotoxicity of blasts and clonogenic cells (CFU-AML) in the AML-193 cell line, in AML patients and in normal bone marrow CFU-GM. The number of surviving blasts and/or DNA synthesis in blasts treated with CSF plus Ara-C or DNR was greater than those treated without CSF in the AML-193 cell line, and in some AML patients. On the other hand, the Ara-C- and DNR-mediated cytotoxicity of CFU-AML was not abrogated by CSF in any instance, but rather, it was significantly enhanced by all the CSF in the majority of instances. Although the enhancement was clearer when Ara-C was used, compared with DNR, there were no significant differences among the enhancing effects of the CSF. Under the same culture conditions as those for CFU-AML, all of the CSF significantly enhanced the Ara-C-mediated cytotoxicity of day 7 normal CFU-GM, although to a lesser extent than in CFU-AML. However, none of the CSF significantly affected the Ara-C-mediated cytotoxicity of day 14 normal CFU-GM or the DNR-mediated cytotoxicity of day 7 or day 14 normal CFU-GM. These results suggest that in the selection of a strategy entailing combined use of cycle-specific drugs plus CSF to increase the antileukemic effectiveness of chemotherapy in AML, G-CSF is preferable to GM-CSF or IL-3, since it has fewer potential clinical side effects, and that, furthermore, DNR may be as useful as Ara-C.
Acute Disease↗
Clinical effect of recombinant human granulocyte colony-stimulating factor (rhG-CSF) on various types of neutropenia including cyclic neutropenia.
Recombinant human granulocyte colony-stimulating factor (rhG-CSF) was investigated for its clinical efficacy in the treatment of various types of neutropenia (3 cases with idiopathic neutropenia of suspected drug induction, 5 cases with idiopathic neutropenia of other origin, and 2 cases with cyclic neutropenia). Treatment with glycosylated rhG-CSF produced in the Chinese Hamster Ovary cells at dose levels of 2-5 micrograms/kg/day caused rapid increases of neutrophil counts associated with an improvement of the infection. In cyclic neutropenia patients, marked reduction in the duration of the neutropenic period was observed with rhG-CSF administration started before the period. Intercurrent stomatitis, which occurred in 1 patient, was markedly milder as compared to a previous episode which occurred during an untreated neutropenic period. The treatment of rhG-CSF was well tolerated and no adverse events were observed, nor was there any detectable anti-rhG-CSF antibody in any patients studied; hence the clinical use of rhG-CSF is considered to be safe. These results suggest beneficial effects of rhG-CSF on the recovery of neutrophil counts in cyclic and other types of idiopathic neutropenias, as well as for the treatment of neutropenia-associated infection.
Adolescent↗
Antileukemic activity of Viva-Natural, a dietary seaweed extract, on Rauscher murine leukemia in comparison with anti-HIV agents, azidothymidine, dextran sulfate and pentosan polysulfate.
An antileukemic activity of partially purified polysaccharide of an edible seaweed. Viva-Natural, against Rauscher murine retrovirus-induced erythroleukemia has been demonstrated. This antileukemic effect is compared with standard anti-human immunodeficiency virus (HIV) agents, azidothymidine (AZT), dextran sulfate and pentosan polysulfate. Pretreatment with Viva-Natural, as an immunomodulator, on day 3 prior to the virus inoculation demonstrated definite prophylactic activity, while pretreatment with the other three anti-HIV agents showed no prophylactic activity. The replication of Rauscher virus in BALB/3T3 cell cultures accompanied by direct cytopathic effect (syncytia formation) was suppressed in the presence of Viva-Natural or the other anti-HIV agents in the culture medium. In spite of the antiviral potentials of the four agents in vitro, only Viva-Natural and AZT demonstrated therapeutic efficacy against Rauscher leukemia in mice.
Animals↗
Preventive effects of a Chinese herb medicine (sho-saiko-to) against lethality after recombinant human tumor necrosis factor administration in mice.
