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金範錫,金星坤,韓必熙,朴樹榮,李宜宣,崔祐榮 明知大學校 産業技術硏究所 2009 産業技術硏究所論文集 Vol.28 No.-
In general, LED display system displays the fixed text in ROM. In this paper, we propose the wireless real-time LED display system in which the text can be easily displayed in any text color and display mode by users And the system can be set up in any place by using Zigbee communication.
Lee, Su Ui,Kim, Mun-Ock,Kang, Myung-Ji,Oh, Eun Sol,Ro, Hyunju,Lee, Ro Woon,Song, Yu Na,Jung, Sunin,Lee, Jae-Won,Lee, Soo Yun,Bae, Taeyeol,Hong, Sung-Tae,Kim, Tae-Don Korean Society for Molecular and Cellular Biology 2021 Molecules and cells Vol.44 No.1
Airway mucus secretion is an essential innate immune response for host protection. However, overproduction and hypersecretion of mucus, mainly composed of the gel-forming MUC5AC protein, are significant risk factors for patients with asthma and chronic obstructive pulmonary disease (COPD). The transforming growth factor β (TGFβ) signaling pathway negatively regulates MUC5AC expression; however, the underlying molecular mechanism is not fully understood. Here, we showed that TGFβ significantly reduces the expression of MUC5AC mRNA and its protein in NCI-H292 cells, a human mucoepidermoid carcinoma cell line. This reduced MUC5AC expression was restored by a TGFβ receptor inhibitor (SB431542), but not by the inhibition of NF-κB (BAY11-7082 or Triptolide) or PI3K (LY294002) activities. TGFβ-activated Smad3 dose-dependently bound to MUC5AC promoter. Notably, TGFβ-activated Smad3 recruited HDAC2 and facilitated nuclear translocation of HDAC2, thereby inducing the deacetylation of NF-κB at K310, which is essential for a reduction in NF-κB transcriptional activity. Both TGFβ-induced nuclear translocation of Smad3/HDAC2 and deacetylation of NF-κB at K310 were suppressed by a Smad3 inhibitor (SIS3). These results suggest that the TGFβ-activated Smad3/HDAC2 complex is an essential negative regulator for MUC5AC expression and an epigenetic regulator for NF-κB acetylation. Therefore, these results collectively suggest that modulation of the TGFβ1/Smad3/HDAC2/NF-κB pathway axis can be a promising way to improve lung function as a treatment strategy for asthma and COPD.
강승계,김수호,김신수,박희명,송근옥,원주희,이명숙,이성옥,이옥제,이은의,이채영,이현미,허필석,Gang Seung-Gye,Kim Su-Ho,Kim Sin-Su,Park Hui-Myeong,Song Geun-Ok,Won Ju-Hui,Lee Myeong-Suk,Lee Seong-Ok,Lee Ok-Je,Lee Eun-Ui,Lee Chae-Yeong,Lee Hyeo 한국호스피스협회 2002 호스피스 학술지 Vol.2 No.1
The hospice activities in Korea have still stood in the premature stage, although the contemporary hospice program, which professionally accommodates terminally ill patients, appeared in the history 35 years ago. Especially, the availability of the facility hospice is not only poor in number, but also lack of a guideline for the conduct of the facility. Saemmul Hospice has keenly felt the necessity of more facility hospices and has interchanged experiences and informations with people interested in hospice. However, the number of facilities has fallen short of one's expectations, and many problems have been revealed in order to maintain the operation. This paper was written in order to improve these atmospheres and to help more terminally ill cancer patients properly. This paper clarifies in detail the principle of management, the method of practice in each departments of Saemmul Hospice, expected effects and supplemental items. We try to provide concrete and practical informations and to help extensively for all peoples who are to begin or currently working. 1.Facility: It secures, maintain, and manage the hospice environment for all around care of patients effectively. 2.Education and Volunteer: It trains and manages hospice volunteers devoted to hospice. 3.Financial: It manages donation by healthy soul with an effective method. 4.Administration and Organization: It executes the administration efficiently and constitutes the organization to operate. 5.Medical and Nursing: It offers the maximum professional supports to a hospital. 6.Medicine and alternative medicine: It improves the quality of life of patients by medical and pharmaceutical approach and by other possible methods available. 7.Nutrition: It helps patients to have diets in accord with the order of the creation. 8.Belief: It offers spiritual care which allows the profound relationship with God. 9. Funeral ceremonies: Funeral ceremonies may heal grieves of families faced with their deaths. 10. Bereaved families: It supports the families after the deaths of patients. 11.Reception and consultation: It seeks to help the patients who meet the purposes for which Saemmul Hospice is established. 12.Publication: It allows publicity activities for Saemmul Hospice. Facility hospice programs are able to overcome the disadvantages that the other type of the hospice possess, like as the economic burdens of the families, and the patients' losses of comforts of home after being transferred to a hospital. Facility hospice can provide home atmosphere with professional manpower and facilities like hospital to the patients. Therefore, it can also improve patients' qualities of life and make them comfortable death. We anticipate that the hospice program in Korea would be more active to let more people be indebted to maintain the nobel human dignity and to cross beautifully in the most painful process of dying in the journey of their lives.
