Metal–organic frameworks (MOFs) with carboxylate ligands as co‐catalysts are very efficient for the oxygen evolution reaction (OER). However, the role of local adsorbed carboxylate ligands around the ...in‐situ‐transformed metal (oxy)hydroxides during OER is often overlooked. We reveal the extraordinary role and mechanism of surface‐adsorbed carboxylate ligands on bi/trimetallic layered double hydroxides (LDHs)/MOFs for OER electrocatalytic activity enhancement. The results of X‐ray photoelectron spectroscopy (XPS), synchrotron X‐ray absorption spectroscopy, and density functional theory (DFT) calculations show that the carboxylic groups around metal (oxy)hydroxides can efficiently induce interfacial electron redistribution, facilitate an abundant high‐valence state of nickel species with a partially distorted octahedral structure, and optimize the d‐band center together with the beneficial Gibbs free energy of the intermediate. Furthermore, the results of in situ Raman and FTIR spectra reveal that the surface‐adsorbed carboxylate ligands as Lewis base can promote sluggish OER kinetics by accelerating proton transfer and facilitating adsorption, activation, and dissociation of hydroxyl ions (OH−).
In the oxygen evolution reaction (OER), surface‐adsorbed carboxylate ligands on bi/trimetallic layered double hydroxides (LDHs)/MOFs demonstrate a synergistic effect. As a Lewis base the carboxylate ligands promote the sluggish OER by accelerating proton transfer and facilitating adsorption, activation, and dissociation of OH− ions, while also facilitating intrinsic electron redistribution and a partially distorted octahedral structure.
The integration of Fe dopant and interfacial FeOOH into Ni‐MOFs Fe‐doped‐(Ni‐MOFs)/FeOOH to construct Fe−O−Ni−O−Fe bonding is demonstrated and the origin of remarkable electrocatalytic performance of ...Ni‐MOFs is elucidated. X‐ray absorption/photoelectron spectroscopy and theoretical calculation results indicate that Fe‐O−Ni−O−Fe bonding can facilitate the distorted coordinated structure of the Ni site with a short nickel–oxygen bond and low coordination number, and can promote the redistribution of Ni/Fe charge density to efficiently regulate the adsorption behavior of key intermediates with a near‐optimal d‐band center. Here the Fe‐doped‐(Ni‐MOFs)/FeOOH with interfacial Fe−O−Ni−O−Fe bonding shows superior catalytic performance for OER with a low overpotential of 210 mV at 15 mA cm−2 and excellent stability with ≈3 % attenuation after a 120 h cycle test. This study provides a novel strategy to design high‐performance Ni/Fe‐based electrocatalysts for OER in alkaline media.
Iron doping and FeOOH decorating leads to interfacial Fe−O−Ni−O−Fe bonding in Fe‐doped‐(Ni‐MOF)/FeOOH. This interfacial bonding can regulate the active Ni site to give the appropriate adsorption behavior of intermediates for the oxygen evolution reaction (OER). As a result, Fe‐doped‐(Ni‐MOF)/FeOOH shows outstanding catalytic performance with low overpotential, small Tafel slope, and high durability.
The intrinsic activity of NiFe layer double hydroxides (LDHs) for the oxygen evolution reaction (OER) suffers from its predominantly exposed (003) basal plane, which is thought to have poor activity. ...Herein, we construct a hierarchal structure of NiFe LDH nanosheet-arrays-on-microplates (NiFe NSAs-MPs) to elevate the electrocatalytic activity of NiFe LDHs for the OER by exposing a high-activity plane, such as the (012) edge plane. It is surprising that the NiFe NSAs-MPs show activity of 100 mA cm
−2
at an overpotential (
η
) of 250 mV, which is five times higher than that of (003) plane-dominated NiFe LDH microsheet arrays (NiFe MSAs) at the same
η
, representing the excellent electrocatalytic activity for the OER in alkaline media. Besides, we analyzed the OER activities of the (003) basal plane and the (012) and (110) edge planes of NiFe LDHs by density functional theory with on-site Coulomb interactions (DFT+U), and the calculation results indicated that the (012) edge plane exhibits the best catalytic performance among the various crystal planes because of the oxygen coordination of the Fe site, which is responsible for the high catalytic activity of NiFe NSAs-MPs.
The (012) edge plane of NiFe layer double hydroxides (LDHs) has been proven to be a highly active plane for water oxidation.
