2,605 research outputs found

    Validation of scramjet exhaust simulation technique at Mach 6

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    Current design philosophy for hydrogen-fueled, scramjet-powered hypersonic aircraft results in configurations with strong couplings between the engine plume and vehicle aerodynamics. The experimental verification of the scramjet exhaust simulation is described. The scramjet exhaust was reproduced for the Mach 6 flight condition by the detonation tube simulator. The exhaust flow pressure profiles, and to a large extent the heat transfer rate profiles, were then duplicated by cool gas mixtures of Argon and Freon 13B1 or Freon 12. The results of these experiments indicate that a cool gas simulation of the hot scramjet exhaust is a viable simulation technique except for phenomena which are dependent on the wall temperature relative to flow temperature

    Validation of scramjet exhaust simulation technique

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    Scramjet/airframe integration design philosophy for hypersonic aircraft results in configurations having lower aft surfaces that serve as exhaust nozzles. There is a strong coupling between the exhaust plume and the aerodynamics of the vehicle, making accurate simulation of the engine exhaust mandatory. The experimental verification of the simulation procedure is described. The detonation tube simulator was used to produce an exact simulation of the scramjet exhaust for a Mach 8 flight condition. The pressure distributions produced by the exact exhaust flow were then duplicated by a cool mixture Argon and Freon 13B1. Such a substitute gas mixture validated by the detonation tube technique could be used in conventional wind tunnel tests. The results presented show the substitute gas simulation technique to be valid for shockless expansions

    N-acetylglucosamine Regulates Virulence Properties in Microbial Pathogens

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    There is growing evidence that the sugar N-acetylglucosamine (GlcNAc) plays diverse roles in cell signaling pathways that impact the virulence properties of microbes and host cells. GlcNAc is already well known as a ubiquitous structural component at the cell surface that forms part of bacterial cell wall peptidoglycan, cell wall chitin in fungi and parasites, and extracellular matrix glycosaminoglycans of animal cells. Chitin and peptidoglycan have been previously linked to cell signaling as they can stimulate responses in plant and animal host cells [1–3]. Recent studies now indicate that GlcNAc released from these polymers can also activate cell signaling via several different mechanisms [4–6]. The role of these new GlcNAc signaling pathways in the regulation of virulence factors will be the focus of this review

    Fir (Abies spp.) stand biomass additive model for Eurasia sensitive to winter temperature and annual precipitation

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    Climate change, especially modified courses of temperature and precipitation, has a significant impact on forest functioning and productivity. Moreover, some alterations in tree biomass allocation (e.g. root to shoot ratio, foliage to wood parts) might be expected in these changing ecological conditions. Therefore, we attempted to model fir stand biomass (t ha(-1)) along the trans-Eurasian hydrothermal gradients using the data from 272 forest stands. The model outputs suggested that all biomass components, except for the crown mass, change in a common pattern, but in different ratios. Specifically, in the range of mean January temperature and precipitation of -30 degrees C to +10 degrees C and 300 to 900 mm, fir stand biomass increases with both increasing temperature and precipitation. Under an assumed increase of January temperature by 1 degrees C, biomass of roots and of all components of the aboveground biomass of fir stands increased (under the assumption that the precipitation level did not change). Similarly, an assumed increase in precipitation by 100 mm resulted in the increased biomass of roots and of all aboveground components. We conclude that fir seems to be a perspective taxon from the point of its productive properties in the ongoing process of climate change.This paper was prepared within the programs of the current scientific research of the Ural Forest Engineering University and Botanical Garden of the Ural Branch of Russian Academy of Sciences. This work was supported by grant "EVA4.0", No. CZ.02.1.01/0.0/0.0/16_019/0000803 financed by OP RDE, by the Slovak Research and Development Agency under contracts No. APVV-15-0265, APVV-16-0325, APVV-18-0086 and the Scientific Grant Agency of the Ministry of Education, Science, Research and Sport of the Slovak Republic under contracts No. VEGA 1/0367/16

