• Tuberculosis and Respiratory Diseases
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• v.43 no.1
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• pp.46-53
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• 1996

Background: Endotoxin or lipopolysaccharide(LPS) can prime phagocytic cells such as polymorphonuclear leukocytes, monocytes or animal peritoneal macrophages to generate increased amounts of secretory products such as oxygen free radicals and tumor necrosis factor, which play an important role in developing adult respiratory distress syndrome in gram negative sepsis. Human alveolar macrophages(HAM) are continuously exposed to various stimuli inhaled into the alveoli, and the response to LPS might be different in HAM. Therefore, we investigated the effect of LPS pre-exposure on HAM adhered to plastic surface and A549 cell(type II human alveolar epithelial cell line) monolayer. Methods: HAM were isolated from bronchoalveolar lavage fluid from normal lung of the patients with localized lung cancer and esophageal cancer. LPS was exposed to HAM for 2hrs before or after adherence to plastic surface of 24-well Linbro plate and A549 cell monolayer. And then HAM was stimulated with PMA(phorbol myristate acetate) or fMLP(N-formyl-methionylleucyl-phenylalanine). The amount of hydrogen peroxide($H_2O_2$) production in the supernatant was measured on the principle of peroxidase-dependent oxidation of phenol red by hydrogen peroxide. Results: LPS pre-exposure could not enhance $H_2O_2$ production in neither HAM adhered to plastic surface nor one to A549 cell monolayer. But LPS even in the absence of PMA or fMLP stimulation directly increased $H_2O_2$ release in HAM if added after the adherence to A549 cell monolayer. Conclusion: Endotoxin does not prime HAM, but may directly activate HAM adhered to alveolar epithelial cells. Further investagation will be necessary.

• Journal of the Korean Institute of Illuminating and Electrical Installation Engineers
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• v.18 no.3
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• pp.34-39
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• 2004

This research investigated the influence on the 4 cell of DC discharge on the side of the discharge characteristic. This DC discharge cells are that composes AND gate of AND gate PDP newly proposed. As for the discharge starting voltage of this discharge cell of 4 pieces, it has been understood that there is deeply a relation up to the space charge generated from the discharge of adjoining discharge cell through the experiment. The discharge voltages which had become each discharge cell optimizations from the experiment result were decided. Moreover, the width of the margin of two AND input voltages is wide and the AND function occurs clearly. However, it has been qualitatively understood that it is difficult enough to obtain the operation margin of the DC priming discharge used to address discharge of PDP.

• IMMUNE NETWORK
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• v.13 no.5
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• pp.194-198
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• 2013

Recent papers have shown that the initial event in the pathogenesis of autoimmune type 1 diabetes (T1D) comprises sensing of molecular patterns released from apoptotic ${\beta}$-cells by innate immune receptors such as toll-like receptor (TLR). We have reported that apoptotic ${\beta}$-cells undergoing secondary necrosis called 'late apoptotic' ${\beta}$-cells stimulate dendritic cells (DCs) and induce diabetogenic T cell priming through TLR2. The role of other innate immune receptors such as TLR7 or TLR9 in the initiation of T1D has also been suggested. We hypothesized that TLR2 blockade could inhibit T1D at the initial step of T1D. Indeed, when a TLR2 agonist, $Pam3CSK_4$ was administered chronically, the development of T1D in nonobese diabetic (NOD) mice was inhibited. Diabetogenic T cell priming by DCs was attenuated by chronic treatment with $Pam3CSK_4$, indicating DC tolerance. For the treatment of established T1D, immune tolerance alone is not enough because ${\beta}$-cell mass is critically reduced. We employed TLR2 tolerance in conjunction with islet transplantation, which led to reversal of newly established T1D. Dipeptidyl peptidase 4 (DPP4) inhibitors are a new class of anti-diabetic agents that have beneficial effects on ${\beta}$-cells. We investigated whether a combination of DPP4 inhibition and TLR2 tolerization could reverse newly established T1D without islet transplantation. We could achieve normoglycemia by TLR2 tolerization in combination with DPP4 inhibition but not by TLR2 tolerization or DPP4 inhibition alone. ${\beta}$-cell mass was significantly increased by combined treatment with TLR2 tolerization and DPP4 inhibition. These results suggest the possibility that a novel strategy of TLR tolerization will be available for the inhibition or treatment of established T1D when combined with measures increasing critically reduced ${\beta}$-cell mass of T1D patients such as DPP4 inhibition or stem cell technology.

