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Notizen: The property of extreme ultraviolet (EUV) generation from Xe clusters irradiated with intense lasers was studied. The Xe cluster jet was well characterized by the interferometric method. In order to obtain the adequate irradiation condition for strong EUV generation, EUV spectra were taken with various laser systems. Then, the wavelength, the pulse width, and the pump energy were widely varied. Through this survey, even with the comparatively low-density Xe jet of ≤5×1018 cm−3 average atomic density, the highest conversion efficiency of over 10% from laser energy to EUV (5–18 nm) was obtained with a subpicosecond KrF laser pulse, where a 4π source was assumed. This EUV source is considered to be attractive as an EUV lithography light source because of its low average atomic density and small Xe cluster. © 2001 American Institute of Physics.

Notizen: A niobium membrane was immersed in hydrogen plasma and could be electrically biased to vary the energy of bombarding ions in the range of 1–200 eV. The fluxes of plasma driven absorption and permeation were almost entirely governed by incident suprathermal neutrals (mostly, thermal atoms), whose energy does not depend on membrane bias, but the ions of controllable energy do affect the neutral-induced permeation through modifying the membrane surface. At the zero bias a high temperature-independent plasma driven permeation (superpermeation) was observed alongside of an enhanced absorption. Bombardment by ions of an energy higher than 50 eV resulted in a sharp decrease of the plasma driven permeation/retention and in an acceleration of boundary processes of absorption/reemission of thermal molecules. At ion energies below 50 eV, the effect of ion bombardment on the plasma driven permeation and the kinetic coefficients of boundary processes were nonmonotonic in ion energy, having a maximum at ∼10 eV. Both an in situ doping with O of the bulk of Nb and a membrane temperature increase reduced the effects of ion bombardment to their complete disappearance. Responsible for that was the replenishment by means of surface segregation of an oxygen monolayer sputtered by ion bombardment. © 2001 American Institute of Physics.

Notizen: summary  This study evaluated the mandibular condyle displacement on the working side while masticating certain foods with different textures. For referencing the mandibular condyle movement, the range of voluntary border movement of the mandibular condyle was determined based on the analysis of the sagittal, left lateral and right lateral border motion using Posselt's figure. The test foods consisted of cheese, peanuts, and beef jerky. During mastication of cheese and peanuts, the amount of displacement of the mandibular condyle in all directions was within the range of border movement. Significant posterior and superior shifts of the mandibular condyle were observed during mastication of beef jerky, compared with the findings obtained during border movement. Accordingly, it is suggested that prolonged mastication of hard fibrous foods, may stimulate the temporomandibular joint structure and mandibular dysfunction patients should limit their intake of such foods.

Notizen: Background : The gastric mucosal alcohol dehydrogenase activity was reported to be reduced in subjects with Helicobacter pylori-associated chronic gastritis. However, the role of H. pylori infection in the metabolism of ingested ethanol has not been fully elucidated.Aim : To clarify whether H. pylori infection exerts any influence on the metabolism of small amounts of ethanol in humans.Subjects and methods : 13C-ethanol (100 μL) diluted in 100 mL water was administered orally to 22 healthy volunteers before breakfast. Breath samples were then collected every 10 min for up to 60 min. The content of 13CO2 (‰) was analysed using a mass-spectrometric method. The excretion rate of labelled CO2 was analysed by calculation of the following mathematical parameters, i.e., Tmax, Cmax, and AUC60.Results : In H. pylori-negative controls (n = 11), the Tmax, Cmax and AUC60 were 0.47 ± 0.13, 19.1 ± 6.0 and 13.7 ± 4.5, respectively. The corresponding values were 0.53 ± 0.16 (n.s.) and 12.7 ± 4.8 (P 〈 0.05) and 9.0 ± 3.6 (P 〈 0.05), respectively, in subjects with H. pylori infection (n = 11). Successful eradication of H. pylori was associated with significant increase of these parameters (Cmax and AUC60, n = 6).Conclusions : The metabolism of small amounts of ethanol is attenuated in subjects with H. pylori infection.

