Trivalent Nickel-Catalyzing Electroconversion of Alcohols to Carboxylic Acids.

The comprehension of activity and selectivity origins of the electrooxidation of organics is a crucial knot for the development of a highly efficient energy conversion system that can produce value-added chemicals on both the anode and cathode. Here, we find that the potential-retaining trivalent nickel in NiOOH (Fermi level, -7.4 eV) is capable of selectively oxidizing various primary alcohols to carboxylic acids through a nucleophilic attack and nonredox electron transfer process. This nonredox trivalent nickel is highly efficient in oxidizing primary alcohols (methanol, ethanol, propanol, butanol, and benzyl alcohol) that are equipped with the appropriate highest occupied molecular orbital (HOMO) levels (-7.1 to -6.5 eV vs vacuum level) and the negative dual local softness values (Δsk, -0.50 to -0.19) of nucleophilic atoms in nucleophilic hydroxyl functional groups. However, the carboxylic acid products exhibit a deeper HOMO level (<-7.4 eV) or a positive Δsk, suggesting that they are highly stable and weakly nucleophilic on NiOOH. The combination (HOMO, Δsk) is useful in explaining the activity and selectivity origins of electrochemically oxidizing alcohols to carboxylic acid. Our findings are valuable in creating efficient energy conversions to generate value-added chemicals on dual electrodes.

Elucidating the mechanisms underlying astrocyte-microglia crosstalk in hippocampal neuroinflammation induced by acute diquat exposure.

The transition from paraquat (PQ) to diquat (DQ), both organic dication herbicides, in China has led to significant increases in the number of acute DQ poisoning cases. Case studies have shown that acute DQ poisoning resulted in injury to the central nervous system (CNS), but the mechanism underlying the injury remains to be explored. The present study aimed to investigate how DQ influenced purinergic signaling between astrocytes and microglia and whether extracellular ATP (eATP) was involved in promoting neuroinflammation induced by acute DQ toxicity through the activation of the P2X4/NLRP3 signaling pathway. We constructed a rat model of acute DQ toxicity to observe the pathological changes in hippocampal tissues after DQ exposure and measure the expression levels of IL-1ß and TNF-α in the hippocampal tissue. We also established an in vitro co-culture model of C6 astrocytes and BV-2 microglia using transwell chambers, measured the amount of eATP secreted into C6 astrocytes after DQ treatment, and assessed the inflammatory response and changes in the P2X4/NLRP3 signaling pathway in BV-2 microglia. The results showed that the neurons in the hippocampal tissue of rats exhibited loose arrangement, nuclear consolidation, and necrosis after DQ exposure, and IL-1ß and TNF-α levels were signification higher in the hippocampal tissue after DQ exposure. DQ exposure to the co-cultured cells induced an increase in ATP secretion from C6 astrocytes as well as a significant increase of P2X4, NLRP3, IL-1ß, and IL-18 expression in BV-2 microglia. In contrast, pretreatment of C6 astrocytes with apyrase (an ATP hydrolase) resulted in a significant decrease of P2X4, NLRP3, IL-1ß, and IL-18 expression in BV-2 microglia. Furthermore, inhibition of P2X4 expression in BV-2 microglia by transfection with si-P2X4 effectively reversed the increase of NLRP3, IL-1ß, and IL-18 in BV-2 microglia induced by DQ when co-cultured with C6 astrocytes. These results indicate that astrocytes can activate the P2X4/NLRP3 signaling pathway in microglia through the DQ-induced extracellular release of ATP to promote neuroinflammation in rat hippocampal tissue.

Continuous strain tuning of oxygen evolution catalysts with anisotropic thermal expansion.

Compressive strain, downshifting the d-band center of transition metal oxides, is an effective way to accelerate the sluggish kinetics of oxygen evolution reaction (OER) for water electrolysis. Here, we find that anisotropic thermal expansion can produce compressive strains of the IrO6 octahedron in Sr2IrO4 catalyst, thus downshifting its d-band center. Different from the previous strategies to create constant strains in the crystals, the thermal-triggered compressive strains can be real-timely tuned by varying temperature. As a result of the thermal strain accelerating OER kinetics, the Sr2IrO4 exhibits the nonlinear lnjo - T-1 (jo, exchange current density; T, absolute temperature) Arrhenius relationship, resulting from the thermally induced low-barrier electron transfer in the presence of thermal compressive strains. Our results verify that the thermal field can be utilized to manipulate the electronic states of Sr2IrO4 via thermal compressive strains downshifting the d-band center, significantly accelerating the OER kinetics, beyond the traditional thermal diffusion effects.

Nonredox trivalent nickel catalyzing nucleophilic electrooxidation of organics.

