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Volcano analyses have been established as a standard tool in the field of electrocatalysis in order to assess the performance of electrodes in a class of materials. The apex of the volcano curve, where the most active electrocatalysts are situated, is commonly defined by a hypothetical ideal material that binds its reaction intermediates thermoneutral at zero overpotential, in correspondence to Sabatier's principle. However, recent studies in the literature reported a right shift of the apex in a volcano curve, in which the most active electrocatalysts bind their reaction intermediates endergonically rather than thermoneutral at zero overpotential. On the example of a two-electron process, this viewpoint addresses the question how the definition of an optimum catalyst needs to be modified with respect to the requirements of Sabatier's principle when kinetic effects and the applied overpotential are included in the analysis. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.BACKGROUND Systemic sclerosis (SSc) is characterized by fibrosis, vascular disease and inflammation. Adenosine signaling plays a central role in fibroblast activation. The aim of the present study was to evaluate the therapeutic effects of adenosine depletion with pegylated adenosine deaminase (PEG-ADA) in preclinical models of SSc. METHODS The effects of PEG-ADA on inflammation, vascular remodeling and tissue fibrosis were analyzed in Fos-related antigen-2 transgenic (Fra2) mice and in the B10.D2→Balb/c(H-2d) model of sclerodermatous-chronic-graft-versus-host-disease (scl-cGvHD). The effects of PEG-ADA were confirmed in vitro in a human full-thickness-skin-model. RESULTS PEG-ADA effectively inhibited myofibroblast differentiation and reduced pulmonary (with decreased collagen expression by 34.3%, p=0.0079, n=6), dermal (51.8%, p=0.0006, n=6) and intestinal fibrosis (17.7%, p=0.0228, n=6) in Fra2 mice. Antifibrotic effects of PEG-ADA were also demonstrated in scl-cGvHD (38.4%, p=0.0063, n=8), and in a human full-thickness-skin model. PEG-ADA decreased inflammation and corrected the M2-Th2-ILC2-bias. Moreover, PEG-ADA inhibited proliferation of pulmonary vascular smooth muscle cells (40.5%, p less then 0.0001, n=6), prevented thickening of the vessel walls (39.6%, p=0.0028, n=6) and occlusions of pulmonary arteries (63.9%, p=0.0147, n=6). Treatment with PEG-ADA inhibited apoptosis of microvascular endothelial cells (65.4%, p=0.0001, n=6) and blunted the capillary rarefication (32.5%, p=0.0199, n=6). RNASeq demonstrated that treatment with PEG-ADA normalized multiple pathways related to fibrosis, vasculopathy and inflammation in Fra2 mice. CONCLUSION Treatment with PEG-ADA ameliorates the three cardinal features of SSc in pharmacologically relevant and well-tolerated doses. These findings may have direct translational implications as PEG-ADA is already FDA-approved for the treatment of patients with ADA-deficient-SCID. This article is protected by copyright. All rights reserved.Intermediates relevant to cobalt-catalyzed alkene hydroformylation have been isolated and evaluated in fundamental organometallic transformations relevant to aldehyde formation. The 18-electron (R,R)-(iPr DuPhos)Co(CO)2 H has been structurally characterized, and it promotes exclusive hydrogenation of styrene in the presence of 50 bar of H2 /CO gas (11) at 100 °C. Deuterium-labeling studies established reversible 2,1-insertion of styrene into the Co-D bond of (R,R)-(iPr DuPhos)Co(CO)2 D. Whereas rapid β-hydrogen elimination from cobalt alkyls occurred under an N2 atmosphere, alkylation of (R,R)-(iPr DuPhos)Co(CO)2 Cl in the presence of CO enabled the interception of (R,R)-(iPr DuPhos)Co(CO)2 C(O)CH2 CH2 Ph, which upon hydrogenolysis under 4 atm H2 produced the corresponding aldehyde and cobalt hydride, demonstrating the feasibility of elementary steps in hydroformylation. Both the hydride and chloride derivatives, (X=H- , Cl- ), underwent exchange with free 13 CO. Under reduced pressure, (R,R)-(iPr DuPhos)Co(CO)2 Cl underwent CO dissociation to form (R,R)-(iPr DuPhos)Co(CO)Cl. © 2020 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.Publication bias undermines the principle of scientific integrity. As generally understood, publication bias refers to selective reporting of positive trial results and non-reporting of negative results. Sodium L-lactate manufacturer However, subtler forms of publication bias also constitute a threat to a balanced understanding of trial results. The anifrolumab story constitutes an illustrative case in point. This article is protected by copyright. All rights reserved.Here, we report the antibacterial properties of two metallocenyl (ferrocenyl and ruthenocenyl) 7-aminocephalosporanic acid (7-ACA) antibiotic bioorganometallic conjugates. Continuing a trend we found in our previous studies, the ruthenocenyl conjugate showed greater antibacterial activity than its ferrocenyl counterpart. Compared with the previously published 7-aminodesacetoxycephalosporanic acid (7-ADCA) conjugates, the 3-acetyloxymethyl group significantly improved the compounds' activity. Furthermore, the Rc-7-ACA compound was more active against clinical S. aureus isolates than the ampicillin reference. Antibacterial activity of the two metallocenyl 7-ACA derivatives was further confirmed by scanning electron microscopy (SEM). Using a CTX-M-14 β-lactamase competition assay based on nitrocefin hydrolysis, we showed that the Rc-7-ACA bound more favorably to CTX-M-14 than its ferrocenyl counterpart, again confirming the superiority of the ruthenocenyl moiety over the ferrocenyl one in interacting with proteins. We also report a 1.47 Å resolution crystal structure of Rc-7-ACA in complex with CTX-M-14 E166A mutant, an enzyme sharing a similar active site configuration with penicillin-binding proteins, the molecular target of β-lactam antibiotics. These results strengthen the case for the antibacterial utility of the Rc and Fc groups. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.Ion homeostasis is essential for cellular survival, and elevated concentrations of specific ions are used to start distinct forms of programmed cell death. However, investigating the influence of certain ions on cells in a controlled way has been hampered due to the tight regulation of ion import by cells. Here, it is shown that lipid-coated iron-based metal-organic framework nanoparticles are able to deliver and release high amounts of iron ions into cells. While high concentrations of iron often trigger ferroptosis, here, the released iron induces pyroptosis, a form of cell death involving the immune system. The iron release occurs only in slightly acidic extracellular environments restricting cell death to cells in acidic microenvironments and allowing for external control. The release mechanism is based on endocytosis facilitated by the lipid-coating followed by degradation of the nanoparticle in the lysosome via cysteine-mediated reduction, which is enhanced in slightly acidic extracellular environment. Thus, a new functionality of hybrid nanoparticles is demonstrated, which uses their nanoarchitecture to facilitate controlled ion delivery into cells.
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