In the process of oxygen evolution reaction (OER) on perovskite, it is of great significance to accelerate the hindered lattice oxygen oxidation process to promote the slow kinetics of water ...oxidation. In this paper, a facile surface modification strategy of nanometer-scale iron oxyhydroxide (FeOOH) clusters depositing on the surface of LaNiO
3
(LNO) perovskite is reported, and it can obviously promote hydroxyl adsorption and weaken Ni-O bond of LNO. The above relevant evidences are well demonstrated by the experimental results and DFT calculations. The excellent hydroxyl adsorption ability of FeOOH-LaNiO
3
(Fe-LNO) can obviously optimize OH
-
filling barriers to promote lattice oxygen-participated OER (LOER), and the weakened Ni-O bond of LNO perovskite can obviously reduce the reaction barrier of the lattice oxygen participation mechanism (LOM). Based on the above synergistic catalysis effect, the Fe-LNO catalyst exhibits a maximum factor of 5 catalytic activity increases for OER relative to the pristine perovskite and demonstrates the fast reaction kinetics (low Tafel slope of 42 mV dec
-1
) and superior intrinsic activity (TOFs of ~40 O
2
S
-1
at 1.60 V vs. RHE).
Rational
Minocycline is a second-generation, semi-synthetic tetracycline, and has broad spectrum-antibacterial activity. Interestingly, many studies have demonstrated that minocycline is beneficial ...for depression, which may be due to its effects on neuroinflammation modulation. Recently, gut microbiota imbalance has been found in depression patient and animal models.
Objectives
Based on the fact of minocycline usually acting as an antibiotic and the relationship between depression, gut microbiota, and neuroinflammation, we designed this study to detect the effects of chronic minocycline treatment on antidepression, neuroinflammation, and gut microbiota modulation.
Results
Our results showed that minocycline treatment for 4 weeks, not acute treatment, exerted antidepressant effect in mice exposed to unpredictable chronic mild stress (CUMS). Further results suggested that chronic minocycline treatment inhibited neuroinflammation of hippocampus and altered species abundance and metabolites of gut microbiota. Meantime, we found that chronic minocycline treatment ameliorated intestinal barrier disruption and reduced the bacteriological indexes, such as diamine oxidase, C-reaction protein, and endotoxin in peripheral blood of CUMS mice.
Conclusions
To sum up, our findings confirm that chronic minocycline treatment exerts the antidepressant effect, inhibits neuroinflammation, and modulates gut microbiota. All of these imply that the antidepressant mechanism of chronic minocycline treatment is maybe due to the combined action of neuroinflammation and gut microbiota modulation, which need further prospective studies.
Astronauts exposed to a gravity-free environment experience cardiovascular deconditioning that causes post-spaceflight orthostatic intolerance and other pathological conditions. Endothelial ...dysfunction is an important factor responsible for this alteration. Our previous study showed enhanced autophagy in endothelial cells under simulated microgravity. The present study explored the cytoprotective role of autophagy under microgravity in human umbilical vein endothelial cells (HUVECs). We found that clinorotation for 48 h induced apoptosis and endoplasmic reticulum (ER) stress in HUVECs. ER stress and the unfolded protein response (UPR) partially contributed to apoptosis under clinorotation. Autophagy partially reduced ER stress and restored UPR signaling by autophagic clearance of ubiquitin-protein aggregates, thereby reducing apoptosis. In addition, the ER stress antagonist 4-phenylbutyric acid upregulated autophagy in HUVECs. Taken together, these findings indicate that autophagy plays a protective role against apoptosis under clinorotation by clearing protein aggregates and partially restoring the UPR.
•Chronic minocycline treatment reduces the anxiety-like behaviors induced by repeated restraint stress in mice.•Minocycline inhibites the microglia activation, and decreases the levels of IL-6 and ...TNF-α in the amygdala.•PPAR-γ/NF-κB pathway in the amygdala is involved in the modulation of the anxiolytic effects of minocycline.•Minocycline may exert the anxiolytic effects through modulating neuroinflammation.
