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Electrochemical oscillations are of interest from the viewpoint of dynamic self-organization of molecular systems. Extensive studies have revealed that N-shaped negative differential resistance (N-NDR) plays an essential role in the majority of the oscillations because an N-NDR induces a positive feedback mechanism. Simple periodic oscillations are explained by the combination of a positive feedback loop and a negative one, latter of which involves a slow process such as the surface concentration of an electroactive species and the surface coverage of an adsorbed species [1]. Among the electrochemical oscillations, the reduction of H2O2 at Pt electrodes in H2SO4 solutions (H2O2 + 2H+ + 2e- → 2H2O) has an especially unique feature because it exhibits ten kinds of oscillations, as we have reported before [2]. One of the oscillations, named oscillation A, appeared in the potential region where under-potential deposited H (upd-H), which suppressed the H2O2 reduction, was formed on Pt surface (see Figure 1a). Another oscillation, named oscillation D, appeared when a small amount of Br- ions, which adsorbed on Pt surface, was added to the solutions. The reduction of S2O8 2- at Pt electrodes in acidic solutions (S2O8 2- + 2e- → 2 SO4 2-) was also unique because it showed several kinds of oscillations. The formation of upd-H also suppressed the S2O8 2- reduction; hence one of the oscillations, named oscillation a, appeared in the potential region of upd-H [3]. The electrochemical oscillations are also of interest from the viewpoint of nonlinear dynamics because they often exhibit transitions among non-oscillatory state, periodic oscillations, quasi-periodic ones, mixed-mode ones, and chaotic ones via period-adding bifurcation, period-doubling bifurcation, and so on. We have been studying bifurcation behavior in the oscillations during the H2O2 and S2O8 2- reductions. The studies showed [3,4] that the complex oscillations such as period-n, mixed-mode, and chaotic oscillations were observed when oscillation A appeared simultaneously with oscillation a (or D) though each was period-1 oscillation (see Figure 1b for the chaotic oscillation induced by the simultaneous occurrence of oscillations A and a). Furthermore, the studies led us to the conclusion that the complex oscillations appeared when two kinds of simple periodic oscillations occurred at the same time, and also that they were caused by the interplay among a positive feedback loop and two negative feedback loops. Recently, we found [5] that oscillation A changed into the complex oscillations when inorganic salts such as Na2SO4 and K2SO4 are added to the solutions (see Figure 1c for the chaotic oscillation). The solutions originally contained (bi)sulfate ions dissociated from H2SO4, and hence we explained that alkali metal ions, i.e., Na+ and K+ ions, caused a negative feedback loop that induced the complex oscillations. This presentation will show the bifurcation behavior in detail and also provide a definitive factor for the appearance of the complex oscillations. REFERENCES [1] M. Orlik, Self-Organization in Electrochemical Systems I, Springer, Berlin, 2012. [2] Y. Mukouyama, H. Kawasaki, D. Hara, M. Kikuchi, Y. Yamada, S, Nakanishi, ECS Trans., 69 (39) 37-45, 2015. [3] Y. Mukouyama, H. Kawasaki, D. Hara, S. Nakanishi, J. Solid State Electrochem., 19, 3253-3263, 2015. [4] Y. Mukouyama, M. Kikuchi, H. Okamoto, J. Solid State Electrochem., 9, 290-295, 2005. [5] Y. Mukouyama, D. Hara, H. Kawasaki, M. Kikuchi, Y. Yamada, S, Nakanishi, ECS Trans., 69 (39) 47-57, 2015. FIGURE CAPTION Figure 1. The I – E curves for a Pt-disc electrode in 0.1 M H2SO4 + 0.2 M H2O2 (a) without Na2S2O8 nor Na2SO4, (b) with 0.1 M Na2S2O8, and (c) with 0.2 M Na2SO4, measured under potential-controlled conditions. The insets in panels a, b, and c are the waveforms of oscillations observed at −0.065, −0.070, and −0.085 V, respectively. Figure 1

