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Posttransplant diabetes mellitus is a frequent complication among transplant recipients. Ligation of advanced glycation end products (AGEs) with their receptor on monocytes/macrophages plays a role in diabetes complications. The enhancement of adhesion molecule expression on monocytes/macrophages activates T cells, reducing allograft survival. In previous work, we found that toxic AGEs, AGE-2 and AGE-3, induced the expression of intracellular adhesion molecule-1, B7.1, B7.2, and CD40 on monocytes, production of interferon-gamma and tumor necrosis factor alpha, and lymphocyte proliferation during human mixed lymphocyte reaction. AGE-induced up-regulation of adhesion molecule expression was involved in cytokine production and lymphocyte proliferation. Prostaglandin E2 (PGE2) concentration-dependently inhibited the actions of AGE-2 and AGE-3. The effects of PGE2 were mimicked by an EP2 receptor agonist, ONO-AE1-259-01 (11,15-O-dimethyl PGE2), and an EP4 receptor agonist, ONO-AE1-329 [16-(3-methoxymethyl)phenyl-omega-tetranor-3,7dithia PGE1]. An EP2 receptor antagonist, AH6809 (6-isopropoxy-9-oxaxanthene-2-carboxylic acid), and an EP4 receptor antagonist, AH23848 [(4Z)-7-[(rel-1S,2S,5R)-5-((1,1'-biphenyl-4-yl)methoxy)-2-(4-morpholinyl)-3-oxocyclopentyl]-4-heptenoic acid], inhibited the actions of PGE2. The stimulation of EP2 and EP4 receptors is reported to increase cAMP levels. The effects of PGE2 were reversed by protein kinase A (PKA) inhibitors and mimicked by dibutyryl cAMP and an adenylate cyclase activator, forskolin. These results as a whole indicate that PGE2 inhibited the actions of AGE-2 and AGE-3 via EP2/EP4 receptors and the cAMP/PKA pathway.

Background and purpose: Post-transplant diabetes mellitus is a frequent complication among transplant recipients. Ligation of advanced glycation end products (AGEs) with their receptor on monocytes/macrophages plays important roles in the genesis of diabetic complications. The enhancement of adhesion molecule expression on monocytes/macrophages activates T-cells, reducing allograft survival. Out of four distinct AGE subtypes (AGE-2, AGE-3, AGE-4 and AGE-5), only AGE-2 and AGE-3 induced expression of intercellular adhesion molecules (ICAMs), output of cytokines and proliferation of lymphocytes, during the mixed lymphocyte reaction (MLR). Here we have assessed the role of histamine in the actions of AGEs during the MLR. Experimental approach: Human peripheral blood cells were used in these experiments. Flow cytometry was used to examine the expression of the ICAM-1, B7.1, B7.2 and CD40. Production of the cytokine interferon-γ, and levels of cAMP were determined by elisa. Lymphocyte proliferation was determined by [3H]-thymidine uptake. Key results: Histamine concentration dependently inhibited the action of AGE-2 and AGE-3. The actions of histamine were antagonized by an H2-receptor antagonist, famotidine, and mimicked by H2/H4-receptor agonists, dimaprit and 4-methylhistamine. The effects of histamine were reversed by a protein kinase A (PKA) inhibitor, H89, and mimicked by dibutyryl cAMP and an adenylate cyclase activator, forskolin. Conclusions and implications: Histamine down-regulated AGE-2- and AGE-3-induced expression of adhesion molecules, cytokine production and lymphocyte proliferation via histamine H2 receptors and the cAMP/PKA pathway.

