The Function and Meaning of Receptor Activator of NF-κB Ligand in Arterial Calcification

Osteoclast-like cells are known to inhibit arterial calcification. Receptor activator of NF-κB ligand（RANKL） is likely to act as an inducer of osteoclast-like cell differentiation. However,several studies have shown that RANKL promotes arterial calcification rather than inhibiting arterial calcification. The present study was conducted in order to investigate and elucidate this paradox. Firstly,RANKL was added into the media,and the monocyte precursor cells were cultured. Morphological observation and Tartrate resistant acid phosphatase（TRAP） staining were used to assess whether RANKL could induce the monocyte precursor cells to differentiate into osteoclast-like cells. During arterial calcification,in vivo and in vitro expression of RANKL and its inhibitor,osteoprotegerin（OPG）,was detected by real-time PCR. The extent of osteoclast-like cell differentiation was also assessed. It was found RANKL could induce osteoclast-like cell differentiation. There was no in vivo or in vitro expression of osteoclast-like cells in the early stage of calcification. At that time,the ratio of RANKL to OPG was very low. In the late stage of calcification,a small amount of osteoclast-like cell expression coincided with a relatively high ratio of RANKL to OPG. According to the results,the ratio of RANKL to OPG was very low during most of the arterial calcification period. This made it possible for OPG to completely inhibit RANKL-induced osteoclast-like cell differentiation. This likely explains why RANKL had the ability to induce osteoclast-like cell differentiation but acted as a promoter of calcification instead.

Differential Notch Activity Is Required for Homeostasis of Malpighian Tubules in Adult Drosophila

Precise regulation of stem cell self-renewal versus differentiation is important for the maintenance of tissue ho- meostasis. Early loss of stem cell activity results in premature ageing, while excess stem cell activity leads to over- proliferation and cancer initiation （Fuchs et al., 2004; Scadden, 2006; Jones and Wagers, 2008; Morrison and Spradling, 2008）. Thus, understanding the mechanism con- trolling stem cell self-renewal and differentiation is critical for development of potential clinic therapy in the future.

Effect of Porous Activated Charcoal Reinforcement on Mechanical and In-Vitro Biological Properties of Polyvinyl Alcohol Composite Scaffolds

The present work focused on developing an innovative composite material by reinforcing polymer matrix with highly porous activated charcoal. Polyvinyl alcohol-activated charcoal（PVA-AC） composite scaffolds were developed by varying the AC concentrations（0, 0.5, 1, 1.5, 2 and 2.5 wt%） in PVA matrix by freeze drying method. The developed scaffolds were characterized for their physicochemical, mechanical and in-vitro biological properties. In addition, the effect of AC on the attachment, proliferation and differentiation of osteoblast MG 63 cells was evaluated by scanning electron microscopy（SEM）, 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide（MTT） assay, alkaline phosphatase（ALP） activity assay and alizarin red stain-based（ARS） assay. All the PVA-AC composite scaffolds exhibited good bioactivity, hemocompatibility and protein adsorption properties. The scaffolds with high AC concentration（2.5 wt%） showed controlled drug release kinetics that are suitable for long term healing. The mechanical properties of all the PVA-AC composite scaffolds were improved when compared to the pure PVA scaffold. The high porosity, swelling degree and hydrophilicity of PVA-AC composite scaffolds facilitated cell attachment and proliferation. This is due to porous AC present in the sample that supported the osteoblast differentiation and formed mineralized nodules without the addition of any extra agents. From the above studies, it can be concluded that PVA-AC composite scaffolds are promising biomaterials for bone tissue engineering applications.