Mg-based materials are promising candidates for high capacity hydrogen storage. However, their poor hydrogenation/dehydrogenation kinetics and high desorption temperature are the main obstacles to their applications. This paper reports a method for in situ formation of cycle stable CeH 2.73 -MgH 2 -Ni nanocomposites, from the hydrogenation of as-melt Mg 80 Ce 18 Ni 2 alloy, with excellent hydrogen storage performance. The nanocomposites demonstrate reversible hydrogen storage capacity of more than 4.0 wt %, at a low desorption temperature with fast kinetics and long cycle life. The temperature for the full hydrogenation/dehydrogenation cycle of the composites is significantly decreased to 505 K, which is about 100 K lower than that for pure Mg. The hydrogen desorption activation energy is 63 ± 3 kJ/mol H 2 for the composites, which is significantly lower than those of Mg 3 Ce alloy and pure Mg (104 ± 7 and 158 ± 2 kJ/mol H 2 , respectively). X-ray diffraction and transmission electron microscopy have been used to reveal the mechanism that delivers this excellent cycle stability and fast hydriding/ dehydriding kinetics. It is found that the hydriding/dehydriding process is catalyzed by the combination of in situ formed extremely fine CeH 2 /CeH 2.73 and Ni to Mg/MgH 2 . In addition, this nanocomposite structure can effectively suppress Mg/MgH 2 grain growth and enable the material to maintain its high performance for more than 500 hydrogenation dehydrogenation cycles.
Semiconducting single-walled carbon
nanotubes (s-SWCNTs) with a
diameter of around 1.0–1.5 nm, which present bandgaps comparable
to silicon, are highly desired for electronic applications. Therefore,
the preparation of s-SWCNTs of such diameters has been attracting
great attention. The inner surface of SWCNTs has a suitable curvature
and large contacting area, which is attractive in host–guest
chemistry triggered by electron transfer. Here we reported a strategy
of host–guest molecular interaction between SWCNTs and inner
clusters with designed size, thus selectively separating s-SWCNTs
of expected diameters. When polyoxometalate clusters of ∼1
nm in size were filled in the inner cavities of SWCNTs, s-SWCNTs with
diameters concentrated at ∼1.3–1.4 nm were selectively
extracted with the purity of ∼98% by a commercially available
polyfluorene derivative. The field-effect transistors built from the
sorted s-SWCNTs showed a typical behavior of semiconductors. The sorting
mechanisms associated with size-dependent electron transfer from nanotubes
to inner polyoxometalate were revealed by the spectroscopic and in situ electron microscopic evidence as well as the theoretical
calculation. The polyoxometalates with designable size and redox property
enable the flexible regulation of interaction between the nanotubes
and the clusters, thus tuning the diameter of sorted s-SWCNTs. The
present sorting strategy is simple and should be generally feasible
in other SWCNT sorting techniques, bringing both great easiness in
dispersant design and improved selectivity.
Retinal pigment epithelium (RPE) cell damage is implicated in the pathogenesis of age-related macular degeneration (AMD). An increase of interferon-c (IFN-c) levels was observed in patients with AMD, but whether inflammatory factors are causally related to AMD progression is unclear. Here, we demonstrate a direct causal relationship between IFN-c and RPE cell death. IFN-c induced human retinal pigment epithelial cell (ARPE-19) death accompanied by increases in Fe 2+ , reactive oxygen species, lipid peroxidation, and glutathione (GSH) depletion, which are main characteristics of ferroptosis. Mechanistically, IFN-c upregulates the level of intracellular Fe 2+ through inhibiting Fe 2+ efflux protein SLC40A1 and induces GSH depletion by blocking cystine/glutamate antiporter, System xc-. At the same time, treatment with IFN-c decreases the level of glutathione peroxidase 4 (GPx4), rendering the cells more sensitive to ferroptosis. JAK1/2 and STAT1 inhibitors could reverse the reduction of SLC7A11, GPx4 and GSH expression induced by IFN-c, indicating IFN-c induces ARPE-19 cell ferroptosis via activation of the JAK1-2/STAT1/SLC7A11 signaling pathway. The above results were largely confirmed in IFN-c-treated mice in vivo. Finally, we used sodium iodate (NaIO 3 )-induced retinal degeneration to further explore the role of ferroptosis in AMD in vivo. Consistent with the role of IFN-c, treatment with NaIO 3 decreased SLC7A11, GPx4 and SLC40A1 expressions. NaIO 3 -induced RPE damage was accompanied by increased iron, lipid peroxidation products (4-hydroxynonenal, malondialdehyde), and GSH depletion, and ferroptosis inhibitors could reverse the above phenomenon. Taken together, our findings suggest that inhibiting ferroptosis or reducing IFN-c may serve as a promising target for AMD.
Diabetic retinopathy (DR) is a common microvascular complication of diabetes mellitus. Abnormal energy metabolism in microvascular endothelium is involved in the progression of diabetic retinopathy. Bile Acid G‐Protein‐Coupled Membrane Receptor (TGR5) has emerged as a novel regulator of metabolic disorders. However, the role of TGR5 in diabetes mellitus‐induced microvascular dysfunction in retinas is largely unknown. Herein, enzyme‐linked immunosorbent assay was used for analyzing bile acid (BA) profiles in diabetic rat retinas and retinal microvascular endothelial cells (RMECs) cultured in high glucose medium. The effects of TGR5 agonist on streptozotocin (STZ)‐induced diabetic retinopathy were evaluated by HE staining, TUNEL staining, retinal trypsin digestion, and vascular permeability assay. A pharmacological inhibitor of RhoA was used to study the role of TGR5 on the regulation of Rho/Rho‐associated coiled‐coil containing protein kinase (ROCK) and western blot, immunofluorescence and siRNA silencing were performed to study the related signaling pathways. Here we show that bile acids were downregulated during DR progression in the diabetic rat retinas and RMECs cultured in high glucose medium. The TGR5 agonist obviously ameliorated diabetes‐induced retinal microvascular dysfunction in vivo, and inhibited the effect of TNF‐α on endothelial cell proliferation, migration, and permeability in vitro. In contrast, knockdown of TGR5 by siRNA aggravated TNF‐α‐induced actin polymerization and endothelial permeability. Mechanistically, the effects of TGR5 on the improvement of endothelial function was due to its regulatory role on the ROCK signaling pathway. An inhibitor of RhoA significantly reversed the loss of tight junction protein under TNF‐α stimulation. Taken together, our findings suggest that insufficient BA signaling plays an important pathogenic role in the development of DR. Upregulation or activation of TGR5 may inhibit RhoA/ROCK‐dependent actin remodeling and represent an important therapeutic intervention for DR.
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