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Biomedical subjects

S Tsuruta

Publications and source records attributed to S Tsuruta.

At least 55 records · Page 3Linked to original sources
PubMed1998

Infantile hemangioendothelioma of the thymus with massive pleural effusion and Kasabach--Merritt syndrome: histopathological, flow cytometrical analysis of the tumor.

Infantile hemangioendothelioma of the thymus is a rare disease. We describe a patient who developed a large anterior mediastinal mass, severe thrombocytopenia and massive pleural effusion at 1 month of age. Glucocorticosteroid and irradiation therapy had no effect on either the tumor size or clinical symptoms and the tumor was resected subtotally. Three months after the subtotal resection, the remaining tumor had almost disappeared and the symptoms had resolved. The patient has now been well for 1 year after surgery without evidence of recurrence. The tumor tissue was characterized by prominent vascular endothelial proliferation intermixed with a normal thymic structure, producing a picture consistent with that of an infantile hemangioendothelioma in the thymus. Immunohistochemically, the tumor cells showed positive staining for vimentin, factor VIII and CD34. The DNA stemline and proliferative activity were examined by flow cytometry, which revealed a diploid stemline with a low growth fraction. DNA content and cell cycle analyses of the tumor tissue may be useful for predicting the biological behavior of the tumor.

DNA, Neoplasm↗
PubMed1998

Retrovirus-mediated gene therapy for human hepatocellular carcinoma transplanted in athymic mice.

Gene therapy using a retrovirus vector carrying herpes simplex virus thymidine kinase gene under the control of the 0.3-kb human alpha-fetoprotein (AFP) gene promoter (LNAF0.3TK virus) in combination with ganciclovir (GCV) treatment was performed in athymic mice harboring AFP-producing HuH-7 human hepatoma cells. GCV treatment resulted in pronounced growth inhibition of the virus-infected HuH-7 xenograft in mice, but did not affect growth of the parental xenograft. These results indicate that the AFP gene promoter sequence allows enough therapeutic gene expression to induce the GCV-mediated cytotoxicity in vivo in AFP-producing human hepatoma cells.

Animals↗
PubMed1998

[Measurement of Candida-specific lymphocyte proliferation by flow cytometry in children with atopic dermatitis].

To study a role of Candida albicans in the development of atopic dermatitis (AD) from the viewpoint of cellular responses, we measured Candida-specific lymphocyte proliferation by flow cytometry in children with AD. There was no apparent age-dependent change in the level of Candida-SIF (stimulation index measured by flow cytometry) in either AD or non-atopic control subjects. The level of Candida-SIF was significantly higher in AD patients than in non-atopic controls (178.0 +/- 89.3 vs 137.9 +/- 37.6, p < 0.02), and the incidence of subjects with the elevated Candida-SIF level (> or = 200) was significantly higher in AD patients than in non-atopic controls (27.9% (17/61) vs 2.6% (1/38), p < 0.005). There was no correlation between the levels of Candida-SIF and Candida-specific IgE antibody. These results suggest that Candida albicans contributes to the development of AD in some patients not only by Type I, but also by Type IV hypersensitivity reactions.

Adolescent↗
PubMed1997

Mechanism of cardiac involvement in the WBN/Kob rat.

The cardiac characteristics of the WBN/Kob rat resemble those of rats with catecholamine-induced myocarditis. To determine the etiology of these WBN cardiac characteristics, we assessed the number and affinity of beta-adrenergic receptors, and investigated adenylate cyclase activity, the cardiac myocyte cyclic adenosine monophosphate (cAMP) concentration and the activity of guanosine triphosphate (GTP)-binding protein in 3-month-old WBN/Kob rats. Age-matched Wistar rats served as controls. The mean number of beta-adrenergic receptors was similar in WBN/Kob and Wistar rats (28.0+/-9.1 v 28.3+/-8.9 fmol/mg protein), and there was no significant difference in beta-adrenergic receptor affinity between groups (1.09+/-0.54 v 1.26+/-0.60 nM). The mean cAMP concentration in cardiac myocytes was significantly higher in WBN/Kob rats than in Wistar rats 1975.6+/-247.8 v 344.9+/-83.6 pmol/g wet tissue), (P=0.0112) as was adenylate cyclase activity (33.61+/-8.32 v 24.3+/-12.78 pmol/mg/min), (P=0.0174). The activity of GTP-binding protein was significantly higher in WBN/Kob rats than in Wistar rats. After a beta-agonist binds to a beta-adrenergic receptor, activated adenylate cyclase produces cAMP in myocytes, which in turn opens the Ca2+ channel, leading to an influx of Ca2+ into myocytes. Our results suggest that the increase in adenylate cyclase activity in WBN/Kob rats have led to an increase in the cAMP concentration in myocytes. This process may have resulted in excessive beta-adrenergic activity due to high activity of GTP binding protein in WBN/Kob rats, which may explain the hypersensitivity of WBN/Kob rats to isoproterenol and the development of catecholamine-induced myocarditis.

