• 치위생과학회지
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• 제17권1호
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• pp.65-72
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• 2017

실험동물의 TMJ 내에 포르말린으로 유도한 염증성 통증 모델에서 홍삼 및 흑삼 추출물이 통증 발생과 조절에 미치는 영향을 평가하고자 하였다. 홍삼 혹은 흑삼 추출물을 TMJ 내에 투여한 후 통증 행위반응의 변화를 관찰하였고, 또한 실험동물의 연수를 적출하여 Nrf2 경로의 활성 변화를 단백정량분석법을 활용해서 분석한 결과 먼저, 포르말린을 TMJ에 주입한 결과 안면부 통증행위반응이 유의하게 증가되었다. 이것을 토대로 홍삼 및 흑삼 추출물의 경구 투여한 결과 포르말린에 의해 유도된 실험동물에서 통증행위 반응이 효과적으로 감소되었고, 단회투여보다 반복투여가 포르말린 2차 통증행위반응 경감에 더 효과적으로 나타났다. 또한 홍삼 및 흑삼 추출물의 반복 투여 시 포르말린에 주입에 의해 증가된 연수에서의 Nrf2 단백 발현량을 감소시켰고, 간과 신장의 독성검사에서도 영향을 미치지 않는 것으로 나타났다. 따라서, 본 연구에서 홍삼 및 흑삼 추출물은 간과 신장을 부작용을 나타내지 않으면서 포르말린으로 유도된 안면부 통증과 Nrf2의 발현의 조절에 효과적인 것으로 나타났다.

• 혜화의학회지
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• 제21권1호
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• pp.33-52
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• 2012

To evaluate the efficacy of Keonkangbujatang (KKBT) in osteoarthritis treatments, C57BL/10 mice were treated with papain to induce osteoarthritis, and anti-arthritic effects were measured. To ensure safety of the KKBT sample, ALT, AST, BUN, and creatinine levels were measured, and they were all within the normal range. Based on the fact that suppression of inflammatory cytokines leads to the improvement of arthritis, IL-1b, IL-6, TNF-a, and MCP-1 production levels were measured. The cytokines were significantly decreased in serum. Also, mRNA levels of IL-1b, IL-6, and iNOS-II were significantly decreased in joint tissues. PGE2, a usual inflammation vector, and LTB4, TXB2, that are involved in the onset and deterioration of inflammation, were all significantly decreased. The levels of white blood cells, neutrophiles, and mononucleophiles also decreased, although the numbers were not significantly large. I*mmune-modulation of KKBT in the pathological mechanism of cartilage deterioration by inflammatory cells and their vectors was proved. This study should provide basis for the development of effective therapeutics as well as use in clinical practice.

• Korean Journal of Acupuncture
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• 제33권4호
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• pp.204-212
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• 2016

Objectives : The aim of the study is to investigate the effects of moxibustion on the pain behavior and expression of TRPM8 in the dorsal root ganglion(DRG) in the rat model of ambient cold(AC) exposed osteoarthritis(OA). Methods : OA was induced by the injection of $50{\mu}l$ of 2% monosodium iodoacetate(MIA) into the knee joint cavity. To examine the level of pain, weight bearing forces(WBFs) of affected limb was measured. For the AC exposure, the animals were housed in 6 h/day at $4^{\circ}C$ for 14 days after MIA injection. Moxibustion treatment was performed at EX-LE4 and EX-LE5 with 5 cons(1, 7 or 10 mg) per day for 13 days from 5 days after MIA injection. The expressions of TRPM8 in DRG were measured by western blotting analysis. Results : The WBFs of MIA-AC group were decreased significantly compared to MIA group at 2, 3, 6, 7, 8 and 9 days after arthritis induction. After the first 6 h-AC exposure, expressions of TRPM8 in MIA-AC group were increased significantly compared to those of naive group. After moxibustion treatment, only the WBFs of 7 mg treated group were restored significantly. Moreover, the over-expressions of TRPM8 were attenuated by the moxibustion treatment in AC exposed rats. Conclusions : The data suggest that AC can increase arthritic knee pain via up-regulated TRPM8 and moxibustion treatment improve the arthritic pain via modulation of TRPM8 expression in DRG in the rat model of AC exposed MIA induced arthritis.

• 대한골관절종양학회지
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• 제3권2호
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• pp.69-79
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• 1997

Objective : The objective of this study was to compare expression of various proto-oncogenes and rates of apoptosis in osteosarcoma patients. Modulation of apoptosis may influence resistance to chemotherapy and therefore affect the outcome of cancer treatment. Osteosarcoma is one of the most fatal malignancies in young adolescents and investigation of the role of apoptotic cell death is warranted in relation to chemotherapy and tumor outcome. Design : The terminal deoxynucleotidyl transferase to exposed 3'-hydroxyl termini of DNA (TUNEL method) staining method has been applied for the in situ detection of DNA double strand breaks. Patients : Thirty-three osteosarcomas in various stages of differentiation from twenty-nine patients were investigated immunohistochemically for p53, Bcl-2 and TUNEL method for apoptosis. Results and conclusion; We have found that higher level of wild type p53 were correlated with enhanced expression of apoptosis. Increased apoptosis rates were found in cases of negative Bcl-2 expression. In the present study, we have concluded that a significant proportion of osteosarcoma, a tumor in which resistance to chemotherapy often occurs, express high levels of p53 and low levels of Bcl-2. Our data provide further evidence for cross-talk between Bcl-2 and p53 and suggests that these genes are important determinants of drug-induced apoptosis.

