IKK‐β‐mediated myeloid cell activation exacerbates inflammation and inhibits recovery after spinal cord injury

Kang, Junghee,Jiang, Mei Hua,Min, Hyun Jung,Jo, Eun‐,Kyeong,Lee, Soojin,Karin, Michael,Yune, Tae Young,Lee, Sung Joong WILEY‐VCH Verlag 2011 European journal of immunology Vol.41 No.5

<P><B>Abstract</B></P><P>Traumatic spinal cord injury (SCI) is followed by massive infiltration and activation of myeloid cells such as neutrophils and macrophages, but the functions of these cells are controversial. In this study, our objective was to elucidate the in vivo role of a signaling pathway involved in activation of these innate immune cells in SCI using myeloid cell‐specific IκB kinase (IKK)‐β conditional knockout (<TEX>${\rm {ikk}}{\rm {\beta}}^{\Delta mye}$</TEX><IMG src='/wiley-blackwell_img/equation/tex2gif-ueqn-1.gif' alt ='equation image'/> ) mice. In these mice, the <I>ikk</I>β gene has been specifically deleted from myeloid cells, compromising their in vivo IKK/NF‐κB‐dependent activation. We found that <TEX>${\rm {ikk}}{\rm {\beta}}^{\Delta mye}$</TEX><IMG src='/wiley-blackwell_img/equation/tex2gif-ueqn-2.gif' alt ='equation image'/> mice had significantly reduced neutrophil and macrophage infiltrations after SCI compared to <I>ikk</I>β<SUP>+/+</SUP> controls. SCI‐induced proinflammatory gene expression was also reduced in <TEX>${\rm {ikk}}{\rm {\beta}}^{\Delta mye}$</TEX><IMG src='/wiley-blackwell_img/equation/tex2gif-ueqn-3.gif' alt ='equation image'/> mice. Reduced neuroinflammation in <TEX>${\rm {ikk}}{\rm {\beta}}^{\Delta mye}$</TEX><IMG src='/wiley-blackwell_img/equation/tex2gif-ueqn-4.gif' alt ='equation image'/> mice was accompanied by attenuated neuronal loss and behavioral deficits in motor activity. In addition, the SCI‐induced expression of CXC ligand 1 was reduced in <TEX>${\rm {ikk}}{\rm {\beta}}^{\Delta mye}$</TEX><IMG src='/wiley-blackwell_img/equation/tex2gif-ueqn-5.gif' alt ='equation image'/> mice, which may be responsible for the reduced neutrophil infiltration in these mice. Our data demonstrate that IKK‐β‐dependent myeloid cell activation potentiates neuroinflammation and neuronal damage after SCI.</P>

Alteration of Mucin Glycosylation in Airway Diseases

Junghee Kang,Jinkuk Kim,Joo-Heon Yoon,Sookyung Hwang,Soohyun Kim 한국당과학회 2006 한국당과학회 학술대회 Vol.2006 No.1

초등학교 영어 교과서 자료의 진정성 고찰

강정희(Kang, Junghee),조미원(Jo, Miwon) 미래영어영문학회 2017 영어영문학 Vol.22 No.1

The purpose of this study is to investigate the authenticity of the expressions in elementary school English textbooks in South Korea. 14 native English speaking instructors from different national backgrounds analyzed 5 elementary school English textbooks for 6<SUP>th</SUP> grade with the 2 criteria of situational and linguistic authenticity. Situational authenticity consists of situational probability and consensus building with students. Linguistic authenticity consists of language expressions, style of formality, and conversation flow. The major results of this study are as follows. First, there are total 43 expressions found of which authenticity is insufficient: 5 in situational authenticity; 38 in linguistic authenticity. Second, most expressions whose linguistic authenticity is insufficient are due to language expressions and conversation flow. Therefore, textbook writers should use more natural and authentic expressions for students to have more confidence when they are using English.

