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Ab initio molecular dynamics simulations confirmed the stability of the studied complexes. Our investigations establish the high potential of the studied complexes for usage in systems for hydrogen storage.Signal amplification by reversible exchange (SABRE) is an effective NMR hyperpolarization technique for signal enhancement using para-hydrogen on iridium catalysts. To date, monodentate chelating nitrogen analogs have been predominantly used as substrates for SABRE because of the limited chelating sites of the Ir-catalyst with different molecular orientations. Herein, for the first time, the use of a tridentate chelating ligand (BPEA) containing pyridine moieties and a secondary amine as a SABRE substrate is demonstrated. For the optimization of the tridentate chelating ligand, alkyl chain lengths were varied with the optimization of the external magnetic field and concentrations of three different ligands. Because many chemically multidentate complexes present in nature have scarcely been studied as SABRE substrates, this optimized tridentate chelating ligand structure with the SABRE catalyst and its polarization transfer from para-hydrogen will broaden the scope of hyperpolarizable substrates and help in the investigation of chelating structures for future applications.Herein, we report the synthesis and investigation of a novel phenazine derivative M1 with oligomeric ethylene glycol ether substituents as a promising anolyte material for non-aqueous organic redox flow batteries (RFBs). The designed material undergoes a reversible and stable reduction at -1.72 V vs. Ag/AgNO3 and demonstrates excellent (>2.5 M) solubility in MeCN. A non-aqueous organic redox flow battery assembled using the novel phenazine derivative as an anolyte and a substituted triarylamine derivative as a catholyte exhibited high specific capacity (∼93% from the theoretical value), >95% Coulombic efficiency, 65% utilization of active materials and good charge-discharge cycling stability.Electrical signals are present in the extracellular spaces between neural cells. To mimic the electrophysiological environment for peripheral nerve regeneration, this study was intended to investigate how conductive graphene-based fibrous scaffolds with aligned topography regulate Schwann cell behavior in vitro via electrical stimulation (ES). To this end, randomly- and uniaxially-aligned polycaprolactone fibrous scaffolds were fabricated by electrospinning, followed by coating with reduced graphene oxide (rGO) via vacuum filteration. SEM revealed that rGO was successfully coated on the fibers without changing their alignment, and also brought about an improvement in mechanical properties and hydrophilicity. The electrical conductivity of the rGO-coated fibrous scaffold was up to 0.105 S m-1. When Schwann cells were seeded on the scaffolds and stimulated by 10 mV in vitro, it was found that either the alignment of the fibers or ES led to a higher level of proliferation and nerve growth factor (NGF) expression of Schwann cells. Further, ES at the aligned fibrous topography enhanced the expression of NGF, the proliferation of Schwann cells, and enhanced the cell migration rate by more than 60% compared to either ES or the oriented fibers alone. The application of exogenous electric cues mediated by templated biomaterials provides profound insights for nerve regeneration.In this work, an NIR-activated fluorescent dye naphthalimide-thioether-cyanine (NPSCY) was developed for the photodynamic treatment of cancer cells. In this dye, naphthalimide and cyanine were selected as the two fluorophores, which were linked by the thioether group. Under 660 nm irradiation, NPSCY could produce 1O2 rapidly, suggesting the potential for photodynamic therapy. Cys can be considered as one of the markers of cancer cells and NPSCY could distinguish Cys from three channels (433 nm, 475 nm, 733 nm) due to the bilateral recognition of the thioether group, which was helpful for accurately locating cancer cells. Fortunately, NPSCY could also produce 1O2 after being reacted with the intracellular biological thiols, which also avoided the inactivation of the photosensitizer in cancer cells. The co-localization coefficient of 0.873 indicated that the cyanine group promoted the aggregation of NPSCY in mitochondria. This photosensitizer showed low dark toxicity and high phototoxicity. Selleck alpha-Naphthoflavone Meanwhile, the half-maximal inhibitory concentration (IC50) was calculated to be 3.7 μM. NPSCY could inhibit cell migration after irradiation at 660 nm.How does a small change in the structure of a phospholipid affect its supramolecular assembly? In aqueous suspensions, the substitution of one ester linkage in DPPC (1,2-dipalmitoyl-sn-glycero-3-phosphocholine) by an ether linkage alters its phase behaviour completely. To unravel the effect of replacing a phospholipid's ester linkage by an ether linkage in lipid monolayers, we characterized pure monolayers of the model lipid DPPC and its sn-2 ether analogue PHPC (1-palmitoyl-2-O-hexadecyl-sn-glycero-3-phosphocholine) as well as mixtures of both by measurements of surface pressure-molecular area (π-Amol) isotherms. In addition, we used infrared reflection absorption spectroscopy (IRRAS) to study lipid condensation, lipid chain orientation, headgroup hydration, and lipid miscibility in all samples. Mixed monolayers consisting of DPPC and PHPC were studied further using epifluorescence microscopy. Our results indicate a strong influence of the sn-2 ether linkage on headgroup hydration and ordering effects in the regions of the apolar chains and the headgroups. Both effects could originate from changes in glycerol conformation. Furthermore, we observed a second plateau in the π-Amol isotherms of DPPC/PHPC mixtures and analysis of the mixed π-Amol isotherms reveals a non-ideal mixing behaviour of both lipids which may be caused by conformational differences in their headgroups.Redox homeostasis is essential for cell function and its disruption is associated with multiple pathologies. Redox balance is largely regulated by the relative concentrations of reduced and oxidized glutathione. In eukaryotic cells, this ratio is different in each cell compartment, and disruption of the mitochondrial redox balance has been specifically linked to metabolic diseases. Here, we report a probe that is selectively activated by endogenous nitroreductases, and releases tributylphosphine to trigger redox stress in mitochondria. Mechanistic studies revealed that, counterintuitively, release of a reducing agent in mitochondria rapidly induced oxidative stress through accumulation of superoxide. This response is mediated by glutathione, suggesting a link between reductive and oxidative stress. Furthermore, mitochondrial redox stress activates a cellular response orchestrated by transcription factor ATF4, which upregulates genes involved in glutathione catabolism.