진단 초음파를 이용한 정상 성인의 정중신경 측정

이정아,임길병,이홍재,정웅태,황현오 최신의학사 2003 最新醫學 Vol.46 No.11-12

Inoue Balloon을 이용한 PMV의 장·단기 결과 분석

진은선,이연아,전숙,김현숙,정승묵,박상선,최락경,임달수,홍석근,황흥곤 대한순환기학회 2003 Korean Circulation Journal Vol.33 No.11

RAW 264.7 세포에 대한 중국산 천연 광물성 섬유 TAFMAG의 독성효과

임영,한진구,김지홍,김현욱,김은경,김경아,장황신 大韓産業醫學會 1999 대한직업환경의학회지 Vol.11 No.3

Objectives : This study was designed to evaluate cytotoxicity of TAFMAG, which is a trade name of natural mineral fiber mined and produced in China. Methods : The cytotoxicity of TAFMAG was evaluated by measuring iron content, lipid peroxidation, erythrocyte hemolysis, and cytotoxicity in vitro. These results were compared with the data of chrystotile and wollastonite as a positive and negative control, respectively. Results : There was significant increase of Fenton activity in TAFMAG and chrysotile with dose-response pattern. The iron chelating agent, desferrioxamine, significantly decreased Fenton activity of the particulates except wollastonite. TAFMAG and chrysotile fibers significantly increased malondialdehyde concentration from lipid peroxidation of the red blood cell membrane. In erythrocyte hemolysis test, TAFMAG & chrysotile had stronger effect on erythrocyte hemolysis than wollastonite with the concentration of 1,000g/ml. Furthermore, TAFMAG was more hemolytic than chrysotile with the concentration of 5,000g/ml. There was a significant cytotoxic effect in TAFMAG and chrysotile on RAW cell compared with wollastonite. Conclusions : In vitro study suggested that TAFMAG may have a similar health hazard as usual asbestos.

Chordoid Glioma Originating in the Intrasellar and Suprasellar Regions: Case Report

Hwang, Jisun,Lee, Aleum,Chang, Kee-Hyun,Moon, Ah Rim,Hwang, Sun-Chul,Hong, Hyun Sook Korean Society of Magnetic Resonance in Medicine 2015 Investigative Magnetic Resonance Imaging Vol.19 No.2

Chordoid glioma is a rare, low-grade brain neoplasm typically located in the third ventricle. Herein, we report an unusual case of histologically confirmed chordoid glioma located in the pituitary fossa and suprasellar region, not attached to the third ventricle. A 57-year-old woman presented with a 2-month history of headache and visual disturbance. Magnetic resonance imaging revealed an ovoid mass in the pituitary fossa and suprasellar region, compressing the optic chiasm without involvement of the third ventricle. The tumor showed low signal intensity on T1-weighted images and iso- to high signal intensity on T2-weighted images, with strong and homogenous contrast enhancement. Subtotal resection was performed via the transcranial approach, and the patient subsequently received adjuvant gamma knife radiosurgery. However, the residual mass showed disease progression 5 months after the initial surgery.

PEP-1-GRX-1 Modulates Matrix Metalloproteinase-13 and Nitric Oxide Expression of Human Articular Chondrocytes

Hwang, Hyun Sook,Park, In Young,Kim, Hyun Ah,Choi, Soo Young S. Karger AG 2017 Cellular physiology and biochemistry Vol.41 No.1