Lee, Seoghyun,Ro, Hyunju,In, Hyun Ju,Choi, Ji-Hee,Kim, Mun-Ock,Lee, Jinhyuk,Hong, Sung-Tae,Lee, Su Ui Elsevier 2018 Cytokine Vol.108 No.-
<P><B>Abstract</B></P> <P>Fisetin (3,7,3′,4′-tetrahydroxyflavone), a natural flavonoid, is a therapeutic agent for respiratory inflammatory diseases such as chronic obstructive pulmonary disease (COPD). However, detailed molecular mechanisms regarding the target protein of fisetin remain unknown.</P> <P>Fisetin significantly reduces tumour necrosis factor alpha (TNF-α)-induced interleukin (IL)-8 levels by inhibiting both nuclear factor kappa B (NF-κB) transcriptional activity and the phosphorylation of its upstream effectors. We show that fisetin prevents interactions between protein kinase C (PKC)δ and TNF receptor-associated factor 2 (TRAF2), thereby inhibiting the inhibitor of kappa B kinase (IKK)/NF-κB downstream signalling cascade. Furthermore, we found that fisetin directly binds to PKCδ <I>in vitro</I>. Our findings provide evidence that fisetin inhibits the TNF-α-activated IKK/NF-κB cascade by targeting PKCδ, thereby mediating inflammatory diseases such as COPD.</P> <P>These data suggest that fisetin is a good therapeutic drug for the treatment of inflammatory lung diseases, such as COPD, by inhibiting the TNF-α/NF-κB signalling pathway.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Fisetin inhibits TNF-α-increased <I>IL-8</I> gene expression by blocking NF-κB activity. </LI> <LI> Fisetin inhibits TNF-α-mediated interactions between PKCδ and TRAF2. </LI> <LI> Fisetin inhibits PKCδ activity. </LI> </UL> </P>
Lee, Su Ui,Ahn, Kyung-Seop,Sung, Min Hee,Park, Ji-Won,Ryu, Hyung Won,Lee, Hyun-Jun,Hong, Sung-Tae,Oh, Sei-Ryang Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.8
The ${\beta}_2$ adrenergic receptor (ADRB2) is a G protein-coupled transmembrane receptor expressed in the human respiratory tract and widely recognized as a pharmacological target for treatments of asthma and chronic obstructive pulmonary disorder (COPD). Although a number of ADRB2 agonists have been developed for use in asthma therapy, indacaterol is the only ultra-long-acting inhaled ${\beta}_2$-agonist (LABA) approved by the FDA for relieving the symptoms in COPD patients. The precise molecular mechanism underlying the pharmacological effect of indacaterol, however, remains unclear. Here, we show that ${\beta}$-arrestin-2 mediates the internalization of ADRB2 following indacaterol treatment. Moreover, we demonstrate that indacaterol significantly inhibits tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-induced NF-${\kappa}B$ activity by reducing levels of both phosphorylated-IKK and -$I{\kappa}B{\alpha}$, thereby decreasing NF-${\kappa}B$ nuclear translocation and the expression of MMP-9, an NF-${\kappa}B$ target gene. Subsequently, we show that indacaterol significantly inhibits TNF-${\alpha}$/NF-${\kappa}B$-induced cell invasiveness and migration in a human cancer cell line. In conclusion, we propose that indacaterol may inhibit NF-${\kappa}B$ activity in a ${\beta}$-arrestin2-dependent manner, preventing further lung damage and improving lung function in COPD patients.
β-Arrestin 2 mediates G protein-coupled receptor 43 signals to nuclear factor-κB.
Lee, Su Ui,In, Hyun Ju,Kwon, Mi So,Park, Bi-oh,Jo, Minmi,Kim, Mun-Ock,Cho, Sungchan,Lee, Sangku,Lee, Hyun-Jun,Kwak, Young Shin,Kim, Sunhong Pharmaceutical Society of Japan 2013 Biological & pharmaceutical bulletin Vol.36 No.11
<P>G-protein coupled receptor 43 (GPR43) serves as a receptor for short-chain fatty acids (SCFAs), implicated in neutrophil migration and inflammatory cytokine production. However, the intracellular signaling pathway mediating GPR43 signaling remains unclear. Here, we show that β-arrestin 2 mediates the internalization of GPR43 by agonist. Agonism of GPR43 reduced the phosphorylation and nuclear translocation of nuclear factor-κB (NF-κB), which was relieved by short interfering RNA (siRNA) of β-arrestin 2. Subsequently, mRNA expression of proinflammatory cytokines, interleukin (IL)-6 and IL-1β, was downregulated by activation of GPR43 and knockdown of β-arrestin 2 recovered the expression of the cytokines. Taken together, these results suggest that GPR43 may be a plausible target for a variety of inflammatory diseases.</P>