We observed the effects of a chinese herb medicine Sho-saiko-to on the lethal and antitumor activities of recombinant human tumor necrosis factor (rhTNF) administered in mice. Sho-saiko-to was noted to protect the rhTNF-induced lethality in galactosamine-hypersensitized mice, and also Sho-saiko-to pretreated mice was protected against the decrease of rectal temperature after rhTNF administration. On the other hand, there was a remarkable enhancement of antitumor activity of rhTNF by Sho-saiko-to pretreatment. These results suggest that Sho-saiko-to drug may protect mice from severe shock syndrome induced by rhTNF.
Animals↗
[Modulation of anthracycline resistance by reserpine in P388 leukemia cells].
The activity of reserpine and a possible mechanism by which it reverses the resistance to both doxorubicin and pirarubicin in doxorubicin-resistant P388 leukemia (P388/DOX) cells were examined in vitro. During 48 hr drug-exposure, the sensitivity of doxorubicin and pirarubicin were potentiated markedly when reserpine was present at the concentration of 1 microgram/ml, which is not toxic to P388 leukemia (P388/S) cells. However, reserpine had little effect on the cytotoxicity of doxorubicin and pirarubicin in the sensitive parent cell. Reserpine at 0.5-20 micrograms/ml increased intracellular accumulation of doxorubicin and pirarubicin in the drug-resistant cells. The potentiating action of reserpine was stronger when the cells were preincubated with reserpine within 30 min. Efflux of doxorubicin and pirarubicin was greater in drug-resistant cells compared to sensitive cells. This enhanced efflux of drug resulted in a decrease in the intracellular accumulation of doxorubicin in the drug-resistant cells. When the resistant cells were exposed to 2 micrograms/ml of reserpine, this enhanced efflux was blocked. A similar effect of reserpine on doxorubicin was seen with the efflux pattern of pirarubicin. From the measurements of drug uptake and efflux, it seems that like other multiple drug resistance modifiers, reserpine modulates anthracycline resistance by increasing intracellular accumulation of drug.
Animals↗
Detection of interleukin 1 in ascites from cats with feline infectious peritonitis.
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Animals↗
[Hematological effect of 14 days treatment of recombinant human granulocyte colony-stimulating factor for neutropenia in myelodysplastic syndromes].
Nineteen patients with myelodysplastic syndromes (MDS) were treated with a glycosylated recombinant granulocyte colony-stimulating factor (rG-CSF) for improvement of neutropenia. rG-CSF was administrated intravenously at a dose of 5 micrograms/kg/day for 14 consecutive days. Most of patients responded to rG-CSF and an approximately 10 fold increase of the peak neutrophil counts was observed. The neutrophil counts were maintained at high level during the treatment period and returned to pretreatment levels several days after stopping rG-CSF. Consistent with the recovery of neutrophil, infectious complications improved in many cases. Effects of rG-CSF were confined to neutrophils, sparing blast cells and other blood cells. Eruption was observed in one patient as toxicity. We conclude that rG-CSF therapy is effective in improving neutropenia with MDS patients.
Adult↗
Myeloid progenitor cell growth characteristics and effect of G-CSF in a patient with congenital cyclic neutropenia.
A 17-year-old male with congenital cyclic neutropenia was treated with recombinant human granulocyte colony stimulating factor (G-CSF) administered subcutaneously at 1 to 2 micrograms/kg per day. The peak and nadir counts of neutrophils and the peak counts of monocytes were significantly elevated, and the period of cycling decreased from 3 to 2 weeks. Bone marrow culture studies revealed the following abnormalities in granulocytic progenitor cells (CFU-G): a decrease in the concentrations of G-cluster forming cells, stimulated by a maximal dose of G-CSF, and a tendency of abnormally low responsive growth of the CFU-G to lower concentrations of G-CSF and GM-CSF. Our findings suggest that administration of G-CSF at relatively low doses overcomes or compensates for these abnormalities, though not completely, as fluctuation in the neutrophil counts persisted.
Bone Marrow↗
Effect of sodium chloride on pirarubicin induced cell killing in P388 mouse leukemia cells.
The effect of sodium chloride on the cytotoxicity of 4'-O-tetrahydropyranyldoxorubicin (pirarubicin), a novel anthracycline derivative, was investigated on P388 mouse leukemia cells in vitro. The modifications in efficiency of uptake and killing action of pirarubicin were found to be dependent on the ionic strength of the medium. The relationship between intracellular drug accumulation into cells and cell killing was pointed out.
Animals↗