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Henoch-$Sch\ddot{o}nlein$ Purpura에서 Interleukin $1{\beta}$ 유전자 다형성과 신장 침범과의 연관성
나형준,고일용,윤준호,예병일,김황민,Na, Hyoung-Joon,Go, Il-Yong,Yoon, Joon-Ho,Yeh, Byung-Il,Kim, Hwang-Min 대한소아신장학회 2006 Childhood kidney diseases Vol.10 No.2
Purpose : High interleukin-1 beta(IL-$1{\beta}$) expression in the skin biopsy specimens of patients with Henoch-$Sch\ddot{o}nlein$ Purpura(HSP) has been observed. We examined IL-$1{\beta}$ gene polymorphism in patients with HSP. The purpose of this study is to examine the relationship between IL-$1{\beta}$ gene polymorphism and renal involvement in HSP. Methods : Patients from mideast Korea with HSP were studied. All patients had at least 6 months of follow up. Patients and ethnically matched controls were genotyped for IL-$1{\beta}$ gene polymorphism by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP). Results : Thirty-four patients(all younger than 15 years old) who had been diagnosed with HSP and 27 controls were examined. No allele or genotype differences between the HSP and control groups were observed. No significant association between the carriage of IL-$1{\beta}$(-511) T allele and renal involvement(P=0.525, OR:1.417, CI:0.545-3.686) was found. Conclusion : In unselected patients with HSP, carriage of IL-$1{\beta}$(-511) T allele does not appear to influence renal involvement.
Baek, Yong-Hyeon,Seo, Byung-Kwan,Lee, Jae-Dong,Huh, Jeong-Eun,Yang, Ha-Ru,Cho, Eun-Mi,Choi, Do-Young,Kim, Deog-Yoon,Cho, Yoon-Je,Kim, Kang-Il,Park, Dong-Suk The Korean Acupuncture Moxibustion Medicine Societ 2005 대한침구의학회지 Vol.33 No.4
Background & Objective: Articular cartilage is a potential target for drugs designed to inhibit the activity of matrix metalloproteinases (MMPs) to stop or slow the destruction of the proteoglycan and collagen in the cartilage extracellular matrix. The purpose of this study was to investigate the effects of Aralia cordata Thunb. in inhibiting the release of glycosaminoglycan (GAG), the degradation of collagen, and MMP activity in rabbit articular cartilage explants. Methods : The cartilage-protective effects of Aralia cordata Thunb. were evaluated by using glycosaminoglycan degradation assay, collagen degradation assay, colorimetric analysis of MMP activity, measurement of lactate dehydrogenase activity and histological analysis in rabbit cartilage explants culture. Results : Interleukin-la (IL-1a) rapidly induced GAG, but collagen was much less readily released from cartilage explants. Aralia cordata Thunb. significantly inhibited GAG and collagen release in a concentration-dependent manner. Aralia cordata Thunb. dose-dependently inhibited MMP-3 and MMP-13 expression and activities from IL-1a-treated cartilage explants cultures when tested at concentrations ranging from 0.02 to 0.2 mg/ml. Aralia cordata Thunb. had no harmful effect on chondrocytes viability or cartilage morphology in cartilage explants. Histological analysis indicated that Aralia cordata Thunb. reduced the degradation of the cartilage matrix compared with that of IL -1a-treated cartilage explants.