Cell-to-cell interaction through binding of intercellular adhesion molecule-1 (ICAM-1) and CD40 on monocytes to their ligands on T-cells plays crucial roles in cytokine production. Advanced glycation end products (AGEs) subtypes induce complications in diabetes. In a previous study, we found that glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) at 100 microg/ml induced the expressions of ICAM-1 and CD40 on monocytes and the production of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha in human peripheral blood mononuclear cells. beta(2)-adrenoceptor stimulation has been demonstrated to modulate the production of inflammatory mediators. In the present study, we found that norepinephrine, epinephrine and isoproterenol inhibited AGE-2- and AGE-3-induced adhesion expression and cytokine production in a concentration-dependent manner. The action of these catecholamines was antagonized by beta(2)-adrenoceptor antagonist, but not by alpha(1)-, alpha(2)- and beta(1)-adrenoceptor antagonist. beta(2)-adrenoceptor agonists, salbutanol and terbutaline inhibited AGE-2- and AGE-3-induced adhesion expression and cytokine production, but alpha(1)-, alpha(2)- and beta(1)-adrenoceptor agonist had no effect, indicating that the stimulation of beta(2)-adrenoceptor might improve AGEs-initiated complications in diabetes.

The up-regulation of adhesion molecule expressions on monocytes enhances cell-to-cell interactions with T cells, leading to cytokine production. Advanced glycation end products (AGEs) are modifications of proteins/lipids that become nonenzymatically glycated after contact with aldose sugars. Among various subtypes of AGEs, glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) induce the expressions of intercellular adhesion molecule-1, B7.1, B7.2, and CD40 on monocytes, the production of interferon-gamma and tumor necrosis factor-alpha, and the lymphocyte proliferation in human peripheral blood mononuclear cells. Nicotine is reported to inhibit the activation of monocytes via nicotinic acetylcholine receptor alpha7 subunit (alpha7-nAChR). In the present study, we found that nicotine inhibited the actions of AGE-2 and AGE-3. A nonselective and selective alpha7-nAChR antagonist, mecamylamine and alpha-bungarotoxin, reversed the inhibitory effects of nicotine, suggesting the involvement of alpha7-nAChR stimulation. Nicotine induced the expression of cyclooxygenase-2, prostaglandin E(2) (PGE(2)), and cAMP in the presence and absence of AGE-2 and AGE-3. PGE(2) is known to activate the EP(2)/EP(4) receptor, increasing the cAMP level and protein kinase A (PKA) activity. The actions of nicotine were reversed in part by an EP(2)-receptor antagonist, AH6809, an EP(4)-receptor antagonist, AH23848, and a PKA inhibitor, N-[2-(p-bromocinnamyl-amino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H89). These results indicate that the mechanism of action of nicotine may be partially via endogenous PGE(2) production.

An enantioselective total synthesis of (−)-cladospolide B was described. The key steps in this synthesis include(a) a Sharpless asymmetric dihydroxylation to elaborate syn diol at C-4 and C-5 positions; (b) a Mitsunobu esterification to reverse the configuration at C-11 from (S) to (R); and (c) a ring-closing metathesis to access the 12-membered macrocyclic ring.

The application of nanoparticles in the biomedical field is an exciting interdisciplinary research area in current materials science. In the present study, size-tunable and water-soluble noble metal silver nanoparticles (Ag NPs) have been successfully synthesized with the assistance of glutathione (GSH). The as-synthesized Ag NPs are ready to bind covalently with a model protein (bovine serum albumin) in mild conditions. The optical property of surface-modifiable Ag NPs was extremely sensitive to their size and the surface modification, suggesting a potential in the biomedical analysis and detection. Furthermore, Ag NPs with an average diameter of ca. 6 nm effectively suppress the proliferation of human leukemic K562 cells in the dose- and time-dependent manners, suggesting the promising potential of Ag NPs in cancer therapy.

The facile total synthesis of the (−)-Heliconol A (ent-1) as well as its diastereoisomer 18 is described, in which different reaction sequences lead to different results. The osmylation of 15 followed by hydrolysis afforded a single isomer 18, otherwise, a mixture of ent-1 and 18 resulted. Other important processes include the catalytic asymmetric CBS reduction and induced osmylation. The synthesis proceeded with a sequence of 11 steps, affording ent-1 in 9.0% and 18 in 22% overall yield, respectively.

