In this paper, we introduce a useful composite layer, comprising hole‐transporting materials with molybdenum oxide. By using the composite as a buffer layer on an anode, an OLED with low drive voltage can be obtained, and pixel defect formation can be effectively suppressed.

A practical enzymatic synthesis of a doubly chiral key compound, (4R,6R)-4-hydroxy-2,2,6-trimethylcyclohexanone, starting from the readily available 2,6,6-trimethyl-2-cyclohexen-1,4-dione is described. Chirality is first introduced at the C-6 position by a stereoselective enzymatic hydrogenation of the double bond using old yellow enzyme 2 of Saccharomyces cerevisiae, expressed in Escherichia coli, as a biocatalyst. Thereafter, the carbonyl group at the C-4 position is reduced selectively and stereospecifically by levodione reductase of Corynebacterium aquaticum M-13, expressed in E. coli, to the corresponding alcohol. Commercially available glucose dehydrogenase was also used for cofactor regeneration in both steps. Using this two-step enzymatic asymmetric reduction system, 9.5 mg of (4R,6R)-4-hydroxy-2,2,6-trimethylcyclohexanone/ml was produced almost stoichiometrically, with 94% enantiomeric excess in the presence of glucose, NAD ؉ , and glucose dehydrogenase. To our knowledge, this is the first report of the application of S. cerevisiae old yellow enzyme for the production of a useful compound.(4R,6R)-4-hydroxy-2,2,6-trimethylcyclohexanone (actinol) is an ideal precursor for the synthesis of naturally occurring, optically active hydroxylated carotenoids, such as zeaxanthin (8), cryptoxanthin, and structurally related compounds (1, 2). Two-step conversion of 2,6,6-trimethyl-2-cyclohexen-1,4-dione (ketoisophorone) to 4-hydroxy-2,2,6-trimethylcyclohexanone ( Fig. 1) by bacterial cells has been reported previously (3,11,12,19). However, in those cases, mixtures of isomers, (4R,6S), (4S,6R), (4R,6R), and (4S,6S), were produced and the productivity was low (ϳ2.5 mg/ml). The enzymes involved in these reactions have not yet been identified.The discovery, purification, and characterization of levodione reductase (LVR), which catalyzes the regio-and stereospecific reduction of (6R)-2,2,6-trimethylcyclohexane-1,4-dione [(6R)-levodione] to actinol, has been reported (17). This LVR has also been cloned and expressed in Escherichia coli (21). Recently, it was also reported that old yellow enzyme (OYE; EC 1.6.99.1) of Candida macedoniensis catalyzes the stereospecific hydrogenation of ketoisophorone to (6R)-levodione (4). However, this enzyme has not yet been cloned, and enzyme purification from C. macedoniensis is needed for (6R)-levodione production. Thus, we tried to use OYE of Saccharomyces cerevisiae, for which the whole-genome sequence is now available. S. cerevisiae has two OYEs: OYE2, encoded by the OYE2 gene (15), and OYE3, encoded by the OYE3 gene (10). Both of them were cloned and expressed in E. coli, and the conversion efficiencies of ketoisophorone to (6R)-levodione were then compared.Here, we report actinol production by the stereoselective hydrogenation of the double bond of ketoisophorone and by the stereoselective reduction of the carbonyl group at the C-4 position of (6R)-levodione. For the first step, hydrogenation, the OYE2 of S. cerevisiae expressed in E. coli was used, and for the second step, carbon...

To examine a possibility that matrix metalloproteinases (MMPs) participate in the pathogenesis of asthma and/or the development of asthma attack, we measured the concentrations of MMP-2, MMP-9, and their respective tissue inhibitors of metalloproteinases (TIMP)-2 and TIMP-1, in induced sputa collected from 28 patients with moderate to severe bronchial asthma. Specimens were collected during both the attack and the remission from 15 age- and sex-matched healthy control subjects. The concentration of MMP-9 was significantly (p < 0.05) higher in the patients, even during the remission, as compared to that in healthy controls. The concentrations of MMP-9 (p < 0.05) and its specific inhibitor TIMP-1 (p < 0.01), and MMP-2 (p < 0.01) in these patients during the attack were significantly higher than those in healthy controls. In these patients, the MMP-9 concentration was significantly higher (p < 0.05) during the attack than during the remission. These results suggest that MMPs and TIMPs may be involved in the pathogenesis of bronchial asthma, and that the increased MMP-9 might be involved in the development of attack in patients with chronic asthma.

The Panic Disorder Severity Scale (PDSS) [Shear et al., 1997] is rapidly gaining world-wide acceptance as a standard global severity measure of panic disorder, however, its cross-cultural validity and reliability have not been reported yet. We developed the Japanese version of the PDSS and examined its factor structure, internal consistency and inter-rater reliability and concurrent validity among Japanese patients with panic disorder with or without agoraphobia. We also established rules of thumb for interpreting PDSS total scores, taking the Clinical Global Impression severity scale as the anchoring criterion. The identical one-factor structure of the PDSS was confirmed among the Japanese patients as among the United States patients. Both internal and inter-rater reliability was excellent (Cronbach's alpha was 0.86, and ANOVA ICCs were all above 0.90). Concurrent validity of the PDSS items with self-report questionnaires tapping similar or overlapping domains was satisfactory (Pearson correlation coefficients were mostly above 0.5). Using the anchor-based approach, the following interpretative guides are suggested: among those with established panic disorder diagnosis, PDSS total scores up to 10 correspond with "mild," those between 11 and 15 with "moderate," and those at or above 16 correspond with "severe" panic disorder. The present findings support the cross-cultural generalizability of panic disorder symptomatology and of the PDSS, in particular.

BackgroundSocial anxiety disorder (SAD) is one of the most common anxiety disorders. The efficacy of cognitive behaviour therapy (CBT) has been examined but to date its effects on Quality of Life (QoL) have not been appropriately evaluated especially in the long term.The study aimed to examine, in the long term, what aspects of Quality of Life (QoL) changed among social anxiety disorder (SAD) patients treated with group cognitive behaviour therapy (CBT) and what predictors at baseline were associated with QoL.MethodsOutpatients diagnosed with SAD were enrolled into group CBT, and assessed at follow-ups for up to 12 months in a typical clinical setting. QoL was evaluated using the Short Form 36. Various aspects of SAD symptomatology were also assessed. Each of the QoL domains and scores on symptomatology were quantified and compared with those at baseline. Baseline predictors of QoL outcomes at follow-up were investigated.ResultsFifty-seven outpatients were enrolled into group CBT for SAD, 48 completed the whole program, and 44 and 40 completed assessments at the 3-month and 12-month follow-ups, respectively. All aspects of SAD symptomatology and psychological subscales of the QoL showed statistically significant improvement throughout follow-ups for up to 12 months. In terms of social functioning, no statistically significant improvement was observed at either follow-up point except for post-treatment. No consistently significant pre-treatment predictors were observed.ConclusionsAfter group CBT, SAD symptomatology and some aspects of QoL improved and this improvement was maintained for up to 12 months, but the social functioning domain did not prove any significant change statistically. Considering the limited effects of CBT on QoL, especially for social functioning, more powerful treatments are needed.