A thorough comprehension of the mechanism behind organic electrooxidation is crucial for the development of efficient energy conversion technology. Here, we find that trivalent nickel is capable of oxidizing organics through a nucleophilic attack and electron transfer via a nonredox process. This nonredox trivalent nickel exhibits exceptional kinetic efficiency in oxidizing organics that possess the highest occupied molecular orbital energy levels ranging from -7.4 to -6 eV (vs. Vacuum level) and the dual local softness values of nucleophilic atoms in nucleophilic functional groups, such as hydroxyls (methanol, ethanol, benzyl alcohol), carbonyls (formamide, urea, formaldehyde, glucose, and N-acetyl glucosamine), and aminos (benzylamine), ranging from -0.65 to -0.15. The rapid electrooxidation kinetics can be attributed to the isoenergetic channels created by the nucleophilic attack and the nonredox electron transfer via the unoccupied eg orbitals of trivalent nickel (t2g6eg1). Our findings are valuable in identifying kinetically fast organic electrooxidation on nonredox catalysts for efficient energy conversions.

Native frustrated Lewis pairs on core-shell In@InOxHy enhances CO2-to-formate conversion.

Strategies to efficiently activate CO2 by strongly inhibiting the competitive hydrogen evolution reaction process are highly desired for practical applications of the electrochemical CO2 reduction technique. Here, we assembled a core-shell In@InOxHy architecture on carbon black by one-step reduction of NaBH4 as a CO2-to-formate catalyst with high selectivity. The stable CO2-to-formate reaction originates from the creation of steritic frustrated Lewis pairs (FLPs) on the InOxHy shell with In-OVs (OVs, oxygen vacancies) Lewis acid, and In-OH Lewis base. During CO2 reduction, the electrochemically stable FLPs are capable of first capturing and stabilizing protons to protonate FLPs to In-H Lewis acid and In-OH2 Lewis base due to its strong steric electrostatic field; then, CO2 is captured and activated by the protonated FLPs to selectively produce formate. Our results demonstrated that FLPs can be created on the surface of oxyphilic single-metal catalysts efficient in accelerating CO2 reduction with high selectivity.

Electrochemically stable frustrated Lewis pairs on dual-metal hydroxides for electrocatalytic CO2 reduction.

The sluggish kinetics of CO2 activation and reduction severely limit the energy conversion efficiency of electrocatalytic CO2 reduction into fuels. Here, ZnSn(OH)6 with an alternating arrangement of Zn(OH)6 and Sn(OH)6 octahedral units and SrSn(OH)6 with an alternating arrangement of SrO6 and Sn(OH)6 octahedral units were adopted to check the effects of frustrated Lewis pairs (FLPs) on electrochemical CO2 reduction. The FLPs were in situ electrochemically reconstructed on ZnSn(OH)6 by reducing the electrochemically unstable Sn-OH to Sn-oxygen vacancies (Sn-OVs) as a Lewis acid site, which are able to create strong interactions with the adjacent electrochemically stable Zn-OH, a Lewis base site. Compared to SrSn(OH)6 without FLPs, the higher formate selectivity of ZnSn(OH)6 originates from the strong ability of FLPs to capture protons and activate CO2via the electrostatic field of FLPs triggering better electron transfer and strong orbital interactions under negative potentials. Our findings may guide the design of electrocatalysts for CO2 reduction with high catalytic performances.

A Template Editing Strategy to Create Interlayer-Confined Active Species for Efficient and Durable Oxygen Evolution Reaction.

Substantial overpotentials and insufficient and unstable active sites of oxygen evolution reaction (OER) electrocatalysts limit their efficiency and stability in OER-related energy conversion and storage technologies. Here, a template editing strategy is proposed to graft highly active catalytic species onto highly conductive rigid frameworks to tackle this challenge. As a successful attempt, two types of NiO6 units of layered Ni BDC (BDC stands for 1,4-benzenedicarboxylic acid) metal organic frameworks are selectively edited by chemical etching-assisted electroxidation to create layered γ-NiOOH with intercalated Ni-O species. In such an interlayer-confined intercalated architecture, the large interlayer space with high ion permeability offers an ideal reaction region to sufficiently expose the OER active sites comprising high-density intercalated Ni-O species, which also suppresses the undesirable γ to ß phase transformation, thus exhibiting efficient and durable OER activity. As a result, water oxidation can occur at an extremely low overpotential of 130 mV and affords 1000 h stability at 100 mA cm-2 . The strategy conceptually shows the possibility of achieving stable homogeneous-like catalysis in heterogeneous catalysis.

Ozone causes depressive-like response through PI3K/Akt/GSK3ß pathway modulating synaptic plasticity in young rats.

