Formation of artificial solid electrolyte interphase by radiolysis

International audienceAmong energy storage devices, Lithium ion batteries (LlBs) are efficient power sources used for many applications inc1uding mobile microelectronics. However, ageing phenomena are not yet fully understood. These 8henomena are a crucial issue to pro vide safe and stable batteries!. LIBs are usually compbsed of a negative electrode where the active material is graphite, a positive electrode usualli a lithium metal oxide and an organic liquid electrolyte. Ortiz et al. have shown that radiolysis is a powerful tool to simulate the degradation of the latter one in short time: minutes/hours instead of weeks/months by electrolysis (Fig. 1). Moreover, radiolysis allows performing experiments at the picosecond time scale thus giving access to reaction mechanisms. During the first cycles of the battery, the reduced surface of the negative electrode reacts with the electrolyte producing a solid interphase (solid electrolyte interphase, SEI) which is responsible for the capacity loss of the battery. In this work, we investigated the SEI formation by radiolysis at the surface of various carbonaceous materials inc1uding crystalline graphite (lithiated or not) and carbon nanoparticles (amorphous as weIl as organized) prepared by laser pyrolysis. Materials were dispersed in a mixture of carbonate solvents containing LiPF. Composition and morphology of SEI were invesigated by XPS and TEM while the composition of gas and liquid phases was studied by gas chromatography and high resolution mass spectrometry, respectively. We show that an artificial SEI can be produced by radiolysis. We observe always the same degradation mechanisms of the electrolyte but interestingly the SEI composition depends on the carbonaceous material. The artificial SEI formed at the surface of graphite is composed of Li carbonate, oxalate and oligomers of poly(ethylene oxide) while the SEI formed at the surface of carbon nanoparticles contains Li salts as Li$_2$CO$_3$. Radiolysis allows producing materials with modified surface that will be tested as new materials for negative electrode

Cholangiocyte chemokine secretion and macrophage accumulation is mediated by osteopontin in murine liver models

Background and aims Progression of chronic liver disease involves accumulation of inflammatory cells towards the peri-portal regions during a ductular inflammatory response. Osteopontin (OPN), an effector of Hh signalling, contributes to liver fibrogenesis and ductular inflammation via activation of hepatic stellate and progenitor cells. In tissue injury, OPN regulates macrophage functions via pro-inflammatory chemoattractant properties. In liver, however, the role of OPN in macrophage activation and recruitment remains unclear. We investigated the role of OPN in cholangiocyte chemokine secretion and macrophage recruitment using in vivo, in vitro, and in silico approaches. Methods In MCD and DDC murine models of liver fibrosis, total liver chemokine expression was measured by qRTPCR and macrophages detected by FACS (CD 11b, F4/80, CCR2, Ly6C). Lentiviral-mediated shRNA (shOPN) was used for OPN knockdown in murine 603B cholangiocytes, and secreted OPN neutralized by specific aptamers. Cholangiocyte chemokine secretion was measured by cytometric bead array and mRNA by qRTPCR. Macrophage migration was assessed in transwells using RAW264.7 cells. To obtain a global perspective of genes affected by OPN, next-generation RNA sequencing was used to compare control and shOPN cholan- giocytes. Transcripts were assessed in DESeq and gene ontologies and pathways by GOrilla, DAVID, and ReviGO software. Results Liver fibrosis in MCD and DDC was accompanied by upregulated total liver OPN, TGF-β, Ccl2, Ccl5, and Cxcll mRNA, and accumulation of liver CDl1b/F4/80(+) CCR2(hi) macrophages. Mice treated with OPN-aptamers had less fibrosis, reduced Ccl2, Ccl5, and Cxcll mRNA, and reduced accumulation of liver CD11b/F4/80(+) CCR2(hi) macrophages and the Ly6C(hi) inflammatory monocyte subset. In shOPN cholangiocytes, RNAseq detected 670 affected genes (Ben- jamini-Hochsberg padj <0.05). Ten chemokines were significantly downregulated: Cxcl16, Cxcl11, Cxcl10, Ccl5, Ccl2, Ccl9, Ccl7 Cxcl1, Cx3cl1 and Cxcl5 (by a range of log2fold between 2.70 and 0.99). Enriched gene ontologies clustered around immunity, chemotaxis and cytokine and chemokine production Altered pathways involved chemokine production and NfKB signalling. Consistent reductions in chemokine secretion and mRNA were verified in shOPN cholangiocytes Additionally, RAW264.7 macrophages cultured with OPN-deficient 603B conditioned media exhibited decreased migration. Conclusions In progressive liver disease OPN promotes chol- angiocyte production of chemokines and the accumulation of macrophages, including a proinflammatory monocyte subset. These data support neutralization of OPN as an anti-inflammatory and anti-fibrotic strategy

Enhanced identification of endocrine disruptors through integration of science-based regulatory practices and innovative methodologies: The MERLON Project [version 1; peer review: 2 approved]

The prevalence of hormone-related health issues caused by exposure to endocrine disrupting chemicals (EDCs) is a significant, and increasing, societal challenge. Declining fertility rates together with rising incidence rates of reproductive disorders and other endocrine-related diseases underscores the urgency in taking more action. Addressing the growing threat of EDCs in our environment demands robust and reliable test methods to assess a broad variety of endpoints relevant for endocrine disruption. EDCs also require effective regulatory frameworks, especially as the current move towards greater reliance on non-animal methods in chemical testing puts to test the current paradigm for EDC identification, which requires that an adverse effect is observed in an intact organism. Although great advances have been made in the field of predictive toxicology, disruption to the endocrine system and subsequent adverse health effects may prove particularly difficult to predict without traditional animal models. The MERLON project seeks to expedite progress by integrating multispecies molecular research, new approach methodologies (NAMs), human clinical epidemiology, and systems biology to furnish mechanistic insights and explore ways forward for NAM-based identification of EDCs. The focus is on sexual development and function, from foetal sex differentiation of the reproductive system through mini-puberty and puberty to sexual maturity. The project aims are geared towards closing existing knowledge gaps in understanding the effects of EDCs on human health to ultimately support effective regulation of EDCs in the European Union and beyond