The work investigates the source of toxicity of copper oxide nanoparticles (CuO NPs) with respect to its leaching characteristic and speciation. Complexation-mediated leaching of CuO NPs by amino acids was identified as the source of toxicity toward Escherichia coli, the model microorganism used in the current study. The leached copper-peptide complex induces a multiple-fold increase in intracellular reactive oxygen species generation and reduces the fractions of viable cells, resulting in the overall inhibition of biomass growth. The cytotoxicity of the complex leachate is however different from that of equivalent soluble copper salts (nitrates and sulfates). A pH-dependent copper speciation during the addition of copper salts gives rise to uncoordinated copper ions, which in turn result in greater toxicity and cell lysis, the latter of which was not observed for CuO NPs even at comparable pH. Since leaching did not occur with micrometer-sized CuO, no cytotoxicty effect was observed, thus highlighting the prominence of materials toxicity at the nanoscale.

Macrophage inhibitory cytokine-1 (MIC-1/GDF15) is associated with cardiovascular disease, inflammation, body weight regulation and cancer. Its serum levels facilitate the diagnosis and prognosis of cancer and vascular disease. Furthermore, its serum levels are a powerful predictor of all-cause mortality, suggesting a fundamental role in biological processes associated with ageing. In cancer, the data available suggest that MIC-1/GDF15 is antitumorigenic, but this may not always be the case as disease progresses. Cancer promoting effects of MIC-1/GDF15 may be due, in part, to effects on antitumour immunity. This is suggested by the anti-inflammatory and immunosuppressive properties of MIC-1/GDF15 in animal models of atherosclerosis and rheumatoid arthritis. Furthermore, in late-stage cancer, large amounts of MIC-1/GDF15 in the circulation suppress appetite and mediate cancer anorexia/cachexia, which can be reversed by monoclonal antibodies in animals. Available data suggest MIC-1/GDF15 may be an important molecule mediating the interplay between cancer, obesity and chronic inflammation.

Summary Macrophage inhibitory cytokine-1 (MIC-1/GDF15) is a member of the TGF-b superfamily, previously studied in cancer and inflammation. In addition to regulating body weight, MIC-1/GDF15 may be used to predict mortality and/or disease course in cancer, cardiovascular disease, chronic renal and heart failure, as well as pulmonary embolism. These data suggested that MIC-1/GDF15 may be a marker of all-cause mortality. To determine if serum MIC-1/GDF15 estimation is a predictor of all-cause mortality we examined a cohort of 876 male subjects aged 35 to 80 years, selected from the Swedish Population Registry, and followed them for overall mortality. Serum MIC-1/GDF15 levels were determined for all subjects from samples taken at study entry. A second (independent) cohort of 324 same-sex twins (69% female) from the Swedish Twin Registry was similarly examined. All the twins had telomere length measured and 183 had serum levels of interleukin 6 (IL-6) and C reactive protein (CRP) available. Patients were followed for up to 14 years and had cause specific and all-cause mortality determined. Serum MIC-1/GDF15 levels predicted mortality in the all-male cohort with an adjusted odds ratio of death of 3.38 (95%CI 1.38–8.26). This finding was validated in the twin cohort. Serum MIC-1/GDF15 remained an independent predictor of mortality when further adjusted for telomere length, IL-6 and CRP. Additionally, serum MIC-1/GDF15 levels were directly correlated with survival time independently of genetic background. Serum MIC-1/GDF15 is a novel predictor of all-cause mortality.

Upon contact with plasma or other protein-containing biological fluids, the surface of nanoparticles is immediately decorated with proteins forming a biologically active protein corona. The biological fates and functions of nanoparticles are determined by physiological responses toward these nanoparticleprotein corona complexes as the effective biological unit of nanoparticles. In this article, we review representative studies on the effects of particle physicochemical characteristics along with the protein profiles in the biological medium on the formation of protein corona and importantly, how the dynamic nature and protein fingerprints of the formed corona govern the biological responses toward nanoparticles. The biological effects arising from the presence of protein corona can be both beneficial and unfavourable to the biomedical applications of nanoparticles. The protein corona-cell interactions open up the feasibility of targeted delivery and cell-specific uptake of therapeutic nanoparticles and in other circumstances, engineering of nanoparticles as adjuvants for vaccine development as well as mitigation of the unintentional cytotoxic effects of nanoparticles. On the other hand, the protein corona-cell interactions could induce rapid clearance of nanoparticles from in vivo circulation as well as activating unwanted inflammatory responses. Taken together, the knowledge on the formation and biological effects of protein corona enables tailored tuning of the physicochemical characteristics of nanoparticles, unique to their intended biological activity.

Reversible antimicrobial photoswitching of nanosilver on a semiconductor support using a facile and optically selective approach is demonstrated. The non‐intrusive cyclical irradiation by UV‐A (300–400 nm) and visible light (>450 nm) result in controlled oxidation state dynamics of the nanosilver, which in turn allows its antimicrobial activity to be switched off and on repeatedly (see image).