KOSEN 한인과학기술자네트워크

아래의 자료들은 산업기술정보원(http://www.kiniti.re.kr)을 통해 검색된 자료들입니다. 웹을 통해 원문신청이 가능합니다. 도움이 되시길 바랍니다. * Osteoclasts are required for bone tumors to grow and destroy bone, Clohisy, Denis R.; Ramnaraine, Margaret L.;, Univ of Minnesota Minneapolis MN USA, Journal of Orthopaedic Research v 16 n 6, p 660-666, 1998, 28 Refs.; TR: G; CODEN: JOREDR Abstract : It has been hypothesized that bone resorption during tumor osteolysis is performed by osteoclasts. Data supporting this hypothesis have been provided from analysis of human biopsy specimens obtained from sites of tumor osteolysis, as well as from experimentation with in vivo animal models. Experiments in this report take this concept one step further by testing the hypothesis that osteoclasts are required for bone tumors to grow and destroy bone. To test this hypothesis, the influence of an osteolytic sarcoma tumor, NCTC clone 2472 (2472), on bone was studied in animals that are osteoclast deficient (microphthalmic, strain B6C3Fe-a/a-Mitf$+mi$/) but whose osteoclast deficiency can be reversed following bone marrow transplantation. Femora of these mice and unaffected wild-type siblings were injected with 10$+5$/ 2472 cells, and after 14 days the femora were analyzed by radiographic and histomorphometric analysis. Macroscopic tumor, tumor-induced osteolysis, and increased osteoclast number were noted in femora of normal mice but not in femora of osteoclast-deficient mice (p $LS 0.001). Bone marrow transplantation converted osteoclast-deficient mice to mice with femora that contained osteoclasts in 4 weeks. Femora of these mice were then injected with 10$+5$/ 2472 tumor cells; after 14 days, in contrast to the findings in the original osteoclast-deficient mice, macroscopic tumor was present, tumor-induced osteolysis was noted on roentgenograms, and osteoclast number was increased when tumor-bearing limbs were compared with sham-injected limbs (p $LS 0.001). These data prove the hypothesis that osteoclasts are required for 2472 tumor-induced osteolysis, and they introduce the exciting possibility that osteoclasts are also required for tumors to grow in bone. * Osteoporosis and bone functional adaptation: Mechanobiological regulation of bone architecture in growing and adult bone, a review, Mosley, John R., Journal of Rehabilitation Research and Development v 37 n 2, p 189-199, 2000, 84 Refs.; TR: GL; Abstract : During life, bone is continually optimized for its load-bearing role by a process of functionally adaptive (re)modelling. This process, which is more active in growing bone, is dominated by high-magnitude, high-rate strains, presented in an unusual distribution. Adaptation occurs at an organ level, involving changes in whole bone architecture and bone mass. The repetitive coordinated bone loading associated with habitual activity may have little role in the preservation of bone mass, and may even reduce the osteogenic potential of an otherwise highly osteogenic stimulus. Cells of the osteocyte/osteoblast network are best placed to appreciate mechanical strain. Among the strain-related responses they show, is a reduced rate of apoptosis. This may serve to regulate and target osteoclast activity. A more complete understanding of the stimuli and pathways involved in both the physiology and pathology of this structural homeostatic mechanism will allow the design of more appropriate exercise regimens and targeted pharmacological interventions to limit morbidity and mortality by reducing bone fragility. * Influence of hydroxyapatite particles on osteoclast cell activities, Sun, Jui-Sheng; Lin, Feng-Huei; Hung, Tsai-Yi; Tsuang, Yang-Hwei; Chang, Walter Hong-Shong; Liu, Hwa-Chang;, Journal of Biomedical Materials Research v 45 n 4, p 311-321, 1999, 48 Abstract : An in vitro osteoblast/osteoclast model was used to test the biocompatibility of