<P><B><I>Background:</I></B> The protein transduction domain (PTD) enables therapeutic proteins to directly penetrate the membranes of cells and tissues, and has been increasingly utilized. Glutaredoxin-1 (GRX-1) is an endogenous antioxidant enzyme involved in the cellular redox homeostasis system. In this study, we investigated whether PEP-1-GRX-1, a fusion protein of GRX-1 and PEP-1 peptide, a PTD, could suppress catabolic responses in primary human articular chondrocytes and a mouse carrageenan-induced paw edema model. <B><I>Methods:</I></B> Human articular chondrocytes were isolated enzymatically from articular cartilage and cultured in a monolayer. The transduction efficiency of PEP-1-GRX-1 into articular chondrocytes was measured by western blot and immunohistochemistry. The effects of PEP-1-GRX-1 on matrix metalloproteinases (MMPs) and catabolic factor expression in interleukin (IL)-1β- and lipopolysaccharide (LPS)-treated chondrocytes were analyzed by real-time quantitative reverse transcription-polymerase chain reaction and western blot. The effect of PEP-1-GRX1 on the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light chain-enhancer of activated B cells (NF-κB) signaling pathway were also analyzed by western blot. Finally, the inhibitory effect of PEP-1-GRX-1 on MMP-13 production was measured <I>in vivo</I> in a mouse carrageenan-induced paw edema model. <B><I>Results:</I></B> PEP-1-GRX-1 significantly penetrated into human chondrocytes and mouse cartilage, whereas GRX-1 did not. PEP-1-GRX-1 significantly suppressed MMP-13 expression and nitric oxide (NO) production in LPS-stimulated chondrocytes, and NO production in IL-1β-stimulated chondrocytes, compared with GRX-1. In addition, PEP-1-GRX-1 decreased IL-1β- and LPS-induced activation of MAPK and NF-κB. In the mouse model of carrageenan-induced paw edema, PEP-1-GRX-1 significantly suppressed carrageenan-induced MMP-13 production as well as paw edema. <B><I>Conclusion:</I></B> These results demonstrate that PEP-1-GRX-1 can be transduced efficiently <I>in vitro</I> and <I>in vivo</I> into human chondrocytes and mouse cartilage tissue and downregulate catabolic responses in chondrocytes by inhibiting the MAPK and NF-κB pathway. PEP-1-GRX-1 thus has the potential to reduce catabolic responses in chondrocytes and cartilage.</P>

Dyspnea and Palpitation during Pregnancy

(Hyun Suk Choi),(Seung Suk Han),(Hyun Ah Choi),(Hae Sung Kim),(Chan Guk Lee),(Youn Yee Kim),(Ji Ju Hwang),(Jeong Bae Park),(Hyun Ho Shin) 대한내과학회 2001 The Korean Journal of Internal Medicine Vol.16 No.4

N/A Objectives: Dyspnea and palpitation are common features of pregnancy. While several theories have been put forward to explain the etiology of gestational dyspnea and palpitation, there have been few systemic studies of its incidence, severity and time-course in a group of normal women. Methods: We interviewed postpartum women, within 3 days after delivery, about dyspnea and palpitation. Separately from this interview, we performed 24-hour ECG monitoring for obstetric patients with palpitation before delivery. Results: The subjects interviewed were 261 women, of whom 37.5 percent and 11.5 percent experienced dyspnea and palpitation, respectively. These symptoms had a tendency to increase to term. The presence of arrhythmias could be documented in only 22% of patients having 24-hour Holter monitoring. Conclusion: Dyspnea and palpitation were common among normal pregnant women and had a tendency to increase to term.

Fibronectin fragment-induced expression of matrix metalloproteinases is mediated by MyD88-dependent TLR-2 signaling pathway in human chondrocytes

Hwang, Hyun Sook,Park, Su Jin,Cheon, Eun Jeong,Lee, Mi Hyun,Kim, Hyun Ah BioMed Central 2015 Arthritis research & therapy Vol.17 No.-