Single and Two-Week Repeated Oral Dose Toxicity Study of DHP2, a Hydrophobic Drug Delivery Vehicle in Mice

Junghee Han,Hesson Chung,Jong-Hwa Lee,Jeong-Eun Suh,Gab-Soo Lee,Jong-Choon Kim,Boo-Hyon Kang 한국독성학회 2004 Toxicological Research Vol.20 No.1

The present study was conducted to investigate the single and 2-week repeated dose toxicity of DHP2, a hydrophobic drug delivery vehicle, in ICR mice. The test article was administered orally to mice at the dose levels of 2.5, 12.5 and 37.5 g/kg for single dose toxicity study and at the dose levels of 0, 2.5, 5, and 10 g/kg for repeated dose toxicity study. In both studies, there were no treatment-related effects on mortality, clinical signs, food and water consumption, ophthalmoscopy, urinalysis, hematology, serum biochemistry, necropsy findings and organ weights of all animals<br/> treated DHP2. Based on these results, it was concluded that the 2-week repeated oral dose of DHP2 may have no toxic effect in mice at a dose level of 10 g/kg. In the condition of this study, the no-observed-adverse-effect level (NOAEL) was considered to be 10 g/kg/day for both sexes.

Single and Two-Week Repeated Oral Dose Toxicity Study of DHP2, a Hydrophobic Drug Delivery Vehicle in Mice

Junghee Han,Hesson Chung,Jong-Hwa Lee,Jeong-Eun Suh,Gab-Soo Lee,Jong-Choon Kim,Boo-Hyon Kang 한국독성학회 2004 Toxicological Research Vol.20 No.2

The present study was conducted to investigate the single and 2-week repeated dose toxicity of DHP2, a hydrophobic drug delivery vehicle, in ICR mice. The test article was administered orally to mice at the dose levels of 2.5, 12.5 and 37.5 g/kg for single dose toxicity study and at the dose levels of 0, 2.5, 5, and 10 g/kg for repeated dose toxicity study. In both studies, there were no treatment-related effects on mortality, clinical signs, food and water consumption, ophthalmoscopy, urinalysis, hematology, serum biochemistry, necropsy findings and organ weights of all animals<br/> treated DHP2. Based on these results, it was concluded that the 2-week repeated oral dose of DHP2 may have no toxic effect in mice at a dose level of 10 g/kg. In the condition of this study, the no-observed-adverse-effect level (NOAEL) was considered to be 10 g/kg/day for both sexes.

A Holistic Approach to Optimizing the Lifetime of IEEE 802.15.4/ZigBee Networks with a Deterministic Guarantee of Real-Time Flows

Kang-Wook Kim,Myung-Gon Park,Junghee Han,Chang-Gun Lee 한국정보과학회 2015 Journal of Computing Science and Engineering Vol.9 No.2

IEEE 802.15.4 is a global standard designed for emerging applications in low-rate wireless personal area networks (LRWPANs). The standard provides beneficial features, such as a beacon-enabled mode and guaranteed time slots for realtime data delivery. However, how to optimally operate those features is still an open issue. For the optimal operation of the features, this paper proposes a holistic optimization method that jointly optimizes three cross-related problems: cluster-tree construction, nodes’ power configuration, and duty-cycle scheduling. Our holistic optimization method provides a solution for those problems so that all the real-time packets can be delivered within their deadlines in the most energyefficient way. Our simulation study shows that compared to existing methods, our holistic optimization can guarantee the on-time delivery of all real-time packets while significantly saving energy, consequently, significantly increasing the lifetime of the network. Furthermore, we show that our holistic optimization can be extended to take advantage of the spatial reuse of a radio frequency resource among long distance nodes and, hence, significantly increase the entire network capacity.

Gold Nanoparticle/Graphene Oxide Hybrid Sheets Attached on Mesenchymal Stem Cells for Effective Photothermal Cancer Therapy

Kang, Seokyung,Lee, Junghee,Ryu, Seungmi,Kwon, Yeji,Kim, Kyung-Hun,Jeong, Dae Hong,Paik, Seung R.,Kim, Byung-Soo American Chemical Society 2017 Chemistry of materials Vol.29 No.8

<P>Cell-mediated nanoparticle delivery has been proposed for an effective cancer therapy. However, there are limitations in loading nanoparticles within cells as the internalized nanoparticles cause cytotoxicity and leak out of the cells via exocytosis. Here, we introduce hybrid sheets composed of gold nanoparticles (AuNPs) and graphene oxide (GO), which stably adhere to the cell surface and exhibit a remarkable photothermal effect. To form AuNP/GO sheets in which GO is sandwiched between two AuNP monolayers, AuNPs are coated with alpha-synuclein protein and subsequently adsorbed onto GO sheets. Attaching AuNP/GO sheets to the tumor-tropic mesenchymal stem cell (MSC) surface enhances the loading efficiency of AuNPs in MSCs by avoiding the cytotoxicity and exocytosis issues. Furthermore, the tight packing of AuNPs on microscaled GO sheets enhances the photothermal effect via strong plasmon coupling between AuNPs. The injection of AuNP/GO sheet-attached MSCs into tumor-bearing mice significantly improves the photothermal therapeutic efficacy by delivering larger amounts of AuNPs to the tumor and generating higher heat at the tumor region compared to injection of AuNP-internalized MSCs. The system of attaching AuNP/GO hybrid sheets to the tumor-tropic cell surface may be an effective platform for cancer therapy.</P>

