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S Chono

Publications and source records attributed to S Chono.

At least 19 recordsLinked to original sources
PubMed2006

Lafutidine can improve the quality of gastric ulcer healing in humans: a randomized, controlled, multicenter trial.

Improving the quality of ulcer healing (QOUH) is one of the valid methods of prevention of relapse of gastric ulcers. We investigated the effect of lafutidine on the QOUH of gastric ulcer compared with famotidine in a randomized, multi-centre controlled trial. Consecutive 80 patients with a gastric ulcer were randomly assigned to receive twice daily either lafutidine (10 mg) or famotidine (20 mg) for 12 weeks. Esophagogastroduodenoscopy was performed to examine the ulcer healing rate and rate of flat type ulcer scars using dye-contrast. The gastric ulcer healing rate was 92.1% in the lafutidine group (35/38) and 94.7% in the famotidine group (36/38). The rate of flat-type ulcer scars was significantly higher in the lafutidine group (68.4%, 26/38) than in the famotidine group (42.1%, 16/38) (P = 0.021). In conclusion, the present study demonstrated that lafutidine, as compared to famotidine, yields a significantly superior QOUH in patients with gastric ulcers in the clinical setting.

Acetamides↗
PubMed2005

Famotidine vs. omeprazole: a prospective randomized multicentre trial to determine efficacy in non-erosive gastro-oesophageal reflux disease.

BACKGROUND: Several studies in Western countries showed that proton-pump inhibitors are superior to histamine2-receptor antagonists or placebo in the treatment of non-erosive gastro-oesophageal reflux disease. The efficacy of acid-suppressive drugs for non-erosive gastro-oesophageal reflux disease in Japan, in which the prevalence of Helicobacter pylori infection is higher compared with Western countries, is unknown. AIM: To compare the efficacy of famotidine and omeprazole in Japanese patients with non-erosive gastro-oesophageal reflux disease by a prospective randomized multicentre trial. METHODS: A total of 98 patients received either famotidine 20 mg b.d. (n = 48) or omeprazole once daily (n = 50). Frequency of gastro-oesophageal reflux disease symptoms and health-related quality of life were evaluated at baseline and after 4 weeks of treatment. Complete relief was defined as no gastro-oesophageal reflux disease symptoms during the 7-day interval in week 4. RESULTS: Complete relief was achieved in 23 (48%) of patients receiving famotidine and 28 (56%) of patients treated with omeprazole. In the famotidine group, complete relief rate in H. pylori-negative patients was significantly lower than H. pylori-positive patients (35% vs. 64%). Both famotidine and omeprazole improved most scales of health-related quality of life. Omeprazole significantly improved reflux score irrespective of H. pylori infection while famotidine significantly improved reflux score in H. pylori-positive patients but not in H. pylori-negative patients. CONCLUSIONS: Omeprazole is more effective than famotidine for the control of gastro-oesophageal reflux disease symptoms in H. pylori-negative patients, while similar efficacy is observed in H. pylori-positive patients with non-erosive gastro-oesophageal reflux disease.

Anti-Ulcer Agents↗
PubMed2005

Effects of ranitidine on quality of gastric ulcer healing compared with famotidine: a randomized, controlled, multicenter trial.

Ranitidine has been found to have anti-inflammatory action as well as antisecretory action in experimental models. However, there are no reports in human gastric ulcer. The aim of this study was to investigate the effects of ranitidine compared with those of famotidine on the quality of gastric ulcer healing. We randomly assigned 69 consecutive patients with gastric ulcers to ranitidine (n = 34) or famotidine (n = 35) for 12 weeks, with endoscopic assessment of the quality of gastric ulcer healing and histological assessment of gastric mucosa 12 weeks after treatment started. Ulcer healing rates of over 95% were very similar in the two groups. The rates of ulcer scars with a flat pattern (good-quality healing) were significantly higher in the ranitidine group than in the famotidine group (per protocol, 63.0% and 34.5%, p = 0.033). The neutrophil infiltration score in the body mucosa treated with famotidine, but not ranitidine, significantly increased after treatment. In contrast, the mononuclear cell infiltration score in the antral mucosa treated with ranitidine, but not in that treated with famotidine, had significantly decreased. In conclusion, initial therapy with ranitidine significantly improved the quality of gastric ulcer healing and the histological scores of gastric mucosa compared with famotidine.

Adult↗
PubMed2001

Effect of dexamethasone palmitate-low density lipoprotein complex on cholesterol ester accumulation in aorta of atherogenic model mice.