Notizen: Background : Helicobacter pylori resistance to clarithromycin, probably due to the frequent use of this antibiotic for the treatment of other diseases, is the greatest obstacle against its eradication.Aim : To clarify the prevalence of clarithromycin-resistant H. pylori in patients with non-tuberculous mycobacterial lung disease receiving multiple antibiotic treatment, including clarithromycin.Methods : We enrolled 88 patients with non-tuberculous mycobacterial lung disease; 29 underwent upper gastrointestinal endoscopy for the diagnosis of H. pylori infection prior to treatment, and 60 underwent it during treatment. The diagnosis of H. pylori infection was confirmed by histological examination, urease test and microaerobic bacterial culture. The minimum inhibitory concentration of clarithromycin was determined and the DNA was analysed for each of the isolated H. pylori strains.Results : Patients during the treatment had a high prevalence rate of clarithromycin-resistant H. pylori (100%). Analysis of DNA of the clarithromycin-resistant H. pylori isolates revealed point mutations at A2142G or A2143G. Moreover, a linear correlation was found between the total cumulative dose of clarithromycin and the minimum inhibitory concentration.Conclusion : All patients with non-tuberculous mycobacterial lung disease being treated long-term with multiple antibiotics, including clarithromycin, harboured clarithromycin-resistant H. pylori in the stomach. Therefore, eradication of H. pylori before commencement of long-term therapy including clarithromycin should be recommended.

Notizen: Background : Although Helicobacter pylori infection is now acknowledged as a major promoter of gastric cancer in humans, the carcinogenetic process of this effect has not been fully elucidated. Precancerous lesions such as intestinal metaplasia, enhanced proliferation of epithelial cells and elevated level of growth factors have been postulated to play a role.Aim : To analyse a relationship between gastric mucosal proliferation, mucosal content of hepatocyte growth factor and prevalence of intestinal metaplasia before and after successful H. pylori eradication therapy.Methods : We evaluated 25 H. pylori-eradicated patients. At initial endoscopic examination, two biopsy tissue samples each were obtained from the antrum and great curvature of the corpus. Tissue content of hepatocyte growth factor and neutrophil myeloperoxidase were measured using an ELISA method, and histological assessment of intestinal metaplasia (haematoxylin and eosin) and proliferating cells (Ki-67 immunostaining) was performed. The patients were treated with a 1-week course of triple therapy. At 10 months after successful eradication, biochemical and histological assessments were repeated.Results : Among all patients (n = 25), no intestinal metaplasia was detected in the corpus mucosa, but was observed in 10 patients (40%) in the antrum. This prevalence ratio was not changed after eradication. A slight decrease in HGF content was demonstrated in both sites, but the level of antral hepatocyte growth factor was significantly decreased in patients with intestinal metaplasia but not in those without. Proliferative index (Ki-67 positive cells/epithelium) was decreased after eradication therapy in both sites. An increase in proliferative index was observed in the antrum with intestinal metaplasia compared with that without, which significantly decreased after eradication therapy.Conclusions : H. pylori eradication therapy in the present study afforded an inhibitory effect on epithelial cell proliferation and on the mucosal content of HGF.

Notizen: Background: CXC chemokines such as interleukin (IL)-8 are neutrophil chemoattractants, the levels of which increase in Helicobacter pylori-infected gastric mucosa. Many investigators have focused on the chemotactic aspects of IL-8; however, CXC chemokines are also reported to have angiogenic activity and to serve as remodelling factors. Rat GRO/CINC-1 is a rodent counterpart of human GROα, a member of the family of CXC chemokines. Gastric mucosa infected with H. pylori is in a state of hyperproliferation, with increases in the amounts of growth factors such as hepatocyte growth factor (HGF). Aim: To investigate whether rat GRO/CINC-1 had growth-stimulating activity for gastric epithelial cells. Methods: The rat gastric epithelial cell line RGM-1 was incubated in serum-free medium for 12 h to adjust the cell cycle to the G0 phase, and GRO/CINC-1 was then added for 24 h. The total cell number was determined by fluorogenic analysis after propidium iodide staining, and cell proliferation was assessed by measuring 5-bromo-2′-deoxyuridine (BrdU) incorporation. The activity of p42/p44 mitogen-activated protein kinase (MAPK) was measured 5–20 min after the start of GRO/CINC-1 exposure. Results: Cultures treated with GRO/CINC-1 showed a significant increase in cell number and BrdU incorporation in a concentration-dependent fashion. The MAPK activity increased within 5 min after GRO/CINC-1 application and returned to the control level at 20 min. Conclusion: The growth-stimulatory effect of GRO/CINC-1 on rat gastric epithelial cells suggests a dual function of this chemokine: proinflammatory action and induction of epithelial proliferation.

