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Three known saponins, chiisanoside, 11-deoxyisochiisanoside, and isochiisanoside, and one novel saponin, 3,4-seco-4(23),20(29)-lupadiene-3,28-dioic acid 28-O-alpha-l-rhamnopyranosyl (1-->4)-beta-d-glucopyranosyl (1-->6)-beta-d-glucopyranoside, referred to as sessiloside, were isolated from a hot water extract of Acanthopanax sessiliflorus leaves. All of these saponins were lupane-type triterpene triglycosides, and their concentrations were 4.1, 1.0, 0.5, and 0.4% (w/w) of the total extract, respectively. Sessiloside and chiisanoside inhibited pancreatic lipase activity in vitro, and addition of the saponin-rich fraction to a high-fat diet suppressed the body weight gain of mice. The possibility of application of the lupane-type saponins from A. sessiliflorus leaves to the treatment of obesity is discussed.

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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.

Gentianae Radix, the dried root and rhizoma of Gentiana lutea L. (Gentianaceae), has long been used as a remedy for liver and stomach inflammation, eye troubles, etc. In this paper, the gastroprotective effects of the methanol extract of Gentian root (GM) were studied using different gastric lesion models. In pylorus-ligated rats, administration of GM in the duodenum suppressed gastric juice secretion and total acid output in a dosedependent manner. Oral or duodenum administration of GM showed significant protection against acute gastric ulcer induced by aspirin plus pylorus ligation, waterimmersion restraint stress-induced ulcers, and gastric mucosal injury induced by ethanol. Furthermore, four secoiridoid glycosides, amarogentin (A1), gentiopicroside (A2), amaroswerin (A3), and swertiamarin (A4), were obtained from Gentian root or Swertia herb, and their protective effects against stress-induced ulcers and ethanol-induced gastric mucosal injury were evaluated. The doses required for 50% inhibition (ID 50 ) of A1, A3, and A4 on stress-induced ulcers were calculated to be 5.76, 2.58, and 167 mg/kg respectively. The protective effect of A2 at 250 mg/kg was 26.5%. On ethanol-induced gastritis, 5.0 mg/kg of A1 and A3 showed remarkable suppressive effects (33.7 and 45.4%, respectively), and 20 mg/kg of A4 exhibited a suppressive effect (30.8%). The effects of A1, A3, and A4 on ethanol-induced gastric lesions were canceled by 5.0 mg/ kg indomethacin pretreatment. These results suggest that the therapeutic effects of Gentian root on gastric lesions are associated with enhanced mucosal defensive factors via the prostaglandin pathway in the cell membrane, and that secoiridoid glycosides contribute to this activity.

We investigate the structure of the relative bicentralizer algebra B(N ⊂ M, ϕ) for inclusions of von Neumann algebras with normal expectation where N is a type III1 subfactor and ϕ ∈ N * is a faithful state. We first construct a canonical flow β ϕ : R * + B(N ⊂ M, ϕ) on the relative bicentralizer algebra and we show that the W * -dynamical system (B(N ⊂ M, ϕ), β ϕ ) is independent of the choice of ϕ up to a canonical isomorphism. In the case when N = M , we deduce new results on the structure of the automorphism group of B(M, ϕ) and we relate the period of the flow β ϕ to the tensorial absorption of Powers factors. For general irreducible inclusions N ⊂ M , we relate the ergodicity of the flow β ϕ to the existence of irreducible hyperfinite subfactors in M that sit with normal expectation in N . When the inclusion N ⊂ M is discrete, we prove a relative bicentralizer theorem and we use it to solve Kadison's problem when N is amenable.2010 Mathematics Subject Classification. 46L10, 46L30, 46L36, 46L37, 46L55.

Based on the analysis on the Ocneanu/Groh-Raynaud ultraproducts and the Effros-Maréchal topology on the space vN(H) of von Neumann algebras acting on a separable Hilbert space H, we show that for a von Neumann algebra M ∈ vN(H), the following conditions are equivalent: (1) M has the Kirhcberg's quotient weak expectation property (QWEP).(2) M is in the closure of the set Finj of injective factors on H with respect to the Effros-Maréchal topology. (3) M admits an embedding i into the Ocneanu ultrapower R ω ∞ of the injective III1 factor R∞ with a normal faithful conditional expectation ε : R ω ∞ → i(M ). (4) For every ε > 0, n ∈ N and ξ1, · · · , ξn ∈ P ♮ M , there is k ∈ N and a1, · · · , an ∈ M k (C)+, such that | ξi, ξj − tr k (aiaj)| < ε (1 ≤ i, j ≤ n) holds, where tr k is the tracial state on M k (C), and P ♮ M is the natural cone in the standard form of M .

The human urinary metabolites of diltiazem were analyzed by thin-layer chromatography (TLC) and gas chromatography-mass spectrometry. Diltiazem was metabolized by deacetylation, N-demethylation, O-demethylation and conjugation. Metabolite MA, N- monodemethyl -diltiazem, was identified as a new major metabolite in human urine, and four metabolites were identified as deacetyl-diltiazem (M1), deacetyl-N- monodemethyl -diltiazem (M2), deacetyl-O-demethyl-diltiazem (M4), deacetyl-N,O-demethyl-diltiazem (M6) which were known as rat urinary metabolites. Metabolite M2, M4 and M6 were converted in part to glucuronides and/or sulfates. Unchanged diltiazem and metabolite MA were determined in human plasma and urine by TLC-densitometry. Diltiazem and metabolite MA excreted in 24-h urine were 44.4 and 48.5% of the total unconjugated form, respectively. The mean plasma level of metabolite MA was approximately one-third of diltiazem level. On the basis of these findings, a probable metabolic pathway of diltiazem in man is presented.