1,892 research outputs found

    Intercalation of graphite in Li-ion batteries: In situ microscopic characterization of the solid-electrolyte interface (SEI)

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    Energy storage technologies are crucial in the next green-energy transition. In particular, Li-ion batteries (LIBs) are nowadays the reference technology for many applications including, in particular, the forthcoming electrical mobility. In the last years, the deep investigation of the plethora of complex phenomena controlling the charge storage mechanism in LIBs allowed a considerable improvement in LIBs performance. In this regard, in situ analysis played a fundamental role in the comprehension of the degradation processes occurring at the electrode/electrolyte interface. In particular, in situ electro chemical atomic force microscopy (EC-AFM), consisting in high-resolution microscopy under electrochemical control, uniquely allowed to monitor the evolution in morphology and mechanical properties of the solid-electrolyte interface (SEI) forming at low potential on the graphitic anodic electrodes of LIBs. In this work, we employed in situ EC-AFM measurements and ex situ ToF-SIMS analysis as representative techniques to provide a comprehensive morphological and compositional overview of the SEI film formed under cyclic voltammetry experiments. The work aims to provide guidelines in the SEI evolution when highly oriented pyrolytic graphite (HOPG), which can be considered a model electrode, is employed. The reported in situ data are in agreement with current interpretative models. The ex situ ToF-SIMS analysis discloses a film composition where different Li compounds are uniformly distributed on the electrode surfac

    Dispareri in materia d'architettvra, et perspettiva. Con pareri di eccellenti, et famosi architetti, che li risoluono.

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    Photocopy (positive)Consists of correspondence between Bassi and Alfonso N, Palladio, Vignola, Vasari and G. B. Bertano on Bassi's controversy with Pellegrino Tibaldi about the plans for the Duomo in Milan.Mode of access: Internet

    The Mucus Slurper: A novel tracheal tube that requires no tracheal tube suctioning : a preliminary report

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    Objective: The buildup of mucus within the endotracheal tube (ETT) progressively reduces its internal volume. We devised the Mucus Slurper as an integral part of the tracheal tube to aspirate all mucus automatically at its distal tip. Design and setting: In vitro, and in vivo studies in sheep at the National Institutes of Health, NHLBI, PCCMB. Subjects: Six sheep, sedated, paralyzed, and mechanically ventilated Interventions: We evaluated the Mucus Slurper in vitro, and we evaluated its efficacy and safety in three healthy sheep during 24 h on volume-controlled mechanical ventilation in comparison to three sheep managed with open tracheal tube suctioning. Measurements and results: In vitro: with the Mucus Slurper connected to a source of vacuum of 450-500 mmHg the total volume of a single suction lasting 0.1, 0.2, and 0.3 s was, respectively, 75.4 ± 7.9, 114.5 ± 4.6, and 143.4 ± 8.7 ml; with the measured vacuum within the lumen of the Mucus Slurper ring of 37 cmH2O. In vivo: during mechanical ventilation we aspirated through the Mucus Slurper 13.4 ± 3.3 cc mucus/24 h. During the course of single aspiration the Mucus Slurper never affected the level of applied PEEP. The tracheal tube was free of tracheal secretions in the Mucus Slurper group while thin secretions were found within the ETT in the control group. Conclusion: The Mucus Slurper is a novel device designed to keep the tracheal tube and proximal trachea free of mucus. In studies in sheep lasting 24 h the Mucus Slurper was safe and prevented all mucus accumulation within the ETT

    Inhaled amikacin for severe Gram-negative pulmonary infections in the intensive care unit: Current status and future prospects

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    Recently, the use of nebulized antibiotics in the intensive care unit, in particular amikacin, has been the subject of much discussion, owing to unconvincing results from the latest randomized clinical trials. Here, we examine and reappraise the evidence in favor and against this therapeutic strategy; we then discuss the potential factors that might have played a role in the negative findings of recent clinical trials. Also, we call attention to several factors that are seldom considered by study developers and regulatory agencies, to promote translational research in this field and improve the design of future randomized clinical trials

    RS4651 suppresses lung fibroblast activation via the TGF-β1/SMAD signalling pathway

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    Background: Idiopathic pulmonary fibrosis (IPF) is a progressive disease resulting in respiratory failure with no efficient treatment options. We investigated the protective effect of RS4651 on pulmonary fibrosis in mice and the mechanism. Methods: Intratracheal injection of bleomycin (BLM) was used to induce pulmonary fibrosis in mice. RS4561 was administered intraperitoneally at different doses. Histopathological changes were observed. The level of alpha-smooth muscle actin (α-SMA) were also tested. In vitro, the proliferation and migratory effects of RS4651 treatment on MRC-5 cells pre-treated with transforming growth factor (TGF-β1) were examined. RNA-sequencing was used to detect differentially expressed target genes. Then, the expression of α-SMA, pSMAD2 and SMAD7 were analysed during RS4651 treatment of MRC-5 cells with or without silencing by SMAD7 siRNA. Results: Histopathological staining results showed decreased collagen deposition in RS4651 administered mice. Additionally, a lower level of α-SMA was also observed compared to the BLM group. The results of in vitro studies confirmed that RS4651 can inhibit the proliferation and migration, as well as α-SMA and pSMAD2 expression in MRC-5 cells treated with TGF-β1. RNA-sequencing data identified the target gene SMAD7. We found that RS4651 could upregulate SMAD7 expression and inhibit the proliferation and migration of MRC-5 cells via SMAD7, and RS4651 inhibition of α-SMA and pSMAD2 expression was blocked in SMAD7-siRNA MRC-5 cells. In vivo studies further confirmed that RS4651 could upregulate SMAD7 expression in BLM-induced lung fibrosis in mice. Conclusions: Our data suggest that RS4651 alleviates BLM-induced pulmonary fibrosis in mice by inhibiting the TGF-β1/SMAD signalling pathway
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