Browsing by Subject "WALL"

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  • Morais de Carvalho, Danila; Lahtinen, Maarit; Bhattarai, Mamata; Lawoko, Martin; Mikkonen, Kirsi S. (2021)
    Hemicellulose-rich wood extracts show efficient capacity to adsorb at emulsion interfaces and stabilize them. Their functionality is enhanced by lignin moieties accompanying the hemicellulose structures, in the form of lignin-carbohydrate complexes (LCCs) and, potentially, other non-covalent associations. The formation and stability of emulsions is determined by their interfacial regions. These are largely unexplored assemblies when formed from natural stabilizers with a complex chemical composition. Understanding the structure of the interfacial region could facilitate both designing the extraction processes of abundant biomasses and unraveling a valuable industrial application potential for the extracts. Herein, we characterized the LCCs from the interface of oil-in-water emulsions stabilized by galactoglucomannan (GGM) or glucuronoxylan (GX)-rich wood extracts, using two-dimensional nuclear magnetic resonance (NMR) spectroscopy analysis. The type of covalent linkage between residual lignin and hemicelluloses determined their partitioning between the continuous and interfacial emulsion phases. Benzylether structures, only found in the interface, were suggested to participate in the physical stabilization of the emulsion droplets. In turn, the phenylglycosides, preferentially observed in the continuous phase, were suggested to interact with adsorbed stabilizers by electrostatic interaction. More hydrophobic lignin structures, such as guaiacyl lignin type, dibenzodioxocin substructures, and certain end groups also contributed to droplet stabilization. The elucidation of such attributes is of paramount importance for the biorefinery industry, enabling the optimization of extraction processes for the preparation of wood-based stabilizers and designed interfaces for novel and sustainable emulsion systems.
  • ASDEX Upgrade Team; EUROfusion MST1 Team; Hakola, A.; Keitaanranta, A.; Kumpulainen, H.; Lahtinen, A.; Likonen, J.; Balden, M.; Cavedon, M.; Krieger, K.; Airila, M.; Groth, M. (2020)
    In this paper, we report experimental and numerical investigations of gross and net erosion of gold (Au) and molybdenum (Mo), proxies for the common plasma-facing material tungsten (W), during L-mode plasma discharges in deuterium (D) in the outer strike-point region of the ASDEX Upgrade tokamak. To this end, erosion profiles of different marker spots (for Au, dimensions 1 x 1 and 5 x 5 mm(2)) and marker coatings (for Mo) have been determined and modelled using the ERO code. The smaller marker spots were designed to quantify the gross-erosion rate while on the bigger markers local prompt re-deposition of Au allowed obtaining data on net erosion. The experimental results indicate relatively uniform erosion profiles across the marker spots or coatings, very little re-deposition elsewhere, and the largest erosion taking place close to the strike point. Compared to W, the markers show up to 15 times higher net erosion but no major differences in the poloidal migration lengths of Au and W can be seen. Gold thus appears to be a proper choice for studying migration of W in the divertor region. The ERO simulations with different background plasmas are able to reproduce the main features of the experimental net erosion profile of Au. Of the studied parameters, electron temperature has the strongest impact on erosion: doubling the temperature enhances erosion by a factor of 2.5-3. In contrast, for Mo, the simulated net erosion is similar to 3 times smaller than what experimental data indicate. The discrepancies can be attributed to the deviations of the background plasma profiles from the measured ones as well as to the applied models or approximations for the ion temperature, plasma potential, and sheath characteristics in ERO. In addition, the surrounding areas of the marker samples being covered with impurities and W from previous experiments may have considerably reduced the actual re-deposition of Mo. All the simulations predict a toroidal tail of re-deposited particles, downstream of the markers, but the particle density seems to be below the experimental detection threshold. The comparison between the 1 x 1 mm(2) and 5 x 5 mm(2) marker spots further reveal that re-deposition drops from >50% to
  • Aoki, Tomohiro; Frösen, Juhana; Fukuda, Miyuki; Bando, Kana; Shioi, Go; Tsuji, Keiichi; Ollikainen, Eliisa; Nozaki, Kazuhiko; Laakkonen, Johanna; Narumiya, Shuh (2017)
    Intracranial aneurysms are common but are generally untreated, and their rupture can lead to subarachnoid hemorrhage. Because of the poor prognosis associated with subarachnoid hemorrhage, preventing the progression of intracranial aneurysms is critically important. Intracranial aneurysms are caused by chronic inflammation of the arterial wall due to macrophage infiltration triggered by monocyte chemoattractant protein-1 (MCP-1), macrophage activation mediated by the transcription factor nuclear factor kappa B (NF-kappa B), and inflammatory signaling involving prostaglandin E-2 (PGE(2)) and prostaglandin E receptor subtype 2 (EP2). We correlated EP2 and cyclooxygenase-2 (COX-2) with macrophage infiltration in human intracranial aneurysm lesions. Monitoring the spatiotemporal pattern of NF-kappa B activation during intracranial aneurysm development in mice showed that NF-kappa B was first activated in macrophages in the adventitia and in endothelial cells and, subsequently, in the entire arterial wall. Mice with a macrophage-specific deletion of Ptger2 (which encodes EP2) or macrophage-specific expression of an I kappa B alpha mutant that restricts NF-kappa B activation had fewer intracranial aneurysms with reduced macrophage infiltration and NF-kappa B activation. In cultured cells, EP2 signaling cooperated with tumor necrosis factor-alpha (TNF-alpha) to activate NF-kappa B and synergistically induce the expression of proinflammatory genes, including Ptgs2 (encoding COX-2). EP2 signaling also stabilized Ccl2 (encoding MCP-1) by activating the RNA-stabilizing protein HuR. Rats administered an EP2 antagonist had reduced macrophage infiltration and intracranial aneurysm formation and progression. This signaling pathway in macrophages thus facilitates intracranial aneurysm development by amplifying inflammation in intracranial arteries. These results indicate that EP2 antagonists may therefore be a therapeutic alternative to surgery.