    Flavodoxin-Like Proteins Protect Candida albicans from Oxidative Stress and Promote Virulence

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    The fungal pathogen Candida albicans causes lethal systemic infections in humans. To better define how pathogens resist oxidative attack by the immune system, we examined a family of four Flavodoxin-Like Proteins (FLPs) in C. albicans. In agreement with previous studies showing that FLPs in bacteria and plants act as NAD(P)H quinone oxidoreductases, a C.albicans quadruple mutant lacking all four FLPs (pst1Δ, pst2Δ, pst3Δ, ycp4Δ) was more sensitive to benzoquinone. Interestingly, the quadruple mutant was also more sensitive to a variety of oxidants. Quinone reductase activity confers important antioxidant effects because resistance to oxidation was restored in the quadruple mutant by expressing either Escherichia coli wrbA or mammalian NQO1, two distinct types of quinone reductases. FLPs were detected at the plasma membrane in C. albicans, and the quadruple mutant was more sensitive to linolenic acid, a polyunsaturated fatty acid that can auto-oxidize and promote lipid peroxidation. These observations suggested that FLPs reduce ubiquinone (coenzyme Q), enabling it to serve as an antioxidant in the membrane. In support of this, a C. albicans coq3Δ mutant that fails to synthesize ubiquinone was also highly sensitive to oxidative stress. FLPs are critical for survival in the host, as the quadruple mutant was avirulent in a mouse model of systemic candidiasis under conditions where infection with wild type C. albicans was lethal. The quadruple mutant cells initially grew well in kidneys, the major site of C. albicans growth in mice, but then declined after the influx of neutrophils and by day 4 post-infection 33% of the mice cleared the infection. Thus, FLPs and ubiquinone are important new antioxidant mechanisms that are critical for fungal virulence. The potential of FLPs as novel targets for antifungal therapy is further underscored by their absence in mammalian cells. Author Summary Oxidative damage is a fundamental problem for cells and a particular challenge for microbial pathogens, which require special mechanisms to resist the oxidative attack by the host immune system. We identified four proteins in the human fungal pathogen Candida albicansthat belong to a large family of enzymes in bacteria and plants that reduce quinone molecules to detoxify them. Interestingly, mutational studies in C. albicans showed that these enzymes also confer resistance to a wide range of oxidants, suggesting they may have broader impact by reducing the major quinone present in cells (ubiquinone or coenzyme Q). In support of this, we found that mutating the COQ3 gene to block ubiquinone synthesis rendered cells highly sensitive to oxidative stress, revealing that it plays a very important antioxidant function in addition to its well known role in energy metabolism. These quinone reductases play a critical role in vivo, as they were required for virulence in mouse infections studies. Since mammalian cells lack this type of quinone reductase, this difference could be exploited to develop much needed novel therapeutic approaches for fungal and bacterial pathogens

    Flavodoxin-Like Proteins Protect Candida albicans from Oxidative Stress and Promote Virulence

