Marine mussel inspired polydopamine (PDA) has received increased attention due to its good thermal and chemical stability as well as strong adhesion on most materials. In this work, high-performance nanofiltration membranes based on interpenetrating polymer networks (IPN) incorporating PDA and polybenzimidazole (PBI) were developed for organic solvent nanofiltration (OSN). Generally, in order to obtain solvent stability, polymers need to be covalently cross-linked under harsh conditions, which inevitably leads to losses in permeability and mechanical flexibility. Surprisingly, by in situ polymerization of dopamine within a PBI support, excellent solvent resistance and permeance of polar aprotic solvents were obtained without covalent cross-linking of the PBI backbone due to the formation of an IPN. The molecular weight cutoff and permeance of the membranes can be fine-tuned by changing the polymerization time. Robust membrane performance was achieved in conventional and emerging green polar aprotic solvents (PAS) in a wide temperature range covering −10 °C to +100 °C. It was successfully demonstrated that the in situ polymerization of PDAcreating an IPNcan provide a simple and green alternative to covalent cross-linking of membranes. To elucidate the nature of the solvent stability, a detailed analysis was performed that revealed that physical entanglement along with strong secondary interaction synergistically enable solvent resistance with as low as 1–3% PDA content.

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Sodium dodecyl sulfate (SDS) is widely used as an irritant. Inflammatory and immune related cytokines/ chemokines are released by keratinocytes following SDS irritation. However, a specific effect of SDS on keratinocytes and the mechanism of skin irritation caused by SDS have not been investigated. To explore the irritant mechanism of SDS on keratinocytes, a gene microarray was used to detect the changes in gene expression after treating keratinocytes with SDS for different amounts of time. After 0.5 h and 1 h SDS exposure, there were changes mainly in genes in the rheumatoid arthritis pathway (CCL5, IL-6, FOS, CSF1, and HLA-DPB1) and TNF signaling pathway (TNF, CSF2, CXCL3, TNFAIP3, PTGS2, CXCL8, CCL20, and PIK3CA) to cause a pro-inflammatory reaction as well as autoimmune activation. After treating with SDS for 2 h and 4 h, there were changes in the expression of genes (LIF, PIM1, MAP3K8, CCNA1, RUNX1, and CYP1) that are related to cell apoptosis and cancerization. This was related to changes in transcriptional activity in the cancer and tryptophan metabolism pathway. Overall, SDS irritation caused different changes in gene expression over time, which altered the state of keratinocytes affecting processes of inflammation, autoimmune response, cell apoptosis, and cancerization. These results provide insight into the irritation process of SDS and provide reference for the future evaluation of skin irritation.