INTRODUCTION Electrochemical oscillations are of interest from the viewpoint of dynamic self-organization of molecular systems. Extensive studies have revealed that an N-shaped negative differential resistance (N-NDR) plays an essential role in the majority of the oscillations. Simple periodic oscillations are explained by the interaction between a positive feedback loop due to an N-NDR characteristic and a negative one where a slow process is involved [1]. Electrochemical oscillations are also of interest from the viewpoint of nonlinear dynamics because they sometimes exhibit chaotic oscillations. Our group has reported that chaotic oscillations appear when two kinds of simple periodic oscillations, named oscillation A and oscillation α, occur simultaneously [2]. Oscillation A (or α) appeared during the reduction of H2O2 (or S2O8 2- dissociated from Na2S2O8) at Pt electrodes in strong acidic solutions such as H2SO4 and HClO4 electrolytes. We concluded that the chaotic oscillations were caused by the interplay among a positive feedback loop due to an N-NDR characteristic, a negative feedback loop where the surface concentration of H2O2 was involved, i.e., that for oscillation A, and a negative feedback loop where the surface concentration of S2O8 2−was involved, i.e., that for oscillation α. On the other hand, the H2O2 reduction at Pt electrodes in H2SO4 solutions was affected by the salts such as Na2SO4 and K2SO4 because the alkali metal ions, Na+ and K+, decreased the electromigration transport of H+ ions from the solution bulk to the electrode surface [3]. Recently, oscillation A was found to appear as a chaotic oscillation in the presence of Na2SO4, indicating that Na+ ions caused a negative feedback loop that induced the chaotic oscillation. In this presentation, the conditions for the appearance of the chaotic oscillation will be discussed. Although the chaotic oscillations due to the simultaneous occurrence of oscillations A and α were also observed in the solutions that contained Na+ ions, they were not induced by Na+ions, which will also be discussed. RESULTS and DISCUSSION Figure 1 shows the current (I) – potential (E) curves for a Pt-disc electrode. When the solution was 0.1 M H2SO4 + 0.2 M H2O2 (Fig. 1a), the H2O2 reduction occurred in the potential region below ca. 0.8 V, and oscillation A appeared at potentials around –0.075 V (vs. SHE) where an N-NDR characteristic appeared. The hydrogen evolution reaction occurred in the potential region below ca. –0.1 V. Oscillation A was simple and periodic as shown in the inset of Fig. 1a. When the solution contained 0.2 M Na2SO4 (Fig. 1b), an aperiodic oscillation, which could be judged as a chaotic oscillation by plotting a next-minimum return map, appeared as shown in the inset. The current values of the higher turning points were almost constant, whereas those of the lower ones were irregular. This indicates that the negative feedback loop for oscillation A played a role in the higher turning points, and also that not only the loop but also another negative feedback loop which was induced by Na+ ions worked in the lower turning points. The chaotic oscillation appeared only when the concentration of Na2SO4 was approximately 0.2 M, and thus the negative feedback loop was induced only when the concentration of Na+was approximately 0.4 M. When the solution contained 0.1 M Na2S2O8 (Fig. 1c), the reduction of S2O8 2− occurred below ca. 0.5 V though the current due to the reduction was too small to affect the I – E curve, and a chaotic oscillation also appeared as shown in the inset [2]. The values of the higher turning points and those of the lower ones were irregular, indicating that two negative feedback loops played roles both in the higher turning points and the lower ones. The loop induced by Na+ ions did not work in higher ones, nor in the lower ones when the Na+ concentration was 0.2 M. We can thus say that the chaotic oscillation was not caused by Na+ions. REFERENCES [1] M. Orlik, Self-Organization in Electrochemical Systems I, Springer, Berlin (2012). [2] Y. Mukouyama, H. Kawasaki, D. Hara, S. Nakanishi, J. Solid State Electrochem., DOI 10.1007/s10008-015-2813-z. [3] Y. Mukouyama, M. Hasegawa, S, Nakanishi, ECS Trans., 64 (2014) accepted. FIGURE CAPTION Figure 1. The I – E curves for a Pt-disc electrode in 0.1 M H2SO4 + 0.2 M H2O2 (a) without Na2SO4 nor Na2S2O8, (b) with 0.2 M Na2SO4, and (c) with 0.1 M Na2S2O8, measured under potential-controlled conditions. The insets in panels a, b, and c are the waveforms of oscillations observed at −0.065, −0.085, and −0.070 V, respectively. Figure 1

We have found that a chaotic oscillation transiently appears when two kinds of current oscillations, named oscillation A and oscillation α, occur simultaneously. Oscillations A and α appear during the reduction of H2O2 and S2O8 2− respectively on the Pt electrode. When the electrode potential is stepped from the rest potential to a potential where both the oscillations appear, a period-1 oscillation first appears, and then a period-doubling bifurcation cascade occurs. After that, the transient chaos appears, which is followed by a sequence of mixed-mode oscillations (MMOs). The appearance of the chaotic behavior and the MMOs can be explained on the basis of the reported mechanisms for oscillations A and α. Both the oscillations are caused by an N-shaped negative differential resistance (N-NDR) due to the formation of under-potential deposited H (upd-H), indicating that a positive feedback mechanism works during the simultaneous occurrence of oscillations A and α. On the other hand, negative feedback mechanisms for oscillations A and α include the surface concentration of H2O2 and S2O8 2−, respectively. We can, then, conclude that the combination of the positive feedback mechanism and the two negative feedback mechanisms of different time scales gives rise to the chaotic behavior and the MMOs, which has been verified by numerical simulations.

We propose that a C-type lectin receptor, SIGNR-1 (also called Cd209b), helps to condition dendritic cells (DCs) in the gastrointestinal lamina propria (LPDCs) for the induction of oral tolerance in a model of food-induced anaphylaxis. Oral delivery of BSA bearing 51 molecules of mannoside (Man(51)-BSA) substantially reduced the BSA-induced anaphylactic response. Man(51)-BSA selectively targeted LPDCs that expressed SIGNR1 and induced the expression of interleukin-10 (IL-10), but not IL-6 or IL-12 p70. We found the same effects in IL-10-GFP knock-in (tiger) mice treated with Man(51)-BSA. The Man(51)-BSA-SIGNR1 axis in LPDCs, both in vitro and in vivo, promoted the generation of CD4(+) type 1 regulatory T (Tr1)-like cells that expressed IL-10 and interferon-γ (IFN-γ), in a SIGNR-1- and IL-10-dependent manner, but not of CD4(+)CD25(+)Foxp3(+) regulatory T cells. The Tr1-like cells could transfer tolerance. These results suggest that sugar-modified antigens might be used to induce oral tolerance by targeting SIGNR1 and LPDCs.

