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Super model for viruses The nematode Caenorhabditis elegans is an ideal model for the study of many aspects of cell biology, including the hot topic of RNA interference (RNAi). But there was a problem in using the worm to study antiviral RNAi responses: C. elegans seemed not to support viral replication. But now the insect pathogen Flock house virus and the mammalian pathogen vesicular stomatitis virus are both shown to infect the worm, and to provoke a strong RNAi-based antiviral defence. So this important genetic model is now available for the study of host–virus interactions, and the antiviral effect of RNAi. The worm Caenorhabditis elegans is a model system for studying many aspects of biology, including host responses to bacterial pathogens 1 , 2 , but it is not known to support replication of any virus. Plants and insects encode multiple Dicer enzymes that recognize distinct precursors of small RNAs and may act cooperatively 3 , 4 , 5 , 6 , 7 . However, it is not known whether the single Dicer of worms and mammals is able to initiate the small RNA-guided RNA interference (RNAi) antiviral immunity as occurs in plants 8 and insects 9 . Here we show complete replication of the Flock house virus (FHV) bipartite, plus-strand RNA genome in C. elegans . We show that FHV replication in C. elegans triggers potent antiviral silencing that requires RDE-1, an Argonaute protein 10 , 11 essential for RNAi mediated by small interfering RNAs (siRNAs) but not by microRNAs. This immunity system is capable of rapid virus clearance in the absence of FHV B2 protein, which acts as a broad-spectrum RNAi inhibitor 9 , 12 upstream of rde-1 by targeting the siRNA precursor. This work establishes a C. elegans model for genetic studies of animal virus–host interactions and indicates that mammals might use a siRNA pathway as an antiviral response.

Autopsy examination of lungs from seven patients who died from Covid-19 showed intussusceptive angiogenesis in greater profusion than was found in lungs from patients who died from influenza or in uninfected lungs that were rejected for transplantation.

\"A circular tale of time travel in a picture book! Max and her dog Boomer accidentally break a vase, a treasured family heirloom-the only thing that Max's great-great-great-great-great-great grandmother managed to save when her houseboat sank. Instead of coming clean, they decide to do the next most logical thing: Build a time machine, travel back to her great-great-great-great-great-great grandmother's home, and smash the vase then so that they can't smash it later! What could possibly go wrong? Building the time machine is surprisingly easy, but controlling the thing proves difficult. After mucking up the time-space continuum, Max and Boomer end up crashing into the family houseboat-and sinking it. Lacking the heart to break anything else, Max and Boomer return to the near-present to warn their near-past selves not to build a time machine. \"I can build a time machine?\" asks the other Max, before tossing the Frisbee that breaks the family's treasured vase....\"-- Provided by publisher.

Telomerase activation through induction of telomerase reverse transcriptase (hTERT) contributes to malignant transformation by stabilizing telomeres. Clinical studies demonstrate that higher hTERT expression is associated with cancer progression and poor outcomes, but the underlying mechanism is unclear. Because epithelial–mesenchymal transition (EMT) and cancer stem cells (CSCs) are key factors in cancer metastasis and relapse, and hTERT has been shown to exhibit multiple biological activities independently of its telomere-lengthening function, we address a potential role of hTERT in EMT and CSCs using gastric cancer (GC) as a model. hTERT overexpression promotes, whereas its inhibition suppresses, EMT and stemness of GC cells, respectively. Transforming growth factor (TGF)-β1 and β-catenin-mediated EMT was abolished by small interfering RNA depletion of hTERT expression. hTERT interacts with β-catenin, enhances its nuclear localization and transcriptional activity, and occupies the β-catenin target vimentin promoter. All these hTERT effects were independent of its telomere-lengthening function or telomerase activity. hTERT and EMT marker expression correlates positively in GC samples. Mouse experiments demonstrate the in vivo stimulation of hTERT on cancer cell colonization. Collectively, hTERT stimulates EMT and induces stemness of cancer cells, thereby promoting cancer metastasis and recurrence. Thus, targeting hTERT may prevent cancer progression by inhibiting EMT and CSCs.

