Large-area uniform dust-free plasma CVD

In the weak magnetic field perpendicular to the discharge electric field, both the electrons and positive ions are transported in the direction of E×B drift by the space charge electric field produced by the preceded electrons. As a result, radicals are generated uniformly outside of discharge space between the electrodes in the direction of E×B drift. On the other hand, negatively charged heavy particles such as dust particles can be removed from discharge space in the direction opposite to E×B drift of plasmas. The authors have studied the transport mechanisms of magnetized dusty plasmas and its applications for the large-area uniform a-Si:H thin film deposition in plasma CVD methods. This paper reviews the transport phenomena and the transport mechanisms of dust particles and the results of film preparation under particle-free process conditions.     

Sulfidation Properties of Ni–20Cr and Ni–13.5Co–20Cr Alloys at 873 K under Low Sulfur Pressures in H2S-H2 Atmospheres

The sulfidation properties of Ni–20Cr and Ni–13.5Co–20Cralloys as well as a nickel-base superalloy AISI685 were investigated at873 K in H₂S–H₂ gas mixtures with sulfur partial pressures of10^–4, 10^–5.5, and 10^–7Pa by mass-gain measurements,electron-probe microanalysis (EPMA), and X-ray diffraction (XRD)analysis. Sulfidation obeyed the parabolic rate law, and the parabolic rateconstants decreased in the order Ni–20Cr, Ni–13.5Co–20Cr,and AISI685 at each sulfur pressure. With decreasing sulfur pressure, therate constants first decreased slowly and then rapidly at a 10–7 Pasulfur pressure. At both 10^–4 and 10^–5.5 Pa sulfur pressures,Ni–20Cr formed a surface scale with a duplex structure of inner(Cr₃S₄) and outer (Ni₃S₂) layers, while Ni–13.5Co–20Cr formeda triplex structure of inner (Cr₃S₄), intermediate(Ni,Co)Cr₂S₄, and outer[Ni₃S₂+(Co,Ni)₉S₈] layers. Thesurface scale formed on AISI685 was verycomplex, comprising at least four layers, a fibrous (Co,Ni)₉S₈ top surface,outer [Ni₃S₂+(Co,Ni)₉S₈], and intermediate [(Cr,Ti)₃S₄] layers, as well asan inner layer containing Cr, Ti, Mo, Al, and S. At the 10^–7 Pa sulfurpressure, which is lower than the dissociation pressure of Ni₃S₂, bothNi–20Cr and Ni–13.5Co–20Cr formed a surface scale ofCr₃S₄ covered by a thin NiCr₂S₄ layer, accompanied by copious internalsulfidation of Cr₃S₄ and/or CrS. On AISI685 there was a surface scale of(Cr,Ti)₃S₄ accompanied by the usual internal sulfidation. It is discussedthat diffusion of cations in the inner Cr₃S₄ layer is the rate-determiningstep for the growth of the multilayer structures. At the 10^–7 Pasulfur pressure, diffusion of Cr and S contribute to form a thin surfacescale and internal sulfidation, respectively.     

Human β-Defensin 3 Inhibits Porphyromonas Gingivalis Lipopolysaccharide-Induced Oxidative and Inflammatory Responses of Microglia by Suppression of Cathepsins B and L

