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- 발행기관 : Blackwell Science Inc (검색결과 3 건)
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Min, J-W,Park, S-M,Rhim, T Y,Park, S-W,Jang, A-S,Uh, S-T,Park, C-S,Chung, I Y Blackwell Science Inc 2007 Clinical and experimental immunology Vol.147 No.3
<P>Interleukin (IL)-5 and eotaxin families regulate the development of eosinophilic inflammation of asthma in a co-operative manner. The exposure to airborne lipopolysaccharide (LPS) induces varying degrees of airflow obstruction and neutrophilic airway inflammation. Production of IL-5 and eotaxin subfamily chemokines was analysed in response to <I>Dermatophagoides pteronyssinus</I> allergen (D.p.) according to the presence of specific IgE to D.p., and investigated the mechanism underlying their LPS-mediated regulation of these cytokines in response to the specific allergen. Peripheral blood cells (PBCs) from asthmatics with (group 1) or without (group 2) specific IgE to D.p. and from non-asthmatics with (group 3) or without (group 4) were stimulated with D.p. or LPS. For LPS-mediated inhibition of IL-5 and eotaxin-2 production, LPS-induced cytokines were added to the D.p.-stimulated PBCs. IL-5 and eotaxin-2, but not eotaxin-1 and 3, were significantly increased by D.p.-stimulated-PBCs from group 1, while only eotaxin-2 was elevated in group 3. Eotaxin-2 production was found in monocytes and correlated with the level of specific IgE to D.p. LPS treatment resulted in the decrease in eotaxin-2 and IL-5 production by the D.p.-stimulated PBCs. LPS-induced IL-10 completely inhibited D.p.-stimulated production of eotaxin-2 and IL-5. The differential responses of the eotaxin family to specific antigens suggest that the predominant role of eotaxin-2 and LPS may attenuate eosinophilic inflammation by inhibiting IL-5 and eotaxin-2 synthesis through IL-10 production.</P>
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Tissue-engineered Cartilage Using Fibrin/Hyaluronan Composite Gel and Its In Vivo Implantation
Park, Sang-Hyug,Park, So Ra,Chung, Soo Il,Pai, Ki Soo,Min, Byoung-Hyun Blackwell Science Inc 2005 Artificial Organs Vol.29 No.10
<P>Abstract: </P><P>The importance of scaffold biomaterials has been emphasized for in vitro culture of tissue-engineered cartilage in a three-dimensional (3D) environment. In this study, we examined the feasibility of fibrin glue, mixed with hyaluronic acid (HA) as a composite scaffold. Fibrin glue has been a useful cell delivery matrix for cartilage tissue engineering and HA is a key component of normal articular cartilage. Our hypothesis is that compared to fibrin itself, a fibrin/HA composite can have significantly enhanced properties, due mainly to the added benefits of HA in the matrix. Pieces of cartilage were isolated from rabbit knees and the chondrocytes were harvested through enzymatic digestion. Both fibrin and fibrin/HA composite were prepared and subsequently implanted in nude mice (<I>n</I> = 9, each group) for 1, 2, and 4 weeks, respectively. The retrieved specimens were then analyzed and the results were compared. Cartilage-like tissue formation was detected earlier with fibrin/HA specimens. They produced significantly higher amounts of the extracellular matrix (ECM) molecules, GAG, and collagen at each time point than those in fibrin. Interestingly, the fibrin/HA composite was also competent in maintaining its initial size. Histology—Safranin O/fast green and Alcian blue—of the retrieved specimens found more intense, uniform staining in the fibrin/HA composites. Analysis of the gene expression of the ECM molecules also confirmed the benefits of the composite with added HA in the maintenance of phenotypic stability. The present study suggests that fibrin/HA composite may serve as a dependable cell delivery vehicle as well as a structural basis for tissue-engineered cartilage.</P>
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Kim, Hyeon Joo,Park, So Ra,Park, Heon Joo,Choi, Byung Hyune,Min, Byoung-Hyun Blackwell Science Inc 2005 Artificial Organs Vol.29 No.5
<P>Abstract: </P><P>The purpose of this study was to investigate age-related changes in the proliferative ability of human articular chondrocytes in culture. In addition, the possible markers for the proliferative capacity of chondrocytes were examined. Chondrocytes obtained from human articular cartilages of young (under 40 years) or old (over 60 years) individuals were expanded until their growth was arrested. The number of cells and the type II collagen phenotype were determined together with the expression levels of proliferating cell nuclear antigen (PCNA) and p21<SUP>WAF1/CIP</SUP> along with the passages of cultured chondrocytes. The results showed that young chondrocytes had higher proliferative capacity and viability than old chondrocytes. The growth arrest and the cessation in the expression of type II collagen were accompanied by down-regulation of PCNA and up-regulation of p21<SUP>WAF1/CIP</SUP> levels in both young and old chondrocytes. Notably, the expression levels of PCNA and p21<SUP>WAF1/CIP</SUP> along with the passages were correlated inversely to each other and showed distinct patterns between young and old chondrocytes. These results suggest that senescence of human articular chondrocytes leads to the decrease in the proliferative capacity and phenotypic stability. In addition, PCNA and p21 could be molecular markers that represent the status of these age-related properties of human articular chondrocytes in vitro.</P>
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