Anxiety disorders are chronic, disabling conditions across the world, and bring a great burden to individuals and society. Although advances have been made in understanding of the pathophysiology of these diseases, no mechanistically new drugs for anxiety disorders have reached the market in the past two decades. Some evidence indicates that stress increases neuroinflammatory signaling, which is related to the development of anxiety and depression. Minocycline, a broad-spectrum tetracycline-antibiotic, has been reported to suppress microglia activation-mediated brain endogenous inflammation. However, it is still unknown whether minocycline can be developed to treat stress-induced anxiety disorders and what is the underlying mechanisms. We chose the anxiety model induced by repeated stress consisting of 2 h of restraint on each of 7 consecutive days. The behavioral test results showed that chronic minocycline treatment, not acute minocycline treatment, increased the time spent in the center area in the open field test and the number of open arm entries and time spent in open arms in the elevated plus maze test, which were comparable with the effect of buspirone. Further mechanism studies demonstrated that chronic minocycline treatment inhibited the microglia activation and decreased the levels of interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α). In addition, peroxisome proliferator-activated receptor gamma/ nuclear factor kappa B (PPAR-γ/NF-κB) signaling pathway was also modulated by chronic minocycline treatment. In conclusion, our findings support the hypothesis that immune dysregulation plays an important role in stress-induced anxiety disorders, and minocycline can be developed to be used in these diseases.
Individuals exposed to long-term spaceflight often experience cardiovascular dysfunctions characterized by orthostatic intolerance, disability on physical exercise, and even frank syncope. Recent ...studies have showed that the alterations of cardiovascular system are closely related to the functional changes of endothelial cells. We have shown previously that autophagy can be induced by simulated microgravity in human umbilical vein endothelial cells (HUVECs). However, the mechanism of enhanced autophagy induced by simulated microgravity and its role in the regulation of endothelial function still remain unclear. We report here that 48 h clinorotation promoted cell migration in HUVECs by induction of autophagy. Furthermore, clinorotation enhanced autophagy by the mechanism of human murine double minute 2 (HDM2)-dependent degradation of cytoplasmic p53 at 26S proteasome, which results in the suppression of mechanistic target of rapamycin (mTOR), but not via activation of AMPK in HUVECs. These results support the key role of HDM2-p53 in direct downregulation of mTOR, but not through AMPK in microgravity-induced autophagy in HUVECs.
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•Ru nanoparticles incorporated into Ni-MOFs and in situ self-assembly grew on the surface of NF.•The formation of Ru-O-Ni interfacial bond at Ru@Ni-MOFs is beneficial for interfacial ...electron transfer.•The form of –COOHOH-Ru can reduce dissociation energy and promote sluggish HER reaction kinetics.•Ru@Ni-MOFs/NF shows superior catalytic performance for HER in alkaline media.
The M@Ni metal–organic frameworks (MOFs) (M = Ru, Pt, Ir, etc.) have been widely recognized as the outstanding electrocatalysts for hydrogen evolution reaction (HER). However, the mechanism of alkaline HER on M@Ni-MOFs remains ambiguous. Here, taking Ru@Ni-MOFs/NF as an example, its HER synergistic catalytic mechanism has been revealed by in situ FT-IR/Raman spectra, H/D isotope experiments, methanol/SCN− poisoning experiments and DFT calculations. Namely, the carboxylate ligands in Ru@Ni-MOFs/NF, apart from regulating the local electronic structure of surface sites, can be used as a Lewis base that exhibits strong affinity toward H2O via intermediate state of –COO-H-OH and subsequently promotes water transfer/activation/dissociation via the form of –COOHOH-Ru with a low kinetic energy barrier. Ru@Ni-MOFs/NF shows a low overpotential of 25 mV at 10 mA cm−2 with a small Tafel slope (31 mV dec−1) and excellent stability.
Microgravity leads to hydrodynamic alterations in the cardiovascular system and is associated with increased angiogenesis, an important aspect of endothelial cell behavior to initiate new vessel ...growth. Given the critical role of Rho GTPase-dependent cytoskeleton rearrangement in cell migration, small GTPase RhoA might play a potential role in microgravity-induced angiogenesis.
We examined the organization of actin filaments by FITC-conjugated phalloidin staining, as well as the expression and activity of RhoA by quantitative PCR and Western blot, in human umbilical vein endothelial cells (HUVECs) under normal gravity and simulated microgravity. Effect of simulated microgravity on the wound closure and tube formation in HUVECs, and their dependence on RhoA, were also analyzed by cell migration and tube formation assays.
We show that in HUVECs actin filaments are disorganized and RhoA activity is reduced by simulated microgravity. Blocking RhoA activity either by C3 transferase Rho inhibitor or siRNA knockdown mimicked the effect of simulated microgravity on inducing actin filament disassembly, followed by enhanced wound closure and tube formation in HUVECs, which closely resembled effects seen on microgravity-treated cells. In contrast, overexpressing RhoA in microgravity-treated HUVECs restored the actin filaments, and decreased wound closure and tube formation abilities.
These results suggest that RhoA inactivation is involved in the actin rearrangement-associated angiogenic responses in HUVECs during simulated microgravity.
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