    Get PDF
    The fungal pathogen Candida albicans causes lethal systemic infections in humans. To better define how pathogens resist oxidative attack by the immune system, we examined a family of four Flavodoxin-Like Proteins (FLPs) in C. albicans. In agreement with previous studies showing that FLPs in bacteria and plants act as NAD(P)H quinone oxidoreductases, a C.albicans quadruple mutant lacking all four FLPs (pst1Δ, pst2Δ, pst3Δ, ycp4Δ) was more sensitive to benzoquinone. Interestingly, the quadruple mutant was also more sensitive to a variety of oxidants. Quinone reductase activity confers important antioxidant effects because resistance to oxidation was restored in the quadruple mutant by expressing either Escherichia coli wrbA or mammalian NQO1, two distinct types of quinone reductases. FLPs were detected at the plasma membrane in C. albicans, and the quadruple mutant was more sensitive to linolenic acid, a polyunsaturated fatty acid that can auto-oxidize and promote lipid peroxidation. These observations suggested that FLPs reduce ubiquinone (coenzyme Q), enabling it to serve as an antioxidant in the membrane. In support of this, a C. albicans coq3Δ mutant that fails to synthesize ubiquinone was also highly sensitive to oxidative stress. FLPs are critical for survival in the host, as the quadruple mutant was avirulent in a mouse model of systemic candidiasis under conditions where infection with wild type C. albicans was lethal. The quadruple mutant cells initially grew well in kidneys, the major site of C. albicans growth in mice, but then declined after the influx of neutrophils and by day 4 post-infection 33% of the mice cleared the infection. Thus, FLPs and ubiquinone are important new antioxidant mechanisms that are critical for fungal virulence. The potential of FLPs as novel targets for antifungal therapy is further underscored by their absence in mammalian cells. Author Summary Oxidative damage is a fundamental problem for cells and a particular challenge for microbial pathogens, which require special mechanisms to resist the oxidative attack by the host immune system. We identified four proteins in the human fungal pathogen Candida albicansthat belong to a large family of enzymes in bacteria and plants that reduce quinone molecules to detoxify them. Interestingly, mutational studies in C. albicans showed that these enzymes also confer resistance to a wide range of oxidants, suggesting they may have broader impact by reducing the major quinone present in cells (ubiquinone or coenzyme Q). In support of this, we found that mutating the COQ3 gene to block ubiquinone synthesis rendered cells highly sensitive to oxidative stress, revealing that it plays a very important antioxidant function in addition to its well known role in energy metabolism. These quinone reductases play a critical role in vivo, as they were required for virulence in mouse infections studies. Since mammalian cells lack this type of quinone reductase, this difference could be exploited to develop much needed novel therapeutic approaches for fungal and bacterial pathogens

    Designing a User-Metaverse Interface for the Industrial-Metaverse

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    The Industrial-Metaverse will create interactions between the physical and virtual worlds to extend operations in the physical industry. This particularity and the demand for increasing immersion in the Metaverse require using XR technologies called User-Metaverse interfaces (UMI). How such a UMI must be designed for the industrial-Metaverse is unknown. This study adopts a design science approach to design a UMI based on social cognitive theory (SCT). According to SCT, creating user-generated Metaverse content is crucial to the UMI design. It empowers users to generate content through their efforts, leading to higher self-efficacy and user engagement. We formulate two theoretically based design principles and instantiate a software artifact, which we evaluate in a laboratory experiment with 57 participants. Our study shows the importance of belief in success in the design of future UMI. Furthermore, our design principles show significant positive outcome expectations of users in their interaction with the software artifact

    Anionic liposomes inhibit human immunodeficiency virus type 1 (HIV-1) infectivity in CD4\u3csup\u3e+\u3c/sup\u3e A3.01 and H9 cells

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    Immunodeficiency viruses undergo fusion with liposomes containing anionic phospholipids (Larsen et al., 1990). We have investigated the effect of liposomes composed of cardiolipin, phosphatidylserine or phosphatidylinositol, on the infectivity of three strains of HIV-1 in A3.01 and H9 cells, measured by p24 (gag) production in the medium. The infectivity of HIV-1 in A3.01 or H9 cells was inhibited by the presence of cardiolipin liposomes during a 2 h infection period, with IC50\u27s of 23.0, 4.8, and 5.0 μM phospholipid, respectively, for the different strains. Liposomes composed of phosphatidylserine or phosphatidylinositol were ineffective under similar conditions. However, prolonged pre-incubation of the virus with these liposomes also inhibited infectivity. Inhibition of virus binding to cells could not account for the inhibition of infectivity. We propose that the fusion products of HIV-1 and anionic liposomes are impaired in their ability to fuse with the plasma membrane
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