Adenylyl Cyclases↗
PubMed1997

Inhibition of nifedipine metabolism in dogs by erythromycin: difference between the gut wall and the liver.

The purpose of this study was to evaluate possible interaction of nifedipine with erythromycin or rokitamycin in the intestinal mucosa. Male beagle dogs were orally administered nifedipine (10 mg), with or without oral pre-medication with erythromycin (300 mg), and 300 mg erythromycin or rokitamycin twice a day for 3 days. The experiments were of randomized cross-over design with a two-week wash-out period between dosing regimens. Erythromycin pre-medication for 3 days resulted in a significant increase in the area under the serum nifedipine concentration-time curve (AUC), whereas the curve for one nifedipine metabolite (M-2) decreased significantly. When the effects of erythromycin on the metabolism of nifedipine were studied using dog liver microsomes it was found that erythromycin significantly inhibited formation of M-2 but not of the metabolite M-1. These results indicate that formation of M-2 from M-1 in the liver might be reduced by erythromycin pre-medication. To avoid possible metabolism in the gut, the dogs were then administered 8 mg nifedipine into the peritoneal cavity, with or without multiple dose pre-treatment with erythromycin for 3 days. After intraperitoneal administration of nifedipine, the maximum concentration (Cmax) of nifedipine increased significantly. After pre-administration of erythromycin the relative bioavailability of nifedipine after oral administration was increased compared with injection into the peritoneal cavity. In-vitro study using rat intestinal microsomes and the in-vivo rat intestinal loop technique also showed that pre-administration of erythromycin inhibits nifedipine metabolism in the small intestine.

Animals↗
PubMed1997

Effects of erythromycin, clarithromycin and rokitamycin on nifedipine metabolism in rats.

The effects of erythromycin, clarithromycin and rokitamycin on the metabolism of nifedipine were studied in vitro and in situ. Erythromycin, clarithromycin or rokitamycin added to nifedipine did not inhibit the formation of metabolite, M-1, of nifedipine, whereas pretreatment with erythromycin or clarithromycin significantly (p < 0.05) inhibited its formation. Only erythromycin significantly (p < 0.05) inhibited the formation of M-2 from M-1. These observations agreed with the results obtained using an in situ rat intestinal loop technique. As assessed by the concentrations of nifedipine and M-2 in jugular and portal vein blood, the inhibition of nifedipine metabolism by erythromycin was greater after multiple doses than after a single dose. Moreover, our results suggest that rokitamycin is a less potent inhibitor of nifedipine metabolism.

Animals↗
PubMed1997

[Enhanced lymphocyte proliferative response to house dust mite in infants with atopic dermatitis].

Allergen-specific lymphocyte proliferation was measured in 24 children with atopic dermatitis and 20 non-atopic controls. The level of house dust mite-specific S.I.F. (stimulation index measured by flow cytometry) in the atopic children was significantly higher than that in the non-atopic controls in every age-group, suggesting that the elevation of the mite-specific S.I.F. level is related to the development of atopic dermatitis. The level of house dust mite-specific S.I.F. correlated significantly with the level of house dust mite-specific IgE-RAST in older children (r < 0.73, p < 0.001), indicating that S.I.F. reflects the activity of lymphocytes competent to promote the production of IgE. In the atopic infants, there was no significant positive correlation between the levels of mite-specific S.I.F. and mite-specific IgE-RAST since, although the former was usually elevated the latter was often very low or negative. The result suggests that the sensitization of T lymphocytes to house dust mite begins as early as in infancy prior to the development of mite-specific IgE antibody.

Adolescent↗
PubMed1997

[Enhanced lymphocyte proliferative response to house dust mite in the older but not in the younger asthmatic children].

