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- 저자 : Jai Suda, S. (검색결과 2 건)
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Giri, S. S.,Jai Suda, S.,Sukumaran, V.,Park, S. C. Springer Science + Business Media 2016 AQUACULTURE INTERNATIONAL Vol.24 No.1
<P>Healthy Labeo rohita (mean bodyweight of 20.1 g) were divided into four groups before being fed for 60 days on diets supplemented with 0 (control), 20 (E1), 30 (E2), or 40 (E3) mg kg(-1) emodin. Various growth and immune parameters were measured after 15, 30, 45, and 60 days of feeding. Fish fed E2 diet exhibited accelerated (p < 0.05) weight gain after 30-60 days of feeding. The most significant improvements (p < 0.05) in immune parameters, such as lysozyme activity, alternative complement pathway activity, respiratory bursts activity, phagocytic activity, superoxide dismutase activity, and myloperoxidase activity, were observed in the E2-fed group after 30 and 45 days of feeding. However, fish groups fed E2 or E3 diets exhibited significantly lower malondialdehyde, aspartate aminotransferase, and alanine aminotransferase activities than did the control group after 30 and 45 days of feeding. The IgM level was significantly elevated in treatment groups after 30 and 45 days of feeding. Further, fish fed E2 diet for 45 days had the highest (p < 0.005) post-challenge survival rate (83.3 %), followed by fish fed E2 diet for 30 days (75 %). Therefore, dietary feeding of emodin at 30 mg kg(-1) to L. rohita for 30-45 days is optimal to enhance the immunity and disease resistance against A. hydrophila.</P>
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Lee, Seoung-Hoon,Rho, Jaerang,Jeong, Daewon,Sul, Jai-Yoon,Kim, Taesoo,Kim, Nacksung,Kang, Ju-Seob,Miyamoto, Takeshi,Suda, Toshio,Lee, Sun-Kyeong,Pignolo, Robert J,Koczon-Jaremko, Boguslawa,Lorenzo, Jo Nature Publishing Group 2006 Nature medicine Vol.12 No.12
Matrix-producing osteoblasts and bone-resorbing osteoclasts maintain bone homeostasis. Osteoclasts are multinucleated, giant cells of hematopoietic origin formed by the fusion of mononuclear pre-osteoclasts derived from myeloid cells. Fusion-mediated giant cell formation is critical for osteoclast maturation; without it, bone resorption is inefficient. To understand how osteoclasts differ from other myeloid lineage cells, we previously compared global mRNA expression patterns in these cells and identified genes of unknown function predominantly expressed in osteoclasts, one of which is the d2 isoform of vacuolar (H<SUP>+</SUP>) ATPase (v-ATPase) V<SUB>0</SUB> domain (Atp6v0d2). Here we show that inactivation of Atp6v0d2 in mice results in markedly increased bone mass due to defective osteoclasts and enhanced bone formation. Atp6v0d2 deficiency did not affect differentiation or the v-ATPase activity of osteoclasts. Rather, Atp6v0d2 was required for efficient pre-osteoclast fusion. Increased bone formation was probably due to osteoblast-extrinsic factors, as Atp6v02 was not expressed in osteoblasts and their differentiation ex vivo was not altered in the absence of Atp6v02. Our results identify Atp6v0d2 as a regulator of osteoclast fusion and bone formation, and provide genetic data showing that it is possible to simultaneously inhibit osteoclast maturation and stimulate bone formation by therapeutically targeting the function of a single gene.
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