Recently, the effects of antibacterial peptides are suggested to have therapeutic potential in Alzheimer’s disease. Furthermore, systemic treatment of Porphyromonas gingivalis (Pg) lipopolysaccharide (LPS) induced Alzheimer’s disease-like neuropathological changes in middle-aged mice. Then, we examined whether human β-defensins (hBDs), antimicrobial peptides produced by the oral mucosa and salivary glands, can suppress Pg LPS-induced oxidative and inflammatory responses by microglia. hBD3 (1 μM) significantly suppressed Pg LPS-induced production of nitric oxide and interleukin-6 (IL-6) by MG6 cells, a mouse microglial cell line. hBD3 (1 μM) also significantly inhibited Pg LPS-induced expression of IL-6 by HMC3 cells, a human microglial cell line. In contrast, neither hBD1, hBD2 nor hBD4 failed to inhibit their productions. Furthermore, hBD3 suppressed Pg LPS-induced p65 nuclear translocation through the IκBα degradation. Pg LPS-induced expression of IL-6 was significantly suppressed by E64d, a cysteine protease inhibitor, and CA-074Me, a known specific inhibitor for cathepsin B, but not by pepstatin A, an aspartic protease inhibitor. Interestingly, hBD3 significantly inhibited enzymatic activities of recombinant human cathepsins B and L, lysosomal cysteine proteases, and their intracellular activities in MG6 cells. Therefore, hBD3 suppressed oxidative and inflammatory responses of microglia through the inhibition of cathepsins B and L, which enzymatic activities are necessary for the NF-κB activation.     

Different Involvement of Vimentin during Invasion by Listeria monocytogenes at the Blood–Brain and the Blood–Cerebrospinal Fluid Barriers In Vitro

The human central nervous system (CNS) is separated from the blood by distinct cellular barriers, including the blood–brain barrier (BBB) and the blood–cerebrospinal fluid (CFS) barrier (BCSFB). Whereas at the center of the BBB are the endothelial cells of the brain capillaries, the BCSFB is formed by the epithelium of the choroid plexus. Invasion of cells of either the BBB or the BCSFB is a potential first step during CNS entry by the Gram-positive bacterium Listeria monocytogenes (Lm). Lm possesses several virulence factors mediating host cell entry, such as the internalin protein family—including internalin (InlA), which binds E-cadherin (Ecad) on the surface of target cells, and internalin B (InlB)—interacting with the host cell receptor tyrosine kinase Met. A further family member is internalin (InlF), which targets the intermediate filament protein vimentin. Whereas InlF has been shown to play a role during brain invasion at the BBB, its function during infection at the BCSFB is not known. We use human brain microvascular endothelial cells (HBMEC) and human choroid plexus epithelial papilloma (HIBCPP) cells to investigate the roles of InlF and vimentin during CNS invasion by Lm. Whereas HBMEC present intracellular and surface vimentin (besides Met), HIBCPP cells do not express vimentin (except Met and Ecad). Treatment with the surface vimentin modulator withaferin A (WitA) inhibited invasion of Lm into HBMEC, but not HIBCPP cells. Invasion of Lm into HBMEC and HIBCPP cells is, however, independent of InlF, since a deletion mutant of Lm lacking InlF did not display reduced invasion rates.     

Visualizing Intramolecular Dynamics of Membrane Proteins

Membrane proteins play important roles in biological functions, with accompanying allosteric structure changes. Understanding intramolecular dynamics helps elucidate catalytic mechanisms and develop new drugs. In contrast to the various technologies for structural analysis, methods for analyzing intramolecular dynamics are limited. Single-molecule measurements using optical microscopy have been widely used for kinetic analysis. Recently, improvements in detectors and image analysis technology have made it possible to use single-molecule determination methods using X-rays and electron beams, such as diffracted X-ray tracking (DXT), X-ray free electron laser (XFEL) imaging, and cryo-electron microscopy (cryo-EM). High-speed atomic force microscopy (HS-AFM) is a scanning probe microscope that can capture the structural dynamics of biomolecules in real time at the single-molecule level. Time-resolved techniques also facilitate an understanding of real-time intramolecular processes during chemical reactions. In this review, recent advances in membrane protein dynamics visualization techniques were presented.     

