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Bio-inspired nanostructures have demonstrated highly efficient mechano-bactericidal performances with no risk of bacterial resistance; however, they are prone to become contaminated with the killed bacterial debris. Herein, a biocompatible mechano-bactericidal nanopatterned surface with salt-responsive bacterial releasing behavior is developed by grafting salt-responsive polyzwitterionic (polyDVBAPS) brushes on a bio-inspired nanopattern surface. Benefiting from the salt-triggered configuration change of the grafted polymer brushes, this dual-functional surface shows high mechano-bactericidal efficiency in water (low ionic strength condition), while the dead bacterial residuals can be easily lifted by the extended polymer chains and removed from the surface in 1 M NaCl solution (high ionic strength conditions). Notably, this functionalized nanopatterned surface shows selective biocidal activity between bacterial cells sand eukaryotic cells. The biocompatibility with red blood cells (RBCs) and mammalian cells was tested in vitro. The histocompatibility and prevention of perioperative contamination activity were verified by in vivo evaluation in a rat subcutaneous implant model. This nanopatterned surface with bacterial killing and releasing activities may open new avenues for designing bio-inspired mechano-bactericidal platforms with long-term efficacy, thus presenting a facile alternative in combating perioperative-related bacterial infection. Bioinspired nanostructured surfaces with noticeable mechano-bactericidal activity showed great potential in moderating drug-resistance. However, the nanopatterned surfaces are prone to be contaminated by the killed bacterial debris and compromised the bactericidal performance. In this study, we provide a dual-functional antibacterial conception with both mechano-bactericidal and bacterial releasing performances not requiring external chemical bactericidal agents. Additionally, this functionalized antibacterial surface also shows selective biocidal activity between bacteria and eukaryotic cells, and the excellent biocompatibility was tested in vitro and in vivo. The new concept for the functionalized mechano-bactericidal surface here illustrated presents a facile antibiotic-free alternative in combating perioperative related bacterial infection in practical application. [Display omitted] [ABSTRACT FROM AUTHOR]

Obesity and related diseases are becoming a growing risk for public health around the world due to the westernized lifestyle. Sema7A, an axonal guidance molecule, has been known to play a role in neurite growth, bone formation, and immune regulation. Whether Sema7A participates in obesity and metabolic diseases is unknown. As several SNPs in SEMA7A and its receptors were found to correlate with BMI and metabolic parameters in the human population, we investigated the potential role of Sema7A in obesity and hepatic steatosis. GWAS and GEPIA database was used to analyze SNPs in SEMA7A and the correlation of Sema7A expression with lipid metabolism related genes. Sema7A−/− mice and recombinant Sema7A (rSema7A) were used to study the role of Sema7A in HFD-induced obesity and hepatic steatosis. Adipose tissue-derived mesenchymal stem cells (ADSCs) were used to examine the role of Sema7A in adipogenesis, lipogenesis and downstream signaling. Deletion of Sema7A aggravated HFD-induced obesity. Sema7A deletion enhanced adipogenesis in both subcutaneous and visceral ADSCs, while the addition of rSema7A inhibited adipogenesis of ADSCs and lipogenesis of differentiated mature adipocytes. Sema7A inhibits adipo/lipogenesis potentially through its receptor integrin β1 and downstream FAK signaling. Importantly, administration of rSema7A had protective effects against diet-induced obesity in mice. In addition, deletion of Sema7A led to increased hepatic steatosis and insulin resistance in mice. Our findings reveal a novel inhibitory role of Sema7A in obesity and hepatic steatosis, providing a potential new therapeutic target for obesity and metabolic diseases. • Sema7A−/− mice are more sensitive to diet-induced obesity, hepatic steatosis and insulin resistance. • Sema7A inhibits adipo/lipogenesis and potentially protects against diet-induced obesity via the integrin β1/FAK axis. • Administration of recombinant Sema7A protects against diet-induced obesity in mice. [ABSTRACT FROM AUTHOR]