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Silver-functionalized textiles, as the most common protective medical materials, have attracted considerable attention. However, poor antibacterial durability and relatively tedious preparation process limit their applications. In this study, a kind of multifunctional cotton fabric was prepared through simultaneous dip-coating of silver-silica hybrid nanoparticles (Ag-MSNs) and fluorinated MSNs (F-MSNs), providing excellent antifouling ability due to superhydrophobicity and long-term antibacterial properties from the sustained release of Ag ions (Ag+). Detailed studies were performed to evaluate their structure and protective performance, especially the long-term antibacterial properties of the obtained fabrics were tested by the inhibition zone experiment for 25 d. The as-prepared fabrics showed good non-wetting properties and sustained antibacterial activity against Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus). Further washing and abrasion experimentations demonstrated that the as-prepared fabrics had stable hydrophobicity and antibacterial properties, much more reliable than commercial antibacterial gauze. Considering the inexpensive and simple preparation process as well as long-term and efficient effect for sterilization, the strategy paves a new and facile way for the fabrication of multifunctional fabrics with robust hydrophobic and antibacterial activity.

The novel KIR3DL1*01507 allele differs from the closest allele KIR3DL1*01502 by a single synonymous mutation.

Endothelial dysfunction and excessively stimulated autophagy, often caused by oxidant injury or inflammation, will lead to atherosclerosis development and progression in diabetes. The aim of this study is to investigate the protective effect of glucagon-like peptide-1 (GLP-1) treatment on preventing oxidative stress-induced endothelial dysfunction and excessively stimulated autophagy. Treatment of endothelial cells with GLP-1 significantly attenuated oxidative stress-induced endothelial dysfunction and autophagy, which was associated with the reduction of intracellular reactive oxygen species (ROS) levels. These protective effects of GLP-1 were likely mediated by reducing phosphorylation of ERK1/2. We further demonstrated that GLP-1 treatment could reverse downregulation of epigenetic factor histone deacetylase 6 (HDAC6), a downstream molecular of the EKR1/2, induced by oxidant injury. In conclusion, our results suggest that GLP-1 produces a protective effect on endothelial cells from oxidant injury by preventing endothelial dysfunction and autophagy, which may be dependent on restoring HDAC6 through a GLP-1R-ERK1/2-dependent manner.

Mannan binding lectin (MBL), initially reported to activate the complement pathway, is also known to be involved in the pathogenesis of autoimmune diseases. We report a thus far unknown function of MBL as a suppressor of T-cell activation. MBL markedly inhibited T-cell proliferation induced by anti-CD3 and anti-CD28 antibodies. Moreover, the presence of MBL during T-cell priming interfered with proximal T-cell receptor signaling by decreasing phosphorylation of Lck, ZAP-70, and LAT. MBL bound to T cells through interaction between the collagen-like region of MBL and calreticulin (CRT) expressed on the T-cell surface. The neutralizing antibody against CRT abrogated MBL-mediated suppression of T-cell proliferation, suggesting that MBL down-modulates T-cell proliferation