In order to confirm the efficacy of dexamethasone palmitate (DP)-low density lipoprotein (LDL) complex on experimental atherosclerosis in vivo, we examined whether DP-LDL complex could be effective for cholesterol ester accumulation in the aorta of atherogenic mice. Nonatherogenic and atherogenic mice were fed with normal and atherogenic diet for 14 weeks, respectively. Dexamethasone (DEX), lipid emulsion containing DP (DP-LE), or DP-LDL complex was intravenously injected once a week from 8 to 14 weeks. Cholesterol levels in serum and aorta in the atherogenic mice were significantly higher than those of nonatherogenic mice. Injection of DP-LDL complex significantly reduced cholesterol ester (CE) accumulation in the aorta of atherogenic mice. The reduction of CE accumulation in aorta treated with DP-LDL complexes was 10 and 100 times more potent than that with DP-LE and DEX, respectively. The radioactivity in the aorta of atherogenic mice treated with 3H-DP-LDL complex was significantly higher than that with 3H-DP-LE and 3H-DEX at 24 h after injection. Even 7 d after injection, a significant amount of radioactivity was present only in the aorta of atherogenic mice treated with DP-LDL complex. This result suggests that DP-LDL complex is selectively delivered to the atherogenic lesions in the aorta of atherogenic mice, and then DP released from the complex inhibits CE accumulation in the aortic intima. Therefore, DP-LDL complex may be a good drug-carrier in drug delivery system for atherosclerosis.

Animals↗
PubMed2000

Inhibitory effect of dexamethasone palmitate-low density lipoprotein complex on low density lipoprotein-induced macrophage foam cell formation.

We used low density lipoprotein (LDL) as a carrier of site-specific delivery of drugs to atherosclerotic lesions, prepared a dexamethasone palmitate (DP)-LDL complex, and examined the effect of the DP-LDL complex on foam cell formation of macrophages in vitro. LDL was isolated from human plasma and the DP-LDL complex was prepared by incubation in the presence of Celite 545. The complex contained about 50 mol of DP in 1 mol of LDL. When macrophages were incubated with LDL for 48 h, cholesterol ester was accumulated in the macrophages, indicating foam cell formation. This accumulation of cholesterol ester was significantly inhibited by incubation with the DP-LDL complex. The potency of the DP-LDL complex was similar to that of dexamethasone alone. The DP-LDL complex also significantly attenuated the accumulation of cholesterol ester induced by incubation with LDL prior to the incubation with the DP-LDL complex. These findings indicated that the DP-LDL complex showed similar characteristics to LDL, and the DP-LDL complex inhibited the foam cell formation of macrophages in in vitro experiments. This DP-LDL complex has a possibility as a drug-carrier complex for use in atherosclerosis.

Animals↗
PubMed1999

Preparation of a complex of dexamethasone palmitate-low density lipoprotein and its effect on foam cell formation of murine peritoneal macrophages.

In the early progression of atherosclerosis, LDL migrates in the subendothelial space of the artery and plays an important role in foam cell formations of macrophages. LDL may serve as a carrier of site-specific delivery of drugs to atherosclerotic lesions. In this exploratory study, dexamethasone palmitate (DP) was incorporated in LDL, and an inhibitory effect of this complex on foam cell formations was examined. LDL was isolated from human plasma, and the DP-LDL complex was prepared by incubation in the presence of Celite 545. No degradation nor modification of LDL was observed. The DP/LDL molar ratio of the complex was 35-50:1. Foam cell formations of murine macrophages were induced by incubation with oxidized LDL. When macrophages were pretreated with the DP-LDL complex, accumulation of cholesterol ester in the macrophages induced by oxidized LDL, i.e., an index of foam cell formation, was decreased. These findings indicated that the DP-LDL complex showed similar characteristics to LDL, and the DP-LDL complex inhibited foam cell formations of macrophages in vitro. This study provides the basis for further study of the DP-LDL complex as a drug-carrier complex for treatment of atherosclerosis.

Animals↗
PubMed1999

Complete regression of recurrent esophageal carcinoma with reduced expression of glutathione S-transferase-pi by treatment with continuous infusion of 5-fluorouracil and low-dose cisplatin infusion.

The mortality rate of recurrent esophageal carcinoma remains high because of its resistance to chemotherapy and radiation therapy. We present a patient with recurrent esophageal carcinoma, which dramatically disappeared after treatment with the combination of continuous infusion of 5-fluorouracil and low-dose cis-Diamminedichloroplatinum-II (cisplatin) infusion (FP therapy). Furthermore, we immunohistologically found that glutathione S-transferases (GST)-pi, a marker of resistance to cisplatin, was faintly expressed both in the endoscopical biopsy specimens of recurrent tumor and in the resected specimens of esophageal carcinoma and metastatic lymph nodes. FP therapy was suggested to be effective for recurrent esophageal carcinoma. Immunostaining for GST-pi might be a prospective marker for the sensitivity of esophageal carcinoma to FP therapy, particularly cisplatin.

Antimetabolites, Antineoplastic↗
PubMed1990

[Immunohistochemical study using a double fluorescent staining on the regional lymph nodes of gastric cancers].

