Biphenyls from aerial parts of Ribes takare

Three new biphenyls, 4,7,8-trimethoxy-2,3-methylenedioxydibenzofuran (1), 7-hydroxy-4,8dimethoxy-2,3-methylenedioxydibenzofuran (2), and 3',5-dimethoxy-3,4-methylenedioxybiphenyl (3), along with eighteen known compounds (4-21) were isolated from the aerial part of Ribes takare D. Don. Their structures were elucidated on the basis of spectroscopic data. Compound 1 and compound 2 showed mild alpha-glucosidase inhibitory activity. (C) 2013 Guo-You Li and Dong-Mei Fang. Published by Elsevier B.V. on behalf of Chinese Chemical Society. All rights reserved

A semi-active H∞ control strategy with application to the vibration suppression of nonlinear high-rise building under earthquake excitations

Different from previous researches which mostly focused on linear response control of seismically excited high-rise buildings, this study aims to control nonlinear seismic response of high-rise buildings. To this end, a semi-active control strategy, in which H∞ control algorithm is used and magneto-rheological dampers are employed for an actuator, is presented to suppress the nonlinear vibration. In this strategy, a modified Kalman–Bucy observer which is suitable for the proposed semi-active strategy is developed to obtain the state vector from the measured semi-active control force and acceleration feedback, taking into account of the effects of nonlinearity, disturbance and uncertainty of controlled system parameters by the observed nonlinear accelerations. Then, the proposed semi-active H∞ control strategy is applied to the ASCE 20-story benchmark building when subjected to earthquake excitation and compared with the other control approaches by some control criteria. It is indicated that the proposed semi-active H∞ control strategy provides much better control performances by comparison with the semi-active MPC and Clipped-LQG control approaches, and can reduce nonlinear seismic response and minimize the damage in the buildings. Besides, it enhances the reliability of the control performance when compared with the active control strategy. Thus, the proposed semi-active H∞ control strategy is suitable for suppressing the nonlinear vibration of high-rise buildings

Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death

<p>Abstract</p> <p>Background</p> <p>Chronic <it>N</it>-Methyl-d-aspartate (NMDA) administration to rats is reported to increase arachidonic acid signaling and upregulate neuroinflammatory markers in rat brain. These changes may damage brain cells. In this study, we determined if chronic NMDA administration (25 mg/kg i.p., 21 days) to rats would alter expression of pro- and anti-apoptotic factors in frontal cortex, compared with vehicle control.</p> <p>Results</p> <p>Using real time RT-PCR and Western blotting, chronic NMDA administration was shown to decrease mRNA and protein levels of anti-apoptotic markers Bcl-2 and BDNF, and of their transcription factor phospho-CREB in the cortex. Expression of pro-apoptotic Bax, Bad, and 14-3-3ζ was increased, as well as Fluoro-Jade B (FJB) staining, a marker of neuronal loss.</p> <p>Conclusion</p> <p>This alteration in the balance between pro- and anti-apoptotic factors by chronic NMDA receptor activation in this animal model may contribute to neuronal loss, and further suggests that the model can be used to examine multiple processes involved in excitotoxicity.</p

Systemic administration of urocortin after intracerebral hemorrhage reduces neurological deficits and neuroinflammation in rats

<p>Abstract</p> <p>Background</p> <p>Intracerebral hemorrhage (ICH) remains a serious clinical problem lacking effective treatment. Urocortin (UCN), a novel anti-inflammatory neuropeptide, protects injured cardiomyocytes and dopaminergic neurons. Our preliminary studies indicate UCN alleviates ICH-induced brain injury when administered intracerebroventricularly (ICV). The present study examines the therapeutic effect of UCN on ICH-induced neurological deficits and neuroinflammation when administered by the more convenient intraperitoneal (i.p.) route.</p> <p>Methods</p> <p>ICH was induced in male Sprague-Dawley rats by intrastriatal infusion of bacterial collagenase VII-S or autologous blood. UCN (2.5 or 25 μg/kg) was administered i.p. at 60 minutes post-ICH. Penetration of i.p. administered fluorescently labeled UCN into the striatum was examined by fluorescence microscopy. Neurological deficits were evaluated by modified neurological severity score (mNSS). Brain edema was assessed using the dry/wet method. Blood-brain barrier (BBB) disruption was assessed using the Evans blue assay. Hemorrhagic volume and lesion volume were assessed by Drabkin's method and morphometric assay, respectively. Pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) expression was evaluated by enzyme-linked immunosorbent assay (ELISA). Microglial activation and neuronal loss were evaluated by immunohistochemistry.</p> <p>Results</p> <p>Administration of UCN reduced neurological deficits from 1 to 7 days post-ICH. Surprisingly, although a higher dose (25 μg/kg, i.p.) also reduced the functional deficits associated with ICH, it is significantly less effective than the lower dose (2.5 μg/kg, i.p.). Beneficial results with the low dose of UCN included a reduction in neurological deficits from 1 to 7 days post-ICH, as well as a reduction in brain edema, BBB disruption, lesion volume, microglial activation and neuronal loss 3 days post-ICH, and suppression of TNF-α, IL-1β, and IL-6 production 1, 3 and 7 days post-ICH.</p> <p>Conclusion</p> <p>Systemic post-ICH treatment with UCN reduces striatal injury and neurological deficits, likely via suppression of microglial activation and inflammatory cytokine production. The low dose of UCN necessary and the clinically amenable peripheral route make UCN a potential candidate for development into a clinical treatment regimen.</p