The development of non-human primate models of asthma requires a period of time (e.g., 0.5 –1 year). To develop the models in a short period, male cynomolgus monkeys were sensitized with dinitrophenyl-Ascaris suum (DNP-As) allergen by intraperitoneal and intramuscular injection and by intratracheal inhalation. All sensitized animals developed positive intradermal skin reaction to DNP-As. Sensitization elevated allergen-specific IgE levels in serum, the number of CCR4-positive T helper lymphocytes in peripheral blood, and IL-4 and IL-5 releases from phorbol 12-myristate 13-acetate- and ionomycin-stimulated peripheral blood. In addition, allergen challenge induced increases in lung resistance, airway inflammation, and hyperresponsiveness to inhaled methacholine. Next, animals were sensitized with house dust mite extracts (HDM) under the similar procedure. In these animals sensitized with DNP-As or HDM, inhaled fluticasone propionate and oral prednisolone inhibited the allergen-induced airway hyperresponsiveness. Taken together, monkey asthma models were successfully developed by sensitization with DNP-As or HDM under a short-term protocol (within 7 weeks). These models should be useful for the evaluation of anti-inflammatory drugs for asthma treatment. Keywords:: airway hyperresponsiveness, bronchoalveolar lavage, CCR4-positive cell, cytokine, methacholine

Tryptophan catabolism, including kynurenine pathway, is known to be involved in immunoregulation and its metabolites play a role in immune modulation. In the context of allergic diseases, it has been proposed that tryptophan degradation pathway, rather than tryptophan deprivation itself, plays an important role in tolerance induction during allergen-specific immunotherapy, which is, by far, the only causal treatment of allergic diseases. In addition, it has recently been demonstrated that kynurenine and, perhaps, its metabolites can act through the aryl hydrocarbon receptor, a unique cellular chemical sensor, and regulate immune functions. The present review intends to highlight the recent development on the involvement of kynurenine pathway in the regulation of allergic diseases.

Scratching behavior was induced in 12 strains of mice and the frequency was compared. An injection of histamine at a dose of 50 nmol induced frequent scratching behavior only in ICR mice, although the same dose of serotonin induced frequent scratching behavior in all strains of mice except for A/J. Histamine (10 nmol), serotonin (1 nmol), substance P (50 nmol) and passive cutaneous anaphylaxis induced significant vascular permeability increase in BALB/c, ICR, ddY and NC/Nga mice. These four stimuli also induced frequent scratching behavior in ICR mice. However, they failed to induce substantial increase in the incidence of scratching in the other three strains, except for ddY, which exhibited a slight but significant increase against substance P injection. These results suggest that the ICR mouse is a good responder for scratching behavior against various stimuli, especially against histamine. Thus ICR mice may be suitable for studying mediators and/or mechanisms for itching.

Anti-scratch effects of oxatomide and epinastine were examined in mice. Scratching behavior and cutaneous reactions were induced in BALB/c, ICR and ddY mice by dinitrofluorobenzene painting, passive cutaneous anaphylaxis and substance P injection, respectively. Although oxatomide and epinastine failed to inhibit scratching behavior in BALB/c mice, they inhibited the cutaneous reaction significantly. The drugs potently inhibited both scratching behavior and cutaneous reaction in ICR mice. They also inhibited scratching behavior and cutaneous reaction in ddY mice, although cetirizine and terfenadine failed to affect them. Histamine did not induce frequent scratching behavior in BALB/c and ddY mice. These results indicate that oxatomide and epinastine inhibit the scratching behavior in ICR mice associated with passive cutaneous anaphylaxis mainly through an antagonistic action on histamine H 1 receptors. The results also indicate that these drugs inhibit substance P-induced scratching behavior in ddY mice through an action independent of the antagonistic action on histamine H 1 receptors.

Background: Itching in humans is attenuated by µ-opioid receptor antagonists. ICR mice display increases in scratching behavior upon induction of IgE-mediated passive cutaneous anaphylaxis (PCA), or intradermal injection of compound 48/80 or histamine. Methods: Cutaneous reactions were induced in ICR mice by IgE-mediated PCA, compound 48/80 and histamine, and the scratching behavior associated with the cutaneous reactions was evaluated. Results: Naloxone and nalmefene reduced the incidence of scratching behavior associated with PCA. Naloxone also inhibited the induction of scratching behavior caused by compound 48/80 and histamine. Naloxone did not affect the increase in vascular permeability caused by PCA and injection of compound 48/80. Conclusion: Scratching behavior in mice may be induced by a sensation or a mechanism similar to itching in humans and should become a useful model for examining itching in humans.

Scratching behavior associated with passive cutaneous anaphylaxis was examined and compared to that induced by compound 48/80 or histamine in ICR mice. Elicitation of passive cutaneous anaphylaxis, and intradermal injections of compound 48/80, histamine or serotonin induced both scratching behavior and vascular permeability increase in ICR mice. In mast cell-deficient WBB6F1-W/Wv mice, although histamine induced scratching behavior and vascular permeability increase, passive cutaneous anaphylaxis was not observed. Cetirizine and terfenadine significantly inhibited the scratching behavior and vascular permeability increase caused by passive cutaneous anaphylaxis, compound 48/80 and histamine. The histamine H1 receptor antagonists inhibited the vascular permeability increase almost completely, whereas they failed to abolish the scratching behavior. Famotidine and ranitidine significantly inhibited the scratching behavior caused by histamine. The histamine H2 receptor antagonists did not affect the vascular permeability increase caused by histamine. The combination of cetirizine and ranitidine abolished the histamine-induced scratching behavior. The combination, however, failed to potentiate the inhibition of passive cutaneous anaphylaxis-induced scratching behavior significantly. The results indicated that histamine induces scratching behavior in ICR mice through both histamine H1 and H2 receptors, and that histamine plays a major role in passive cutaneous anaphylaxis-induced scratching behavior. Histamine might also play an important role in compound 48/80-induced scratching behavior.