• IMMUNE NETWORK
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• v.11 no.3
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• pp.163-168
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• 2011

Background: Nanoparticles (NPs) prepared from biodegradable polymers, such as poly (D,L-lactic acid-co-glycolic acid) (PLGA), have been studied as vehicles for the delivery of antigens to phagocytes. This paper describes the preparation of antigen-loaded PLGA-NPs for efficient cross-priming. Methods: NPs containing a similar amount of ovalbumin (OVA) but different sizes were produced using a micromixer-based W/O/W solvent evaporation procedure, and the efficiency of the NPs to induce the cross-presentation of OVA peptides were examined in dendritic cells (DCs). Cellular uptake and biodistribution studies were performed using fluorescein isothiocyanate (FITC)-loaded NPs in mice. Results: The NPs in the range of $1.1{\sim}1.4{\mu}m$ in size were the most and almost equally efficient in inducing the cross-presentation of OVA peptides via $H-2K^b$ molecules. Cellular uptake and biodistribution studies showed that opsonization of the NPs with mouse IgG greatly increased the percentage of FITC-positive cells in the spleen and lymph nodes. The major cell type of FITC-positive cells in the spleen was macrophages, whereas that of lymph nodes was DCs. Conclusion: These results show that IgG-opsonized PLGA-NPs with a mean size of $1.1{\mu}m$ would be the choice of biodegradable carriers for the targeted-delivery of protein antigens for cross-priming in vivo.

• Proceedings of the KIEE Conference
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• 2003.10a
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• pp.192-194
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• 2003

In this paper, we present a 2-Dimensional simulation model of the discharge in an ac plasma display panel cell. Therefore, we study a ramp reset waveform in an ac plasma display panel discharge cell using 2-Dimensional simulation. Finally We research a connection between priming particles' density and stability.

• Proceedings of the KIEE Conference
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• 2007.07a
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• pp.1406-1407
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• 2007

본 논문에서 제안한 ac-PDP(Plasma display panel) 셀구조는 Long gap의 전극 사이에 보조 전극을 삽입한 구조이다. 일반적으로, long gap 구조를 가진 PDP cell은 높은 방전 개시 전압을 가지므로, Long gap 전극 사이에 보조전극을 삽입하여 방전 개시 전압을 낮춤과 동시에 휘도 상승, 소비 전력의 감소효과로 발광효율의 향상을 가져왔다. 제안한 구조의 구동을 위하여 asymmetric mode와 long gap mode라는 2가지 파형을 가지고 실험하였다. 두 파형은 공통적으로 기존의 ADS(Address and Display period Separated)파형을 Y(Scan), Z(Common), A(Address) 전극에 인가하였으며, 보조적극에는 Z(Common) 전극의 파형을 수정한 형태로 인가하였다. Asymmetric mode는 보조전극에 Z(Common) 전극에 인가되는 파형과 같은 형태의 파형을 인가하여 Long gap의 구조를 가지지만 Short gap에서 방전이 가능하도록 설계하였고, long gap mode는 보조전극에 인가되는 Z(Common) 파형 중 sustain pulse를 초기 3개만을 주어 Short gap에서 방전을 개시함과 동시에 priming 입자를 생성하고, 나머지 sustain 구간에서는 floating시켜 이미 생성된 priming 입자를 long gap에서 구동을 가능하도록 하였다.

• Proceedings of the KIEE Conference
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• 2004.07c
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• pp.1751-1754
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• 2004

Effects of delay on the discharge time lag and the controllability of weak discharge mode were studied under single cell driving circumstances of ac PDP. It was found that sufficient number of priming particle is necessary for inducing weak discharge in ramp voltage driving. Discharge time lag was reduced dramatically under priming condition. It is speculated that the increasement of strong discharge is related to the reduction of the $Xe^*(^3P_1)$ particles during the after glow.