Notizen: We previously reported that attenuated epithelial apoptosis and enhanced proliferation in comparison with mice might link to the specific carcinogenesis in Mongolian gerbils and suggested that the difference in both strains might be due to a difference in genetic background. p53 is a well-known tumour suppressor gene, mutation of which is also known to be involved in gastric cancer formation.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:The present study was designed to examine the level of gastric epithelial apoptosis and proliferation in p53 heterozygous knockout mice (p53+/−) colonized with Helicobacter pylori(Sydney strain: SS1).〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Female p53+/− mice and wild-type controls were orally inoculated with SS1 and the stomachs were examined 24 weeks later. DNA fragmentation was measured by levels of cytoplasmic mono- & oligo-nucleosomes as well as by the TUNEL method. Gastric mucosal proliferative activity was morphometrically evaluated from the PCNA-stained tissue specimens. Gastric mucosal myeloperoxidase (MPO) activity was measured to evaluate mucosal inflammation.〈section xml:id="abs1-4"〉〈title type="main"〉Results:DNA fragmentation and the number of TUNEL-positive cells, as well as PCNA-positive cell number increased significantly in both groups of H. pylori-infected mice, suggesting that levels of apoptosis and proliferation may be independent of a deficiency of one p53 allele. MPO activity in p53+/− mice and wild-type controls increased to the same level.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion:Although H. pylori inoculation per se induces an increase in cell turnover in mice, heterozygous mutation of p53 did not significantly modify the balance in cell apoptosis and proliferation.

Notizen: We previously demonstrated that Helicobacter pylori colonization evokes gastric mucosal inflammation and an extensive increase in lipid peroxides and glutathione in Mongolian gerbils. Zinc and its derivative, polaprezinc, have been reported to be potent antioxidants in gastric mucosa.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To examine the effect of polaprezinc on gastric mucosal oxidative inflammation in H. pylori-colonized Mongolian gerbils.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Sixty-eight male Mongolian gerbils were orally inoculated with H. pylori (ATCC43504, 5 × 108 CFUs/gerbil; H. pylori group) and 35 gerbils were inoculated with the culture media (control group). Twenty-two gerbils in the H. pylori and 13 gerbils in the control group were fed with diets containing polaprezinc (0.06%, 100 mg/kg, 10 times the usual clinical dose) (H. pylori + polaprezinc group, polaprezinc group). The remaining gerbils were fed a standard laboratory chow diet. Neutrophil infiltration, assessed histologically and by the activity of myeloperoxidase, the contents of CXC-chemokine (GRO/CINC-1-like protein) and the contents of thiobarbituric acid-reactive substances, was evaluated in each group 12 weeks after the inoculation. Separately, gastric mucosal leucocyte activation and capillary perfusion were also assessed using intravital microscopy 2, 4, 8 and 12 weeks after the inoculation.〈section xml:id="abs1-4"〉〈title type="main"〉Results:In all H. pylori-inoculated animals, the bacterial infection persisted throughout the experimental period. Gastric mucosal lesion formation in the H. pylori group was significantly inhibited in the H. pylori + polaprezinc group. Elevated levels of myeloperoxidase activity, GRO/CINC-1 and thiobarbituric acid-reactive substances in the H. pylori group at 12 weeks were attenuated significantly by polaprezinc treatment. Enhanced levels of venular leucocyte activation observed in the H. pylori group were attenuated significantly in the H. pylori + polaprezinc group during both the early phase (2 weeks) and late phase (12 weeks).〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion:Polaprezinc inhibited H. pylori-associated gastric mucosal oxidative inflammation, including initial micro-vascular leucocyte activation, in Mongolian gerbils.

Notizen: Background: Matrix metalloproteinases (MMPs), enzymes capable of degrading collagens and other extracellular matrix components, have been implicated in gastric ulcer formation. However, the effect on MMP expression of Helicobacter pylori, also implicated in these lesions, has not been studied to our knowledge. Aim: To seek links between H. pylori and MMP expression likely to affect gastric ulcer formation. After fibroblasts from human gastric wall were cocultured with H. pylori, concentrations of MMP-1 and -2 in the medium were determined by enzyme-linked immuno-sorbent assays. Results: Whereas MMP-1 was not detected in media from fibroblasts or H. pylori culture alone, MMP-1 was detected in cocultures (P 〈 0.01). Similar amounts of MMP-2 were detected in medium from fibroblasts cultured alone and with H. pylori. No MMP-2 production by H. pylori cultured alone was detected. Conclusions: MMP-1 appears to be important in gastric ulcer pathogenesis, and MMP-1 induction by H. pylori may impede gastric ulcer healing.