We investigated the effects of KF19514 (5-phenyl-3-(3-pyridyl)methyl-3H-imidazo[4,5-c][1,8]naphthyridin-4 (5H)-one) on bronchoconstriction and allergic inflammation in guinea pigs and on tumor necrosis factor-alpha production in mice. KF19514 inhibited phosphodiesterase 4 (IC50 = 0.40 microM) and phosphodiesterase 1 (IC50 = 0.27 microM) derived from canine tracheal smooth muscles. KF19514 relaxed contracted tracheal smooth muscle and had a potent inhibitory effect on antigen-induced bronchoconstriction (EC50 = 0.058 microM) in vitro. Intravenous administration of KF19514 inhibited histamine-induced bronchoconstriction (ID50 = 2.8 microg/kg i.v.). Moreover, oral administration of KF19514 inhibited anaphylactic bronchoconstriction (ID50 = 0.2 mg/kg p.o.), and eosinophil infiltration in airway stimulated with platelet-activating factor (PAF) or antigen. KF19514 also produced a significant inhibition of tumor necrosis factor-alpha production in mice (ID50 = 0.023 mg/kg p.o.). Finally, KF19514 completely inhibited antigen-induced hyperreactivity at 0.1 mg/kg p.o. These results demonstrate that KF19514 may have efficacy in the treatment of asthma.

Background Tryptophan metabolites have been suggested to play a role in immune modulation, wherein those have recently been shown to be endogenous ligands of aryl hydrocarbon receptor (AhR; a unique cellular chemical sensor). However, the involvement of tryptophan metabolites and AhR in modulating mast cell function remains to be fully defined. We therefore investigated that the functional impacts of tryptophan metabolites on human and mouse mast cell responses in vitro and their functional importance in vivo. Methods Three tryptophan metabolites, kynurenine (KYN), kynurenic acid (KA) and quinolinic acid (QA), were examined in terms of their effect on IgE-mediated responses in mouse bone marrow-derived mast cells (BMMCs) and in human peripheral blood-derived cultured mast cells (HCMCs) and on in vivo anaphylactic responses. For evaluation of AhR involvement, we examined the responses of mast cells from AhR-null or AhR-wild-type mice with the use of a known AhR antagonist, CH223191. Results Kynurenine, but not KA and QA, enhanced IgE-mediated responses, including degranulation, LTC4 release, and IL-13 production in BMMCs through the activation of PLCγ1, Akt, MAPK p38, and the increase of intracellular calcium. KYN also enhanced cutaneous anaphylaxis in vivo. These enhancing effects of KYN were not observed in AhR-deficient BMMCs and could be inhibited by CH223191 in BMMCs. Further, KYN had similar enhancing effects on HCMCs, which were inhibited by CH223191. Conclusion The AhR-KYN axis is potentially important in modulating mast cell responses and represents an example of AhR's critical involvement in the regulation of allergic responses.

Some cameras, especially in the case of assembling line-sensor 3CCD cameras, may generate non-suitable images which include phenomena called "pixel shifts." This paper describes such a phenomenon, its numerical analysis and comparison between professional determination and machine detection. If there is such a pixel shift in the image, a user of camera may be suffering from a lack of precision of the image to be measured or utilized for image understanding. In a conventional approach of manufacturing line-sensor 3CCD cameras, some specialists have determined whether phenomena of "pixel shifts" occurs or not in the image. They have reported performance evaluation for the relevant camera which monitors the image before shipping camera. We had already proposed a numerical method to detect occurrence of pixel shift in the image with Lagrange interpolation function, calculated the values of the level for occurrence of pixel shift quantitatively. In the previously comparison, our calculated results had been perfectly consistent with determination by some specialist. And moreover, we have applied our approach into another kind sets of 20 samples of camera-monitored image and compared determination by another specialist with our corresponding results. By means of Kansei Evaluation of human sensitivity, we have discriminated difference of specialist's determination and our numerical approach.

We propose that the aryl hydrocarbon receptor (AhR), a unique chemical sensor, is critical in controlling mast cell differentiation, growth, and function in vitro and in vivo. In antigen-stimulated mast cells, exposure to AhR ligands resulted in a calcium- and reactive oxygen species (ROS)-dependent increase of reversible oxidation in and reduced activity of SHP-2 phosphatase, leading to enhanced mast cell signaling, degranulation, and mediator and cytokine release, as well as the in vivo anaphylactic response. Surprisingly, significant mast cell deficiency was noted in AhR-null mice due to defective calcium signaling and mitochondrial function, concomitant with reduced expression of c-kit and cytosolic STAT proteins, as well as enhanced intracellular ROS and apoptosis. Consequently, AhR-null mast cells responded poorly to stimulation, demonstrating a critical role of AhR signaling in maintaining mast cell homeostasis.

Histamine release from purified rat peritoneal mast cells (PMC) was examined and compared to that from a non-purified preparation (PEC). Both PEC and PMC released similar amounts of histamine upon stimulation with compound 48/80, calcium ionophore A23187 and substance P. In contrast, IgE-dependent histamine release from PMC caused by antigen, anti-IgE and concanavalin A was very low compared to that of PEC. The reduced IgE-dependent histamine release from PMC, however, was recovered when PMC was reconstituted with non-mast cells (NMC) present in the peritoneal cavity. The effect was time-dependent and reached a plateau in 30 min. NMC from both sensitized and non-sensitized rats recovered the reduced histamine release from PMC dose-dependently. The potentiating effect of NMC was observed even in the presence of excess amount of phosphatidylserine. Supernatants of NMC and a mixture of PMC and NMC incubated for 1 hr at 37 degrees C, however, failed to potentiate the histamine release. These results demonstrate that IgE-dependent histamine release from rat peritoneal mast cells is upregulated by other cells present in the peritoneal cavity, and that the mechanism involved is distinct from that of phosphatidylserine.