The synthesis of heliannuol D along with the first synthesis of heliannuol B has been achieved using Mitsunobu reaction and ring-closing metathesis as the key steps.

The facile enantioselective synthesis of the di-O-methyl ethers of (-)-agatharesinol (1b), (-)-sugiresionl (2b), (+)-nyasol (3b) and (+)-tetrahydronyasol (4) were achieved in high yield. The absolute configuration of (+)-3a was confirmed via first total synthesis of (+)-3b and (+)-4.

The first efficient asymmetric total syntheses of xestodecalactones B and C have been accomplished in 10 steps with an overall yield of 22 and 20.2%, respectively. The key steps involve the utility of Evans oxazolidinone-mediated syn-aldol condensations to establish the C-9 configuration and the macrolide ring formation by intramolecular acylation. The absolute configurations of xestodecalactones B and C have been determined via these syntheses.

A general and efficient route for the synthesis of 5,6- seco -hexahydrodibenzopyran and trans -hexahydrodibenzopyran analogues was established, via a highly regio- and stereoselective S N 2′ reaction of arylcyanocuprates to enol silyl ether of α,β-epoxycyclohexanone. It was applied to the first facile total synthesis of (+)-Machaeridiol B and (+)-Machaeriol B.

Pro-inflammatory cytokines contribute to hypoxic–ischemic brain injury. Blood–brain barrier (BBB) dysfunction represents an important component of hypoxic–ischemic brain injury in the fetus. Hypoxic–ischemic injury could accentuate systemic cytokine transfer across the fetal BBB. There has been considerable conjecture suggesting that systemic cytokines could cross the BBB during the perinatal period. Nonetheless, evidence to support this contention is sparse. We hypothesized that ischemia–reperfusion increases the transfer of systemic interleukin-1β (IL-1β) across the BBB in the fetus. Ovine fetuses at 127 days of gestation were studied 4 hours after 30 minutes of bilateral carotid artery occlusion and compared with a nonischemic group. Recombinant ovine IL-1β protein was expressed from an IL-1β pGEX-2 T vector in E. coli BL-21 cells and purified. The BBB function was quantified in 12 brain regions using a blood-to-brain transfer constant with intravenous 125I-radiolabeled IL-1β (125I-IL-1β). Interleukin-1β crossed the intact BBB in nonischemic fetuses. Blood-to-brain transport of 125I-IL-1β was higher ( P < 0.05) across brain regions in fetuses exposed to ischemia–reperfusion than nonischemic fetuses. We conclude that systemic IL-1β crosses the intact fetal BBB, and that ischemia–reperfusion increases transfer of this cytokine across the fetal BBB. Therefore, altered BBB function after hypoxia–ischemia facilitates entry of systemic cytokines into the brain of the fetus.

The one-pot synthesis of 1H-inden-1-one from 1-(2-bromoaryl)prop-2-en-1-ol was described. The reaction involved a sequential intramolecular Heck reaction followed by an aerial oxidation of allylic alcohol.

A series of naturally occurring C-7 oxidized abietane diterpenes have been synthesized from racemic ferruginyl methyl ether in high yields. 6-Hydroxyl-5,6-dehydrosugiol (7) can be converted into stable xanthoperol (12) using high temperature. Among the products, the structures of sugiyl methyl ether (2) and 6(-hydroxysugiyl methyl ether (8) were determined by X-ray analysis.

Unit commitment problem (UCP) is a large scale nonlinear hybrid integer programming problem and it involves determining on/off states of units and generations of units. This paper proposes an improved particle swarm optimization (IPSO) for the solution of UCP. In the proposed approach, the on/off states of units are limited into feasible schedules by providing a new method related to a time order at first. After that, the problem is transformed into a simple economic load dispatch problem. Then this dispatch problem is solved by an improved priority list technique instead of the classical equal lambdaiteration method. All the above improvements are embedding into the framework of PSO approach for UCP. It is seen from the numerical results that the presented algorithm surely possesses a high quality and a high convergence speed. Keywords-unit commitment problem; particle swarm optimization; time order; priority list