Won, Cheolhee,Kim, Byung‐,Hak,Yi, Eun Hee,Choi, Kyung‐,Ju,Kim, Eun‐,Kyung,Jeong, Jong‐,Min,Lee, Jae‐,Ho,Jang, Ja‐,June,Yoon, Jung‐,Hwan,Jeong, Won‐,Il,P John Wiley and Sons Inc. 2015 Hepatology Vol.62 No.4
<P>Enhanced expression of the cancer stem cell (CSC) marker, CD133, is closely associated with a higher rate of tumor formation and poor prognosis in hepatocellular carcinoma (HCC) patients. Despite its clinical significance, the molecular mechanism underlying the deregulation of CD133 during tumor progression remains to be clarified. Here, we report on a novel mechanism by which interleukin‐6/signal transducer and activator of transcription 3 (IL‐6/STAT3) signaling up‐regulates expression of CD133 and promotes HCC progression. STAT3 activated by IL‐6 rapidly bound to CD133 promoter and increased protein levels of CD133 in HCC cells. Reversely, in hypoxic conditions, RNA interference silencing of STAT3 resulted in decrease of CD133 levels, even in the presence of IL‐6, with a concomitant decrease of hypoxia‐inducible factor 1 alpha (HIF‐1α) expression. Active STAT3 interacted with nuclear factor kappa B (NF‐κB) p65 subunit to positively regulate the transcription of HIF‐1α providing a mechanistic explanation on how those three oncogenes work together to increase the activity of CD133 in a hypoxic liver microenvironment. Activation of STAT3 and its consequent induction of HIF‐1α and CD133 expression were not observed in Toll‐like receptor 4/IL‐6 double‐knockout mice. Long‐term silencing of CD133 by a lentiviral‐based approach inhibited cancer cell‐cycle progression and suppressed <I>in vivo</I> tumorigenicity by down‐regulating expression of cytokinesis‐related genes, such as TACC1, ACF7, and CKAP5. We also found that sorafenib and STAT3 inhibitor nifuroxazide inhibit HCC xenograft formation by blocking activation of STAT3 and expression of CD133 and HIF‐1α proteins. <I>Conclusion</I>: IL‐6/STAT3 signaling induces expression of CD133 through functional cooperation with NF‐κB and HIF‐1α during liver carcinogenesis. Targeting STAT3‐mediated CD133 up‐regulation may represent a novel, effective treatment by eradicating the liver tumor microenvironment. (H<SMALL>EPATOLOGY</SMALL> 2015;62:1160‐1173)</P>
Baek, Yong-Hyeon,Seo, Byung-Kwan,Lee, Jae-Dong,Huh, Jeong-Eun,Yang, Ha-Ru,Cho, Eun-Mi,Choi, Do-Young,Kim, Deog-Yoon,Cho, Yoon-Je,Kim, Kang-Il,Park, Dong-Suk The Korean AcupunctureMoxibustion Medicine Society 2005 대한침구의학회지 Vol.22 No.2
Background & Objective: Articular cartilage is a potential target for drugs designed to inhibit the activity of matrix metalloproteinases (MMPs) to stop or slow the destruction of the proteoglycan and collagen in the cartilage extracellular matrix. The purpose of this study was to investigate the effects of Aralia cordata Thunb. in inhibiting the release of glycosaminoglycan (GAG), the degradation of collagen, and MMP activity in rabbit articular cartilage explants. Methods : The cartilage-protective effects of Aralia cordata Thunb. were evaluated by using glycosaminoglycan degradation assay, collagen degradation assay, colorimetric analysis of MMP activity, measurement of lactate dehydrogenase activity and histological analysis in rabbit cartilage explants culture. Results : Interleukin-la (IL-1a) rapidly induced GAG, but collagen was much less readily released from cartilage explants. Aralia cordata Thunb. significantly inhibited GAG and collagen release in a concentration-dependent manner. Aralia cordata Thunb. dose-dependently inhibited MMP-3 and MMP-13 expression and activities from IL-1a-treated cartilage explants cultures when tested at concentrations ranging from 0.02 to 0.2 mg/ml. Aralia cordata Thunb. had no harmful effect on chondrocytes viability or cartilage morphology in cartilage explants. Histological analysis indicated that Aralia cordata Thunb. reduced the degradation of the cartilage matrix compared with that of IL -1a-treated cartilage explants.