Effect of stem cell factor on histamine release from rat peritoneal mast cells was studied. Although stem cell factor did not evoke histamine release by itself, it clearly potentiated histamine release from sensitized mast cells caused by antigen, anti-IgE and concanavalin A. However, stem cell factor did not affect histamine release caused by compound 48/80, calcium ionophore A23187 and substance P. Although maximum potentiation of antigen-induced histamine release by stem cell factor was accomplished after 1–10 minute-preincubation, potentiation was declined after a longer incubation period. Potentiation of histamine release by phosphatidylserine and non-mast cells in the rat peritoneal cavity was incubation time-dependent. Potentiation by stem cell factor was additive to that by phosphatidylserine or non-mast cells. These results indicate that stem cell factor selectively potentiates IgE-dependent histamine release from rat peritoneal mast cells, and suggest that the mechanism involved is distinct from that of phosphatidylserine or non-mast cells in the rat peritoneal cavity.

The hydrogen peroxide reduction reaction (HPRR) has attracted attention because it is involved in the oxygen reduction reaction, which is an important cathode reaction in several fuel cell systems. Thus, it has been widely studied, including effects of electrolyte components and additives on the HPRR at Pt electrodes. Katsounaros and Mayrhofer have reported the influence of the adsorption of (bi)sulfate and halide ions to the HPRR in acidic electrolytes [1]. The strength of the inhibition of the HPRR increases as the degree of the adsorption increases. They also reported [2] that alkali metal cations, e.g., Li+, Na+, and K+, suppress the HPRR in basic electrolytes. The hydrated alkali metal cations and chemisorbed OH species on Pt, denoted as M+(H2O) x and OHads respectively, non-covalently stabilize each other, leading to the formation of quasi-specifically adsorbed hydrated metal ion clusters, OHads-M+(H2O) x clusters, that blocks electrochemical reactions. The suppression becomes large as the strength of the non-covalent interaction increases (K+ < Na+ < Li+), and as a consequence the rest potential decreases in the following order: K+ < Na+ < Li+, as reproduced in Figure 1a. On the other hand, inorganic salts which are composed of the alkali metal cations, e.g., Na2SO4 and K2SO4, are often used as supporting electrolytes for electrochemical reactions. However, as we have reported before [3], the salts generally affect the hydrogen evolution reaction (HER) on various kinds of metals, namely, Pt, Au, Rh, Ag, Cu, Fe, Ni, W, Zn, Sn, and In, in strong acidic solutions. The rate of the HER decreased in the presence of the cations because the transport rate of H+ ions to the electrode surface due to electromigration decreased in the presence of the cations. Thus, the reduction current due to the HER decreased as the concentration of the salts increased. We have reported [4] that the HPRR in acidic electrolytes is also affected when the inorganic salts, Na2SO4 and K2SO4, are added to the electrolytes. The local pH at the electrode surface became basic during the HPRR because of the decrease in the transport rate of H+ in the presence of the alkali metal cations. Furthermore, we have tentatively suggested [5] that the HPRR in acidic electrolytes is affected by the non-covalent interaction between the cations and OHads. Then, in order to verify this, this work focuses on studying how the cations affect the HPRR. Although the rest potential is independent on the kind of alkali metal cations, the HPRR is suppressed due to the presence of the cations. The H2O2 reduction current decreases (in absolute value) in the following order: Li+ < Na+ < K+, as shown in Fig. 1b. This order is in the reverse order of the strength of the non-covalent interaction observed for basic electrolytes. Thus, the suppression cannot be explained on the basis of the non-covalent interaction but rather on the basis of the decrease in the transport rate of H+, which will be discussed in this work. REFERENCES [1] I. Katsounaros, W. B. Schneider, J. C. Meier, U. Benedikt, P. U. Biedermann, A. Cuesta, A. A. Auer and K. J. Mayrhofer, Physical Chemistry Chemical Physics, 15, 8058 (2013). [2] I. Katsounaros and K. J. J. Mayrhofer, Chem. Commun., 48, 6660-6662 (2012). [3] Y. Mukouyama, R. Nakazato, T. Shiono, S. Nakanishi and H. Okamoto, J. Electroanal. Chem., 713, 39 (2014). [4] Y. Mukouyama, H. Kawasaki, D. Hara, M. Kikuchi, Y. Yamada, S. Nakanishi, ECS Trans., 69 (39), 37-45 (2015). [5] Y. Mukouyama, D. Hara, H. Kawasaki, M. Kikuchi, Y. Yamada, S. Nakanishi, ECS Trans., 69 (39), 47-57 (2015). FIGURE CAPTION Figure 1. The current (I) – potential (E) curves for a Pt-plate electrode in basic and acidic solutions measured under potential controlled conditions at a scan rate of 0.01 Vs-1. The basic solutions are 0.05 M alkali hydroxide (denoted as MOH) + 0.01 M H2O2, and the acidic ones are 0.05 M H2SO4 + 0.01 M H2O2 with or without 0.05 M alkali sulfate (denoted as M2SO4). Figure 1

Peritoneal mast cell hyperplasia was investigated in rats after evoking IgE antibody-antigen reaction. Rats were immunized with antigen and then passively sensitized with monoclonal IgE antibody before antigen challenge. A significant increase in the number of peritoneal mast cells was observed 3 weeks after the antigen challenge in the peritoneal cavity, although the histamine content of the mast cells was decreased significantly. In rats without prior immunization, these changes were not observed. Stimulation with compound 48/80 or calcium ionophore A23187 did not affect the number of mast cells. This model may prove to be a useful tool for studying the mechanisms of mast cell hyperplasia and recruitment of mast cell precursors in vivo.