<P><B>Introduction</B></P><P>Fibronectin fragments (FN-fs) are increased in the cartilage of patients with osteoarthritis (OA) and have a potent chondrolytic effect. However, little is known about the cellular receptors and signaling mechanisms that are mediated by FN-fs. We investigated whether the 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) regulates cartilage catabolism via the Toll-like receptor (TLR)-2 signaling pathway in human chondrocytes.</P><P><B>Methods</B></P><P>Small interfering RNA was used to knock down TLR-2 and myeloid differentiation factor 88 (MyD88). TLR-2 was overexpressed in chondrocytes transfected with a TLR-2 expression plasmid. The expression levels of matrix metalloproteinase (MMP)-1, MMP-3, and MMP-13 were analyzed using quantitative real-time reverse transcription polymerase chain reactions, immunoblotting, or enzyme-linked immunosorbent assay. The effect of TLR-2 on 29-kDa FN-f-mediated signaling pathways was investigated by immunoblotting.</P><P><B>Results</B></P><P>TLR-2, TLR-3, TLR-4, and TLR-5 mRNA were significantly overexpressed in OA cartilage compared with normal cartilage, whereas no significant difference of TLR-1 mRNA expression was found. 29-kDa FN-f significantly increased TLR-2 expression in human chondrocytes in a dose- and time-dependent manner. Knockdown of TLR-2 or MyD88, the latter a downstream adaptor of TLR-2, significantly inhibited 29-kDa FN-f-induced MMP production at the mRNA and protein levels. Conversely, TLR-2 overexpression led to enhanced MMP production by 29-kDa FN-f. In addition, TLR-2 knockdown apparently inhibited 29-kDa FN-f-mediated activation of phosphorylated nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha, and p38, but not of c-Jun N-terminal kinase or extracellular signal-regulated kinase. Exposure to synovial fluid (SF) from affected joints of patients with OA elevated MMP-1, MMP-3, and MMP-13 expression markedly in primary chondrocytes without reducing cell viability. However, TLR-2 knockdown in chondrocytes significantly suppressed SF-induced MMP induction.</P><P><B>Conclusions</B></P><P>Our data demonstrate that the MyD88-dependent TLR-2 signaling pathway may be responsible for 29-kDa FN-f-mediated cartilage catabolic responses. Our results will enhance understanding of cartilage catabolic mechanisms driven by cartilage degradation products, including FN-f. The modulation of TLR-2 signaling activated by damage-associated molecular patterns, including 29-kDa FN-f, is a potential therapeutic strategy for the prevention of cartilage degradation in OA.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1186/s13075-015-0833-9) contains supplementary material, which is available to authorized users.</P>

Inhibitory Effects of Asparagus cochinchinensis in LPS-Stimulated BV-2 Microglial Cells through Regulation of Neuroinflammatory Mediators, the MAP Kinase Pathway, and the Cell Cycle

Hyun Ah Lee(이현아),Ji Eun Kim(김지은),Jun Young Choi(최준영),Ji Eun Sung(성지은),Woo Bin Youn(윤우빈),Hong Joo Son(손홍주),Hee Seob Lee(이희섭),Hyun-Gu Kang(강현구),Dae Youn Hwang(황대연) 한국생명과학회 2020 생명과학회지 Vol.30 No.4

