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Biomedical subjects

M Toki

Publications and source records attributed to M Toki.

15 recordsLinked to original sources
PubMed2005

A prospective randomized trial of either famotidine or omeprazole for the prevention of bleeding after endoscopic mucosal resection and the healing of endoscopic mucosal resection-induced ulceration.

BACKGROUND: It has been reported that inhibitors of gastric acid secretion prevent bleeding after endoscopic mucosal resection for mucosal gastric neoplasm. However, uncertain whether an histamine2-receptor antagonist or proton-pump inhibitor is more effective. AIM: To evaluate prospectively the effectiveness of famotidine or omeprazole for ulcer management after endoscopic mucosal resection. METHODS: From July 2003 to October 2004, 57 patients were randomly assigned to famotidine or omeprazole for the management of endoscopic mucosal resection. Both drugs were given intravenously for the first 2 days, thereafter by mouth. The bleeding rates after endoscopic mucosal resection, the effects on the healing of endoscopic mucosal resection-induced ulceration, and cost-benefits were compared. RESULTS: Twenty-eight patients received famotidine and 29 received omeprazole. No significant difference was observed between the two groups in patient characteristics. The bleeding rates after endoscopic mucosal resection were not significantly different (18% vs. 14%) between the groups. Similarly, no differences were seen in the size of the endoscopic mucosal resection-induced ulceration at 1, 30 and 60 days after resection between groups. The total costs of anti-secretory agents demonstrated a significant cost-benefit to those treated with famotidine (10,420 yen vs. 17,782 yen). CONCLUSIONS: Famotidine is suggested as a better alternative to omeprazole for the management of endoscopic mucosal resection, as it showed a clear cost-benefit, and the healing results after endoscopic mucosal resection were similar for the two treatment strategies.

Aged↗
PubMed1999

Identification of IFN-gamma-producing cells in IL-12/IL-18-treated mice.

Both IL-12 and IL-18 have been characterized as effective IFN-gamma-inducing cytokines. Concomitant treatment with IL-12 and IL-18 has been shown to synergistically induce IFN-gamma and may be an effective therapy for treating cancer, allergy, and infectious diseases. To understand the mechanisms underlying the strong induction of IFN-gamma by IL-12/IL-18 in mice, we focused our studies on the IFN-gamma-producing cells in various lymphoid organs and tissues and utilized the intracellular cytokine staining method to detect such cells in situ. After combined treatment with IL-12 and IL-18, IFN-gamma-positive cells in C57BL/6 mice were detected in the liver (12.18%), spleen (0.68%), bone marrow (1.80%), and peritoneum (2.12%), but not in the thymus or lymph nodes (<0.05 and <0.08%, respectively). A two-color staining method revealed that the majority of IFN-gamma-producing cells in the liver were NK1.1(+) cells, while those in the spleen were mostly CD3(+) cells, and to a lesser degree NK1.1(+) cells. Both CD4(+) and CD8(+) cells in the liver and in the spleen produced IFN-gamma. The CD19(+) B cell population was not definitely shown to produce IFN-gamma in our induction experiments. NKT cells, which are a subpopulation of NK1. 1(+) CD3(+) cells, were diminished in the liver and did not seem to contribute to IFN-gamma production arising from IL-12/IL-18 treatment. Further in vitro experiments confirmed the responsiveness of hepatic mononuclear cells to IL-12/IL-18 stimulation. This study is the first to show the IFN-gamma-producing mechanisms of IL-12/IL-18 treatment at the phenotypic level.

Animals↗
PubMed1999

Interobserver and intraobserver variation in endoscopic assessment of GERD using the "Los Angeles" classification.

BACKGROUND: A new endoscopic classification of gastroesophageal reflux disease (GERD) has been proposed, and the term mucosal break has been introduced to describe mucosal damage. This new classification was evaluated by endoscopists with different levels of experience. METHODS: Fifty endoscopic photographs for each of 20 randomly selected patients with GERD were assessed retrospectively by three groups of seven endoscopists classified by experience: group 1 (100 to 500 procedures), group 2 (500 to 3000), and group 3 (more than 3000). The new classification was modified by adding grade 0 to describe healed mucosal breaks, so that there were five grades. All photographs were assessed twice at an interval of more than 1 week, and kappa statistics were used to determine observer variation. RESULTS: Interobserver variation within group 3 (kappa = 0.39, n = 21) and between groups 3 and 2 (kappa = 0.36, n = 49) was significantly different (p < 0.01) from that between groups 3 and 1 (kappa = 0.26, n = 49). Intraobserver variation in group 1 (kappa = 0.39, n = 7) was significantly different (p < 0.01) from that in group 2 (kappa = 0.51, n = 7) and group 3 (kappa = 0.54, n = 7). CONCLUSIONS: Observer variation depends on level of endoscopic experience. Only experienced endoscopists should use the new classification for grading of GERD.