Numerical Analysis is one of the most useful subjects to combine mathematics, physics, computer science, especially programming language, algorithm and/or practical exercises in several domains of Engineering. However, it has been considered to be one of the typically fundamental subjects by not only instructors but also learners themselves. This paper focuses Problem-based Educational Visualization as an application of Numerical Analysis on solving the real problems from industry and demonstrates activity of “Industry — University Collaboration” to build co-working relationship among higher education and outside society. The paper also introduces how to apply Numerical Analysis into performance evaluation of camera, especially determining whether images obtained by camera are well-adjusted or not.

Fucosylated glycans on pathogens are known to shape the immune response through their interaction with pattern recognition receptors, such as C-type lectin receptors (CLRs), on dendritic cells (DCs). Similar fucosylated structures are also commonly found in a variety of allergens, but their functional significance remains unclear. To test a hypothesis that allergen-associated glycans serve as the molecular patterns in functional interaction with CLRs, an enzyme-linked immunosorbent assay-based binding assay was performed to determine the binding activity of purified allergens and allergen extracts. THP-1 cells and monocyte-derived DCs (MDDCs) were investigated as a model for testing the functional effects of allergen-CLR interaction using enzyme-linked immunosorbent assay, Western blotting, and flow cytometry. Significant and saturable bindings of allergens and allergen extracts with variable binding activities to DC-specific ICAM3-grabbing non-integrin (DC-SIGN) and its related receptor, L-SIGN, were found. These include bovine serum albumin coupled with a common glycoform (fucosylated glycan lacking the alpha1,3-linked mannose) of allergens and a panel of purified allergens, including BG60 (Cyn dBG-60; Bermuda grass pollen) and Der p2 (house dust mite). The binding activity was calcium-dependent and inhibitable by fucose and Lewis-x trisaccharides (Le(x)). In THP-1 cells and human MDDCs, BG60-DC-SIGN interaction led to the activation of Raf-1 and ERK kinases and the induction of tumor necrosis factor-alpha expression. This effect could be blocked, in part, by Raf-1 inhibitor or anti-DC-SIGN antibodies and was significantly reduced in cells with DC-SIGN knockdown. These results suggest that allergens are able to interact with DC-SIGN and induce tumor necrosis factor-alpha expression in MDDCs via, in part, Raf-1 signaling pathways.

INTRODUCTION Electrochemical oscillations, which are attractive phenomena from the viewpoint of dynamic self-organization of molecular systems, have been reported in a variety of electrochemical reactions [1]. Among them, the H2O2 reduction at Pt electrodes in H2SO4 solutions (H2O2 + 2H+ + 2e- → 2H2O) has an especially unique feature where nine kinds of oscillations, named oscillations A, B, C, D, E, F, G, H, and I are observed [2-4]. Oscillation A appeared in the potential region of the formation of under-potential deposited H (upd-H) which suppressed the H2O2 reduction, whereas oscillation B appeared in the region of hydrogen evolution reaction (HER). Oscillations C and D appeared when a small amount of Cl- or Br- ions, which adsorbed on a Pt surface, were added to electrolysis solutions. Oscillation E appeared when a single-crystal Pt(111) electrode was used because H2O2 was autocatalytically reduced especially on the Pt(111) surface. Oscillations F and G appeared in the presence of a small amount of Br- ions when a Pt(111) or Pt(100) electrode was used. Oscillations H and I appeared when the cations such as Na+ and K+ were added to electrolysis solutions [2-4]. In the presence of the cations, the transport rate of H+ to the electrode surface by the electromigration decreased and consequently the local pH at the electrode surface became basic during the H2O2 reduction. In the vicinity of the surface where the pH was basic, H2O2 dissociated to form HO2 - ion, which was electrochemically reduced to OH- or oxidized to O2. Oscillation H was tentatively caused by the interaction between the autocatalytic H2O2 reduction and the electrooxidation of HO2 - [2, 3]. On the other hand, oscillation I was probably caused by the suppression of the reduction of HO2 - due to the formation of upd-H [4]. Recently, a new oscillation, which was named oscillation J, was found to appear during the H2O2 reduction in the presence of the cations. In this presentation, the conditions for the appearance of oscillation J and its mechanism will be discussed. RESULTS and DISCUSSION Figure 1 shows the current (I) – potential (E) curves for a Pt-disc electrode. When the solution was 0.1 M H2SO4 + 0.1 M H2O2 (Fig. 1a), the H2O2 reduction occurred in the potential region below ca. 0.8 V under potential controlled conditions. The reduction was suppressed, that is, an N-shaped negative differential resistance (N-NDR) appeared, at around ca. –0.1 V due the formation of upd-H. Oscillation A appeared as a current oscillation at the potentials of the N-NDR and the HER due to the H+ reduction occurred in the potential region below ca. –0.15 V. Oscillation A did not appeared under current controlled conditions (Fig. 1b). When the concentration of H2O2 was 0.3 M, oscillation B appeared both under potential controlled conditions and under current controlled ones (Figs. 1c and 1d). The I – E curves were strongly affected by adding Na2SO4 or K2SO4 to the solution because the local pH at the electrode surface became basic during the H2O2 reduction in the presence of Na+ or K+ [2-4]. When the solution was 0.1 M H2SO4 + 0.3 M H2O2 + 0.1 M Na2SO4 (Figs. 1e and 1f), oscillations A and B did not appear. However, oscillation I appeared at around –0.8 V under potential controlled conditions. The HER due to the water reduction occurred in the potential region below ca. –1.0 V. When the H2O2 concentration was high, e.g., 0.9 M (Figs. 1g and h), oscillations I and H appeared under potential controlled conditions and under current controlled conditions, respectively. The new oscillation, oscillation J, appeared at around –1.15 V under potential controlled conditions and also appeared in the potential range between –0.4 and –1.5 V under current controlled conditions. Oscillation J synchronized with the behavior of hydrogen bubbles formed by the HER. Thus, the bubble evolution probably played a role in the mechanism of oscillation J. REFERENCES [1] M. Orlik, Self-Organization in Electrochemical Systems I, Springer, Berlin (2012). [2] Y. Mukouyama, M. Hasegawa, S. Yamamoto, S. Nakanishi, H. Okamoto, ECS Trans., 58 (25) 99-107, 2014. [3] Y. Mukouyama, M. Hasegawa, S. Nakanishi, ECS Trans., 64 (2014) accepted. [4] Y. Mukouyama, M. Hasegawa, S. Nakanishi, ECS Trans., 64 (2014) accepted. FIGURE CAPTION Figure 1. The I – E curves for 0.1 M H2SO4 + x M H2O2 + y M Na2SO4, where (x, y) = (0.1, 0), (0.3, 0), (0.3, 0.1), and (0.9, 0.1) from top to bottom, measured (left) under current controlled conditions and (right) under current controlled conditions. Figure 1

