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Biomedical subjects

K Furusho

Publications and source records attributed to K Furusho.

At least 73 records · Page 4Linked to original sources
PubMed1995

Interleukin 8 (IL-8) inhibits the interleukin 4 (IL-4)-induced but not the spontaneous growth of human B cells via mechanisms that may involve protein kinase C.

IL-8 inhibited the IL-4-induced but not the spontaneous growth of both a human B cell line, CBL, and in vivo activated B cells. This inhibition was specific to IL-8, since anti-IL-8 mAb, but not control IgG1, blocked inhibition. Phorbol 12, 13 dibutyrate did not affect the IL-4-induced B cell growth; however, it reversed the IL-8-mediated inhibition, and this reversal was blocked by H7 (a protein kinase C inhibitor), but not by H8 (a protein kinase A inhibitor). These results indicate that IL-8 inhibits IL-4-induced B cell growth via specific mechanisms that may involve protein kinase C.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1995

Involvement of interleukin (IL)-13, but not IL-4, in spontaneous IgE and IgG4 production in nephrotic syndrome.

Nephrotic syndrome (NS) is a renal disease characterized by proteinuria and hypoalbuminemia. In NS patients without any allergic disease, serum IgE and IgG4 levels were selectively increased, and peripheral blood mononuclear cells (MNC) spontaneously produced IgE and IgG4. T cells produced interleukin (IL)-13 spontaneously, and B cells constitutively expressed IL-13 receptors (IL-13R). In addition, T cells stimulated surface IgE-negative (sIgE-) and sIgG4- B cells to produce IgE and IgG4, respectively, and IgE and IgG4 production was specifically blocked by anti-IL-13 antibody (Ab). MNC from atopic dermatitis (AD) patients also produced IgE and IgG4 spontaneously. However, in AD patients, T cells spontaneously produced IL-4, but not IL-13, and B cells constitutively expressed IL-4R, but not IL-13R. T cells stimulated sIgE- and sIgG4- B cells to produce IgE and IgG4, respectively, and the production was specifically blocked by anti-IL-4 Ab. On the other hand, sIgE+ and sIgG4+ B cells from both NS and AD patients spontaneously produced IgE and IgG4, respectively, and this production was not affected by T cells, anti-IL-4 Ab, or anti-IL-13 Ab. These results indicate that IL-13 is involved in the enhanced production of IgE and IgG4 in NS, while IL-4 is involved in these responses in AD.

Adolescent↗
PubMed1995

Physical interaction with monocytes rescues human mature CD4+ T-cell lines from anti-CD3-induced apoptosis.

Crosslinking of the TcR-CD3 complex with immobilized anti-CD3 antibodies without sufficient co-stimulation induced cell death in human mature CD4+ T-cell lines. In these T cells, DNA fragmentation and morphological characteristics of apoptosis were seen. The anti-CD3-induced apoptosis was inhibited by co-culture with monocytes. The rescue signal provided by monocytes does not need to be present simultaneously with signals mediated by anti-CD3. When T cells were precultured with monocytes for 24 h before anti-CD3 stimulation and then the monocytes were removed from the culture, anti-CD3-induced T-cell apoptosis was also inhibited. To determine whether the monocyte-derived rescue signals were transduced by soluble factors or by direct cell-to-cell interaction with monocytes, we precultured T cells with monocytes separated by a micropore membrane which prevented T cell-monocyte physical interaction but not the diffusion of secreted molecules. In this system, rescue signals could not reach the T cells. To further assess the importance of physical interaction, we precultured T cells with fixed monocytes. T cells could not be rescued from apoptosis under these experimental conditions, either. The results considered collectively suggest that sufficient physical interaction with viable monocytes is important for the rescue of anti-CD3-induced apoptosis of CD4+ T cells.

Antibodies, Monoclonal↗
PubMed1995

Somatic cell mutation frequency at the HPRT, T-cell antigen receptor and glycophorin A loci in Cockayne syndrome.

Skin fibroblasts of patients with Cockayne syndrome (CS) are hypersensitive to the lethal or mutagenic effect of ultraviolet light, which may cause genetic instability. Up to now, however, no systematic study of in vivo somatic cell mutation in CS cells has been reported. This article describes our investigation of the mutation frequencies (Mfs) at three different loci, i.e. hypoxanthine-guanine phosphoribosyl transferase (HPRT), T-cell antigen receptor (TCR) and glycophorin A (GPA), in six patients with CS. Mfs at the HPRT and TCR loci were found to be within the normal range as determined in age-matched controls. In the GPA locus of two patients, there was a slight increase, but it was much smaller than that reported in other DNA repair deficient syndromes. The frequency of spontaneous HPRT mutation in Epstein-Barr virus transformed B-lymphoblastoid cells derived from CS patients was similar to that in cells from normal children. The molecular characterization of the representative HPRT mutant T cell clones from CS patients did not show any structural alterations. These results may explain, at least in part, why CS is not associated with predisposition to cancer.

Adolescent↗
PubMed1995

Role of LFA-1/ICAM-1-dependent cell adhesion in CD40-mediated inhibition of anti-IgM antibody-induced B-cell death.