Information on the effects of injury on neovascularization in the immature brain is limited. We investigated the effects of ischemia on cerebral cortex neovascularization after the exposure of fetuses to 30 minutes of cerebral ischemia followed by 48 hours of reperfusion (I/R-48), 30 minutes of cerebral ischemia followed by 72 hours of reperfusion (I/R-72), or sham control treatment (Non-I/R). Immunohistochemical and morphometric analyses of cerebral cortex sections included immunostaining for glial fibrillary acidic protein and collagen type IV (a molecular component of the vascular basal lamina) to determine the glial vascular network in fetal brains and Ki67 as a proliferation marker. Cerebral cortices from I/R-48 and I/R-72 fetuses exhibited general responses to ischemia, including reactive astrocyte morphology, which was not observed in Non-I/R fetuses. Cell bodies of reactive proliferating astrocytes, along with large end-feet, surrounded the walls of cerebral cortex microvessels in addition to the thick collagen type IV-enriched basal lamina. Morphometric analysis of the Non-I/R group with the I/R-48 and I/R-72 groups revealed increased collagen type IV density in I/R-72 cerebral cortex microvessels (p0.01), which also frequently displayed a sprouting appearance characterized by growing tip cells and activated pericytes. Increases in cerebral cortex basic fibroblast growth factor were associated with neovascularization. We conclude that increased neovascularization in fetal cerebral cortices occurs within 72 hours of ischemia.

article i nfo We have previously shown that increases in blood-brain barrier permeability represent an important compo- nent of ischemia-reperfusion related brain injury in the fetus. Pro-inflammatory cytokines could contribute to these abnormalities in blood-brain barrier function. We have generated pharmacological quantities of mouse anti-ovine interleukin-1β monoclonal antibody and shown that this antibody has very high sensitivity and specificity for interleukin-1β protein. This antibody also neutralizes the effects of interleukin-1β protein in vitro. In the current study, we hypothesized that the neutralizing anti-interleukin-1β monoclonal antibody at- tenuates ischemia-reperfusion related fetal blood-brain barrier dysfunction. Instrumented ovine fetuses at 127 days of gestation were studied after 30 min of carotid occlusion and 24 h of reperfusion. Groups were sham operated placebo-control- (n = 5), ischemia-placebo- (n = 6), ischemia-anti-IL-1β antibody- (n = 7), and sham-control antibody- (n = 2) treated animals. Systemic infusions of placebo (0.154 M NaCl) or anti- interleukin-1β monoclonal antibody (5.1 ± 0.6 mg/kg) were given intravenously to the same sham or ischemic group of fetuses at 15 min and 4 h after ischemia. Concentrations of interleukin-1β protein and anti-interleukin- 1β monoclonal antibody were measured by ELISA in fetal plasma, cerebrospinal fluid, and parietal cerebral cortex. Blood-brain barrier permeability was quantified using the blood-to-brain transfer constant (Ki) with α-aminoisobutyric acid in multiple brain regions. Interleukin-1β protein was also measured in parietal ce- rebral cortices and tight junction proteins in multiple brain regions by Western immunoblot. Cerebral cortical interleukin-1β protein increased (P b 0.001) after ischemia-reperfusion. After anti-interleukin-1β monoclonal antibody infusions, plasma anti-interleukin-1β monoclonal antibody was elevated (P b 0.001), brain anti- interleukin-1β monoclonal antibody levels were higher (P b 0.03), and interleukin-1β protein concentrations (P b 0.03) and protein expressions (P b 0.001) were lower in the monoclonal antibody-treated group than in placebo-treated-ischemia-reperfusion group. Monoclonal antibody infusions attenuated ischemia-reperfusion- related increases in Ki across the brain regions (P b 0.04), and Ki showed an inverse linear correlation (r = �0.65, P b 0.02) with anti-interleukin-1β monoclonal antibody concentrations in the parietal cortex, but had little effect on tight junction protein expression. We conclude that systemic anti-interleukin-1β mono- clonalantibody infusionsafter ischemiaresult inbrainanti-interleukin-1βantibodyuptake, andattenuate ische- mia-reperfusion-related interleukin-1β protein up-regulation and increases in blood-brain barrierpermeability across brain regions in the fetus. The pro-inflammatory cytokine, interleukin-1β, contributes to impaired blood- brain barrier function after ischemia in the fetus.

