Hemostatic fabrics are most commonly used in baseline emergency treatment; however, the unnecessary blood loss due to the excessive blood absorption by traditional superhydrophilic fabrics is overlooked. Herein, for the first time, superhydrophobic/superhydrophilic Janus fabrics (superhydrophobic on one side and superhydrophilic on the other) are proposed: the superhydrophilic part absorbs water in the blood to expedite the clotting while the superhydrophobic part prevents blood from further permeating. Compared with the common counterparts, effective bleeding control with reducing blood loss more than 50% can be achieved while the breathability largely remain by using Janus fabrics. The proposed prototypes can even prolong the survival time in the rat model with serious bleeding. This strategy for reducing blood loss via simply tuning wettability is promising for the practical applications.

Nanotechnology is an interdisciplinary science that has developed rapidly in recent years. Metallic nanoparticles (NPs) are increasingly utilized in dermatology and cosmetology, because of their unique properties. However, skin exposure to NPs raises concerns regarding their transdermal toxicity. The tight junctions of epithelial cells form the skin barrier, which protects the host against external substances. Recent studies have found that NPs can pass through the skin barrier into deeper layers, indicating that skin exposure is a means for NPs to enter the body. The distribution and interaction of NPs with skin cells may cause toxic side effects. In this review, possible penetration pathways and related toxicity mechanisms are discussed. The limitations of current experimental methods on the penetration and toxic effects of metallic NPs are also described. This review contributes to a better understanding of the risks of topically applied metallic NPs and provides a foundation for future studies.

BackgroundThe extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known.MethodsIn this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro.ResultsThis analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the Ca2+-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level.ConclusionThis study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis.Electronic supplementary materialThe online version of this article (10.1186/s12989-018-0274-0) contains supplementary material, which is available to authorized users.