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Surface structure of Pt(3 1 0) = 3(1 0 0)–(1 1 0), which contains kink atoms in the step, has been determined with the use of in situ surface X-ray scattering (SXS) in the double layer region (0.50 V(RHE)) in 0.1 M HClO 4 . Clean Pt(3 1 0) surface has pseudo (1 × 1) structure on which lateral displacements of 2–9% and 0.3–1% are found along a and b directions, respectively, whereas the surfaces of Pt(1 1 0) = 2(1 1 1)–(1 1 1) and Pt(3 1 1) = 2(1 0 0)–(1 1 1) are reconstructed to (1 × 2) according to previous reports. Interlayer spacing between the first and the second layers d 12 is contracted about 5% compared with the bulk spacing, whereas those between underlying layers are expanded down to fourth layer. Fully adsorbed CO has no effect on the surface structure of Pt(3 1 0). This result differs from that on Pt(1 1 1), where d 12 is expanded after CO adsorption.

Purpose To present the results of proton beam therapy for patients with esophageal cancer. Methods and materials This study reviewed 46 patients with esophageal cancer who were treated between 1985 and 1998 using proton beams with or without X-rays. All patients had locoregionally confined disease; all but one had squamous cell carcinoma. Of the 46 patients, 40 received combinations of X-rays (median, 48 Gy) and protons (median, 31.7 Gy) as a boost. The median total dose of combined X-ray and proton radiation for the 40 patients was 76.0 Gy (range, 69.1–87.4 Gy). The remaining 6 patients received only proton beam therapy (median, 82.0 Gy; range, 75–89.5 Gy). Results The 5-year actuarial survival rate for the 46 patients, patients with T1 ( n = 23), and those with T2–T4 ( n = 23) was 34%, 55%, and 13%, respectively. The 5-year disease-specific survival rate for the 46 patients, those with T1, and those with T2–T4 was 67%, 95%, and 33%, respectively. The 5-year local control rate for patients with T1 and T2–T4 lesions was 83% and 29%, respectively. The site of the first relapse was locoregional for 16 patients and distant organs for 2 patients. Conclusion The results suggest that proton beam therapy is an effective treatment for patients with locally confined esophageal cancer. Additional studies are required to determine the optimal total dose, fractionation schedule, and best combinations of protons and conventional X-rays with or without chemotherapy.

We investigated the role of xanthine oxidase-derived oxygen radicals in the development of endothelin-1-induced gastric ulcer. Mucosal lipid peroxidation showed a peak 24 h after injection, while gastric mucosal haemodynamics were fully restored 26 h after endothelin-1 injection. Allopurinol and oxypurinol, but not superoxide dismutase or catalase, protected the gastric mucosa 24 h after endothelin-1 injection. Oxypurinol antagonized both the vasoconstrictor effect of endothelin-1 and the decrease in gastric ATP. All treatments on the second day after endothelin-1 injection significantly reduced gastric mucosal damage. Xanthine oxidase-derived oxygen radicals contributed largely to the exacerbation but they did not mediate the onset of endothelin-1-induced gastric ulcer. Pretreatment with probucol (500 mg/kg, p.o.) also protected the gastric mucosa from endothelin-1-induced mucosal injury by its antioxidant activity. Oxypurinol was gastroprotective through its vasoactive and energy saving actions. The haemodynamic background of endothelin-1-induced gastric ulcer consists of long lasting ischaemia and subsequent “reperfusion” which may be responsible for the late burst of oxygen radicals.

Carbothermic reduction was adapted to convert mixtures of cerium oxide and praseodymium oxide into cerium–praseodymium mixed dicarbides (Ce x Pr 1− x C 2 ). XRD results indicate that the lattice parameters of Ce x Pr 1− x C 2 vary continuously with x and that the complete miscibility exists between CeC 2 and PrC 2 .

Endothelin-1 (ET-1) is produced from inactive precursor big ET-1 by endothelin-converting enzyme-1 (ECE-1), a membrane-bound metalloprotease, structurally similar to another metalloprotease, neutral endopeptidase 24.11 (NEP). Although both phosphoramidon and thiorphan are metalloprotease inhibitors, the ECE activity is inhibited by phosphoramidon but not by thiorphan, a specific inhibitor of NEP. Therefore, to investigate whether an ECE inhibitor can prevent indomethacin-induced gastric mucosal damage in rats, we compared the effects between the two metalloprotease inhibitors on both gastric mucosal integrity and the levels of ET-1 and big ET-1 in gastric tissue. Phosphoramidon significantly decreased ET-1 levels, causing a concomitant big ET-1 increase and dose-dependently attenuated indomethacin-induced gastric mucosal damage. By contrast, thiorphan neither changed the ratio of ET-1/big ET-1 nor attenuated the damage. In conclusion, the prevention of gastric mucosal damage by an ECE inhibitor indicates that endogenous ET-1 may play an important role in the pathogenesis of indomethacin-induced gastric mucosal damage.

