RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      검색결과 좁혀 보기

      선택해제
      • 좁혀본 항목 보기순서

        • 원문유무
        • 원문제공처
        • 등재정보
        • 학술지명
          펼치기
        • 주제분류
        • 발행연도
          펼치기
        • 작성언어

      오늘 본 자료

      • 오늘 본 자료가 없습니다.
      더보기
      • 무료
      • 기관 내 무료
      • 유료
      • KCI등재후보

        무지의 피질골 파괴를 동반한 골내 표피 봉입 낭종 - 증례 보고 -

        박진성,문동규,박형빈,조세현 대한수부외과학회 2011 대한수부외과학회지 Vol.16 No.3

        Intraosseous epidermal inclusion cyst is a rare benign, cystic lesion. It is thought to result from traumatic implantation of epidermal elements into bone. Radiologic findings of intraosseous epidermal inclusion cysts are well-defined,lytic lesions. It is difficult to diagnose intraosseous epidermal inclusion cyst without pathologic diagnosis. We experienced a 43-year-old man with a history of trauma followed by painless expansion of his left thumb. Radiographs demonstrated a severe expansile, ill-defined lytic lesion with cortical destruction in the distal phalanx of left thumb,mimicking neoplastic bone lesion or infectious lesion. An intraosseous epidermal inclusion cyst was confirmed by pathologic diagnosis, which was lined by stratified squamous epithelium, containing keratinized cellular debris. 골내 표피 봉입 낭종은 드문 양성 종양으로 외상과 관련이 있으며 손상된 골 조직 내부로 표피 세포가 감입되어 발생한다고 알려져 있다. 골내 표피 봉입 낭종의 단순방사선 소견은 피질골의 팽대를 보이며, 비교적 경계가 명확한 용해성 골 병변이다. 골내 표피 봉입 낭종의 감별 진단은 수부의 다른 골 종양과 염증성 질환이 있으며 확진을 위해서는 조직학적 진단이 필수적이다. 저자들은 43세 남자의 좌측 무지의 원위지골에서 발생한 골내 표피 봉입 낭종을 경험하였으며 단순방사선 소견상 심한 피질골의 팽대와 파괴를 동반하여 다른 골 종양과의 감별이 필요하였고, 이에 대해 문헌고찰과 함께 증례 보고를 하는 바이다.

      • MS-275, a benzamide histone deacetylase inhibitor, prevents osteoclastogenesis by down-regulating c-Fos expression and suppresses bone loss in mice

        Kim, H.N.,Lee, J.H.,Jin, W.J.,Ko, S.,Jung, K.,Ha, H.,Lee, Z.H. North-Holland ; Elsevier Science Ltd 2012 european journal of pharmacology Vol.691 No.1

        Histone deacetylase (HDAC) enzymes play important roles in physiological and pathological processes by catalyzing the deacetylation of lysine residues in histone and non-histone proteins. Inhibition of HDACs has emerged as an attractive therapeutic strategy for various diseases including cancer and inflammatory diseases. We recently found that MS-275, a class I-specific HDAC inhibitor, exhibits an anabolic effect on bone through promoting expression of alkaline phosphatase in osteoblasts. MS-275 has also been suggested to inhibit inflammatory bone destruction, but the underlying mechanisms are still poorly understood. In this study, we investigated the effects and mechanism of action of MS-275 on osteoclast differentiation and activation. We found that MS-275 inhibits osteoclast differentiation in coculture of osteoblasts and bone marrow cells without affecting expression of receptor activator of NF-κB ligand (RANKL), a key cytokine for osteoclast differentiation, in osteoblasts. MS-275 inhibited RANKL-mediated osteoclast differentiation from its precursors by suppressing RANKL-induced expression of c-Fos, a crucial transcription factor for osteoclastogenesis. The inhibitory effect of MS-275 on osteoclast differentiation was blunted by ectopic overexpression of c-Fos. In addition to osteoclast differentiation, MS-275 decreased bone resorbing activity of mature osteoclasts. Consistent with the in vitro effects, MS-275 decreased osteoclast number and bone destruction in IL-1-induced mouse calvarial bone destruction model. Taken together, our results demonstrate that MS-275 suppresses bone destruction by inhibiting osteoclast differentiation and activation, suggesting a potential therapeutic value of MS-275 for bone disorders associated with increased bone resorption.

      • KCI등재

        Knockdown of EMMPRIN (OX47) in MRMT-1 Carcinoma Cells Inhibits Tumor Growth and Decreases Cancer-Induced Bone Destruction and Pain

        Yanke Chen,Jing Luan,Ting Jiang,Donghui Cai,Chao Sun,Xiaofei Wang,Xiaoge Zhao,Xingchun Gou 대한암학회 2021 Cancer Research and Treatment Vol.53 No.2