Background Glycoproteins containing Lewis-x (Le x ) trisaccharides are often associated with the host's adaptive T H 2-type immunity, but the mechanisms underlying the T H 2-biased response are at present unclear. Objective The modulatory effect of Le x or its glycoconjugates on IgE/T H 2 responses was investigated. Methods The levels of serum antibodies and cytokines were analyzed by means of ELISA, RT-PCR, or both. Results In C3H mice Le x coupled with BSA (Le x -BSA) elicited higher levels of specific IgE and IgG1, but not IgG2a, which were associated with increased levels of splenic T H 2 cytokines when compared with those seen in BSA-sensitized mice. In BALB/c mice sensitized with Le x -BSA or Le x mixed with ovalbumin, significantly increased levels of specific IgE and IgG2a antibodies were found concomitant with reduced levels of serum IL-12p70. These effects were attenuated in IL-12–deficient BALB/c mice. Le x and an isomer, Le y , but not other isomers, inhibited the production of LPS-induced IL-12p70, associated with a significant reduction of nuclear NF-κB, in bone marrow–derived dendritic cells from BALB/c mice, suggesting that Le x -induced suppression of IL-12p70 results in an enhanced T H 2 response. The addition of mannan, a known ligand for dendritic cell–specific intercellular adhesion molecule 3–grabbing nonintegrin, abrogated the suppressive effect of Le x trisaccharides. Conclusion These results provide evidence for a potential role of Le x trisaccharides in shaping the immune responses through, at least in part, its suppressive effect on IL-12p70 production. Considering the relative ubiquity of glycoproteins with Le x or similar oligosaccharides, including plant-derived (or food-derived) allergens, these findings might have a broad implication. Clinical implications The adjuvant activity of Le x trisaccharides might aid in vaccine design and might be important in determining the allergenicity of proteins containing this or other similar structures.

Immunoglobulin E (IgE)-dependent histamine release from purified rat peritoneal mast cells (PMC) is very low in comparison to that from a non-purified preparation (PEC). The reduced histamine release from PMC is recovered or potentiated by reconstitution with separated non-mast cells (NMC). In the present study, further characterization was undertaken to elucidate the mechanisms involved. Sensitized mast cells were recovered from peritoneal cavities of rats, and purified by density gradient centrifugation with Percoll. Effects of NMC reconstitution, membrane fraction of NMC, NMC incubation supernatant, adhesion molecules and extracellular matrix proteins on IgE-dependent histamine release from PMC were examined. IgE-dependent histamine release was significantly potentiated by NMC reconstitution to PMC. The potentiation was dependent on the concentration of NMC reconstituted and reached a plateau after 30 min incubation. Increasing concentration of PMC did not affect the histamine release. Membrane fraction prepared from NMC also potentiated PMC histamine release in a dose-dependent manner. The potentiation reached a plateau in 5 min. Furthermore, incubation supernatant of NMC potentiated PMC histamine release. Antibodies against intercellular adhesion molecule (ICAM)-1, lymphocyte function-associated antigen (LFA)-1, very late activation antigen (VLA)-1, VLA-4 and VLA-6, and fibronectin did not affect the potentiation of PMC histamine release by NMC reconstitution. Fibronectin, laminin and collagen failed to potentiate PMC histamine release. These results indicate that the membrane component(s) of NMC in the rat peritoneal cavity seems to modulate IgE-dependent histamine release from peritoneal mast cells of rats, and that the active molecule(s) may be released from NMC. Adhesion molecules such as ICAM-1, LFA-1 and VLA are not involved.

IgE-dependent histamine release from rat mesenteric mast cells was investigated. Excised mesenterium was cut into pieces and incubated with IgE overnight at 4 degrees C for sensitization. Over 10 pieces of mesenterium specimen could be prepared from a rat. Antigen-induced histamine release from mesenterium specimen was initiated rapidly and reached a plateau in 5 min. In an optimal condition, over 50% of total histamine was released. In contrast, unpurified and purified peritoneal mast cells released only 22.5% and 5.3% of total histamine, respectively, upon IgE stimulation. Tranilast, a mast cell stabilizer, inhibited the histamine release from mesenteric mast cells significantly. The mesenterium might be useful material for studying tissue-associated mast cell activation.