Accurate Indoor Location Tracking Exploiting Ultrasonic Reflections

Kim, Kang-Wook,Kwon, Jihye,Lee, Chang-Gun,Han, Junghee IEEE 2016 IEEE SENSORS JOURNAL Vol.16 No.24

<P>Time difference of arrivals) (TDoA)-based location tracking systems using RF and ultrasonic signals often give unacceptable errors due to the line-of-sight limitation of the ultrasonic signal. To overcome this limitation, many researchers have devoted their efforts using various methods. To further enhance accuracy and improve performance, this paper proposes a novel TDoA-based location tracking technique that explicitly exploits ultrasonic reflections in location estimation. We also propose a reflection plane detection method, which makes system configuration easy for the proposed reflection-aware location tracking algorithm. The proposed system can achieve a high location accuracy with errors smaller than 35 cm even when the lines of sight of ultrasonic signals are frequently blocked and hence they are received through reflections.</P>

System-Wide Time versus Density Tradeoff in Real-Time Multicore Fluid Scheduling

Kim, Kang-Wook,Cho, Youngeun,Eo, Jeongyoon,Lee, Chang-Gun,Han, Junghee IEEE 2018 IEEE Transactions on Computers Vol.67 No.7

<P>Recent parallel programming frameworks such as OpenCL and OpenMP allow us to enjoy the parallelization freedom for real-time tasks. The parallelization freedom creates the time versus density tradeoff problem in fluid scheduling, i.e., more parallelization reduces thread execution times but increases the density. By system-widely exercising this tradeoff, we propose optimal parameter tuning of real-time tasks aiming at maximizing the schedulability of multicore fluid scheduling. Our experimental study by both simulation and actual implementation shows that the proposed approach well balances the time and the density, and results in up to 80 percent improvement of the schedulability.</P>

A peptide containing Noxa mitochondrial-targeting domain induces cell death via mitochondrial and endoplasmic reticulum disruption

Park, Junghee,Han, Ji-Hye,Myung, Seung-Hyun,Kang, Hyuno,Cho, Ju-Yeon,Kim, Tae-Hyoung Academic Press 2019 Biochemical and biophysical research communication Vol. No.

<P><B>Abstract</B></P> <P>Noxa is a weak apoptosis activator consisting of a BH3 domain and a mitochondrial-targeting domain (MTD). BH3 binds Mcl-1 and Bcl2A1 and inactivates their anti-apoptotic activities, while MTD delivers BH3 to mitochondria. Previously we revealed that MTD may also function as an inducer of necrosis via conjugation with octa-arginine, which induces cytosolic Ca<SUP>2+</SUP> influx from mitochondria. However, the mechanism(s) underlying this process has not been elucidated yet. Here, we show that calcium influx induced by an MTD peptide fused with octa-arginine residue (R8:MTD) originates not only from mitochondria but also from the extracellular space. However, calcium spikes were not sufficient for necrosis. R8:MTD induced mitochondrial permeability transition pore opening, fragmentation, and swelling. These mitochondrial events induced by MTD appeared to be necessary for necrosis induction, since DIDS, a VDAC inhibitor, inhibited the mitochondrial swelling and cell death induced by MTD. We show that R8:MTD disrupted endoplasmic reticulum (ER) structures but not peroxisomes or Golgi, indicating that R8:MTD causes necrosis by inducing ER events as well.</P> <P><B>Highlights</B></P> <P> <UL> <LI> MTD peptide fused with 8-arginine (R8:MTD) induced necrotic cell death. </LI> <LI> R8:MTD induced Ca<SUP>2+</SUP> influx from mitochondria and extracellular space. </LI> <LI> MTD interacted with VDAC, and induced mitochondrial catastrophe. </LI> <LI> VDAC inhibitor DIDS inhibited cell death and mitochondrial disruption. </LI> <LI> R8:MTD disrupted ER where VDAC was expressed. </LI> </UL> </P>