Background Calcium phosphate cement （CPC） is a favorable bone-graft substitute, with excellent biocompatibility and osteoconductivity. However, its reduced osteoinductive ability may limit the utility of CPC. To increase its osteoinductive potential, this study aimed to prepare tissue-engineered CPC and evaluate its use in the repair of bone defects. The fate of transplanted seed cells in vivo was observed at the same time. Methods Tissue-engineered CPC was prepared by seeding CPC with encapsulated bone mesenchymal stem cells （BMSCs） expressing recombinant human bone morphogenetic protein-2 （rhBMP-2） and green fluorescent protein （GFP）. Tissue-engineered CPC and pure CPC were implanted into rabbit femoral condyle bone defects respectively. Twelve weeks later, radiographs, morphological observations, histomorphometrical evaluations, and in vivo tracing were performed. Results The radiographs revealed better absorption and faster new bone formation for tissue-engineered CPC than pure CPC. Morphological and histomorphometrical evaluations indicated that tissue-engineered CPC separated into numerous small blocks, with active absorption and reconstruction noted, whereas the residual CPC area was larger in the group treated with pure CPC. In the tissue-engineered CPC group, in vivo tracing revealed numerous cells expressing both GFP and rhBMP-2 that were distributed in the medullar cavity and on the surface of bony trabeculae. Conclusion Tissue-engineered CPC can effectively repair bone defects, with allogenic seeded cells able to grow and differentiate in vivo after transplantation.
LIU Chun-rongMIAO JunXIA QunHUANG Hong-chaoGONG ChenYANG QiangLI Lan-ying
Background Iodine deficiency is a major factor affecting thyroid auto-regulation,the quantity of iodine may greatly influence the synthesis of thyroid hormones （THs）.It has long been believed that TH enters the cell through passive diffusion.Recent studies have suggested that several transporters could facilitate transportation of TH.The monocarboxylate transporter 8 （MCT8） was identified as a very active and specific TH transporter.The purpose of this study was to investigate whether iodine insufficient affected the expression of MCT8 in the thyroid gland.Methods Sixty BALB/c mice were randomly divided into two groups：control group was fed with standard feed （iodine concentration of 300 μg/kg）; while low-iodine （LI） group received iodine-insufficient feed （iodine concentration of 20-40 μg/kg）.After 3 months,10 mice of each group were sacrificed.The remaining 20 mice of each group were kept till 6 months.From the LI group,we randomly selected 15 mice and injected triiodothyronine （T3,100 μg/kg body weight per day） intraperitoneally for 24,48 or 72 hours （5 mice for each time-point）.Then,all the mice were sacrificed.Mouse serum thyroxine （T4）,T3,and thyroid-stimulating hormone （TSH） levels were determined by chemiluminescence immunoassay （CIA）.The protein content or messenger RNA （mRNA） level of thyroid MCT8 was measured by Western blotting analysis or real time RT-PCR respectively.MCT8 subcellular location in thyroid tissues was probed with immunohistochemistry （IHC） assay.Results We found that mouse serum T3 and T4 levels decreased and TSH level increased by the end of the third month.Consistent with these findings,there was significant goiter and hypothyroidism in the LI group.Meanwhile,the MCT8 mRNA increased to 1.36-fold of the level in the control group at the 3rd month.At 6th month,the serum T4 level in LI mice remained at a lower level,and MCT8 mRNA expression continued rising to nearly 1.60-fold compared with the control group.The protein content was al
Hu ZhimeiZhuo XiaohuaShi YananLiu XinYuan JihongLi LanyingSun Yina