Effects of 11 histamine H 1 receptor antagonists on IgE-mediated biphasic cutaneous reaction in mice were examined. The immediate phase reaction (IPR) assessed at 1 hour after antigen application was significantly inhibited by all antihistamines' examined. The inhibition of IPR by cetirizine and mequitazine were potent, but those by cyproheptadine and diphenhydramine were weak. The later phase reaction (LPR) assessed at 24 hours after antigen application was inhibited by chlorphemramine, oxatomide, ketotifen, mequitazine, emedastine, terfenadine and azelastine. The inhibition of LPR by emedastine was potent, but those by ketotifen and terfenadine were only partial. Emedastine inhibited both IPR and LPR comparably. Present results indicate that H 1 receptor activation is involved in the IPR of the biphasic cutaneous reaction, and that the blockade of H 1 receptors at IPR does not contribute to the attenuation of following LPR. Histamine H 1 receptor antagonists inhibiting the LPR have a property distinct from H 1 receptor antagonism, which may have an additional benefit for the treatment of allergic diseases.

Inhibitory mechanisms of isoproterenol and clenbuterol for immunoglobulin E (IgE)-mediated experimental allergic reactions in rats were studied. IgE-mediated passive cutaneous anaphylaxis, histamine-induced cutaneous reaction and serotonin-induced cutaneous reaction were evoked at the same time in the same rats. Isoproterenol administered intravenously immediately before challenge inhibited all these reactions significantly. Clenbuterol administered intravenously 0–3 h before challenge also significantly inhibited the three cutaneous reactions. The inhibition was maximum when drugs were given 1 h before challenge. Passive cutaneous anaphylaxis was always inhibited more potently than histamine-induced cutaneous reaction and serotonin-induced cutaneous reaction by these β -adrenoceptor agonists. Passive peritoneal anaphylaxis was caused by injecting an antigen intravenously. Isoproterenol administered intravenously immediately before challenge inhibited the reaction significantly. Clenbuterol administered intravenously 0–3 h before challenge also significantly inhibited passive peritoneal anaphylaxis, maximally so when given 1 h before challenge. In vitro IgE-dependent histamine release from sensitized peritoneal mast cells or mesenteric mast cells was not affected by isoproterenol and clenbuterol. Mouse monoclonal IgE, a foreign protein, administered intravenously decreased rapidly in the circulation. About 50% of the mouse IgE given disappeared in 20 min. The decrease of mouse IgE was partly but significantly inhibited by the β -adrenoceptor agonists, and the inhibition was abolished by simultaneous treatment with propranolol. These results indicate that direct inhibition of mast cell activation does not contribute to the potent inhibition of in vivo allergic reactions in rats by β -adrenoceptor agonists, and that inhibition of the allergic cutaneous reaction is partially explained by the inhibition of vascular permeability increases caused by mast cell mediators. Penetration of intravenously administered antigen from blood vessels to peripheral tissues to cause mast cell activation might be inhibited by β -adrenoceptor agonists, and this could play some role in inhibiting intravenous antigen-induced allergic reactions in rats. Clenbuterol exhibited its maximum action with some latency in vivo, suggesting that some time-requiring process may be involved in the manifestation of its action.

We investigated the effect of KW-4679 ((Z)-11-[(3-dimethylamino)propylidene]-6, 11-dihydrodibenz[b, e]oxepin-2-acetic acid monohydrochloride), an orally active anti-allergic drug, on antigen-induced airway hyperresponsiveness using two different indicators, pulmonary resistance (RL) and dynamic lung compliance (Cdyn), in actively sensitized guinea pigs. Oral administration of KW-4679 (0.1 and 1 mg/kg) 1 hr before aerosolized antigen exposure significantly inhibited the development of airway hyperresponsiveness to inhaled acetylcholine in RL and Cdyn in a dose-dependent manner. Terfenadine (10 mg/kg) also inhibited the development of airway hyperresponsiveness. These results indicate that KW-4679 could be useful in the treatment of bronchial asthma.

Rat peritoneal mast cells, which had been sensitized two days earlier by an intraperitoneal injection of rat monoclonal IgE antibodies, were purified by density gradient centrifugation with 60% Percoll (cell purity > 95%). Histamine release from the purified mast cells (PMC) was then compared to that of a non-purified preparation (peritoneal exudate cells; PEC). Both PEC and PMC released similar amounts of histamine upon stimulation with calcium ionophore A23187 and compound 48/80. In contrast, antigen-induced histamine release from PMC was very low compared to that of PEC. PEC released up to 30% of total histamine upon challenge with 1 microgram/ml of antigen, whereas histamine release from PMC was only one third or less than that of PEC. When PEC was suspended in 60% Percoll and treated for a period needed for purification, the reduction of antigen-induced histamine release was negligible. Mast cells purified by centrifugation on a metrizamide gradient released only small amount of histamine similar to Percoll-purified mast cells. Non-mast cells (NMC) recovered from the interface of the 60% Percoll potentiated the antigen-induced histamine release from PMC concentration- and time-dependently. The supernatant of the NMC suspension which was incubated at 37 degrees C for 60 min, however, failed to potentiate histamine release in PMC. We concluded therefore that separation media such as Percoll and metrizamide do not cause the low antigen-induced histamine release in PMC, but that the separation of mast cells from other cells present in the peritoneal cavity itself causes it. Antigen-induced mast cell histamine release is potentiated through a direct interaction between mast cells and NMC, and some cell surface molecules also seem to be involved.