Cross-linking of surface IgM by anti-IgM antibody caused activation-induced cell death of a surface IgM+, IgD+ human B lymphoma cell line, B104. The dying B104 cells did not show the morphology of apoptosis but did show that of necrosis. However, anti-IgM antibody caused apoptosis of another surface IgM+, IgD+ human B lymphoma cell line, DND-39. The influx of extracellular Ca2+ was necessary for the cell deaths of B104 and DND-39 caused by anti-IgM antibody. Their cell deaths were inhibited by cyclosporine. The anti-IgM antibody-induced cell death of DND-39, but not that of B104, was prevented by costimulation with anti-CD40 antibody. In human peripheral blood B-cells, anti-IgM antibody inhibited cell cycle transition induced by Staphylococcus aureus Cowan I at the G2/M interphase without inhibition of DNA synthesis. In this system, too, anti-CD40 antibody canceled the inhibitory signal transduced through surface IgM and increased the number of M phase cells. Blocking antibodies against the leukocyte function-associated antigen-I/intercellular adhesion molecule-1 system decreased the rescue effect of anti-CD40 antibody in both DND-39 cells and peripheral B-cells, which shows that leukocyte function-associated antigen-1/intercellular adhesion molecule-1-dependent cell adhesion plays an important role in the CD40-mediated inhibition of surface IgM-mediated negative signals.

Animals↗
PubMed1995

Interferon-alpha treatment for severe atopic dermatitis.

Patients with both severe atopic dermatitis (AD) and chronic myeloid leukemia, chronic hepatitis B, or chronic hepatitis C were treated with interferon-alpha (IFN-alpha). IFN-alpha treatment improved AD. Moreover, there were also significant decreases in serum IgE and IgG4 levels and in in vitro spontaneous IgE and IgG4 production by patients' mononuclear cells.

Adolescent↗
PubMed1995

IgM-mediated B cell apoptosis.

Cross-linking of surface immunoglobulin M (sIgM) on normal mature B cells induces different signaling consequences, including DNA synthesis (positive signaling) and cell cycle arrest and/or death by apoptosis (negative signaling). Presumably, the difference depends on the intensity of sIgM cross-linking: relatively weak cross-linking induces DNA synthesis, moderate cross-linking induces DNA synthesis with cell cycle arrest at the G2/M interphase, and intense cross-linking induces apoptosis. In vivo experiments with transgenic mice have shown that relatively weak cross-linking of sIgM by soluble antigens induces anergy in autoreactive B cells, whereas intense sIgM cross-linking by membrane-bound forms of antigens induces deletion of them. However, it is still unknown whether the different intensities of sIgM cross-linking generate qualitatively different signals responsible for DNA synthesis or cell death or whether they generate qualitatively the same but quantitatively different signals, and the quantitative difference is responsible for the induction of positive or negative signaling. The sIgM-mediated negative signaling presumably plays an important role in the induction and maintenance of B cell tolerance, and sIgD and sIgG also possess the machinery necessary for negative signaling. Negative signaling through sIgM is dependent on tyrosine kinase(s) and Ca2+ influx and is sensitive to cyclosporin A in certain types of B cells but not in all B cells. It has been suggested that there are different intracellular signaling pathways that transduce negative signaling via sIgM, and that activation-induced B cell death by sIgM cross-linking does not necessarily show DNA fragmentation and the morphology of apoptosis. On the other hand, sIgM-mediated B cell death may be inhibited in the presence of appropriate co-stimulators such as IL-4, alpha-, and beta-interferons and CD40-mediated signaling. The CD40-mediated signaling effectively inhibits sIgM-mediated B cell apoptosis in many but not all experimental systems. Although homotypic cell adhesion through the LFA-1/ICAM-1 dependent pathway was shown to be involved in certain types of CD40-mediated inhibition of sIgM-mediated negative signaling, it is still not known how the cytokines and CD40-mediated signaling inhibit sIgM-mediated B cell death. The molecular mechanisms responsible for sIgM-mediated negative signaling and for the inhibitory signaling against sIgM-mediated negative signaling need further elucidation.

Animals↗
PubMed1994

A multicenter, randomized, controlled trial of intravenous gamma globulin therapy in children with acute Kawasaki disease.

We studied the effect of intravenous, polyethyleneglycol-treated, human immunoglobulin, administered at 200 mg/kg per day (group A: n = 147; male 86, female 61; age < 1 year, 50) or 400 mg/kg per day (group B: n = 152; male 87, female 65; age < 1 year, 52) for five consecutive days and compared it with freeze-dried, sulfonated human immunoglobulin [group C: n = 152; male 87, female 65; age < 1 year, 51), administered at 200 mg/kg per day for five consecutive days, on the prevention of coronary artery abnormalities in Kawasaki disease. Echocardiograms were interpreted blindly and independently. Proportions of 87.1%, 95.4%, and 82.3% in groups A, B, and C, respectively, had no coronary artery abnormalities. The confidence limits of difference between the proportions of groups A and C, groups B and C, and groups B and A were -4.4% and 10.4%, 7.8% and 15.9%, and 4.0% and 10.8%, respectively. Duration of fever and serum immunoglobulin G (IgG) levels were correlated with the prevalence of coronary artery abnormalities. We concluded that intravenous, polyethyleneglycol-treated, human immunoglobulin and freeze-dried, sulfonated human immunoglobulin had clinically equivalent effects on coronary artery abnormalities, and that five daily doses of 400 mg/kg of intravenous, polyethyleneglycol-treated, human immunoglobulin is more effective than that of 200 mg/kg gamma globulin.