Recently increased production of endothelin-1 has been implicated in the pathogenesis of gastric ischemia-reperfusion injury. We have investigated the effects of endothelin converting enzyme inhibition on local gastric ischemia-reperfusion injury in rats by using two metalloprotease inhibitors, phosphoramidon and thiorphan. In presence of exogenous 0.15M HCI intragastrically, local ischemia was induced by the clamping of left gastric artery for 15 min and reperfusion was done for 30 min. In separate group of rats, phosphoramidon (10-60 mg/kg) or thiorphan (60 mg/kg) were given as i.v. bolus injection immediately before the induction of ischemia. Phosphoramidon dose dependently attenuated the macroscopic and microscopic mucosal injuries while thiorphan did not. These results indicate that phosphoramidon-sensitive endothelin converting enzyme activity is highly present in stomach and phosphoramidon, by inhibiting the conversion of big endothelin-1 to endothelin-1 attenuated the gastric mucosal damage in this model.

Bosentan, a new type of orally effective, mixed (ETA+ETB) endothelin receptor antagonist has been recently introduced and tested in a variety of experimental models. We studied the effect of bosentan on the changes in gastric mucosal hemodynamics and mucosal integrity, induced by the exogenous application of endothelin-1, in rats. Bosentan (10 mg/kg iv) pretreated rats were injected with endothelin-1 (500-1000-2000 pmol/kg, iv) and gastric mucosal hemodynamics were monitored. After combined oral (30 mg/kg) and systemic pretreatment with bosentan we studied the effects of submucosal injection of endothelin-1 (50 pmol) on blood flow and gastric mucosa. Bosentan antagonized the vasodilator, vasoconstrictor and ulcerogenic effects of endothelin-1 in the rat gastric mucosa. These results show that bosentan can be a useful probe in the study of endogenous endothelin in the gastrointestinal tract.

We investigated the effect of the anti-ulcer drug cetraxate on the development of the gastric ulcer induced by the submucosal injection of endothelin-1 in the rat gastric body, and its effects on gastric mucosal hemodynamics and tissue oxygenation by Laser doppler flowmetry and tissue spectrophotometry. Endothelin-1 induced gastric ulcer (ulcer length: 11.85 +/- 0.89 mm, mean +/- SEM, n = 4) which was strongly attenuated by cetraxate (ulcer length: 3.27 +/- 0.3 mm, mean +/- SEM, n = 8, p < 0.0001). Cetraxate maintained also tissue oxygenation without causing any significant effect on the endothelin-1-induced changes in gastric mucosal blood flow and volume. These results show that cetraxate exerts its cytoprotective action partly by maintaining mucosal oxygenation.

Background and Aims:We have already reported that gastric mucosal autofluorescence intensity increased in accordance with gastric mucosal lesions formation induced by dicrofenac sodium administration in rats. In this study, we have established an endoscopic apparatus composed with an image processor and a highly-sensitive camera for fluorescence observation named SEFAS: a simultaneous endoscopic fluorescence analyzing system. Using this system, we clarified whether NSAID-treatment increased gastric mucosal fluorescence intensity in human volunteers or not. Moreover, we examined relations of distributions between tissue peroxidation and fluorescent substance. Methods: Healthy human volunteers who completely agreed to take part in this study were administrated 50 mg dicrofenac per os. Mucosal fluorescence intensity were measured with SEFAS before and 1, 2 hour(s) after the dicrofenac treatment. Moreover, volunteers were also administrated 50 mg teprenone, a mucosal prostaglandin inducing agent, 30 min before the dicrofenac treatment, and were also measured mucosal intensities. In each study, some pieces of mucosa were taken from each area of the mucosal fluorescence measurement. These biopsies were rapidly made into specimens of cryosections. They were immunohistochemicaly stained with anti-4-hydroxynonenal antibody, a specific monoclonal antibody for peroxidized tissue, and analyzed distributions of tissue peroxidation. Distributions of autofluorescent substance were also observed. Moreover, autofluorescent substance was analyzed with HPLC. Results: The dicrofenac treatment increased mucosal fluorescence intensity. The administrations of teprenone completely restrained this phenomenon. Fluorescence substances were porphyrins. These fluorescence substances were localized at the disrupted surface layer of the gastric mucosa. Peroxidized tissue was located in middle part of the mucosa. Conclusions: It suggested that tissue peroxidation was induced before mucosal injury formation, and fluorescent porphyrins were generated with tissue disruption. Mucosal fluorescence observations with SEFAS can diagnose NSAID-induced gastric lesions.