미세교세포(Microglial cells)에서 신경염증반응(neuroinflammatory responses)의 억제는 알츠하이머질환, 파킨슨질환, 헌팅턴질환과 같은 신경퇴행성질환(neurodegenerative diseases)을 치료하기 위한 주요 표적으로 고려되고 있다. 천문동(Asparagus cochinchinesis)은 열, 기침, 신장 질환, 유방암, 염증성질환 및 뇌질환을 치료하는 데 오랫동안 사용 되어온 전통 치료제(Traditional medicine)이다. 본 연구에서는 lipopolysaccharide (LPS)로 활성화된 BV-2 미세교세포에서 항염증효과가 있는 천문동 뿌리 열수추출물(Aqueous extract from A. cochinchinesis root, AEAC)의 신경보호 메커니즘을 연구하였다. 먼저, 어떤 유의적인 세포독성은 플라보노이드(flavonoid), 페놀(phenol), 사포닌(saponin)을 함유하는 AEAC를 4가지 농도로 처리된 BV-2세포에서 검출되지 않았다. 또한, nitric oxide (NO), cyclooxygenase-2 (COX-2) mRNA 및 inducible nitric oxide synthase (iNOS) mRNA 수준은 AEAC+LPS 처리군에서 비하여 21%정도 감소하였다. 전염증성 사이토카인(TNF-α과 IL-1β) 및 항염증성 사이토카인(IL-6와 IL-10)농도에 대한 유사한 감소는 비록 감소비율은 다르지만, Vehicle+LPS 처리군에 비해 AEAC+LPS 처리군에서 검출되었다. 더불어, LPS 처리 후 mitogen-activated protein (MAP) kinase의 인산화수준의 증가는 AEAC 전처리군에서 유의하게 회복되었고, 세포주기에서 G2/M의 억제(arrest)는 AEAC+LPS 처리군에서 개선되었다. 또한, LPS 처리로 유도된 ROS의 증가도 AEAC 전처리군에서 감소되었다. 따라서, 이러한 결과는 AEAC가 MAPK 신호전달 경로, 세포주기 및 ROS (reactive oxygen species) 생성의 조절을 통해 LPS 자극에 대한 항신경염증 활성을 유도함을 제시하고 있다. The suppression of neuroinflammatory responses in microglial cells can be considered a key target for improving the progression of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and Huntington’s disease (HD). Asparagus cochinchinensis has traditionally been used as a medicine to treat fever, cough, kidney disease, breast cancer, inflammatory diseases, and brain diseases. In this study, we investigated the neuroprotective mechanism of an aqueous extract from A. cochinchinensis root (AEAC), particularly its anti-inflammatory effects on lipopolysaccharide (LPS)-activated BV-2 microglial cells. BV-2 cells were treated with four different concentrations of AEAC. No significant toxicity was detected in BV-2 cells treated with AEAC. Nitric oxide (NO), cyclooxygenase-2 (COX-2) mRNA, and inducible nitric oxide synthase (iNOS) mRNA levels were 21% lower in the AEAC+LPS group than in the Vehicle+LPS group. Lower proinflammatory (TNF-α and IL-1 β) and anti-inflammatory cytokine (IL-6 and IL-10) levels were also detected in the AEAC+LPS group than in the Vehicle+LPS group, albeit at varying rates. Moreover, the phosphorylation of mitogen-activated protein kinase (MAPK) members after LPS treatment was significantly recovered in the AEAC-pretreated group compared to the Vehicle+LPS group, enhancement of the phosphorylation of mitogen-activated protein kinase (MAPK) members after LPS treatment was significantly recovered in the AEAC-pretreated group, while cell cycle arrest at the G2/M phase caused by LPS treatment was less severe in the AEAC+LPS group. The increase in reactive oxygen species (ROS) generation induced by LPS treatment was also lower in the AEAC-pretreated group than in the Vehicle+LPS group. This is the first study to show that AEAC exerts anti-neuroinflammatory activity against LPS stimulation by regulating the MAPK signaling pathway, the cell cycle, and ROS production.

PEP-1-FK506BP12 inhibits matrix metalloproteinase expression in human articular chondrocytes and in a mouse carrageenan-induced arthritis model

( Hyun Sook Hwang ),( In Young Park ),( Dae Won Kim ),( Soo Young Choi ),( Young Ok Jung ),( Hyun Ah Kim ) 생화학분자생물학회(구 한국생화학분자생물학회) 2015 BMB Reports Vol.48 No.7

The 12 kDa FK506-binding protein (FK506BP12), an immunosuppressor, modulates T cell activation via calcineurin inhibition. In this study, we investigated the ability of PEP-1-FK506BP12, consisting of FK506BP12 fused to the protein transduction domain PEP-1 peptide, to suppress catabolic responses in primary human chondrocytes and in a mouse carrageenan-induced paw arthritis model. Western blotting and immunofluorescence analysis showed that PEP-1-FK506BP12 efficiently penetrated chondrocytes and cartilage explants. In interleukin-1 (IL-1 )-treated chondrocytes, PEP-1-FK506BP12 significantly suppressed the expression of catabolic enzymes, including matrix metalloproteinases (MMPs)-1, -3, and -13 in addition to cyclooxygenase-2, at both the mRNA and protein levels, whereas FK506BP12 alone did not. In addition, PEP-1-FK506BP12 decreased IL-1 -induced phosphorylation of the mitogen-activated protein kinase (MAPK) complex (p38, JNK, and ERK) and the inhibitor kappa B alpha. In the mouse model of carrageenan-induced paw arthritis, PEP-1-FK506BP12 suppressed both carrageenan-induced MMP-13 production and paw inflammation. PEP-1-FK506BP12 may have therapeutic potential in the alleviation of OA progression. [BMB Reports 2015; 48(7): 407-412]

Cloning and Sequencing of an aprL gene of Bacillus licheniformis NS70 Encoding an Alkaline Protease

Hyun-Ah Hwang,Jong Hwa Kim,Hee-Sop Nam,Hyung-Jae Lee,Tae Kwang Oh,Moon-Sik Yang,Keon-Sang Chae 한국식품과학회 1997 Food Science and Biotechnology Vol.6 No.4