Adult↗
PubMed1999

Sesterterpenoids and diterpenoids of the wax excreted by a scale insect, Ceroplastes pseudoceriferus.

A new sesterterpene, (2Z,6Z,10E)-cericerene-15,24-diol (1), and its 30-hydroxytriacontanoate (2) were isolated from the wax exuded by the scale insect Ceroplastes pseudoceriferus, together with the acetates and 30-hydroxytriacontanoates of 3,15-dihydroxy- and 15, 20-dihydroxylabda-7,13-diene (3-6). The absolute configurations of the labdadiene alcohols were antipodal to the ordinary labdanes isolated from terrestrial plants.

Animals↗
PubMed1997

In vitro study using leukemia cell line panel to demonstrate rapid thymic T cell death due to contact with HIV-1 carrier cell clones.

A rapid (within 1 h) and profound cytotoxic cell death of immature TdT+CD4+CD8+ and/or TdT+CD4+ thymic T cell type leukemia cell lines, and of normal thymocyte populations rich in TdT+CD4+CD8+ cells was induced by contact with some human immunodeficiency virus type-1 (HIV-1) carrier T cell clones. This cytotoxic reaction, without requiring a complete viral replication cycle in the thymic T cells, did not occur in any mature CD4+CD8+ and/or CD4+ T cells which are otherwise permissive for virus infection. Although it was not an antigen-specific cytotoxic reaction, the rapid and profound thymic T cell destruction was shown, at the individual clonal level, to be triggered specifically by the binding of CD4 molecules on thymic T cells with gp120/gp160 on HIV-1 carrier clones. The present study suggesting direct elimination of immature T cells by contact with some HIV-1-infected T cells, may provide a novel insight into the mechanism responsible for the mature CD4+ T cell depletion in HIV-1 infection.

Antigens, CD↗
PubMed1997

Acquired cytotoxic activity of CD8+ HIV-1IIIB carrier immature T cell clones specific to CD4+CD8+ (parental) human T cell clones and normal thymocytes.

By infecting human leukemia cell lines in vitro with HIV-1IIIB' a number of HIV-1 carrier clones were generated. Among them, 5 of 13 CD8+ HIV-1 carrier T cell clones were shown to acquire a rapid cytotoxic activity (within 1 hour) specific to TdT+CD4+CD8+ immature T cells including normal thymocytes. This novel cytotoxic reaction, without requiring virus infection and indicating a rapid T cell precursor elimination during active lymphopoiesis, suggests a mechanism responsible for mature CD4+ T cell depletion in HIV-1 infected individuals.

Antigens, CD↗
PubMed1991

Comparative efficacy of acid reflux inhibition by drug therapy in reflux esophagitis.

The advent of histamine H2 receptor antagonists (H2-RA) has allowed the treatment of reflux esophagitis (RE) to be controlled over a relatively long term. The authors have experienced some cases resistant to H2-RA, but it was revealed that these cases can be successfully treated with proton pump inhibitors. It has been suggested that esophagogastric dysmotility can lead to RE. RE has been treated for many years by using GI-prokinetic agents, which theoretically inhibit acid reflux and improve esophageal acid clearance. In order to compare the effects on acid reflux of an H2-RA (famotidine), a proton pump inhibitor (omeprazole) and a GI-prokinetic agent (cisapride), we measured the 24-hour pH in the esophagus and stomach simultaneously, before and after treatment in 17 patients with RE. It was found that the proton pump inhibitor was the most effective drug for inhibiting esophageal acidification, followed by famotidine and then cisapride. Furthermore, we found that cisapride often actually exacerbated acid reflux. The differences in inhibitory effects on acidification allowed us to draw conclusions regarding the treatment of RE. It was concluded that the stronger the inhibitory effect of a drug on acid secretion, the more useful it was in the treatment of RE. The GI-prokinetic drug did not inhibit acid reflux as much as we had expected.

Adult↗