        Purpose Bone destruction and pain caused by cancer is one of the most devastating complications of cancer patients with bone metastases, and it seriously affects the quality of patients’ life. Extracellular matrix metalloproteinase inducer (EMMPRIN) is a cell adhesion molecule with increased expression in a variety of tumors. This study focused to clarify the specific function of EMMPRIN in bone metastasis of breast cancer.Materials and Methods Adenovirus with shRNA-EMMPRIN was transfected into MRMT-1 rat breast carcinoma cells, and the MRMT-1 cells with different expression levels of EMMPRIN were implanted into the bone marrow cavity of rat tibia. Next, the effect of down-regulation of EMMPRIN was evaluated as follows: bone damage was detected by X-ray radiological and tartrate-resistant acid phosphatase staining; the tumor burden was evaluated by hematoxylin and eosin staining; the test of pain-related behaviors was assessed used the bilateral paw withdrawal mechanical threshold; and the levels of secretory factors in tumor conditioned medium were determined by using enzyme-linked immunosorbent assay.ResultsWe found that down-regulation of EMMPRIN in tumor cells can simultaneously reduce tumor burden, relieve cancer-induced bone destruction and pain. ConclusionMaterials and Methods EMMPRIN is expected to be a therapeutic target for relieving bone metastasis of breast cancer and alleviating cancerinduced bone destruction and pain. The method of targeting EMMPRIN may be a promising strategy for the treatment of cancer in the future.

      • The natural flavonoid galangin inhibits osteoclastic bone destruction and osteoclastogenesis by suppressing NF-κB in collagen-induced arthritis and bone marrow-derived macrophages

        Huh, J.E.,Jung, I.T.,Choi, J.,Baek, Y.H.,Lee, J.D.,Park, D.S.,Choi, D.Y. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.698 No.1

        We investigated the effect of galangin, a natural flavonoid, on osteoclastic bone destruction in collagen-induced arthritis and examined the molecular mechanisms by which galangin affects osteoclastogenesis in bone marrow derived macrophages. In mice with collagen-induced arthritis, administration of galangin significantly reduced the arthritis clinical score, edema and severity of disease without toxicity. Interestingly, galangin treatment during a later stage of collagen-induced arthritis, using mice with a higher clinical arthritis score, still significantly slowed the progression of the disease. Extensive cartilage and bone erosive changes as well as synovial inflammation, synovial hyperplasia and pannus formation were dramatically inhibited in arthritic mice treated with galangin. Furthermore, galangin-treated arthritic mice showed a significant reduction in the concentrations of IL-1β, TNF-α and IL-17 . We found that galangin inhibited osteoclastogenic factors and osteoclast formation in bone marrow-derived macrophages and osteoblast co-cultured cells, and increased osteoprotegerin (OPG) levels in osteoblasts. Galangin and NF-κB siRNA suppressed RANKL-induced phosphorylation of the c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), but not AKT and extracellular signal-regulated kinase ½ (ERK½). Also, the JNK inhibitor SP600125 and p38 inhibitor SB203580 reduced RANKL-induced expressions of phospho-c-Jun, c-fos and NFATc1 genes during osteoclast development. In addition, galangin suppressed RANKL-induced phosphorylation of NF-κB, phospho-IκBα, inflammatory cytokines and osteoclast formation in bone marrow-derived macrophages. Our data suggest that galangin prevented osteoclastic bone destruction and osteoclastogenesis in osteoclast precursors as well as in collagen-induced arthritis mice without toxicity via attenuation of RANKL-induced activation of JNK, p38 and NF-κB pathways.

      • KCI등재
      • SCIESCOPUSKCI등재

        치주질환에 이환된 환자에서 구치 상실 치열 수복을 위한 임플란트 수복

        이승원,김영수,Yi, Seung-Won,Kim, Young-Soo 대한치주과학회 2005 Journal of Periodontal & Implant Science Vol.35 No.1

        Number of fixtures supporting prosthesis for rehabilitation of partial edentulism in distal area is an important factor in distal area to the bone tissue response around dental implant. Optimal number and optimal positioning of dental implant has leaded to the stable condition of bone tissue and successful long-term treatment outcome. This clinical and radiographic study was performed to document and evaluate the short-term result of occlusal rehabilitation by means of implant-supported fixed prostheses (ISPs) especially for partial edentulism in distal area in patients treated for advanced periodontal disease and to verify the number of fixture affecting the bone tissue response. A total of 30 consecutive patients referred because of advanced periodontal disease were included. Before the implant therapy was initiated, periodontal treatment was performed and the outcome evaluated during at least a 6-month period. An individual maintenance care program was designed for each patient. All 75 implants were placed using a 2-stage surgical approach. The patients were divided into 2 groups, in one of which two fixtures were placed and in the other of which three fixtures were placed with tripodal geometry. Following installation of the ISPs, all patients underwent a baseline examination including evaluation of i) oral hygiene, and ii) periodontal/ peri-implant conditions, and iii) radiographs. These examinations were repeated annually during the 1 or 2-year observation period. The results were as follows: 1.No single implant was lost during the observation follow-up period. 1.The percentage of plaque harboring surfaces and bleeding units upon probing were found to be low (<10%), and no soft tissue complications were recorded. 1.Two-fixture group showed bone destruction ranged from 0.0mm to 1.5mm and the mean was 0.31mm. Three-fixture group showed more bone destruction of 0.51mm. There was no statistically difference between two groups. These results suggested that the factor for success is not the number of fixture but the strict maintenance of peri-implant tissue health and initial stability of fixture.