Traditional Double-fed Wind Generation systems are based on the vector control method, and it is dependent on motor parameters. The performance of the control system will be affected with the parameters changing,. This paper proposes a new control method based on inverse system and variable structure sliding mode(VSS) theories, through the inverse system theory, the structure of its state’s equation, obtaining the structure of the inverse system, the establishment of Wind Power Generation closed-loop control system is established. The VSS controller, designed with exponential reaching law, can improve the dynamic performance in normal operation range effectively. When the system operates with variable speed constant frequency (VSCF) and the phase voltage drops, the simulations show that the control system can control the DC link voltage steabily, maintain unity power factor, achieve the decoupling of the active and reactive power. And experiments show that the control method used in VSCF wind power system is feasible. DOI: http://dx.doi.org/10.11591/telkomnika.v11i11.3534 Full Text: PDF

Objective: High mobility group box-1 (HMGB1) plays an important role in triggering inflammatory responses in many types of diseases. In this study, we examined the involvement of HMGB1 in traumatic brain injury (TBI) and evaluated the ability of intravenously administered neutralizing anti-HMGB1 monoclonal antibody (mAb) to attenuate brain injury. Methods: Traumatic brain injury was induced in rats or mice by fluid percussion. Anti-HMGB1 mAb or control mAb was administered intravenously after TBI. Results: Anti-HMGB1 mAb remarkably inhibited fluid percussion-induced brain edema in rats, as detected by T2-weighted magnetic resonance imaging; this was associated with inhibition of HMGB1 translocation, protection of blood–brain barrier (BBB) integrity, suppression of inflammatory molecule expression, and improvement of motor function. In contrast, intravenous injection of recombinant HMGB1 dose-dependently produced the opposite effects. Experiments using receptor for advanced glycation end product (RAGE)−/−, toll-like receptor-4 (TLR4)−/−, and TLR2−/− mice suggested the involvement of RAGE as the predominant receptor for HMGB1. Interpretation: Anti-HMGB1 mAb may provide a novel and effective therapy for TBI by protecting against BBB disruption and reducing the inflammatory responses induced by HMGB1. ANN NEUROL 2012;72:373–384

Vector control method is the common way in traditional Double-fed Wind Generation, but it is more dependent on motor parameters, once the operational situation changes, the effect of the system control will be affected. This paper proposes a control method based on inverse system, through the inverse system theory, the state equation of doubly-fed induction motor (DFIG) and power converter, to construct the structure of the DFIG wind power generation inverse control system. Finally, the corresponding wind power generation closed-loop control system is established. When the system operates in variable speed constant frequency (VSCF) and the phase voltage drops, the simulation results show that the control system can keep the DC link voltage steady, maintain unity power factor, achieve the decoupling of the active and reactive power. It proves that this control method used in VSCF wind power generation is feasible.

Consumer decision support systems (CDSSs) help online users make purchasing decisions in e-commerce Web sites. To more effectively compare the usefulness of the various functionalities and interface features of such systems, we have developed a simulation environment for decision tasks of any scale and structure. Furthermore, we have identified three criteria in an evaluation framework for assessing the quality of such CDSSs: users’ cognitive effort, preference expression effort, and decision accuracy. A set of experiments carried out in such simulation environments showed that most CDSSs employed in current e-commerce Web sites are suboptimal. On the other hand, a hybrid decision strategy based on four existing ones was found to be more effective. The interface improvements based on the new strategy correspond to some of the advanced tools already developed in the research field. This result is therefore consistent with our earlier work on evaluating CDSSs with real users. That is, some advanced tools do produce more accurate decisions while requiring a comparable amount of user effort. However, the simulation environment will enable us to efficiently compare more advanced tools among themselves, and indicate further opportunities for functionality and interface improvements.