• 한국컴퓨터정보학회논문지
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• 제15권6호
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• pp.49-56
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• 2010

본 논문은 직교주파수분할다중접속방식 기반의 마이크로 기지국을 위한 PHY-MAC 계층에서 최적화된 자원할당 기법에 대해 연구한다. 본 논문에서는 PHY-MAC 계층 간 제어 정보 흐름 및 기능 구현을 포함하여 계층 간 최적화된 2단계 자원할당 기법을 제안한다. 제안하는 2단계 자원할당 기법은 사용자 그룹핑 단계 및 자원할당 단계로 구성된다. 사용자 그룹핑 단계에서는 각 사용자별 PHY-MAC 계층 특성에 따라 사용자들을 매크로 기지국 자원을 할당받을 사용자 그룹과 마이크로 기지국 자원을 할당받을 사용자 그룹으로 분류한다. 자원할당 단계에서는 사용자 그룹 내의 각 사용자별로 실제 할당 받을 자원의 형태 및 양을 결정하는 스케줄러를 정의한다. 제안하는 기법에서는 다이버시티 및 AMC 기법을 스케줄러 정의에 활용한다. 시뮬레이션 결과는 제안하는 방법이 마이크로 기지국을 고려하지 않는 기존 방법에 비해 평균 셀 수율을 40~80% 증가시킬 수 있음을 보인다.

• 한국통신학회논문지
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• 제33권3A호
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• pp.311-318
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• 2008

FCC 스펙트럼을 만족하는 초광대역(UWB) 무선을 위한 새로운 펄스 파형을 제안한다. POCS(projections onto convex sets) 기술은 UWB 신호의 제반특성(FCC 스펙트럼 마스크하에서의 효율적인 스펙트럼 이용, 시간 제한성, 좋은 자기상관)의 제약 조건하에서 UWB 펄스의 시간 및 스펙트럼의 파형을 최적화한다. 시뮬레이션 결과에 의하면 펄스 파형의 모든 값에 대해 새로운 펄스 파형은 FCC 스펙트럼 마스크를 매우 효율적으로 만족할 뿐만 아니라 거의 동일한 자기상관함수를 갖고 있음을 보여준다. 또한 동일한 펄스폭에 대해 제안된 펄스의 절단된(즉 엄격히 시간 제한된) 펄스 파형은 이진 TH-PPM(time-hoping pulse position modulation) 시스템의 BER 성능에서 절단된 가우시안 모노싸이클(Gaussian monocycle)보다 우수하다. POCS 기술은 이 기술의 본질적인 설계 유연성 및 결합 최적화 능력 관점에서 UWB 펄스 파형 설계에 매우 효과적인 방법을 제공한다.

• 동의생리병리학회지
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• 제22권4호
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• pp.871-877
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• 2008

Heme oxygenase-1 (HO-1), an inducible heme-degrading enzyme, is expressed by macrophages and endothelial cells in response to various stresses and mediators of inflammation. HO-1 has been recently implicated in regulation of angiogenesis via expression of VEGF. The purpose of this study was to determine the effects of HO-1 modulation on the collagen-induced arthritis (CIA) model and on angiogenesis via up- regulation of VEGF expression in human synovial fibroblast. DBA/1J mice were treated with an inhibitor of HO-1, tin protoporphyrin IX (SnPP), or with an inducer of HO-1, cobalt protoporphyrin IX (CoPP), from day 1 to day 35 after CIA induction. The clinical evolution of disease was monitored visually. At the end of the experiment, histopathologic changes were examined on the joints. VEGF expression in paws were measured by immunohistochemical stain. mRNA expression of HO-1 and VEGF stimulated with various concentration of $TNF-{\alpha}$, CoPP accessed on human synovial fibroblast by RT-PCR. Effects of pretreatment with SnPP on mRNA expression of HO-1 and VEGF in the presence of CoPP and $TNF-{\alpha}$ in synovial fibroblast was accessed by Real-time RT-PCR. Administration of cobalt protoporphyrin IX significantly induced the inflammatory response, with increased arthritis index and expression of VEGF in the paws of the arthritis models. Treatment with SnPP significantly reduced the severity of CIA through inhibition of joint inflammation and cartilage destruction. The expression of VEGF were also significantly reduced by SnPP treatment in the paw. CoPPIX as inducer of HO-1, increased HO-1 and VEGF expression dose dependently in synovial fibroblast. In contrast, inhibition of HO-1 activity by SnPPIX abrogated CoPPIX-induced HO-1 and VEGF production in synovial fibroblast. Stimulation with $TNF-{\alpha}$ increased HO-1 and VEGF expression itself and showed additive effect on HO-1 and VEGF expression when it treated with CoPP. When SnPP was treated with CoPP and $TNF-{\alpha}$, it abrogated the CoPP induced HO-1 and VEGF expression and also abrogated $TNF-{\alpha}$ induced HO-1 and VEGF expression in synovial fibroblast. The effects of HO-1 induction in rheumatoid arthritis results in aggravation of arthritis via up-regulation of VEGF. I concluded that inhibition of the expression or activity of HO-1 could be a therapeutic target of rheumatoid arthritis.