various-sized hydroxyapatite (HA) particles. Cellular responses to the HA particles were evaluated by changes in cell counts and the secretion of transforming growth factor, alkaline phosphatase, tumor necrosis factor, prostaglandin, and lactate dehydrogenase in the supernatant of the culture media. The results led to the conclusion that larger HA particles may be quite compatible with bone cells while smaller-sized HA particles can both activate the osteoclasts and decrease the cell population of the osteoblasts. * Activation of osteoclast-mediated bone resorption by the supernatant from a rabbit synovial cell line in response to polyethylene particles, Kim, Kang Jung; Itoh, Tatsuo; Tanahashi, Masahiko; Kumegawa, Masayoshi;, Journal of Biomedical Materials Research v 32 1, p 3-9, 1996, 29 Refs.; TR: X; CODEN: JBMRBG Abstract : It is unknown whether the soluble factors produced from cells activated by wear particles in the fibrous tissue around failed joint prostheses really activate osteoclastic bone resorption. In this study, the activation of osteoclast-mediated bone resorption by the products from a rabbit synovial cell line (HIG-82) stimulated by various particles was investigated using rabbit unfractionated bone cells cultured on a dentin slice. The HIG cells were challenged with the following laboratory-made particles: high-density polyethylene (PE), cobalt alloy (Co-Cr), titanium alloy (Ti6Al4V), pure titanium (Ti), and sintered hydroxyapatite (HA). The size of each particle was $LS@2 $mu@m. The supernatants from HIG cells cultured with the appropriate concentration of wear particles were added to unfractionated bone cells on a dentin slice, and then resorbed areas were determined for each particle. Interestingly, resorbed areas significantly increased only when the culture medium from HIG cells with PE particles was added to unfractionated bone cells. This study demonstrates that PE particles stimulate the rabbit synovial cells to produce soluble factors that induce osteoclast-mediated bone resorption. Moreover, this experimental model is a useful method sensitively to evaluate the effects of soluble factors from the cells stimulated by particulate biomaterials from joint prostheses on osteoclastic bone resorption. * Improvement of the adaptive bone remodeling theory and its application for simulation of osteoporosis, Sakamoto, Jiro; Oda, Juhachi; Aoyama, Kazuhiro; Sueyoshi, Yashunobu; Sawaguchi, Takeshi; Tomita, Katsuro;, Proceedings of the 1995 Bioengineering Conference American Society of Mechanical Engineers, Bioengineering Division (Publication) BED v 29, p 475-476, 1995, 1 Abstract : An improved theory of mechanical adaptive bone remodeling that is applicable to bone healing and osteoporosis is proposed. The theory is applied to remodeling problems of proximal femur corresponding to normal and osteoporosis state. Efficiency of the theory is discussed from the results. > 안녕하세요. 비교해부학을 배우는 학부생입니다. > 얼마전에 수업시간에 다음과 같은 것을 배웠습니다. > > 뼈가 부러지고 난 다음 뼈가 붙으면 불룩해지며 뼈에 상흔이 남는다고 합니다. 여기에 Osteoclast가 작용하여 다시 편편해 진다고 배웠습니다. 어떻게 Osteoclast가 불룩했던 곳을 나란하고도 반듯하게 바꿀수 있는지 그 메카니즘에 대해서 알고 싶습니다. > > 제가 학부생이라 많이 알지 못함을 기억해주시고 좋은답변 부탁드립니다.

>안녕하세요. 비교해부학을 배우는 학부생입니다.> 얼마전에 수업시간에 다음과 같은 것을 배웠습니다.>> 뼈가 부러지고 난 다음 뼈가 붙으면 불룩해지며 뼈에 상흔이 남는다고 합니다. 여기에 Osteoclast가 작용하여 다시 편편해 진다고 배웠습니다. 어떻게 Osteoclast가 불룩했던 곳을 나란하고도 반듯하게 바꿀수 있는지 그 메카니즘에 대해서 알고 싶습니다. >> 제가 학부생이라 많이 알지 못함을 기억해주시고 좋은답변 부탁드립니다. 간단한 설명 보통 뼈가 부러지면 osteocyte가 기계적 손상을 인식함을 통해 bone remodeling을 시작하게 되는데 피가 고이게 되고 bone marrow mesencymal stem cell에서 유래된 preosteoblast가 많이 생성되는데 preosteoblast는 rankl ligand가 있어 bone marrow hemotopoietic stem cell에서 유래한 preosteoclast의 rank receptor 결합하게 되어 osteoclast를 활성화 시켜 osteoclast는 손상 받은 뼈를 녹이기 시작하게 되는데 어느 정도 진행되면 preosteoblast에서 OPG라는 단백질을 배출해 더이상의 osteoblast를 활성화시키지 않고 osteoblast를 많이 만들어 osteoblast가 뼈를 생성하여 손상 받은 뼈를 잇게만드는 것 입니다.