Description: Ocean acidification events are recognized as important drivers of change in biological systems. Particularly, the impacts of acidification are more severe in estuarine systems than in surface ocean due to their shallowness, low buffering capacity, low salinity and high organic matter from land drainage. Moreover, because they are transitional areas, estuaries can be seriously impacted by a vast number of anthropogenic activities and in the last decades, carbon nanomaterials (CNMs) are considered as emerging contaminants in these ecosystems. Considering all these evidences, chronic experiment was carried out, trying to understand the possible alteration on the chemical behaviour of two different CNMs (functionalized and pristine) in predicted climate change scenarios and consequently, how these alterations could modify the sensitivity of one the most common marine and estuarine organisms (the polychaeta Hediste diversicolor) assessing a set of biomarkers related to polychaetes oxidative status as well as the metabolic performance and neurotoxicity. Our results demonstrated that all enzymes worked together to counteract seawater acidification and CNMs, however oxidative stress in the exposed polychaetes to both CNMs, especially under ocean acidification conditions, was enhanced. In fact, although the antioxidant enzymes tried to cope as compensatory response of cellular defense systems against oxidative stress, the synergistic interactive effects of pH and functionalized CNMs indicated that acidified pH significantly increased the oxidative damage (in terms of lipid peroxidation) in the cotaminated organisms. Different responses were observed in organisms submitted to pristine CNMs under pH control, where the lipid peroxidation did not increase along with the increasing exposure concentrations. The present results further demonstrated neurotoxicity caused by both CNMs, especially noticeable at acidified conditions. The mechanism of enhanced toxicity could be attributed to slighter aggregation and more suspended NMs in acidified seawater (as demonstrated by the DLS analysis). Therefore, ocean acidification may cause a higher risk of CNMs to marine ecosystems.

Description: We evaluated whether genetic predisposition is sufficient to induce changes due to chronic high glucose (HG; 25 mmol/L) in the presence or absence of insulin (HGI; 10 µg/mL) on osteogenic differentiation and markers in bone-marrow mesenchymal stem cells (BMSCs) from young Wistar (WBMSCs) and spontaneous hypertensive rats (SBMSCs) without hypertension. HG suppressed osteogenic differentiation in both the strains, observed by mineralization inhibition and decreased levels of the osteogenic markers Runx2 , osterix , osteopontin , and bone sialoprotein , compared to osteogenic medium (OM) cells. In WBMSCs, the effects of HG were associated with the down regulation of ERK1/2 and up regulation of p38 activities; however, HGI did not revert the effects of HG on MAPK activities. Moreover, HG did not affect MAPK signaling in SBMSCs compared to that in OM. HGI increased mineralization in WBMSCs compared to that in OM, but not in SBMSCs. High expression of peroxisome proliferator-activated receptor-gamma and glucose transporter type 4 in OM could be related with the predisposition to adipogenic differentiation noted in SBMSCs and was confirmed by emergence of adipocyte-like cells by HGI treatment. Downregulation of p38 and upregulation of JNK activities were observed in both BMSCs treated with HGI compared to those treated by HG. Ma (osmotic control) also suppressed osteogenic differentiation in both the strains. In conclusion, we demonstrated that SBMSCs from young spontaneous hypertensive rats, without hypertension but with genetic and epigenetic predisposition, exhibited decreased osteoblastic differentiation under HG and HGI did not revert the effects of HG in SBMSCs but increased adipogenic differentiation. This article is protected by copyright. All rights reserved

Description: Colistin-resistant Klebsiella pneumoniae co-harboring KPC and MCR-1 in a Hematopoietic Stem Cell Transplantation Unit Colistin-resistant 〈i〉Klebsiella pneumoniae〈/i〉 co-harboring KPC and MCR-1 in a Hematopoietic Stem Cell Transplantation Unit, Published online: 30 November 2018; doi:10.1038/s41409-018-0416-x Colistin-resistant Klebsiella pneumoniae co-harboring KPC and MCR-1 in a Hematopoietic Stem Cell Transplantation Unit