Comparative Study on Epidermal Moisturizing Effects and Hydration Mechanisms of Rice-Derived Glucosylceramides and Ceramides

Ceramide (Cer) plays an important role in skin barrier functions in the stratum corneum (SC). The ingestion of food-derived glucosylceramides (GlcCer) attenuates transepidermal water loss (TEWL). However, the moisturizing effects of single molecules of GlcCer and Cer remain unclear. Therefore, we herein purified 13 GlcCer and 6 Cer, including elasticamide, which has the same structure as human Cer[AP], from rice and compared their epidermal moisturizing effects in a reconstructed human epidermal keratinization model. The results obtained showed that 10 µM of 5 GlcCer[d18:2] with a 4E,8Z sphingadienine and C18 to C26 fatty acids and 10 µg/mL of 3 Cer with C23 or C24 fatty acids significantly reduced TEWL. The moisturizing effects of these GlcCer were dependent on the length of fatty acids. Furthermore, 10 µg/mL of elasticamide increased the SC Cer contents by promoting the expression of GlcCer synthase. Electron microscopic observations revealed that 1 µM of GlcCer[d18:2(4E,8Z)/26:0] increased the number of keratohyalin granules and desmosomes. Immunostaining and Western blotting indicated that 1 µM of GlcCer[d18:2(4E,8Z)/26:0] up-regulated the expression of filaggrin and corneodesmosin, which contribute to epidermal hydration. This comparative study on epidermal moisturization by GlcCer and Cer isolated from rice revealed differences in their hydration mechanisms.     

Behavior of shock waves formed by unsteady supersonic jet injected into cell

The unsteady behavior of flow driven by a jet suddenly injected into a cell is numerically studied by solving the axisymmelric two-dimensional compressible Navier-Stokes equations. The system of the calculation is a model of the laser ablation of a certain duration followed by a discharging process through the exit hole at the down- stream end of the cell. In the calculations, the contour of the cell is changed while other parameters such as the Mach number of the jet, its duration, and the diameter of the cell exit are fixed. Monitoring the velocity at the exit hole is used to investigate the influence of the shape on the interaction between the shock wave and the jet. As the result, it was found that the velocity peak value and its arrival time at the downstream end of the cell exit are determined by the diameter of the cell.     

CCL4 Regulates Eosinophil Activation in Eosinophilic Airway Inflammation

Eosinophilic chronic rhinosinusitis (ECRS) is a refractory airway disease accompanied by eosinophilic inflammation, the mechanisms of which are unknown. We recently found that CCL4/MIP-1β—a specific ligand for CCR5 receptors—was implicated in eosinophil recruitment into the inflammatory site and was substantially released from activated eosinophils. Moreover, it was found in nasal polyps from patients with ECRS, primarily in epithelial cells. In the present study, the role of epithelial cell-derived CCL4 in eosinophil activation was investigated. First, CCL4 expression in nasal polyps from patients with ECRS as well as its role of CCL4 in eosinophilic airway inflammation were investigated in an in vivo model. Furthermore, the role of CCL4 in CD69 expression—a marker of activated eosinophils—as well as the signaling pathways involved in CCL4-mediated eosinophil activation were investigated. Notably, CCL4 expression, but not CCL5, CCL11, or CCL26, was found to be significantly increased in nasal polyps from patients with ECRS associated with eosinophil infiltration as well as in BEAS-2B cells co-incubated with eosinophils. In an OVA-induced allergic mouse model, CCL4 increased eosinophil accumulation in the nasal mucosa and the bronchoalveolar lavage (BALF). Moreover, we found that CD69 expression was upregulated in CCL4-stimulated eosinophils; similarly, phosphorylation of several kinases, including platelet-derived growth factor receptor (PDGFR)β, SRC kinase family (Lck, Src, and Yes), and extracellular signal-regulated kinase (ERK), was upregulated. Further, CCR5, PDGFRβ, and/or Src kinase inhibition partially restored CCL4-induced CD69 upregulation. Thus, CCL4, which is derived from airway epithelial cells, plays a role in the accumulation and activation of eosinophils at inflammatory sites. These findings may provide a novel therapeutic target for eosinophilic airway inflammation, such as ECRS.