Allergen-specific lymphocyte proliferation was measured by flow cytometry in 16 children with atopic dermatitis (AD). 26 with bronchial asthma (BA) and 13 non-atopic controls. Although the level of mite-S.I.F. (stimulation index measured by flow cytometry) in the younger AD children (2-7 y) was significantly higher than that in the non-atopic subjects (189.6 +/- 70.7 vs 113.9 +/- 11.0, p < 0.02), there was no elevation in the younger BA children (122.6 +/- 23.4). It is therefore likely that the elevated mite-S.I.F. level is related to the development of the allergic cellular inflammation representing the pathology of AD, rather than the IgE-mediated allergic reaction as a mechanism of childhood BA. Because the level of mite-specific IgE antibody in the younger BA children is elevated (93.6 +/- 41.2 PRU/ml), the result also indicates that mite-specific peripheral T lymphocytes do not play a critical role in stimulating the mite-specific IgE synthesis. On the contrary, the older BA children (8-15 y) showed an elevated mite-S.I.F. level (176.0 +/- 54.6) significantly higher than that in the non-atopic subjects (114.6 +/- 13.9, p < 0.05) as well as that in the younger BA children (p < 0.05). Because other investigators have reported that the level of mite-specific lymphocyte proliferation is increased in the adult BA patients, the transition from childhood BA to adult-type BA may start at the age of about 8 y.

Adolescent↗
PubMed1997

[Close positive correlation between the level of mite-specific lymphocyte proliferation and the percentage of peripheral blood eosinophils in infants with atopic dermatitis].

Eosinophils (Eo) are known to play a critical role in the chronic allergic inflammation, featuring pathologically in atopic dermatitis (AD), and the Eo percentage in the peripheral blood is elevated in AD infants (0 y) as well as in older AD children (3-15 y). In search of the most important factor in the increase of Eo percentage, we analyse the correlation between the level of Eo percentage in the peripheral blood and the levels of various allergy-related parameters. In AD infants, the level of Eo percentage was found to be correlated most strongly with the level of mite-specific lymphocyte proliferation expressed by S.I.F. (stimulation index measured by flow cytometry) (r = 0.88, p < 0.001). It also correlated significantly with the levels of serum IgE (r = 0.56, p < 0.05), egg white-specific IgE-RAST (r = 0.64, p < 0.01) and egg white-specific S.I.F.(r = 0.59, p < 0.02), but not with the levels of mite-specific IgE-RAST or candida-specific S.I.F. On the contrary, the level of Eo percentage correlated most intimately with the levels of serum IgE (r = 0.73, p < 0.001) and mite-specific IgE-RAST (r = 0.71, p < 0.001) in older AD children. These results suggest that mite-specific peripheral blood helper T lymphocytes, the proliferation of which is thought to be represented by S.I.F., play a more essential role in AD infants than in older AD children in the increase of Eo percentage in the peripheral blood.

Adolescent↗
PubMed1996

Preparation of specific antiserum to 17 alpha-estradiol 17-N-acetylglucosaminide.

A specific enzyme immunoassay (EIA) method has been developed for 17 alpha-estradiol 17-N-acetylglucosaminide as a model compound instead of 15 alpha-hydroxyestrogen 15-N-acetylglucosaminides. Two new haptens, 3-(omega-carboxyalkyl) ether derivatives of 17-alpha-estradiol 17-N-acetylglucosaminide, were synthesized and conjugated with bovine serum albumin (BSA). The EIA was newly established using specific antiserum elicited against 3-(1-carboxypropyl) ether of 17 alpha-estradiol 17-N-acetylglucosaminide (17NAG CPE)-BSA conjugate and beta-galactosidase-labeled 17NAG CPE as a labeled antigen. An appropriate dose-response curve of EIA for 17 alpha-estradiol 17-N-acetylglucosaminide was obtained in the range of 20-1000 pg/tube. The specificity of EIA proved to be satisfactory in terms of cross-reactivities to related compounds including 15 alpha-N-acetylglucosaminides. The proposed method will be applicable to the preparation of antisera for use in EIA of 15 alpha-hydroxyestrogen 15-N-acetylglucosaminides.

Acetylglucosamine↗
PubMed1996

Influence of storage humidity on hardness of light-cured glass polyalkenoate cements.

The influence of storage in various environments on the hardness of four commercial light-cured glass polyalkenoate cements and one conventional glass polyalkenoate cement was investigated. Specimens with or without light exposure were stored for 7 days in different humidity conditions. A hardness tester with a diamond indenter point was used and Vickers hardness numbers under minor load conditions were determined. Non-light-exposed specimens did not increase in hardness in either dry or wet conditions. Light-exposed specimens became harder with time in dry conditions. Light-exposed specimens stored in wet conditions hardened only slightly. To investigate the effects of humidity, some light-exposed specimens stored first in wet conditions were stored another 7 days in dry conditions. They became as hard as those first stored in dry conditions for 7 days. It is concluded that the hardness of these cements corresponds with the humidity of the storage environment.

