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We aimed to determine if successful or failed eradication of Helicobacter pyloriwith triple therapy causes any difference in gastric mucosal histology. Japanese H. pylori-positivepatients with a healed peptic ulcer received high (n= 112) or low (n= 113) doses of triple therapy (omeprazole, amoxicillin and clarithromycin) for 1 week. Biopsies from the greater curvature of the central antrum and upper corpus were taken 6 weeks and 30 weeks after treatment completion, and gastric mucosal histology compared between successful (n= 171) and failed (n= 34) eradication groups. Morphological variables of gastritis were graded according to the updated Sydney System. Successful eradication therapy was defined as improvement in inflammation, neutrophil activity and atrophy; failed eradication therapy as improvement in inflammation and neutrophil activity only. Gastric mucosal atrophy gradually improved (in addition to improvements in inflammation and neutrophil activity) with successful eradication of H. pyloriinfection.Conclusions: Improvements in atrophy, inflammation and neutrophil activity were confirmed histopathologically following successful H. pylorieradication therapy, but improvements in inflammation and neutrophil activity were also seen after failed eradication therapy. No improvement in metaplasia was observed, irrespective of the success or failure of treatment. Since atrophy is known to be involved in the aetiology of gastric cancer, H. pylorieradication might prevent development of gastric cancer.

The OH reaction rate constants have been measured for CH3OCF2CHF2, CHF2OCH2CF2CHF2, CHF2OCH2CF2CF3, and CF3CH2OCF2CHF2 over the temperature range 250−430 K. Kinetic measurements have been carried out using the flash photolysis, laser photolysis, and discharge flow methods, combined respectively with the laser-induced fluorescence technique to monitor the OH radical concentrations. The influence of impurities contained in the samples of fluorinated ethers has been investigated by means of sample purification using gas chromatography. No sizable effect of impurities was found on the measured rate constants of these fluorinated ethers, if the purified samples were used in the kinetic measurements. The Arrhenius rate constants have been determined from the respective kinetic data as k(CH3OCF2CHF2) = 2.60 × 10^-12 exp[−(1420 ± 170)/T], k(CHF2OCH2CF2CHF2) = 2.49 × 10^-12 exp[−(1500 ± 170)/T], k(CHF2OCH2CF2CF3) = 2.14 × 10^-12 exp[−(1580 ± 170)/T], and k(CF3CH2OCF2CHF2) = 1.49 × 10^-12 exp[−(1520 ± 170)/T] cm³ molecule^-1 s^-1, where the quoted errors represent the 95% confidence level and included systematic errors. Uncertainty factors at 298 K (with the formulation of the NASA panel for data evaluation¹⁴) for these fluorinated ethers were 1.1.

Ab initio calculations have been carried out for the PH2 + O2 reaction by using Gaussian-2 theory, which is considered a key reaction to understand low-temperature phosphine combustion. It has been suggested that the reaction proceeds through two main routes at low temperatures. One is the reaction to yield OH radicals, and the other yields hydrogen atoms. Of the two reactions, the latter seems to be the chain branching process, which enables the spontaneous ignition of phosphine at room temperature.

The OH reaction rate constants have been measured for CF3CH2OH, CF3CF2CH2OH, and CF3CH(OH)CF3 over the temperature range 250−430K. Kinetic measurements have been carried out using the discharge flow, laser photolysis, and flash photolysis methods, combined respectively with the laser-induced fluorescence technique to monitor the OH radical concentrations. The influence of impurities contained in the sample of CF3CF2CH2OH has been investigated by means of sample purification using gas chromatography. No sizable effect of impurities was found on the measured rate constants of these three fluorinated alcohols. The Arrhenius rate constants have been determined from the respective kinetic data as k(CF3CH2OH) = (2.00 ± 0.37) × 10^-12 exp[−(890 ± 60)/T], k(CF3CF2CH2OH) = (1.40 ± 0.27) × 10^-12 exp[−(780 ± 60)/T], and k(CF3CH(OH)CF3) = (6.99 ± 1.56) × 10^-13 exp[−(990 ± 70)/T] cm³ molecule^-1 s^-1. A method of predicting the OH reaction rate constants for fluorinated alcohols, hydrofluorocarbons, alkanes, and alcohols has been proposed.

Ab initio G-2 calculations have been carried out for a number of elementary reactions relevant to low-temperature silane oxidation. The calculations have been made to identify the chain-branching process which enables the spontaneous ignition of silane at room temperature. Extensive calculations have also been made for the reactions of major intermediates with hydrogen atoms and water vapor.