Background and Purpose— High mobility group box-1 (HMGB1) exhibits inflammatory cytokine-like activity in the extracellular space. We previously demonstrated that intravenous injection of anti-HMGB1 monoclonal antibody (mAb) remarkably ameliorated brain infarction induced by middle cerebral artery occlusion in rats. In the present study, we focused on the protective effects of the mAb on the marked translocation of HMGB1 in the brain, the disruption of the blood–brain barrier (BBB), and the resultant brain edema. Methods— Middle cerebral artery occlusion in the rat was used as the ischemia model. Rats were treated with anti-HMGB1 mAb or control IgG intravenously. BBB permeability was measured by MRI. Ultrastructure of the BBB unit was observed by transmission electron microscope. The in vitro BBB system was used to study the direct effects of HMGB1 in BBB components. Results— HMGB1 was time-dependently translocated and released from neurons in the ischemic rat brain. The mAb reduced the edematous area on T2-weighted MRI. Transmission electron microscope observation revealed that the mAb strongly inhibited astrocyte end feet swelling, the end feet detachment from the basement membrane, and the opening of the tight junction between endothelial cells. In the in vitro reconstituted BBB system, recombinant HMGB1 increased the permeability of the BBB with morphological changes in endothelial cells and pericytes, which were inhibited by the mAb. Moreover, the anti-HMGB1 mAb facilitated the clearance of serum HMGB1. Conclusions— These results indicated that the anti-HMGB1 mAb could be an effective therapy for brain ischemia by inhibiting the development of brain edema through the protection of the BBB and the efficient clearance of circulating HMGB1.

Advanced glycation end product (AGE) subtypes, proteins or lipids that become glycated after exposure to sugars, induce complications in diabetes. Among the various AGE subtypes, glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) have been indicated to play roles in inflammation in diabetic patients. The engagement of AGEs and receptor for AGEs activates monocytes. Because the engagement of intercellular adhesion molecule-1 (ICAM-1), B7.1, B7.2, and CD40 on monocytes with their ligands on T cells plays roles in cytokine production, we investigated the effects of AGE-2 and AGE-3 on the expressions of ICAM-1, B7.1, B7.2, and CD40 on monocytes, the production of interferon gamma and tumor necrosis factor alpha, and the lymphocyte proliferation in human peripheral blood mononuclear cells and their modulation by prostaglandin E(2) (PGE(2)). AGE-2 and AGE-3 induced the expressions of adhesion molecule, the cytokine production, and the lymphocyte proliferation. PGE(2) concentration-dependently inhibited the actions of AGE-2 and AGE-3. The effects of PGE(2) were mimicked by an E-prostanoid (EP)(2)-receptor agonist, 11,15-O-dimethyl prostaglandin E(2) (ONO-AE1-259-01), and an EP(4) receptor agonist, 16-(3-methoxymethyl)phenyl-omega-tetranor-3,7-dithia prostaglandin E(1) (ONO-AE1-329). An EP(2)-receptor antagonist, 6-isopropoxy-9-oxaxanthene-2-carboxylic acid (AH6809), and an EP(4)-receptor antagonist, (4Z)-7-[(rel-1S,2S,5R)-5-(1,1'-biphenyl-4-yl)methoxy)-2-(4-morpholinyl)-3-oxocyclopentyl]-4-heptenoic acid (AH23848), inhibited the actions of PGE(2). The stimulation of EP(2) and EP(4) receptors is reported to increase cAMP levels. The effects of PGE(2) were reversed by a protein kinase A (PKA) inhibitor, H89, and mimicked by a dibutyryl cAMP and an adenylate cyclase activator, forskolin. These results as a whole indicated that PGE(2) inhibited the actions of AGE-2 and AGE-3 via EP(2)/EP(4) receptors and the cAMP/PKA pathway.