\"Is wind power the answer to our energy supply problems? Is there enough wind for everyone? Is offshore generation better than onshore generation? Can a roof-mounted wind turbine generate enough electricity to supply a typical domestic household? Electricity Generation Using Wind Power (2nd Edition) answers these pressing questions through its detailed coverage of the different types of electrical generator machines used, as well as the power electronic converter technologies and control principles employed. Also covered is the integration of wind farms into established electricity grid systems, plus environmental and economic aspects of wind generation. Written for technically minded readers, especially electrical engineers concerned with the possible use of wind power for generating electricity, it incorporates some global meteorological and geographical features of wind supply plus a survey of past and present wind turbines. Included is a technical assessment of the choice of turbine sites. The principles and analysis of wind power conversion, transmission and efficiency evaluation are described. This book includes worked numerical examples in some chapters, plus end of chapter problems and review questions, with answers.\" -- Publisher's description

Chronic behavioral stress and beta-adrenergic signaling have been shown to promote cancer progression, whose underlying mechanisms are largely unclear, especially the involvement of epigenetic regulation. Histone deacetylase-2 (HDAC2), an epigenetic regulator, is critical for stress-induced cardiac hypertrophy. It is unknown whether it is necessary for beta-adrenergic signaling-promoted cancer progression. Using xenograft models, we showed that chronic behavioral stress and beta-adrenergic signaling promote angiogenesis and prostate cancer progression. HDAC2 was induced by beta-adrenergic signaling in vitro and in mouse xenografts. We next uncovered that HDAC2 is a direct target of cAMP response element-binding protein (CREB) that is activated by beta-adrenergic signaling. Notably, HDAC2 is necessary for beta-adrenergic signaling to induce angiogenesis. We further demonstrated that, upon CREB activation, HDAC2 represses thrombospondin-1 (TSP1), a potent angiogenesis inhibitor, through epigenetic regulation. Together, these data establish a novel pathway that HDAC2 and TSP1 act downstream of CREB activation in beta-adrenergic signaling to promote cancer progression.

The electrochemical conversion of CO and H 2 O into liquid fuel is made feasible at modest potentials with the use of oxide-derived nanocystalline Cu as the catalyst. A new catalyst with energy-saving potential Renewable electricity is often produced when it is not needed. If the surplus could be harnessed to drive the conversion of CO 2 and water into liquid fuel, the energy would not go to waste and a use would be found for CO 2 produced by carbon capture. All this requires efficient electrocatalysts that reduce CO 2 not only to CO, but also further into fuel chemicals. Copper does this but with low efficiency and selectivity. Christina Li et al . now show that the intrinsic catalytic properties of copper can be improved by producing it from its oxide as interconnected nanocrystallites. Their enhanced catalyst generates primarily ethanol, demonstrating that a two-step conversion of CO 2 to liquid fuel powered by renewable electricity might be possible. The electrochemical conversion of CO 2 and H 2 O into liquid fuel is ideal for high-density renewable energy storage and could provide an incentive for CO 2 capture. However, efficient electrocatalysts for reducing CO 2 and its derivatives into a desirable fuel 1 , 2 , 3 are not available at present. Although many catalysts 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 can reduce CO 2 to carbon monoxide (CO), liquid fuel synthesis requires that CO is reduced further, using H 2 O as a H + source. Copper (Cu) is the only known material with an appreciable CO electroreduction activity, but in bulk form its efficiency and selectivity for liquid fuel are far too low for practical use. In particular, H 2 O reduction to H 2 outcompetes CO reduction on Cu electrodes unless extreme overpotentials are applied, at which point gaseous hydrocarbons are the major CO reduction products 12 , 13 . Here we show that nanocrystalline Cu prepared from Cu 2 O (‘oxide-derived Cu’) produces multi-carbon oxygenates (ethanol, acetate and n -propanol) with up to 57% Faraday efficiency at modest potentials (–0.25 volts to –0.5 volts versus the reversible hydrogen electrode) in CO-saturated alkaline H 2 O. By comparison, when prepared by traditional vapour condensation, Cu nanoparticles with an average crystallite size similar to that of oxide-derived copper produce nearly exclusive H 2 (96% Faraday efficiency) under identical conditions. Our results demonstrate the ability to change the intrinsic catalytic properties of Cu for this notoriously difficult reaction by growing interconnected nanocrystallites from the constrained environment of an oxide lattice. The selectivity for oxygenates, with ethanol as the major product, demonstrates the feasibility of a two-step conversion of CO 2 to liquid fuel that could be powered by renewable electricity.