Acrylic Resins↗
PubMed1996

[Measurement of proliferation of allergen-stimulated peripheral blood lymphocytes by flow cytometry].

The percentage of S-phase cells in peripheral blood mononuclear cells (PBMC) from 14 atopic and 6 non-atopic subjects was measured by flow cytometry after stimulation with mite allergen (Der f) for 6 days and converted to the stimulation index (S.I.F.: stimulation index measured by flow cytometry). S.I. F. showed a close positive correlation with the serum IgE level (r = 0.67, p = 0.001). S.I.F. in the atopic subjects was significantly higher than in the non-atopic subjects (165.6 +/- 49.8 vs 113.2 +/- 12.2, p < 0.05). S.I.F. in subjects with a high (> or = 100 PRU/ml) IgE-RAST level for mite allergen Der p was significantly higher than that in subjects with a negative RAST level (178.4 +/- 53.8 vs 113.2 +/- 12.2, p < 0.02). Flow-cytometric measurement of the proliferation of PBMC in response to allergenic stimulation may be a useful method for studying the immunological abnormality present in atopic subjects.

Adolescent↗
PubMed1995

[Two-color flow cytometry analysis of lymphocyte subsets in patients with acute myocardial infarction and post-myocardial infarction syndrome].

Serial changes in lymphocyte subsets were analyzed in 37 patients with acute myocardial infarction (AMI), in 2 patients with postmyocardial infarction syndrome (PMIS), and in healthy subjects (control group) using two-color flow cytometry to investigate cellular immunity after AMI and PMIS. Peripheral blood lymphocyte subsets were measured on admission and at weeks 2, 4, 8, and 16 after the onset of AMI. The white blood cell count was significantly higher on admission and at week 2 in the AMI group compared with the control group. The percentage of CD4-positive helper T cells was significantly higher on admission and at weeks 2 and 4 in the AMI group compared with the control group, and the percentage of CD8-positive suppressor T cells was significantly lower in the AMI group at week 2 than in the control group. The ratio of helper-to-suppressor T cells peaked 2 weeks after the AMI and then decreased gradually. There were no significant changes in the CD4/CD8 ratio, the percentage of cytotoxic T cells, or the percentage of inducer T cells, throughout the observation period. There were no significant differences in the percentage of T cells, B cells, CD4-positive T cells, CD8-positive T cells, and natural killer cells between AMI patients and control subjects. The percentage of activated CD4- and CD8-positive cells was higher in the AMI group at weeks 4 and 8 than in the control group. There was no significant correlation between changes in lymphocyte subsets and infarct size. The percentage of activated CD8-positive cells was consistently higher in the PMIS group compared with the control and AMI groups. The percentage of cytotoxic T cells in one of the PMIS patients was significantly higher than in the AMI group. There were no significant differences in the proportions of other subsets between PMIS and AMI patients. The changes in lymphocyte subsets observed in patients with AMI suggested that immunological competence was enhanced in these patients. Abnormalities in humoral immunity, such as the appearance of anticardiac antibody, have been observed in patients with PMIS. Our results suggest that PMIS is also associated with changes in cellular immunity.

Adult↗
PubMed1994

Homologous dinucleotide (GT or TG) deletion in Japanese patients with chronic granulomatous disease with p47-phox deficiency.

The cytosolic 47-kDa protein designated as p47-phox (phagocyte oxidase) is one of the essential components of the superoxide-generating system in phagocytes, and its defect is known to cause chronic granulomatous disease (CGD). Five unrelated CGD patients with p47-phox deficiency were found among 82 CGD patients in Japan. We sequenced the cDNAs and the genomic DNAs corresponding to p47-phox derived from these patients. In all cases examined, the defect was identified to be a GT (or TG) dinucleotide deletion at bases 75/76 (or 74/75, respectively) in the coding sequence for the protein. The same mutation was reported previously for a total of 9 alleles from 5 CGD patients in England and in the United States. It seems, therefore, that the dinucleotide GT deletion is the common mutation in 47-phox deficient CGD due to certain structural issues.

Adolescent↗
PubMed1994

Treatment of hepatocellular carcinoma with transcatheter arterial embolization. Analysis of prognostic factors.