Bae, Eun-Ah,Seo, Hyungseok,Kim, Byung-Seok,Choi, Jeongwon,Jeon, Insu,Shin, Kwang-Soo,Koh, Choong-Hyun,Song, Boyeong,Kim, Il-Kyu,Min, Byung Soh,Han, Yoon Dae,Shin, Sang Joon,Kang, Chang-Yuil American Association for Cancer Research 2018 Cancer Research Vol.78 No.18
<P>These findings provide mechanistic insights into the application of NKT cell stimulation as a potent adjuvant for immunotherapy against advanced cancer.</P><P>PD-1–based cancer immunotherapy is a successful example of immune checkpoint blockade that provides long-term durable therapeutic effects in patients with cancer across a wide spectrum of cancer types. Accumulating evidence suggests that anti-PD-1 therapy enhances antitumor immunity by reversing the function of exhausted T cells in the tumor environment. However, the responsiveness rate of patients with cancer to anti-PD-1 therapy remains low, providing an urgent need for optimization and improvement. In this study, we designed an anti-PD-1–resistant mouse tumor model and showed that unresponsiveness to anti-PD-1 is associated with a gradual increase in CD8 T-cell exhaustion. We also found that invariant natural killer T cell stimulation by the synthetic ligand α-galactosylceramide (αGC) can enhance the antitumor effect in anti-PD-1–resistant tumors by restoring the effector function of tumor antigen–specific exhausted CD8 T cells. IL2 and IL12 were among the cytokines produced by αGC stimulation critical for reinvigorating exhausted CD8 T cells in tumor-bearing mice and patients with cancer. Furthermore, we observed a synergistic increase in the antitumor effect between αGC-loaded antigen-presenting cells and PD-1 blockade in a therapeutic murine tumor model. Our study suggests NKT cell stimulation as a promising therapeutic strategy for the treatment of patients with anti-PD-1–resistant cancer.</P><P><B>Significance:</B> These findings provide mechanistic insights into the application of NKT cell stimulation as a potent adjuvant for immunotherapy against advanced cancer. <I>Cancer Res; 78(18); 5315–26. ©2018 AACR</I>.</P>
마이크로 프로세서에 의한 自己制御형 永久磁石 同期 電動機의 驅動 및 運轉 特性의 改善
윤병도,김윤호,김일환,이용석 중앙대학교 기술과학연구소 1989 기술과학연구소 논문집 Vol.19 No.-
전력 전자 공학의 발달에 의해 영구자석 동기전동기의 운전 분야가 대단히 진보되고 있음이 최근 논문을 통해서 보고 되고 있다. 영구자석 동기전동기는 크기와 중량의 감소로 인한 장점, 회전자의 동손이 없으므로 효율이 높다는 장점이 있어 각종 분야의 응용에 유리하다. 본 연구는 마이크로프로세서와 전압원 인버터를 사용한 자기제어형 영구자석 동기전동기의 구동장치를 제안한다. 영구자석 동기전동기의 운전은 고정자 전류와 역기전력을 동기화 시킴으로서 가능하게 한다. 고 분해능의 인크리멘탈 엔코더를 사용하여 영구자석 동기전동기에 적합한 자기제어형 PWM. 인버터 설계를 가능하게 하였다. 저속 영역에서 토오크 리플을 감소 시키기 위해 펄스 수를 제어하였으며 운전중 최적 부하각의 제어는 토오크-속도 특성을 개선시킴을 검토 하였다. Recent research has indicated that the permanent magnet synchronous motor(PMSM) drives are considerably improved by the development of power electronics. The PMSMs are favoured in many applications as there are advantages in size and weight reduction, and in efficiency due to elimination of the field copper losses. This paper presents a Self-Controlled PMSM, fed by voltage suource inverter based on the microprocessor. The proper operation of the PMSM can be ensured only if the stator current is always synchronized with is Back-EMF. The use of incremantal encoder with high resolution makes it possible to design a Self-Controlled PWM inverter for a PMSM. The pulse ratios are controlled to reduce the torque ripple in the low-speed drive region. In addition, torque-speed characteristics are improved by the control of optimal load angle.
RAW264.7 세포에서 interferon-r 및 LPS에 의해 유도되는 NO생성에 미치는 TALT-35의 영향
박종일,박경석,김종석,박지훈,윤은진,송경섭,서강식,김훈,윤완희,박승길,임규,황병두 충남대학교 생물공학연구소 2006 생물공학연구지 Vol.12 No.-
TALP-35 purified from human term placenta is known to increase microtubule polymerization and stabilize the polymerized microtubule. To examine the effect of TALP-35 on immune system this study was performed. MTT assay was performed to investigate the effect of TALP-35 on the proliferation of RAW264.7 cells. TALP-35 dose dependently suppress the proliferation of RAW264.7 cells at high concentration (above 1 μM) in unstimulated cells, in case of 10 μM TALP-35 treated cells the suppression was 25% but in stimulated cells it was only 15%. Cosedimentation assay was carried out to investigate whether TALP-35 can bind to tubulin of RAW264.7, monocyte/macrophage lineage of mouse, and polymerize it. TALP-35 polymerize the tubulin of RAW264.7 cells and sedimented in dose-dependent manner. To investigate the effect of TALP-35 on the expression of iNOS protein western blotting was performed. The expression level of iNOS was decreased dose dependently in high concentration of TALP-35 treatment. To examine the activity of iNOS, secreted NO was determined by method based on Griess reaction. Interferon-γ and LPS-stimulated production of NO from RAW264.7 cells was decreased dose dependently above 0.1 μM concentration of TALP-35 and 50% is decreased at 10μM of it. This study shows TALP-35 can control cytokine induced-iNOS expression therefore it might control inflammatory diseases.