Ozone pollution has been associated with several adverse effects, including memory impairment, intellectual retardation, emotional disturbances. However, the potential mechanisms remain uncertain. The present study aimed to investigate whether ozone (O3) regulates synaptic plasticity through PI3K/Akt/GSK3ß signaling pathway and induces neurobehavioral modifications among the young rats. In vivo, the newborn rats were used to construct the animal model of early postnatal O3 treatment. In vitro, this study measured the effect of different concentrations of serum from O3 treated rats on the viability of the PC12 cells, and investigated the modifications of synaptic plasticity and PI3K/Akt/GSK3ß signaling pathway in the hippocampus and PC12 cells after O3 treated. The results revealed significant depression-like behavior and increased hippocampal histopathological damage in the young rats after O3 treated. Compared with the control group, the expression levels of synaptic related proteins including Drebrin, PSD95, Synaptophysin and PIK3R1, p-Akt, and p-GSK3ß were decreased in the O3 treated group. In vitro assays, a significant reduction in Drebrin, PSD95, Synaptophysin, PIK3R1, p-Akt, and p-GSK3ß was found in PC12 cells after O3 serum treated. While 740Y-P (a specific PI3K activator) administered, the expression levels of Drebrin, PSD95, Synaptophysin, PIK3R1, p-Akt, and p-GSK3ß in the 740Y-P + O3 group were significantly elevated in vivo and vitro compared with the O3-only group. In addition, miRNAs modulating PIK3R1 were screened on bioinformatics website, the study found aberrant expression of miR-221-3p in the hippocampus and serum of O3 treated group. Inhibition of miR-221-3p expression effectively reversed the reduction of Drebrin, PSD95, Synaptophysin, PIK3R1, p-Akt, and p-GSK3ß in PC12 cells induced by O3 treatment. Altogether, these studies indicate that O3 restrained the expression of PI3K/Akt/GSK3ß signaling pathway and impaired synaptic plasticity that resulted in depressive-like behavior in young rats. Moreover, miR-221-3p plays an important role in this procedure by regulating PIK3R1.

JAK2/STAT3 pathway regulates microglia polarization involved in hippocampal inflammatory damage due to acute paraquat exposure.

OBJECTIVE: To explore the effects of acute paraquat (PQ) exposure on the phenotypic polarization of hippocampal microglia and its mechanism. METHODS: An acute PQ exposure rat model was established. Male SD rats were exposed to 0, 5, 25, and 50 mg/kg PQ, and brain hippocampal tissue was collected after 1, 3, and 7 days of exposure, respectively. Hippocampal pathological changes were examined by H&E staining, and immunohistochemistry (IHC) was used to detect changes in the number of Iba-1-positive cells, the average number of endpoints, and the average process length. The protein expression of Iba-1 was detected by western blotting. BV-2 microglia were treated with 0, 0.01, 0.025, 0.05, or 0.1 µmol/L PQ for 24 h. ELISA and western blotting assays were performed to detect the expression of TNF-α and IL-1ß in vivo and in vitro. The M1 microglia marker iNOS, the M2 microglia marker Arg-1, and the p-JAK2 and p-STAT3 protein were detected by western blotting. JAK2/STAT3 pathway activation role in regulating microglia phenotypic polarization was further validated in vivo and in vitro by JAK2-specific inhibitor AG490 administration. RESULTS: After acute PQ exposure, hippocampal neurons showed pathological changes such as loose arrangement and nuclear pyknosis, the number of Iba-1 positive cells and the expression of Iba-1 protein increased, and the average number of endpoints and average process length of microglia decreased. Histological examination revealed that compared with the control group, in the 50 mg/kg PQ group on the 3rd and 7th day, the expression of TNF-α, IL-1ß, and iNOS significantly increased, while that of Arg-1 significantly decreased. p-JAK2 and p-STAT3 expression significantly increased in the 50 mg/kg PQ group on the 1st, 3rd, and 7th day. In vitro, compared with the control group, the expression of TNF-α, IL-1ß, iNOS, p-JAK2, and p-STAT3 significantly increased, while Arg-1 expression was significantly reduced in the 0.025, 0.05, and 0.1 µmol/L PQ groups. After AG490 administration, the expression levels of p-JAK2, p-STAT3, iNOS, TNF-α, and IL-1ß in the AG490 +PQ group were significantly inhibited in vivo and in vitro compared with the PQ-only group. On the contrary, Arg-1 expression was significantly increased. CONCLUSION: Our results suggest that acute PQ exposure may induce M1-type polarization of hippocampal microglia by activating the JAK2/STAT3 pathway, which in turn releases pro-inflammatory factors such as TNF-α and IL-1ß, leading to hippocampal inflammatory damage.

N-Doped Graphene-Coated Commercial Pt/C Catalysts toward High-Stability and Antipoisoning in Oxygen Reduction Reaction.

Stability and antipoisoning effects are the main challenges for the application of commercial Pt/C catalysts. Herein, we soaked and adsorbed polydopamine to coat Pt particles on commercial Pt/C and subsequently converted the coatings to few-layer N-doped graphene by calcination to produce Pt/C@NC. The coatings effectively block the direct contact of Pt nanoparticles and electrolyte, thus enhancing the catalyst stability by avoiding Ostwald ripening and suppressing the competitive adsorption of toxicants, contributing to the enhancement of the antipoisoning ability. More importantly, the coatings do not hurt the oxygen reduction reaction (ORR) activity of commercial Pt/C, which exhibits a half wave potential of 0.84 V in an acidic electrolyte. The spectroscopic and theoretical results confirmed that the coatings originate from a strong Pt bonding to pyridinic N of N-doped graphene and that the high ORR activity results from the coordinately unsaturated carbon atoms, as the real ORR active sites, to strongly capture electrons from Pt.