Biomedical subjects
Publications and source records attributed to S Hase.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
To evaluate the usefulness of endoscopic ultrasonography for carcinoid tumors, we examined 29 patients with gastrointestinal carcinoid tumors (5 gastric, 7 duodenal, and 17 rectal). The smallest size detectable by endoscopic ultrasonography was 2 mm in diameter histologically. The cross-sectional image of the tumors was primarily oval to round. The internal echo was generally hypoechoic and homogeneous. The margins were clearly visualized, and the contour was somewhat smooth. The tumors were mainly located in the third layer. The second layer covered the tumor with the third layer at its base, and it abutted the tumor and became indistinct near its upper interface. These findings were especially recognized in lesions with submucosal invasion and were similar at all sites. The overall accuracy of determining the depth of invasion using endoscopic ultrasonography was 75% (27 of 36 lesions). Limited to the lesions detectable by endoscopic ultrasonography, the accuracy was 90%. Endoscopic ultrasonography was useful in determining the presence of local metastases. Moreover, endoscopic ultrasonography allowed direct detection of perigastrointestinal lymph node metastases (75%, three of four patients). In conclusion, endoscopic ultrasonography was found to be useful for the staging of gastrointestinal carcinoid tumors by determining depth of involvement and presence of perigastrointestinal lymph node metastases.
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We examined the gastric ulcerogenic property of selective COX-1 and/or COX-2 inhibitors in rats, and investigated whether COX-1 inhibition is by itself sufficient for induction of gastric damage. Animals fasted for 18 h were given various COX inhibitors p.o., either alone or in combination, and they were killed 8 h later. The nonselective COX inhibitors such as indomethacin, naproxen and dicrofenac inhibited PG production, increased gastric motility, and provoked severe gastric lesions. In contrast, the selective COX-2 inhibitor rofecoxib did not induce any damage in the stomach, with no effect on the mucosal PGE(2) contents and gastric motility. Likewise, the selective COX-1 inhibitor SC-560 also did not cause gastric damage, despite causing a significant decrease in PGE(2) contents. The combined administration of SC-560 and rofecoxib, however, provoked gross damage in the gastric mucosa, in a dose-dependent manner. SC-560 also caused a marked gastric hypermotility, whereas rofecoxib had no effect on basal gastric motor activity. On the other hand, the COX-2 mRNA was expressed in the stomach after administration of SC-560, while the normal gastric mucosa expressed only COX-1 mRNA but not COX-2 mRNA. These results suggest that the gastric ulcerogenic property of conventional NSAIDs is not accounted for solely by COX-1 inhibition and requires the inhibition of both COX-1 and COX-2. The inhibition of COX-1 up-regulates the COX-2 expression, and this may counteract the deleterious influences, such as gastric hypermotility and the subsequent events, due to a PG deficiency caused by COX-1 inhibition.
Most of non-steroidal anti-inflammatory drugs (NSAIDs) except aspirin (ASA) produce intestinal damage in rats. In the present study, we re-examined the intestinal toxic effect of ASA in rats, in comparison with various NSAIDs, and investigated why ASA does not cause damage in the small intestine, in relation to its metabolite salicylic acid (SA). Various NSAIDs (indomethacin; 10 mg/kg; flurbiprofen; 20 mg/kg; naproxen; 40 mg/kg; dicrofenac; 40 mg/kg; ASA; 20-200 mg/kg) were administered s.c., and the small intestinal mucosa was examined macroscopically 24 h later. All NSAIDs tested, except ASA, caused hemorrhagic lesions in the small intestine, with a decrease of mucosal PGE(2) contents. ASA did not provoke any damage, despite inhibiting (prostaglandin) PG production, and prevented the occurrence of intestinal lesions induced by indomethacin, in a dose-related manner. This protective action of ASA was mimicked by the equimolar doses of SA (17.8-178 mg/kg). Indomethacin caused intestinal hypermotility, in preceding to the occurrence of lesion, and this event was followed by increases of enterobacterial translocation in the mucosa. Both ASA and SA prevented both the intestinal hypermotility and the bacterial translocation seen after indomethacin treatment. In addition, the protective effect of SA was not significantly influenced by either the adenosine deaminase or the adenosine receptor antagonists. Following administration of ASA, the blood SA levels reached a peak within 30 min and remained elevated for more than 7 h. These results suggest that SA has a cytoprotective action against indomethacin-induced small intestinal lesions, and this action may be associated with inhibition of the intestinal hypermotility and the bacterial translocation, but not mediated by endogenous adenosine. Failure of ASA to induce intestinal damage may be explained, at least partly, by a protective action of SA, the metabolite of ASA.