Artificially layered Bi2Sr2Can-1CunO4+n films were synthesized by sequential sputter deposition of BiO, SrCu0.5O1.5 and CaCuO2 layers. Annealing behavior of these films which were irradiated by Ar ions was studied. Defect assisted improvement of their crystalline perfection is expected which might results in the improvement of the superconducting properties of these films. An artificial film, such as an intergrowth of 2223 and 2234 phases, and superstructure films of (2245)1(2201)1 and (2234)1(2212)1, were irradiated by Ar ions (150 keV, 2-10×1012 ions/cm2) and annealed at 730 °C. An improvement of superconducting transition temperatures were observed.

Biologically active amidated gastrin is synthesized by carboxyl-terminal alpha-amidation of a glycine-extended progastrin post-translational processing intermediate (G-Gly). Although plasma levels of G-Gly are equivalent to those of gastrin, G-Gly has essentially no acute effect on gastric acid secretion. However, we have observed that inhibition of gastrin amidation leads to increased plasma concentrations of G-Gly and enhanced gastric acid secretion. We hypothesized, therefore, that G-Gly might have a chronic effect to increase H+,K(+)-ATPase expression in gastric parietal cells. In the present studies, we observed that a 2-day preincubation with G-Gly significantly enhanced histamine-stimulated [14C]aminopyrine uptake by isolated canine gastric parietal cells but acutely administered G-Gly had no effect. On Northern blot analysis, both G-Gly and gastrin dose-dependently increased H+,K(+)-ATPase alpha-subunit gene expression with maximal induction (225 +/- 35 and 170 +/- 29% of basal, mean +/- S.E.) achieved at concentrations of 10(-9) M G-Gly and 10(-8) M gastrin, respectively. Using an H+,K(+)-ATPase alpha-subunit gene-luciferase chimeric reporter construct transfected into primary cultured parietal cells, we observed that both G-Gly and gastrin increased luciferase activity in a manner similar to that obtained by Northern blot analysis. L365,260, a specific gastrin/CCKB receptor antagonist, completely reversed the stimulation of luciferase activity induced by gastrin but had no effect on G-Gly-stimulated activity. Gastrin increased [Ca2+]i, although G-Gly did not, however, genistein (a tyrosine kinase inhibitor) significantly reduced induction of luciferase activity by both G-Gly and gastrin. Specific binding of 125I-Leu15-G2-17-Gly to gastric parietal cells was dose-dependently displaced by G2-17-Gly but not by gastrin nor L365,260. Gastrin peptides truncated at the carboxyl- (G1-13) and amino terminus (G5-17-Gly) both induced H+,K(+)-ATPase alpha-subunit gene expression and inhibited 125I-Leu15-G2-17-Gly binding, but were less potent than G2-17-Gly. These data indicate that G-Gly may have a functional role in potentiating gastric acid secretagogue action via enhanced expression of the gene responsible for H+ generation through action at a novel receptor that can be distinguished from the gastrin/CCKB receptor. Thus, both the substrate and product of the terminal progastrin processing reaction appear to have complementary functions in regulation of gastric acid secretion.

Epidermal growth factor (EGF) acutely inhibits acid secretion; however, prolonged administration of EGF has been reported to increase acid production. We undertook these studies to examine whether the physiological effects of EGF on acid secretion are mediated by regulation of gastric H+,K+-ATPase, the principle enzyme responsible for acid secretion. EGF in concentrations equivalent to those in plasma increased H+,K(+)-ATPase alpha-subunit mRNA levels. Using H+,K(+)-ATPase-luciferase constructs transfected into primary cultured parietal cells, a significant step up in EGF inducibility was observed between bases -162 and -156 (5'-GACATGG-3') relative to the cap site. This EGF response element (ERE) conferred EGF inducibility when linked to homologous and heterologous promoters. The ERE is homologous to the 3' half-site of the c-fos serum response element to which rNFIL-6, rE12, and SRE-ZBP bind. Electrophoretic mobility shift assays using an ERE probe and parietal cell nuclear extracts revealed a specific DNA-protein complex, the formation of which was changed by neither E12 and NFIL-6 consensus oligonucleotides nor antibodies for NFIL-6, SRE-ZBP, and E12. Our studies indicate that EGF induces gastric H+,K(+)-ATPase alpha-subunit gene expression via an interaction between a specific ERE and a novel transcriptional factor and that this may be a physiologic mechanism by which EGF regulates acid secretion.

Perturbation effects of additional linkers on the spin−spin coupling in biphenyl-4,4‘-dinitrene (1) were examined by introducing a linking group between 2- and 2‘-positions of 1. Five different doubly linked systems showed triplet ESR spectra corresponding to quinonoid dinitrenes. Curie law analyses suggested that all those triplet states were thermally excited triplet states. In addition, the singlet−triplet energy gaps, which were determined by the Curie law analyses, were well correlated with their corresponding zero-field-splitting (zfs) D values. The result could be explained by the stability of dinitrene character which is estimated from the resonance energy of the intervening π-system. Our semiempirical molecular orbital calculations supported the experimental correlation between the singlet−triplet energy gap and the zfs D value.