BACKGROUND: Transcatheter arterial embolization (TAE) is a useful treatment modality for hepatocellular carcinoma (HCC). To study the prognostic factors, survival time of patients with HCC after TAE was analyzed retrospectively using clinical manifestations of coexisting liver cirrhosis and clinical features of HCC. METHODS: Eighty-seven patients with HCC were treated with TAE between 1984 and 1991 and observed at Nagasaki University Hospital. All the patients also had liver cirrhosis. RESULTS: The survival time of the 87 patients after TAE ranged from 2 months to 8.1 years (mean +/- standard deviation, 2.7 +/- 0.3 years). Survival curves after TAE did not differ between men and women (P > 0.5) or between hepatitis B and C viral infection (P > 0.8), but they depended on clinical stages of coexisting liver cirrhosis (P < 0.01). The cumulative survival after TAE was significantly longer in patients with uninodular tumors than in patients with multinodular tumors (P < 0.0001) (3-year survival, 53.3% vs. 13.3%; 5-year survival, 32.2% vs. 3.3%, respectively). In contrast, patients' survival time was not associated with the size of the tumor detected at the time of treatment with TAE (P > 0.1). CONCLUSIONS: Treatment of HCC with TAE is well indicated regardless of tumor size for patients with nonadvanced liver cirrhosis and uninodular tumors. Alternatively, treatment of HCC with TAE alone is still insufficient in patients with multinodular tumors. Other treatment modalities in combination with TAE should be considered to achieve a more favorable prognosis of these patients.

Adult↗
PubMed1994

Involvement of CD11b/CD18 in enhanced neutrophil adhesion by Fc gamma receptor stimulation.

Neutrophils showed a rapid and transient adhesion to immunoglobulin G (IgG)-coated plates compared with their adhesion to bovine serum albumin (BSA)-coated plates: the adhesion reached a peak after 15 min of incubation and then gradually returned to almost the basal state in 60 min. The addition of monomeric IgG or anti-Fc gamma RII monoclonal antibody (mAb) (IV.3) suppressed the increase in adhesion, whereas anti-Fc gamma RIII mAb (3G8) was hardly effective, indicating that the interaction of Fc gamma R, especially Fc gamma RII, with coated IgG is involved in the process. Adhesion was also blocked by cytochalasin B, suggesting that functional actin filament structures are crucial. Protein kinase inhibitors, erbstatin and genistein, inhibited the adhesion in a dose-dependent manner. The adhesion was inhibited by anti-CD11b (M1/70) and anti-CD18 (MHM23, TS1/18) mAbs. Moreover, neutrophils from a patient with complete leukocyte adhesion deficiency syndrome did not show increased adhesion to IgG-coated plates. The adhesion of neutrophils to fibrinogen- and BSA-coated plates was also increased when Fc gamma R was stimulated in the fluid phase with soluble aggregated IgG, which was also inhibited by anti-CD11b mAb. Stimulation of neutrophil Fc gamma R with soluble aggregated IgG enhanced the expression of CD11b in concert with the enhanced adhesion. These data collectively suggest that stimulation via Fc gamma R evokes a tyrosine kinase-dependent and actin filament-dependent intracellular signal that enhances the specific and nonspecific adhesive activity of neutrophils, presumably through the activation of CD11b/CD18.

Adult↗
PubMed1994

Genotoxic activities in vivo of cobaltous chloride and other metal chlorides as assayed in the Drosophila wing spot test.

A series of metal chlorides were subjected to the wing spot test of Drosophila melanogaster. In the test, larvae trans-heterozygous for the wing-hair mutations mwh and flr were orally treated at the third instar stage with a test compound and the wings were inspected at the adult stage for spots expressing phenotypes of the markers. CoCl2, MnCl2, MoCl3, NiCl2 and ZnCl2 were clearly effective in inducing spots with one or two mutant hairs (small spots). CoCl2 was clearly effective in inducing spots with three or more mutant hairs (large spots) as well. CrCl3, FeCl2 and FeCl3 were negative under the conditions used. Based on estimated frequencies of small spots induced at the LD50, the genotoxic effectiveness of the positive metal salts were ranked in a sequence of CoCl2 > ZnCl2 > MoCl3 > (MnCl2, NiCl2). Since CoCl2 did not induce large spots in the wings of the mwh/TM3 flies with a suppressed ability of mitotic crossing-over, the large spots induced by this compound in the mwh/flr system were ascertained as mutant clones due to mitotic crossing-overs.

Animals↗