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This paper presents a the study on air curtain system of top and bottom bi-directional jet air discharge for blocking the spread of smoke in case of tunnel fire. The five kinds different air curtains of A, B, C, D, and E of models for various performance tested after manufactured. A results of the various performance test obtained the best efficiency from E model air curtain. And optimize the injection angle of the air curtain nozzle through the three-dimensional computational fluid dynamics (CFD) analysis and analyzed the effects of external pressure of tunnel. and also single factor design have been applied. At present, our attention is focused on the velocity distribution(flow width and flow position) of 1.5m on the ground in tunnel. Also, analyzed the influence of draft in the tunnel. Detailed effects of discharge angle of air curtain and velocity at nozzle exit are discussed. 1. 서 론 터널 방연 에어커튼이란 터널 내부에서 화재가 발생했을 때 운전자들이 안전하게 대피할 수 있는 피난공간을 확보하기 위해 고압 공기를 분사해 화재시 발생되는 유독성 연기를 차단하는 시설이다. 현재 전국 고속도로 상에 있는 500 ∼1,000m 터널 123개소 가운데 93개소의 터널에는 피난연결통로가 설치되지 않은 것으로 파악됐다.

This study investigated whether anti-CD40 Ab and 8-oxo-dG attenuate mast cell migration and EAE development. Anti-CD40 Ab and 8-oxo-dG reduced EAE scores, mast cell numbers, expression of adhesion molecules, OX40L and Act1, levels of TNF-α, LTs, expression of cytokines, and co-localization of Treg cells and mast cells, all of which are increased in EAE-brain tissues. Each treatment enhanced Treg cells, expression of OX40, and cytokines related to suppressive function of Treg cells in EAE brain tissues. Act-BMMCs with Treg cells reduced expression of OX40L and CCL2/CCR2, VCAM-1, PECAM-1, [Ca²⁺]i levels, release of mediators, various signaling molecules, Act1 related to IL-17a signals versus those in act-BMMCs without Treg cells. The data suggest that IL-10- and IL-35-producing Foxp3⁺-Treg cells, enhanced by anti-CD40 Ab or 8-oxo-dG, suppress migration of mast cells through down-regulating the expression of adhesion molecules, and suppress mast cell activation through cell-to-cell cross-talk via OX40/OX40L in EAE development.

Bacterial diseases in soybean are bacterial pustule by Xanthomonas axonopodis pv. glycines, wildfire by Pseudomonas syringae pv. tabaci, bacterial blight by Pseudomonas savastanoi pv. glycines and bacterial brown spot by Pseudomonas syringae pv. syringae in Korea. It is difficult to identify each disease by early symptoms in fields, because the initial symptoms of these diseases are very similar to each other. In this study, we developed multiplex PCR detection method for rapid and accurate diagnosis of bacterial diseases. The glycinecin A of X. axonopodis pv. glycines, the tabtoxin of P. syringae pv. tabaci, the coronatine of P. savastanoi pv. glycines and the syringopeptin of P. syringae pv. syringae have been reported previously. These bacteriocin or phytotoxin producing genes were targeted to design the specific diagnostic primers. The primer pairs for diagnosis of each bacterial diseases were selected without nonspecific reactions. The studies on simultaneous diagnosis method were also conducted with primarily selected 21 primers. As a result, we selected PCR primer sets for multiplex PCR. Sizes of the amplified PCR products using the multiplex PCR primer set consist of 280, 355, 563 and 815 bp, respectively. This multiplex PCR method provides a efficient, sensitive and rapid tool for the diagnosis of the bacterial diseases in soybean.

Mast cells are major effector cells of allergic diseases related to IgE. This study was undertaken to determine whether IgE or IgA, produced by CD40-CD40L or OX40-OX40L interactions between B cells and mast cells, re-activate FceRI or FcαRI on mast cell surface. C57BL mice were sensitized and subjected to OVA challenge to induce asthma. Bone marrow-derived mast cells (BMMCs) and primary B cells were co-cultured. Mast cell recruitment into airways was stained by May-Grunwald Giemsa, the expression of markers or signaling molecules were determined by immunohistochemistry or Western blotting, and co-localization of B cells and mast cells by immunofluorescence. Anti-CD40 plus anti-OX40L Abs synergistically reduced IgE and IgA production, and mediators (histamine, LTs and cytokines) released in mast cells, and additively reduced other responses, such as, numbers of mast cells, the expression of markers (tryptase, mMCP5, B220 and CD19), surface molecules (CD40, CD40L, OX40 and OX40L), FceRI or FcαRI and the co-localization of BMMCs and B cells, and IgE- or IgA-producing cells, as compared with individual blocking Ab treatment which reducedresponses in BAL cells or lung tissues of OVA-challenged mice or in co-culture of B and mast cells. The data suggest that IgE and IgA, produced by OX40-OX40L or CD40-CD40L interaction between B cells and mast cells, may re-activate receptors of FCeRI and FcαRI on mast cell surfaces, followed by more mediator release, and furthermore, that treatment with anti-CD40 plus anti-OX40L Abs offers a potential treatment for allergic asthma.