We studied the chronic effect of ammonia, which is one of the pathogenic factors of Helicobacter pylori in gastroduodenal diseases, on the healing of acetic acid-induced gastric ulcers in rats with special reference to the collagen metabolism. Rats were given either tap water or 0.1 or 0.02% ammonia solution before and after ulcer induction. We measured the ulcer index, hydroxyproline concentrations and type III collagen/total hydroxyproline ratios in the ulcer base. Epithelialization was achieved 4 weeks later under the influence of ammonia. Nevertheless, ammonia treatment significantly increased the collagen deposition in the ulcer base compared with the nonammonia treatment group, 4 weeks after ulcer induction. In the nonammonia treatment group, the type III collagen/total hydroxyproline ratio decreased 3 weeks after ulcer induction. On the contrary, in the groups treated with ammonia throughout the experiment, type III collagen/total hydroxyproline ratio remained high until 4 weeks after ulcer induction. In conclusion, intragastric ammonia delayed the ulcer healing process in its early phase, but did not affect the achievement of re-epithelialization. However, it disturbed the collagen metabolism in the ulcer base. Excessive deposition of collagen and an abnormally high proportion of its immature type may be unfavorable for ulcer healing. These findings may explain in part why H. pylori-induced ulcer is so difficult to treat.
BACKGROUND: We previously reported that lafutidine ((I)-2-(furfurylsulfinyl)-N-[4-[4-(piperidinomethyl)-2-pyridyl]oxy-(Z)-2-butenyl] acetamide), a novel histamine H(2)-receptor antagonist, protects the small intestine against indomethacin-induced damage, mediated by capsaicin-sensitive afferent neurons (CSN). MATERIAL AND METHODS: In the present study, we investigated whether or not the protective action of lafutidine against indomethacin-induced intestinal damage is mediated by endogenous nitric oxide (NO). Male SD rats were given indomethacin (10 mg/kg, s.c), killed 24 hr later, and the small intestinal mucosa was examined. Lafutidine (10 mg/kg) and capsaicin (10 mg/kg) was given p.o. twice 0.5 hr before and 9 hr after indomethacin. The NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME: 10 mg/kg) or the selective iNOS inhibitor aminoguanidine (10 mg/kg) was given s.c. 1 hr before lafutidine, while L-arginine (200 mg/kg) was given i.p. 10 min before L-NAME. RESULTS: Indomethacin produced severe lesions in the small intestine, accompanied by increases in enterobacterial translocation in the mucosa. Both lafutidine and capsaicin significantly reduced the severity of these lesions, together with suppression of bacterial translocation. The protective action of lafutidine as well as capsaicin was almost totally abolished by L-NAME but not aminoguanidine, in a L-arginine-sensitive manner. Both lafutidine and capsaicin significantly increased intestinal mucus secretion, and these effects were also attenuated by prior administration of L-NAME. The exogenous NO donor NOR-3 prevented indomethacin-induced intestinal lesions at the dose that stimulated the mucus secretion and inhibited the bacterial translocation. CONCLUSIONS: These results suggest that lafutidine protects the small intestine against indomethacin-induced damage, the action being dependent on CSN and mediated by endogenous NO produced by cNOS. The protective action of lafutidine may be attributable to suppression of the bacterial translocation following indomethacin, probably due to stimulation of intestinal mucus secretion.
An education model developed in response to various education needs identified by nurses is outlined. The modular format and its advantages are described and set in the context of changes in the educational environment.
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