• Journal of Life Science
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• v.30 no.7
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• pp.651-659
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• 2020

Cardiovascular disease is one of the leading causes of death across the world, and gold-standard treatments such as percutaneous coronary intervention and artery bypass grafting have various limitations including myocardial damage and subsequent maladaptive cardiac remodeling. To overcome this, stem-cell therapies are emerging as a promising strategy for cardiovascular regeneration. Endothelial progenitor cells (EPCs) have high potential to proliferate and differentiate into endothelial cells for vascularization and tissue regeneration, and several clinical trials have explored EPC function in tissue repair in relation to clinical safety and improving cardiac function. Consequently, EPC has been suggested as a feasible stem-cell therapy. However, autologous EPC transplantation in cardiovascular disease patients is restricted by risk factors such as age, smoking status, and hypertension that lead to reduced bioactivity in the EPCs. New approaches for improving EPC function and stem-cell efficacy have therefore been suggested, including cell priming, organoid culture systems, and enhancing transplantation efficiency through 3D bioprinting methods. In this review, we provide a comprehensive understanding of EPC characteristics, therapeutic approaches, and the current state of clinical research into EPCs as stem-cell therapy for cardiovascular disease.

• 한국균학회소식:학술대회논문집
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• 2015.11a
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• pp.23-23
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• 2015

Rice blast disease caused by M. oryzae is the most devastating fungal disease in rice. During the infection process, M. oryzae secretes a large number of glycosyl hydrolase (GH) proteins into the apoplast to digest host cell wall and assist fungal ingress into host tissues. In this study, we identified a novel M. oryze arabinofuranosidase B (MoAbfB) which is secreted during fungal infection. Live-cell imaging exhibited that fluorescent labeled MoAbfB was highly accumulated in fungal invasive structures such as appressorium, tips of penetration peg, biotrophic interfacial complex (BIC), as well as invasive hyphal tip. Deletion of MoAbfB mutants extended biotrophic phase followed by enhanced disease severity, whereas, over-expression of OsMoAbfB mutant induced rapid defense responses and enhanced rice resistance to M. oryzae infection. Furthermore, exogenous treatment of MoAbfB protein showed inhibition of fungal infection via priming of defense gene expression. We later found that the extract of MoAbfB degraded rice cell wall fragments could also induce host defense activation, suggesting that not MoAbfB itself but oligosaccharides (OGs) derived from MoAbfB dissolved rice cell wall elicited rice innate immunity.

• Journal of Life Science
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• v.32 no.7
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• pp.567-577
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• 2022

Recently, the prevalence of ischemic diseases, such as ischemic heart disease, cerebral ischemia, and peripheral arterial disease, has been continuously increasing due to the aging population. The current standardized treatment for ischemic diseases is reperfusion therapy through pharmacotherapy and surgical approaches. Although reperfusion therapy may restore the function of damaged arteries, it is not effective at restoring the function of the surrounding tissues that have been damaged due to ischemia. Therefore, it is necessary to develop a new treatment strategy that can safely and effectively treat ischemic damage and restore the function of surrounding tissues. To overcome these limitations, stem cell-based therapy to regenerate the damaged region has been studied as a promising strategy for ischemic vascular diseases. Mesenchymal stem cells (MSCs) can be isolated from diverse tissues and have been shown to be promising for the treatment of ischemic disease by regenerating damaged tissues through immunomodulation, the promotion of angiogenesis, and the secretion of various relevant factors. Moreover, new approaches to enhancing MSC function, such as cell priming or enhancing transplantation efficiency using a 3D culture method, have been studied to increase stem cell therapeutic efficacy. In this review, we provide various strategies by which MSCs are used to treat ischemic diseases, and we discuss the challenges of MSC transplantation, such as the differentiation, proliferation, and engraftment of MSCs at the ischemic site.