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Much research has been focused on developing bone morphogenetic protein-2(BMP-2) delivery systems to enhance bone formation in bone defect repair and bone tissue engineering. However, many of these current systems have several drawbacks associated with low loading efficiencies and reduced biological activities after release. Collagen scaffolds can be used as in delivery systems because of their biocompatibility. However, growth factors have naturally low affinity to collagen, which is disadvantageous for maintaining a sufficient growth factor concentration at the delivery sites. To enhance BMP-2 binding to collagen scaffolds, we chose a porous collagen scaffold that was chemically modified using Traut's reagent. The modified collagen scaffold allows cross-linking of the collagen fibers and is able to immobilize more BMP-2 after treatment with Sulfo-SMCC. We demonstrated that cross-linking led to a slower release rate of BMP-2, but did not reduce its biological activity. Moreover, more ectopic bone formation was induced by subcutaneous implants of cross-linked collagen treated with BMP-2. We concluded that collagen scaffolds chemically conjugated with BMP-2 using Traut's reagent and Sulfo-SMCC was an effective delivery system for use in bone defect repair and in bone tissue engineering.

Abstract. We present a new product with explicit aerosol corrections, POMINO-TROPOMI, for tropospheric nitrogen dioxide (NO2) vertical column densities (VCDs) over East Asia, based on the newly launched TROPOspheric Monitoring Instrument with an unprecedented high horizontal resolution. Compared to the official TM5-MP-DOMINO (OFFLINE) product, POMINO-TROPOMI shows stronger concentration gradients near emission source locations and better agrees with MAX-DOAS measurements (R2=0.75; NMB=0.8 % versus R2=0.68, NMB=-41.9 %). Sensitivity tests suggest that implicit aerosol corrections, as in TM5-MP-DOMINO, lead to underestimations of NO2 columns by about 25 % over the polluted northern East China region. Reducing the horizontal resolution of a priori NO2 profiles would underestimate the retrieved NO2 columns over isolated city clusters in western China by 35 % but with overestimates of more than 50 % over many offshore coastal areas. The effect of a priori NO2 profiles is more important under calm conditions.

ObjectivesToll‐like receptor 4 (TLR4) is abnormally expressed in oral cancer tissues and promotes cancer cell invasion. The purpose of this study was to clarify the mechanism by which autophagy regulates oral cancer invasion through the TLR4‐NF‐κB pathway.Subjects and MethodsWe examined TLR4 expression in oral cancer tissues and analysed the relationship between its expression and clinicopathological features. The invasion and migration of LPS‐stimulated oral cancer cells with up‐ or downregulation of TLR4 expression was detected in addition to NF‐κB signalling and autophagy levels. Furthermore, the role of autophagy in regulating TLR4‐mediated cell invasiveness was explored by silencing the expression of key autophagy genes ATG7 and p62.ResultsWe found that TLR4 overexpression was closely related to cervical lymphatic metastasis and poor survival. TLR4 activated the NF‐κB pathway to promote the invasiveness of OSCC cells, and autophagy partly inhibited invasiveness by suppressing the NF‐κB pathway. We observed that p62 translocated from the cytoplasm to the nucleus when autophagy was activated by LPS. Finally, silencing p62 further promoted LPS‐mediated cell invasiveness.ConclusionToll‐like receptor 4 significantly enhanced the invasiveness of OSCC cells. Autophagy may regulate cell invasiveness through the NF‐κB pathway by modulating both the cytoplasmic and nuclear levels of p62.