For the purpose to investigate the immunological anti-tumor function of lymphocytes in the regional lymph nodes of gastric cancer, a double staining procedure using several monoclonal antibodies against the surface membranes of T and NK cells with fluorescent antibody technique was conducted. The number of CD11b+ cells out of CD8+ cells was small with almost all being CD11b- belonging to cytotoxic T cells. Leu8+ cells and Leu8- cells out of CD4+ cells were recognized in equal numbers and were reciprocal. The ratio of CD4+ Leu8-/CD4+ demonstrated an increase in the group injected with OK-432. The ratio of OKT9+ or OKIa1+ occupied in CD8+ or CD4+ cells was only several percent, and few in number. An increase for the ratio of CD4+ OKT9+/CD4+ was observed in the group injected with IL-2. Similar increases for the ratio of CD4+ OKIa1+/CD4+ were obtained in the group injected with OK-432 and in the metastatic group, respectively. The Leu7+ CD16+ cells were not observed. The Leu7- CD16+ cells were observed in a part where metastases were focused. These results indicated that lymphocytes in regional lymphocyte of gastric cancer might hold the hidden anti-tumor effect, but did not display the full function without preoperative intratumor injection of BRM such as IL-2 or OK-432.

Antibodies, Monoclonal↗
PubMed1989

Absence of effect of 16,16-dimethyl prostaglandin E2 on reduction of gastric mucosal blood flow caused by indomethacin in rats.

The effects of 16,16-dimethyl prostaglandin E2 PGE2 on gastric mucosal blood flow and gastric mucosal damage were tested in rats given indomethacin. Blood flow was measured by hydrogen gas clearance. Indomethacin given intragastrically reduced the blood flow in nonlesion areas and the levels of PGE2 and 6-keto-PGF1 alpha in the gastric mucosa and caused mucosal damage in a dose-related way. Indomethacin (20 mg/kg) significantly reduced the blood flow 30 min after administration, and the reduction increased until 90 min. Then the flow plateaued until 240 min. Gastric mucosal damage caused by 20 mg/kg of indomethacin and evaluated by only gross observations, began at 60 min and developed with time until 240 min after administration. 16,16-Dimethyl PGE2 (5 micrograms/kg) did not affect the reduction of blood flow caused by indomethacin during 240 min of measurements, but it significantly inhibited the indomethacin-induced mucosal damage evaluated by gross observations. These results suggest that prevention by 16,16-dimethyl PGE2 of grossly observed gastric mucosal damage caused by indomethacin was not related by preservation of the gastric mucosal blood flow in the areas without lesions.

16,16-Dimethylprostaglandin E2↗
PubMed1989

[Effects of indomethacin on cellular resistance and synthesis of prostaglandins in epithelial cells isolated from rat gastric mucosa].

This study was done to test effects of indomethacin (IND) on cell damage and prostaglandin (PG) synthesis in mucosal epithelial cells isolated from rat stomach in vitro. IND caused the cell damage in a dose-related way at concentrations over 5 X 10(-4) M. This damage was inhibited by 16,16-dimethyl PGE2 (10(-6) M). IND abolished the synthesis of PGE2, PGI2, and TXA2 at the concentration of 10(-4) M at which IND alone did not cause cell damage. The cells treated with 10(-4) M IND were significantly susceptible to damage caused by 15% ethanol compared to the cells not treated with IND. 16,16-Dimethyl PGE2 also inhibited the damage caused by IND + ethanol. These results suggest that the IND-induced susceptibility of the cells to damage is related to PG deficiency.

16,16-Dimethylprostaglandin E2↗
PubMed1987

Analysis of tissue lymphocytes by double fluorescent staining--gastric cancer tissue and regional lymph nodes.

An immunohistochemical study was performed on human lymphocytes in the tissue of gastric cancer, and also in the regional lymph nodes, by double fluorescent staining, using monoclonal antibodies. Leu3a+8+ cells (inducer T cells) which consist about 30 per cent of Leu 3a+ cells were seen in the tissue surrounding the gastric cancer. The other 70 per cent of Leu 3a+ cells were Leu3a+8- cells (helper T cells). In the lymph nodes they were noted in T cell areas in almost the same proportions, while in germinal centers, only Leu3a+8- cells were found. On the other hand, OKT8+Leu15- cells (cytotoxic T cells) were noted in a large number, while OKT8+Leu15+ cells (suppressor T cells) were few. Further, an increase of OKT8+Leu15- cells was seen around gastric cancer or metastatic cancer in lymph nodes. These immunohistochemical findings suggest that cytotoxic T cells are the main component in the tissue of gastric cancers and the regional lymph nodes. Increases in inducer T cells and helper T cells are probably required to induce cytotoxic T cells around the cancer tissue.

Antibodies, Monoclonal↗