Effect of Bordered Pit Torus Position on Permeability in Chinese Yezo Spruce

The effect of different bordered pit torus positions on wood permeability was studied by air-drying and ethanol-exchange drying for green wood and by soaking in water, then followed by ethanol-exchange drying for air-dried wood of Chinese yezo spruce (Picea jezoensis var. komarovii). The results showed that different treatments caused different pit torus positions and different wood permeability. The air-drying treatment resulted in pit torus aspiration and low permeability for sapwood. The ethanol-exchange drying treatment left the pit torus in an unaspirated position and resulted in high permeability for sapwood. Soaking in water followed by ethanol-exchange drying caused deaspiration of a part of pit torus and increased permeability for both sapwood and heartwood

Enzyme catalysed Pictet-Spengler formation of chiral 1,1'-disubstituted- and spiro-tetrahydroisoquinolines

The Pictet-Spengler reaction (PSR) involves the condensation and ring closure between a β-arylethylamine and a carbonyl compound. The combination of dopamine and ketones in a PSR leads to the formation of 1,1′-disubstituted tetrahydroisoquinolines (THIQs), structures that are challenging to synthesize and yet are present in a number of bioactive natural products and synthetic pharmaceuticals. Here we have discovered that norcoclaurine synthase from Thalictrum flavum (TfNCS) can catalyse the PSR between dopamine and unactivated ketones, thus facilitating the facile biocatalytic generation of 1,1′-disubstituted THIQs. Variants of TfNCS showing improved conversions have been identified and used to synthesize novel chiral 1,1′-disubstituted and spiro-THIQs. Enzyme catalysed PSRs with unactivated ketones are unprecedented, and, furthermore, there are no equivalent stereoselective chemical methods for these transformations. This discovery advances the utility of enzymes for the generation of diverse THIQs in vitro and in vivo

Demand response from the control of aggregated inverter air conditioners

Inverter air conditioners (ACs) account for a large proportion of air conditioning loads in many countries and, thus, contribute significantly to the peak loads in these areas, especially in summer. On the other hand, as an important category of thermostatically controlled load with thermal energy storage capability, inverter ACs also have the potential to provide considerable flexibility for electric power systems that are faced with increasing challenges posed by high penetration of renewable power generation. This paper focuses on the demand response from the control of the aggregated inverter ACs for load reduction. A virtual energy storage system (VESS) model that encapsulates the room with an inverter AC was established based on the electric model of an inverter AC and the thermodynamic model of a room. Based on the VESS model, a virtual state of charge (VSOC) priority-based load reduction control method with temperature holding and linear recovery strategies was proposed. The VSOC priority based control was designed to decrease the negative impact of load reduction on customers’ thermal comfort from the perspective of the whole AC population. The temperature holding strategy was designed to reduce the electric power of an AC while ensuring that the indoor temperature is always below the allowable limit. The linear recover strategy was proposed to reduce the load rebound after load reduction. Four cases were studied regarding the operation and load reduction of the 100 inverter ACs, and the simulation results verified the models established and the effectiveness and advantages of the proposed load reduction control method

Glucosylceramide synthase upregulates MDR1 expression in the regulation of cancer drug resistance through cSrc and β-catenin signaling

<p>Abstract</p> <p>Background</p> <p>Drug resistance is the outcome of multiple-gene interactions in cancer cells under stress of anticancer agents. <it>MDR1 </it>overexpression is most commonly detected in drug-resistant cancers and accompanied with other gene alterations including enhanced glucosylceramide synthase (GCS). <it>MDR1 </it>encodes for P-glycoprotein that extrudes anticancer drugs. Polymorphisms of <it>MDR1 </it>disrupt the effects of P-glycoprotein antagonists and limit the success of drug resistance reversal in clinical trials. GCS converts ceramide to glucosylceramide, reducing the impact of ceramide-induced apoptosis and increasing glycosphingolipid (GSL) synthesis. Understanding the molecular mechanisms underlying <it>MDR1 </it>overexpression and how it interacts with GCS may find effective approaches to reverse drug resistance.</p> <p>Results</p> <p><it>MDR1 </it>and <it>GCS </it>were coincidently overexpressed in drug-resistant breast, ovary, cervical and colon cancer cells; silencing <it>GCS </it>using a novel mixed-backbone oligonucleotide (MBO-asGCS) sensitized these four drug-resistant cell lines to doxorubicin. This sensitization was correlated with the decreased <it>MDR1 </it>expression and the increased doxorubicin accumulation. Doxorubicin treatment induced GCS and <it>MDR1 </it>expression in tumors, but MBO-asGCS treatment eliminated "in-vivo" growth of drug-resistant tumor (NCI/ADR-RES). MBO-asGCS suppressed the expression of <it>MDR1 </it>with GCS and sensitized NCI/ADR-RES tumor to doxorubicin. The expression of P-glycoprotein and the function of its drug efflux of tumors were decreased by 4 and 8 times after MBO-asGCS treatment, even though this treatment did not have a significant effect on P-glycoprotein in normal small intestine. GCS transient transfection induced <it>MDR1 </it>overexpression and increased P-glycoprotein efflux in dose-dependent fashion in OVCAR-8 cancer cells. GSL profiling, silencing of globotriaosylceramide synthase and assessment of signaling pathway indicated that GCS transfection significantly increased globo series GSLs (globotriaosylceramide Gb3, globotetraosylceramide Gb4) on GSL-enriched microdomain (GEM), activated cSrc kinase, decreased β-catenin phosphorylation, and increased nuclear β-catenin. These consequently increased <it>MDR1 </it>promoter activation and its expression. Conversely, MBO-asGCS treatments decreased globo series GSLs (Gb3, Gb4), cSrc kinase and nuclear β-catenin, and suppressed <it>MDR-1 </it>expression in dose-dependent pattern.</p> <p>Conclusion</p> <p>This study demonstrates, for the first time, that GCS upregulates <it>MDR1 </it>expression modulating drug resistance of cancer. GSLs, in particular globo series GSLs mediate gene expression of <it>MDR1 </it>through cSrc and β-catenin signaling pathway.</p