      • KCI등재
      • SCOPUSKCI등재

        심한 하악골 파괴를 동반한 화농성 육아종

        신정원,허민석,이삼선,최순철,박태원,Shin Jeong-Won,Heo Min-Suk,Lee Sam-Sun,Choi Soon-Chul,Park Tae-Won 대한영상치의학회 2000 Imaging Science in Dentistry Vol.30 No.2

        Pyogenic granuloma is a overzealous proliferation of a vascular type connective tissue as a result of some minor trauma and is a well circumscribed elevated, pedunculated or sessile benign inflammatory lesion of skin and mucous membrane. The clinical features of pyogenic granuloma are indicative but not specific and nearly all cases of pyogenic granulomas are superficial in nature, and there is little if any mention in the literature of these lesions producing alveolar bone even jaw bone loss. This case is somewhat unique in that the lesion was an obvious histologic pyogenic granuloma; however, it appeared to invade the mandibular bone which resulted in the loss of the adjacent teeth. A 12-year-old boy came to Seoul National University Dental Hospital with chief complaints of left facial swelling. The features obtained were as follows; Plain radiograms showed a large well-circumscribed radiolucent lesion on left mandibular ramus area, which made severe expansion of lingual cortex and displacement of lower left 3rd molar tooth germ. Computed tomograms showed large soft tissue mass involving left masticator space with destruction of left mandibular ramus. Histologically, sections revealed loose edematous stroma with intense infiltration of inflammatory cells and proliferation of vascular channels. Also, there were focal areas of extensive capillary proliferation, bone destruction and peripheral new bone formation.

      • Trichostatin A inhibits osteoclastogenesis and bone resorption by suppressing the induction of c-Fos by RANKL

        Kim, H.N.,Ha, H.,Lee, J.H.,Jung, K.,Yang, D.,Woo, K.M.,Lee, Z.H. North-Holland ; Elsevier Science Ltd 2009 european journal of pharmacology Vol.623 No.1

        Histone deacetylases are enzymes involved in the remodeling of chromatin structure, in the regulation of transcriptional activity, and in epigenetic integrity. Histone deacetylase inhibitors such as trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA) have emerged as potent anticancer drugs that have proved useful in preclinical and early clinical trials. The role of histone deacetylase inhibitors in regulating osteoclast differentiation, however, is not well established. In this study, we analyzed the effects of TSA on osteoclast differentiation induced by the differentiation factor RANKL (receptor activator of NF-κB ligand). TSA strongly inhibited osteoclast formation in coculture of bone marrow cells and osteoblasts without reducing RANKL expression in osteoblasts. Furthermore, TSA suppressed RANKL-induced osteoclast formation from primary bone marrow-derived macrophages. TSA was only effective when present during the early stage of osteoclast differentiation. This effect was accompanied by a significant decrease in the RANKL-stimulated induction of c-Fos and NFATc1, which are key transcription factors during early osteoclastogenesis. The ectopic introduction of c-Fos and a constitutively active form of NFATc1 reversed the TSA-induced antiosteoclastogenic effect. Consistent with the in vitro results, TSA inhibited lipopolysaccharide- and interleukin-1-induced bone resorption and osteoclast formation in an in vivo model. Taken together, our findings suggest a novel action of TSA: inhibiting RANKL-induced osteoclast formation by suppressing the induction of the osteoclastogenic transcription factor c-Fos. Also, the inhibitory effect of TSA on bone destruction in vivo suggests that histone deacetylase inhibitors may be novel therapeutics for treating typical bone diseases.

      • Metastatic bone disease: current concepts of clinicopathophysiology and modern surgical treatment

        Frassica,D A,Frassica,F J,Sim,F H 가톨릭중앙의료원 가톨릭암센터 1997 암심포지움 Vol.- No.1

        Metastatases to bone are a common problem confronting both the orthopaedic oncologist and cancer specialists. Early diagnosis requires a knowledge of the pathogenesis of bone metastases. A primary route of metastatic cells in via Batson's vertebral vein plexus. An understanding of the pathophysiology enables the surgeon to plan effective treatment. As many patients continue to survive for prolonged periods following the detection of bone metastases, it is important to plan treatment that is durable and functional. Non-operative treatment is utilised for small lesions (less than 25 percent of the cortical diameter). Radiotherapy (generally 3000 cGy in ten fractions), patient education (to avoid excessive torsional loads), and systemic chemotherapy or hormonal therapy are the mainstays of non-operative treatment. The indications for surgical treatment include: (1) lesions greater than 50 percent the diameter of the cortex, (2) permeative lesions in high stress areas (subtrochanteric region of the hip, mid-femoral diaphysis, mid humeral metaphysis), and (3) lesions in which pain persists following external beam irradiation. Early and effective treatment improves the remaining quality of life in patients with metastatic bone disease. A knowledge of the pathogenesis and pathophysiology aids the clinician in making an early diagnosis.

      연관 검색어 추천

      이 검색어로 많이 본 자료

      활용도 높은 자료

      해외이동버튼