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Aws S Salim - One of the best experts on this subject based on the ideXlab platform.

  • use of scavenging oxygen derived free radicals to protect the rat against aspirin and ethanol induced Erosive Gastritis
    Journal of Pharmaceutical Sciences, 1992
    Co-Authors: Aws S Salim
    Abstract:

    Abstract Oxygen-derived free radicals are cytotoxic and produce tissue damage. The effect of the radical scavengers allopurinol and dimethyl sulfoxide (DMSO) on aspirin‐ and ethanol‐induced acute gastric mucosal injury was studied in the rat. Orogastric instillation of aspirin at 200 mg/kg produced, after 4 h, gastric mucosal injury in 30% of rats without pyloric ligation [score, 3.1 ± 0.8 mm 2 , mean ± standard error of the mean (SEM); n = 10] and in 80% of rats with this ligation (score, 10.4 ± 1.2 mm 2 , mean ± SEM; n = 10). Gavage with 1 mL of 2 or 5% allopurinol or DMSO at 24 h before and again just before aspirin administration completely protected rats with or without pyloric ligation against injury. Orogastric instillation of ethanol (1 mL of a 40% solution) produced, after 1 h, gastric mucosal injury in all rats with or without pyloric ligation (24.1 ± 1.7 and 14.1 ± 1.3 mm 2 , respectively, mean ± SEM; n = 10). Gavage with 1 mL of 5% allopurinol or DMSO at 24 h before and again just before ethanol administration completely protected rats with or without pyloric ligation against injury. Protection against the aspirin‐ and ethanol‐induced injury was not associated with any significant effect on the H + output. The results suggest that oxygen‐derived free radicals are directly implicated in the mechanism of aspirin‐ and ethanol‐induced acute gastric mucosal injury and that scavenging these free radicals protects against injury by maintaining the integrit of the gastric mucosa.

  • role of sulfhydryl containing agents in the healing of Erosive Gastritis and chronic gastric ulceration in the rat
    Journal of Pharmaceutical Sciences, 1992
    Co-Authors: Aws S Salim
    Abstract:

    One milliliter of 1, 2, or 5% DL-cysteine (cysteine) or DL-methionine methylsulfonium chloride (MMSC) was instilled into the rat stomach 1, 24, and 48 h after giving ethanol (1 mL of 40% solution) by gavage. One hour following the administration of ethanol, gastric mucosal injury was seen in all the animals (22.6 ± 1.1 mm2, mean ± SEM; n = 10). Twenty-four hours after giving the ethanol, all the rats treated with cysteine or MMSC still had the mucosal injury. Treatment with 2% cysteine or MMSC significantly (p < 0.01) reduced the extent of this injury (10.2 ± 0.6 and 10.1 ± 0.5 mm2, respectively, versus 20.7 ± 1.2 mm2, mean ± SEM; n = 10), an action that was similarly achieved by the 5% solutions (10.1 ±0.5 and 9.9 ± 0.3 mm2, respectively, versus 20.7 ± 1.2 mm2, mean ± SEM; n = 10). Forty-eight hours following the administration of ethanol, 30% of the animals given 1% cysteine or MMSC still had gastric mucosal injury, which was significantly (p < 0.001) less extensive than that seen with ethanol alone (3.8 ± 0.3 and 4.1 ± 0.3 mm2, respectively, versus 13.1 ± 0.8 mm2, mean ± SEM; n = 10). At this time period, however, none of the animals treated with 2 or 5% solutions of cysteine or MMSC still had any injury. Healing of the ethanol-induced injury was confirmed microscopically and was achieved by regeneration. Chronic gastric ulceration was produced in the rat by administering 5 mg/kg of reserpine ip every day for 5 days, then housing the animals for 2 weeks. Cysteine and MMSC (1 mL by gavage daily) demonstrated a dose-dependent and time-related power to stimulate the healing of this ulceration. After gavaging for 5 days, 80% of the rats given 1% cysteine and 70% of those given 1% MMSC had gastric ulceration, whereas only 20% of the animals given 10% solutions had the ulceration. After gavaging for 10 days, 20% of the rats given 1% cysteine and 30% of those given 1% MMSC had gastric ulceration, whereas none gavaged with 5 or 10% solutions of these agents still had any ulceration. At this stage, 70% of the animals gavaged with distilled water still had the ulceration. These cysteine and MMSC actions were independent of any effect on the gastric acid secretion. The results show that sulfhydryl-containing agents stimulate the healing of ethanol-induced acute gastric mucosal injury and chronic gastric ulceration in the rat.

Sang Yong Seol - One of the best experts on this subject based on the ideXlab platform.

  • da 9601 for Erosive Gastritis results of a double blind placebo controlled phase iii clinical trial
    World Journal of Gastroenterology, 2004
    Co-Authors: Sang Yong Seol, Myunghwan Kim, Jong Sun Ryu, Myunggyu Choi, Dong Wook Shin, Byoung Ok Ahn
    Abstract:

    DA-9601 for Erosive Gastritis: Results of a double-blind placebo-controlled phase III clinical trial