A Novel Metagenomic Short-Chain Dehydrogenase/Reductase Attenuates Pseudomonas aeruginosa Biofilm Formation and Virulence on Caenorhabditis elegans

In Pseudomonas aeruginosa, the expression of a number of virulence factors, as well as biofilm formation, are controlled by quorum sensing (QS). N-Acylhomoserine lactones (AHLs) are an important class of signaling molecules involved in bacterial QS and in many pathogenic bacteria infection and host colonization are AHL-dependent. The AHL signaling molecules are subject to inactivation mainly by hydrolases (Enzyme Commission class number EC 3) (i.e. N-acyl-homoserine lactonases and N-acyl-homoserine-lactone acylases). Only little is known on quorum quenching mechanisms of oxidoreductases (EC 1). Here we report on the identification and structural characterization of the first NADP-dependent short-chain dehydrogenase/reductase (SDR) involved in inactivation of N-(3-oxo-dodecanoyl)-L-homoserine lactone (3-oxo-C12-HSL) and derived from a metagenome library. The corresponding gene was isolated from a soil metagenome and designated bpiB09. Heterologous expression and crystallographic studies established BpiB09 as an NADP-dependent reductase. Although AHLs are probably not the native substrate of this metagenome-derived enzyme, its expression in P. aeruginosa PAO1 resulted in significantly reduced pyocyanin production, decreased motility, poor biofilm formation and absent paralysis of Caenorhabditis elegans. Furthermore, a genome-wide transcriptome study suggested that the level of lasI and rhlI transcription together with 36 well known QS regulated genes was significantly (≥10-fold) affected in P. aeruginosa strains expressing the bpiB09 gene in pBBR1MCS-5. Thus AHL oxidoreductases could be considered as potent tools for the development of quorum quenching strategies

Formation mechanism and control of flaring in forward tube spinning

Forward tube spinning (or flow forming) is usually employed to produce cylindrically tubular components to meet the increasing requirements for manufacturing high-performance and light-weight products at low cost and short lead-time. In forward tube spinning, flaring defect may easily occur at the opening end of tubes, which would deteriorate the quality of the spun tubular parts and reduce the material utilization. In addition, an additional operation is needed to trim away the flared end of the spun tabular parts. Efficient control of flaring formation is thus a non-trivial issue in forward tube spinning process and thus become one of the critical bottleneck issues to be addressed in this unique forming process. In this study, the formation mechanism of flaring was systematically studied via finite element (FE) simulation and an in-depth understanding was thus established, which forms basis for control of flaring forming in forward tube spinning. Based on the simulated material flow behaviour, it is found that flaring is formed by the material in non-spun zone flowing away from the mandrel. This material flow behaviour is caused by the pile up and the decreasing stiffness of the non-spun zone. In addition, the effects of process parameters on flaring were investigated to reduce flaring. The results show that the smaller feed rate and thickness reduction per pass can reduce the maximum flaring to a certain extent, but is very limited. To increase productivity and shorten forming lead-time, an efficient method to control flaring was proposed using a pressing ring in front of the roller based on the formation mechanism of flaring. FE simulation was further used to study the feasibility and demonstrates the validity of the method in terms of reducing and even eliminating the flaring with a short production lead-time. Finally, the forward tube spinning experiments were carried out to validate the formation mechanism of flaring and the method to avoid or eliminate the flaring formation in forward tube spinning