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锐赛恭喜丁磊老师成功发文：
Effects of CCN3 on rat cartilage endplate chondrocytes cultured under serum deprivation in vitro. Molecular Medicine Reports。
Lentiviral-mediated RNAi targeting caspase-3 inhibits apoptosis induced by serum deprivation in rat endplate chondrocytes in vitro. Brazilian Journal of Medical and Biological Research
锐赛一如既往的“为客户赢得荣誉”，并且在坚实的技术服务中，始终以转化医学理念，为病患之需而先行。
对于丁老师的支持“The combined sequences of the enhanced green fluorescent protein (EGFP) gene and the caspase-3 siRNA were cloned into the AscI and PmeI sites of the pLenti6.3- MCS vector (R&S Biotechnology, China) containing a CMV-driven GFP reporter.”，我们同样并将一直支持下去。
锐赛转化医学理念
作为一家成长中的生物技术医药公司；我们致力于发展独特，高质量的病毒载体介导的基因传递技术以更好地服务于科学研究和药物开发；并且运用病毒载体技术，通过系统生物学研究手段改变生物技术服务和药物开发的模式，从而实现生物制药的产业化。
基因传导 锐赛致力于使用最先进的病毒载体包装技术将RNAi, microRNA和基因导入到靶细胞。
锐赛致力于通过发展独特，新颖的病毒包装技术为科学研究提供理解基因组和蛋白质组功能的工具。我们的使命是在转化医学的研究路上，为在全基因组水平系统地理解细胞调控机制和药物开发，提供病毒载体介导的基因导入技术。
锐赛生物成功地将多年的分子生物学和病毒研究经验结合并运用于重组腺病毒(Adenovirus)，腺相关病毒(Adeno-associated virus, AAV)，慢病毒(Lentivirus)，逆转录病毒(Retrovirus)，狂犬病病毒（rabies virus）和杆状病毒（baculovirus）的制备。锐赛拥有生产全世界滴度最高的六大病毒包装技术，能稳定地制备出高质量地病毒载体，并确保可以高效地用于感染体外细胞和动物体内注射。锐赛也一直努力将最好的病毒载体制备技术呈献给科学研究和药物开发工作者们。
Abstract.
The presence of apoptotic cells and loss of extracellular matrix (ECM) are common characteristics of degenerated cartilage endplates (CEPs). In addition, therapeutic efficacy is hampered by an incomplete understanding regarding the mechanisms underlying CEP homeostasis and degeneration. The CCN proteins have recently emerged as important regulators of cell‑ECM interactions, and have been identified as key mediators of nucleus pulposus ECM composition and tissue homeostasis. However, whether CCN3 is associated with CEP homeostasis has yet to be elucidated. The present study aimed to investigate the effects of CCN3 on the apoptosis and ECM synthesis of CEP cells cultured under serum deprivation. Rat CEP cells were confirmed to be of the chondrocytic phenotype by toluidine blue staining. The mRNA expression levels of CCN3 were markedly increased, and a dose‑dependent increase of apoptotic rate was detected under serum deprivation conditions following treatment with recombinant CCN3, whereas CCN3 did not exert a proapoptotic effect on cells cultured under normal conditions. Furthermore, CCN3‑treated cells exhibited a decrease in the expression levels of aggrecan and collagen II in both groups. These results suggested that CCN3 may act as a regulator, rather than an initiator, of serum deprivation‑induced cellular apoptosis, and that CCN3 has a catabolic effect on the mediation of ECM synthesis under both normal and serum deprivation conditions. Therefore, CCN3 may represent a novel therapeutic target for the prevention of CEP degeneration.