  • a phase iii clinical trial of stillentm for Erosive Gastritis
    Clinical Endoscopy, 2004
    Co-Authors: Sang Yong Seol, Myunghwan Kim, Jongsun Rew, Myunggyu Choi
    Abstract:

    a novel cytoprotectant, for Gastritis showed 180 mg of Stillen, t.i.d. for 2 weeks results in a significant increase of cure rate when compared with a placebo group. It is reported that antioxidative effect and strengthening the endogenous cytoprotective molecules of the gastric mucosa play a pivotal role for cytoprotective action of . The aim of this phase III multicenter, double-blind comparative study was to assess the efficacy of for the treatment of Erosive Gastritis. Methods: Five hundred and twelve patients with Erosive Gastritis were enrolled and divided into three groups. Each group received 180 mg or 360 mg of or 600 mg of cetraxate (NeuerTM) t.i.d. for 2 weeks, respectively and a follow-up endoscopic examination for evaluation. Results: Patients treated with 180 mg and 360 mg of had a significantly improved endoscopic cure rate of Gastritis (55.6% and 57.5%, respectively) compared with patients treated with 600 mg of cetraxate (35.5%, p＜0.001). Endoscopic improvement rate was also significantly higher in 180 mg group (67.3%) and 360 mg group (65.0%) of treated patients than cetraxate treated group (46.4%, p＜0.001). During the study, both and cetraxate were well tolerated. Conclusions: These results clearly demonstrate that is an efficacious, safe, and well-tolerated treatment for Gastritis.

Myunggyu Choi - One of the best experts on this subject based on the ideXlab platform.

  • da 9601 for Erosive Gastritis results of a double blind placebo controlled phase iii clinical trial
    World Journal of Gastroenterology, 2004
    Co-Authors: Sang Yong Seol, Myunghwan Kim, Jong Sun Ryu, Myunggyu Choi, Dong Wook Shin, Byoung Ok Ahn
    Abstract:

    DA-9601 for Erosive Gastritis: Results of a double-blind placebo-controlled phase III clinical trial

  • a phase iii clinical trial of stillentm for Erosive Gastritis
    Clinical Endoscopy, 2004
    Co-Authors: Sang Yong Seol, Myunghwan Kim, Jongsun Rew, Myunggyu Choi
    Abstract:

    a novel cytoprotectant, for Gastritis showed 180 mg of Stillen, t.i.d. for 2 weeks results in a significant increase of cure rate when compared with a placebo group. It is reported that antioxidative effect and strengthening the endogenous cytoprotective molecules of the gastric mucosa play a pivotal role for cytoprotective action of . The aim of this phase III multicenter, double-blind comparative study was to assess the efficacy of for the treatment of Erosive Gastritis. Methods: Five hundred and twelve patients with Erosive Gastritis were enrolled and divided into three groups. Each group received 180 mg or 360 mg of or 600 mg of cetraxate (NeuerTM) t.i.d. for 2 weeks, respectively and a follow-up endoscopic examination for evaluation. Results: Patients treated with 180 mg and 360 mg of had a significantly improved endoscopic cure rate of Gastritis (55.6% and 57.5%, respectively) compared with patients treated with 600 mg of cetraxate (35.5%, p＜0.001). Endoscopic improvement rate was also significantly higher in 180 mg group (67.3%) and 360 mg group (65.0%) of treated patients than cetraxate treated group (46.4%, p＜0.001). During the study, both and cetraxate were well tolerated. Conclusions: These results clearly demonstrate that is an efficacious, safe, and well-tolerated treatment for Gastritis.

Byoung Ok Ahn - One of the best experts on this subject based on the ideXlab platform.

Kyunghwan Cho - One of the best experts on this subject based on the ideXlab platform.

  • which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Fast Eating Speed Increases the Risk of Endoscopic Erosive Gastritis in Korean Adults
    2016
    Co-Authors: Minkyung Kim, Eyeon Kim, Byoungduck Han, Kyunghwan Cho, Et Al. Eating Speed, Erosive Gastritis
    Abstract:

    Background: Fast eating or overeating can induce gastrointestinal diseases such as Gastritis. However, the associa-tion between Gastritis and speed of eating is unclear. The aim of this study was to determine whether eating speed is associated with increased risk of endoscopic Erosive Gastritis (EEG). Methods: We carried out a cross-sectional study involving 10,893 adults who underwent a general health checkup between 2007 and 2009. Two groups, EEG patients and EEG-free patients, were compared by using the t-test and the chi-square test. Multiple logistic regression analyses were performed to investigate the association between eat-ing speed and EEG. Results: The group with EEG had a higher proportion of males, average age, body mass index, and percentages of current smokers and risky drinkers than those without EEG. After adjusting for anthropometric, social, and endo-scopic parameters, the group with the highest eating speed (<5 min/meal) had 1.7 times higher risk for EEG than the group with the lowest eating speed (≥15 min/meal) (odds ratio, 1.71; 95 % confidence interval, 1.20–2.45). Conclusion: High eating speed is an independent risk factor for EEG. Our results indicate the need for further stud

  • fast eating speed increases the risk of endoscopic Erosive Gastritis in korean adults
    Korean Journal of Family Medicine, 2015
    Co-Authors: Minkyung Kim, Eyeon Kim, Byoungduck Han, Kyunghwan Cho
    Abstract:

    Background Fast eating or overeating can induce gastrointestinal diseases such as Gastritis. However, the association between Gastritis and speed of eating is unclear. The aim of this study was to determine whether eating speed is associated with increased risk of endoscopic Erosive Gastritis (EEG). Methods We carried out a cross-sectional study involving 10,893 adults who underwent a general health checkup between 2007 and 2009. Two groups, EEG patients and EEG-free patients, were compared by using the t-test and the chi-square test. Multiple logistic regression analyses were performed to investigate the association between eating speed and EEG. Results The group with EEG had a higher proportion of males, average age, body mass index, and percentages of current smokers and risky drinkers than those without EEG. After adjusting for anthropometric, social, and endoscopic parameters, the group with the highest eating speed ( Conclusion High eating speed is an independent risk factor for EEG. Our results indicate the need for further studies to clarify the role of eating speed in Gastritis.