Background-It has been reported that the acidity of gastric contents could be an important factor in regulating jejunal flora. Aims-To investigate the eVects of omeprazole induced changes in gastric pH on jejunal flora and bile acid metabolism. Methods-Twenty one patients with gastric ulcer and 19 healthy volunteers were studied. Deconjugation of bile acids was detected using a bile acid breath test. Jejunal fluid was aspirated using a double lumen tube with a rubber cover on the tip and deconjugation was examined using thin layer chromatography. Fat malabsorption was detected by a triolein breath test. Results-In the bile acid breath test, expired breath samples from all patients and healthy volunteers showed significantly greater 14 CO 2 specific activity after omeprazole treatment (20 mg/day) than before treatment. Bacterial overgrowth was found in the jejunal fluid and gastric juice of both ulcer patients and healthy volunteers after omeprazole treatment. The following species were identified: Escherichia coli, Candida albicans, enterococcus, Lactobacillus bifidus, Bacteroides vulgatus, B uniformis, Eubacterium lentum, Eu parvum, and Corynebacterium granulosum. All of these species, except E coli and C albicans, deconjugate bile acids. There was a significant correlation between 14 CO 2 activity and gastric pH, both before and after omeprazole treatment in both groups. The triolein breath test revealed impaired fat absorption in both groups after omeprazole treatment. Conclusions-Both patients with gastric ulcer and healthy volunteers exhibited increased deconjugation of bile acids caused by bacterial overgrowth in the jejunum and fat malabsorption after omeprazole treatment. The bacterial overgrowth consisted of both anaerobes and aerobes with deconjugation ability and was probably associated with an omeprazole induced shift to neutral pH in the gastric juice. (Gut 1998;42:266-271)

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We isolated and characterized 23 compounds, including a new iridoid named gentiolutelin and its dimethyl acetal, and a new lignan named gentioluteol from fresh roots (including small amounts of rhizome) of Gentiana lutea cultivated in Japan (Hokkaido). The structures of gentiolutelin and gentioluteol were determined as (1S,2R,3S,5R)-3-hydroxy-2-methyl-5-(2-oxoethyl)-cyclopentanecarboxylic acid methyl ester and (7R,8S,8¢S)-4,4¢,8,9-tetrahydroxy-3,3¢,5-trimethoxy-7,9¢-epoxylignan, respectively, on the basis of chemical and spectroscopic evidence. It was noteworthy that gentiopicroside, known to be a major secoiridoid glycoside in Gentian root, was not detected from the fresh roots of 3-year-old G. lutea.

Abstractof phospholipase A 2 and acetyltransferase on membrane alkylacyl phospholipids. PAF was Background -The role of platelet activating factor (PAF) in asthma remains originally described as a substance released from basophils sensitised with IgE.1 controversial. The priming effect of PAF on leukotriene B 4 (LTB 4 ) release, 5-lipThe stimulation of neutrophils by PAF results in the release of lysosomal enzymes and oxygenase activity, and intracellular calcium levels in asthmatic neutrophils was superoxide anions and the generation of leukotriene (LT) B 4 . 2 3 The biological effects of examined. Methods -LTB 4 and other lipoxygenase PAF, including airway microvascular leakage, bronchoconstriction, sustained increase in metabolites in neutrophils obtained from 17 asthmatic patients and 15 control sub-bronchial smooth muscle responsiveness, and pulmonary vasoconstriction, mimic many clinjects were measured by reverse phase-high performance liquid chromatography (RP-ical features of asthma. Thus, PAF has been considered an important mediator in asthma HPLC). Intracellular calcium levels were monitored using the fluorescent probe as well as in other lung disorders. 4 However, clinical studies 5 6 with PAF receptor antagonist fura-2. Results -The mean (SD) basal LTB 4 re-have not provided evidence for a pivotal role for PAF in asthma. lease from neutrophils was not significantly different between the two groups It was recently reported that PAF acetylhydrolase activity is absent in 4% of the Japan-(0.05 (0.01) vs 0.03 (0.02) ng/10 6 cells); however, when stimulated with calcium iono-ese population.7 This deficiency, inherited in an autosomal recessive fashion and observed phore A23187 (2.5 M), neutrophils from asthma patients released more LTB 4 than thus far only in the Japanese population, 7 completely abolishes enzymatic activity.8 Acquired cells from control subjects (15.7 (1.2) vs 9.9 (1.6) ng/10 6 cells). Although PAF alone deficiency of PAF acetylhydrolase activity has been reported in patients with asthma. 9 Indid not alter LTB 4 release, it enhanced the response to subsequent A23187 stimu-terestingly, the prevalence of this trait is higher in children with severe asthma, suggesting that lation. This effect was observed following treatment for five minutes with PAF at the decreased ability to degrade PAF allows the accumulation of phospholipid to provoke or concentrations >1.0 M. The maximal effect was seen with 5.0 M PAF+2.5 M amplify the asthmatic response. This discovery may allow the identification of individuals pre-A23187 (62.7 (2.2) vs 18.6 (2.3) ng/10 6 cells). Pretreatment with PAF also increased 5-disposed to asthma, and also provides strong evidence that PAF plays an important role in lipoxygenase activity and intracellular calcium levels in neutrophils from asthmatic asthma. 10On the other hand, early and late phase patients to a greater extent than in those from non-asthmatic patients.reactions have been observed in asthmatic Keywords: platelet activating factor (PAF), priming phils from asth...