Allergic asthma is characterized by chronic airway remodeling, which is associated with the expression of extracellular matrix proteins (ECM) by TGF-β. However, to date there are no reports demonstrating that structural proteins are directly expressed in mast cells. This study aimed to investigate whether ECM proteins are expressed in mast cells activated with antigen/antibody reaction, and whether the resolution effects of irradiation or 8-oxo-dG may contribute to allergic asthma prevention. Bone marrow-derived mast cells (BMMCs) were activated with DNP-HSA/anti-DNP IgE antibody (act-BMMCs). C57BL/6 mice were sensitized and challenged with ovalbumin (OVA) to induce allergic asthma. Mice were treated orally with 8-oxo-dG or exposed to whole body irradiation (using (137)Cs gamma ray at a dose of 0.5 Gy) for three consecutive days 24 h after OVA challenge. Expression of extracellular matrix (ECM) proteins, TGF-β signaling molecules and NF-κB/AP-1 was determined in the BMMCs, bronchoalveolar lavage (BAL) cells or lung tissues using Western blot, polymerase chain reaction (PCR) and electrophoretic mobility shift assay (EMSA), respectively. Act-BMMCs increased expression of ECM proteins, TGF-β/TGF-β receptor I, TGF-β signaling molecules and cytokines; and increased both NF-κB and AP-1 activity. In addition, the population of mast cells; expression of mast cell markers, TGF-β signaling molecules, ECM proteins/amounts; OVA-specific serum IgE level; numbers of goblet cells; airway hyperresponsiveness; cytokines/chemokines were increased in BAL cells and lung tissues of OVA-challenged mice. All of the above end points were reduced by irradiation or 8-oxo-dG in vitro and in vivo, respectively. The data suggest that mast cells induce expression of ECM proteins through TGF-β produced in inflammatory cells of OVA mice and that post treatment of irradiation or 8-oxo-dG after OVA-challenge may reduce airway remodeling through down-regulating mast cell re-activation by TGF-β/Smad signals.

Mast cells play important roles via FceRI-mediated activation in allergic asthma. A nonpolymorphic MHC I-like molecule CD1d, which is mainly expressed in APCs, presents glycolipid Ag to iTCR on iNKT cells and modulates allergic responses. This study aimed to investigate the role of CD1d on IgE production and mast cell activation related to allergic asthma. Bone marrow-derived mast cells (BMMCs) from C57BL/6 Wild type (WT) or KO (CD1d(-/-)) mice were activated with Ag/Ab (refer to WT-act-BMMCs and KO-act-BMMCs, respectively) or α-Galactosylceramide (WT-αGal-BMMCs, KO-αGal-BMMCs) in the presence of iNKT cells. WT, KO or BMMC-transferred KO mice were sensitized and/or challenged by OVA or α-Gal to induce asthma. KO-act-BMMCs reduced intracellular Ca(2+) levels, expression of signaling molecules (Ras, Rac1/2, PLA2, COX-2, NF-κB/AP-1), mediator release (histamines, leukotrienes and cytokines/chemokines), and total IgE levels versus the corresponding WT-BMMCs. KO mice reduced total and OVA-specific serum IgE levels, number of mast cells, recruiting molecules (CCR2/CCL2, VCAM-1, PECAM-1), expression of tryptase, c-kit, CD40L and cytokine mRNA, co-localization of c-kit and CD1d or iNKT cells in BAL cells or lung tissues, and PCA responses, compared with the corresponding WT mice. BMMC-transferred KO-both mice showed the restoration of all allergic responses versus KO-both mice (Ag/Ab reaction plus α-Gal). KO-αGal-BMMCs or KO-αGal mice did not show any responses. Our data suggest that CD1d-expressed mast cells may function as APC cells for iNKT cells and exacerbate airway inflammation and remodeling through up-regulating IgE production via B cell Ig class switching and mediator release in mast cells of OVA-challenged mice.

FEBRUARY 2013 AB44 Abstracts S A T U R D A Y 159 Effect of Cholesterol Depletion On Interleukin-8 Production in Human Respiratory Epithelial Cells Min Jung Kim, MD, Jung Yeon Hong, Kyung Eun Lee, PhD, Hwan Soo Kim, MD, Yoon Ki Han, MD, Hye Mi Jee, MD, Kyung Won Kim, MD, PhD, Myung Hyun Sohn, MD, PhD, Kyu-Earn Kim, MD, PhD; Yonsei University College of Medicine, Seoul, Korea, Yonsei University School of Medicine, Seoul, Korea, CHA University School of Medicine, Seongnam, Korea. RATIONALE: Lipid rafts in epithelial cell membrane plays multifunctions, including components of immune system and important mediators in inflammatory process. But the role of cholesterol, composing lipid rafts, has not been described in the inflammatory response. The aim of this study is to investigate the effect of cholesterol depletion to inflammatory process via expression of interleukin (IL)-8 in airway epithelial cells. METHODS: The human epithelial-like lung carcinoma cell line(A 549) was treated with 0.5% methyl-b-cyclodextrin as a selective cholesterol extractor. IL-8 levels were assessed by enzyme-linked immunosorbent assay (ELISA) and rechecked after cholesterol repletion. Mitogen-activated protein kinase (MAPK) inhibitors were used to find upstream signaling pathway for IL-8 production in cholesterol-depleted cells. RESULTS: IL-8 production in cholesterol-depleted epithelial cells increased in a time-dependent manner. The maximum production of IL-8 recorded at 24 hwas almost 3.5 timesmore than control cells. In addition, it reversed after cholesterol repletion. And IL-8 production decreased followed by pretreatment with extracellular signal-regulated kinase (ERK) inhibitor U0126, but not with JNK inhibitor II or p38 MAPK inhibitor SB202190. CONCLUSIONS: These results suggested that inflammatory responses could be increased in cholesterol-depleted cells, and it was regulated by MAPK signaling system, predominantly by ERK pathway. We concluded that lipid component in airway epithelial cells may play a role in inflammatory process.