Acute Disease↗
PubMed1992

A case of Farber disease.

We report a case of Farber disease (Farber lipogranulomatosis). The main features were a shrill voice, joint swelling, subcutaneous nodules and retarded psychomotor development. Cytological investigation revealed intracytoplasmic inclusion bodies characteristic of Farber disease. Lipid analysis of liver tissue indicated an accumulation of ceramide containing non-hydroxy fatty acids. It was found that the acid ceramidase activity in the liver was reduced to 31% of the control value. In this patient there was also persistent diarrhea, cholelithiasis, transient proteinuria and increased urinary total sialic acids. These features have not been noted in previously reported cases.

Acid Ceramidase↗
PubMed1992

The effects of rice bran broth bathing in patients with atopic dermatitis.

We determined the effects of rice bran broth bathing therapy in 17 outpatients with atopic dermatitis. The rice bran broth used in this study was made in our hospital and distributed to the patients who dissolved it in the bathtub as a medicinal bath. In the case of one patient, redness and itching of the skin increased just after bathing. The patient subsequently discontinued therapy. We followed the other 16 patients who performed rice bran broth bathing for 2-5 months and examined their skin symptoms once a month. The efficacy of this therapy in alleviating skin symptoms was excellent in four of the 16 evaluated patients, good in seven, slightly effective in four, and ineffective in one. None of the 16 patients experienced negative effects of treatment. Recurrence of initial symptoms was not detected in any patient during rice bran broth bathing. Rice bran broth bathing therapy appears to be safe and clinically useful.

Adolescent↗
PubMed1991

Intravenous gamma-globulin for Kawasaki disease.

We studied the effect of gamma-globulin (IVGG) and aspirin (ASA) on the development of the coronary artery lesions (CAL) of Kawasaki disease (KD) in three different protocols. Within 29 days of the onset of KD the echocardiographic evidence of CAL had developed in 39-42% of the patients in the ASA group, but only in 13.7-20.8% of the patients treated with IVGG (200 or 400 mg/kg X 5). In long-term follow-up observation of CAL of these patients the evidence of CAL in both the ASA and the IVGG group regressed gradually; however, the residual rate of CAL was significantly low in the IVGG group at all times up to 24 months after onset. These facts suggest that when using IVGG for KD, we should select a dose of intact gamma-globulin, 1,000 mg/kg or more in total, to prevent the occurrence of CAL. We have demonstrated not only a significant reduction in the occurrence of CAL in patients treated with IVGG but a reduction in the residual rate of CAL for two years as compared with those treated by ASA.

Aspirin↗
PubMed1984

High-dose intravenous gammaglobulin for Kawasaki disease.

The ability of high-dose intravenous gammaglobulin (IVGG) to prevent the coronary artery lesion of Kawasaki disease has been studied in a multicentre controlled trial of IVGG plus aspirin versus aspirin alone, aspirin being the conventional treatment for Kawasaki disease. Patients were allocated at random to aspirin (45 cases) or IVGG (40 cases), there being no significant intergroup differences in age, sex ratio, duration of disease until the start of treatment, or severity. The development of coronary artery dilatation was monitored by two-dimensional echocardiography. Within 29 days of the onset of the disease, this lesion had developed in 19 cases (42%) in the aspirin group and in 6 cases (15%) in the IVGG group. There were no new instances of this lesion: in the period 30-60 days coronary artery dilatation persisted in 14 and 3 cases, respectively. In patients found to have echocardiographic abnormalities selective coronary arteriography was done 30-60 days after onset of Kawasaki disease and the lesion was confirmed in 1 of the 6 cases in the IVGG group and in 11 of the 19 controls. High-dose IVGG seems to reduce the frequency of coronary artery abnormalities in patients with Kawasaki disease.

Acute Disease↗
PubMed1982

A study of a female with congenital sideroblastic anemia.

A female infant with congenital refractory sideroblastic anemia is described. A marked reduction of delta-aminolevulinic acid (ALA) synthetase activity of erythroblasts was noticed with and without treatment of pyridoxal phosphate. Mitochondrial neutral protease activity of erythroblasts, which inactivates specifically the apo form of ALA synthetase, was normal and the sensitivity of apo form of ALA synthetase to the neutral protease was also normal. It was speculated that the reduction of ALA synthetase activity is not due to the high speed of destruction, but rather due to the impairment in production of ALA synthetase, which could explain the unresponsiveness to pyridoxine therapy in this case.

5-Aminolevulinate Synthetase↗