Emergencies have been bringing huge damage, even worse when emergency event chain reaction is formed. Different emergency evolution models have been studied in the systematic perspective to find out common characters and correlation among four various emergency events. We propose an academic framework with four hierarchies including single event, event chain, event network, and event supernetwork and discuss how to response to the emergency in different hierarchies. We also prove its efficiency by discussing a real case. This paper can provide useful guidelines to prevent broadcasting of disaster and macro precaution.

The facile total synthesis of the (−)-Heliconol A (ent-1) as well as its diastereoisomer 18 is described, in which different reaction sequences lead to different results. The osmylation of 15 followed by hydrolysis afforded a single isomer 18, otherwise, a mixture of ent-1 and 18 resulted. Other important processes include the catalytic asymmetric CBS reduction and induced osmylation. The synthesis proceeded with a sequence of 11 steps, affording ent-1 in 9.0% and 18 in 22% overall yield, respectively.

The one-pot synthesis of 1H-inden-1-one from 1-(2-bromoaryl)prop-2-en-1-ol was described. The reaction involved a sequential intramolecular Heck reaction followed by an aerial oxidation of allylic alcohol.

A simple and efficient synthesis of tribenzohexadehydro[12]annulene and related derivatives in the ionic liquid 1-butyl-3-methylimidazolium tetrafluoroborate is described. A Sonogashira coupling reaction is the key step. In this system, the amount of CuI normally used can be reduced so that homocoupling is minimized.

The technology of headspace coupled GC/MS was used to study the volatile components of both fresh and dry Perilla frutescens. Twenty-three components were identified of which β-caryophyllene (24.2%), thujopsene (13.0–20.8%), perillaldehyde (14.2–15.1%) and (Z)-β-farnesene (3.3–10.9%) were major.

Two diastereoisomers of silybin, silybin A and silybin B, were separated from silymarin by HPLC in our previous study. The present study assessed the effects of the diastereoisomers on cell apoptosis, and compared these with their mixture, silybin, in human chronic myeloid leukemia K562 cells. Both isomers showed stronger effects on cell growth inhibition and apoptosis induction than silybin. Compared with silybin B, silybin A showed higher effects on the production of intracellular reactive oxygen species and Ca2+. These results suggest that silybin A and silybin B have similar potency on apoptosis induction with different oxidative effects. Antagonistic effects may exist between silybin A and silybin B, partially through ROS production and Ca2+ increase.

Critiquing techniques provide an easy way for users to feedback their preferences over one or several attributes of the products in a conversational recommender system. While unit critiques only allow users to critique one attribute of the products each time, a well-generated set of compound critiques enables users to input their preferences on several attributes at the same time, and can potentially shorten the interaction cycles in finding the target products. As a result, the dynamic generation of compound critiques is a critical issue for designing the critique-based conversational recommender systems. In earlier research the Apriori algorithm has been adopted to generate compound critiques from the given data set. In this paper we propose an alternative approach for generating compound critiques based on the multi-attribute utility theory (MAUT). Our approach automatically updates the weights of the product attributes as the result of the interactive critiquing process. This modification of weights is then used to determine the compound critiques according to those products with the highest utility values. Our experiments show that the compound critiques generated by this approach are more efficient in helping users find their target products than those generated by the Apriori algorithm. © Springer-Verlag Berlin Heidelberg 2006.

Preference-based search (PBS) is a popular approach for helping consumers find their desired items from online catalogs. Currently most PBS tools generate search results by a certain set of criteria based on preferences elicited from the current user during the interaction session. Due to the incompleteness and uncertainty of the user's preferences, the search results are often inaccurate and may contain items that the user has no desire to select. In this paper we develop an efficient Bayesian filter based on a group of users' past choice behavior and use it to refine the search results by filtering out items which are unlikely to be selected by the user. Our preliminary experiment shows that our approach is highly promising in generating more accurate search results and saving user's interaction effort. Copyright 2007 ACM.