A Facile Li_(2)TiO_(3) Surface Modification to Improve the Structure Stability and Electrochemical Performance of Full Concentration Gradient Li-Rich Oxides

Full concentration gradient lithium-rich layered oxides are catching lots of interest as the next generation cathode for lithium-ion batteries due to their high discharge voltage,reduced voltage decay and enhanced rate performance,whereas the high lithium residues on its surface impairs the structure stability and long-term cycle performance.Herein,a facile multifunctional surface modification method is implemented to eliminate surface lithium residues of full concentration gradient lithium-rich layered oxides by a wet chemistry reaction with tetrabutyl titanate and the post-annealing process.It realizes not only a stable Li_(2)TiO_(3)coating layer with 3D diffusion channels for fast Li^(+)ions transfer,but also dopes partial Ti^(4+)ions into the sub-surface region of full concentration gradient lithium-rich layered oxides to further strengthen its crystal structure.Consequently,the modified full concentration gradient lithium-rich layered oxides exhibit improved structure stability,elevated thermal stability with decomposition temperature from 289.57℃to 321.72℃,and enhanced cycle performance(205.1 mAh g^(-1)after 150 cycles)with slowed voltage drop(1.67 mV per cycle).This work proposes a facile and integrated modification method to enhance the comprehensive performance of full concentration gradient lithium-rich layered oxides,which can facilitate its practical application for developing higher energy density lithium-ion batteries.

Acquired sensorineural hearing loss,oxidative stress,and microRNAs

Hearing loss is the third leading cause of human disability.Age-related hearing loss,one type of acquired sensorineural hearing loss,is largely responsible for this escalating global health burden.Noise-induced,ototoxic,and idiopathic sudden sensorineural are other less common types of acquired hearing loss.The etiology of these conditions is complex and multi-fa ctorial involving an interplay of genetic and environmental factors.Oxidative stress has recently been proposed as a likely linking cause in most types of acquired sensorineural hearing loss.Short non-coding RNA sequences known as microRNAs(miRNAs)have increasingly been shown to play a role in cellular hypoxia and oxidative stress responses including promoting an apoptotic response.Sensory hair cell death is a central histopathological finding in sensorineural hearing loss.As these cells do not regenerate in humans,it underlies the irreversibility of human age-related hearing loss.Ovid EMBASE,Ovid MEDLINE,Web of Science Core Collection,and ClinicalTrials.gov databases over the period August 1,2018 to July 31,2023 were searched with"hearing loss,""hypoxamiRs,""hypoxia,""microRNAs,""ischemia,"and"oxidative stress"text words for English language primary study publications or registered clinical trials.Registe red clinical trials known to the senior author we re also assessed.A total of 222studies were thus identified.After excluding duplicates,editorials,retra ctions,secondary research studies,and non-English language articles,39 primary studies and clinical trials underwent full-text screening.This resulted in 11 animal,in vitro,and/or human subject journal articles and 8 registered clinical trial database entries which form the basis of this narrative review.MiRNAs miR-34a and miR-29b levels increase with age in mice.These miRNAs were demonstrated in human neuroblastoma and murine cochlear cell lines to target Sirtuin 1/peroxisome proliferato r-activated receptor gamma coactivator-1-alpha(SIRT1/P GC-1α),SIRT1p53,and SIRT1/hypoxia-inducible factor 1-alpha signaling pathways resulting in increased apoptosis.Furthermore,hypoxia and oxidative stress had a similar adve rse apoptotic effect,which was inhibited by resve ratrol and a myocardial inhibitorassociated transcript,a miR-29b competing endogenous mRNA.Gentamicin reduced miR-182-5p levels and increased cochlear oxidative stress and cell death in mice-an effect that was corrected by inner ear stem cell-derived exosomes.There is ongoing work seeking to determine if these findings can be effectively translated to humans.

Targeting sepsis through inflammation and oxidative metabolism

Infection is a public health problem and represents a spectrum of disease that can result in sepsis and septic shock.Sepsis is characterized by a dysregulated immune response to infection.Septic shock is the most severe form of sepsis which leads to distributive shock and high mortality rates.There have been significant advances in sepsis management mainly focusing on early identification and therapy.However,complicating matters is the lack of reliable diagnostic tools and the poor specificity and sensitivity of existing scoring tools i.e.,systemic inflammatory response syndrome criteria,sequential organ failure assessment(SOFA),or quick SOFA.These limitations have underscored the modest progress in reducing sepsis-related mortality.This review will focus on novel therapeutics such as oxidative stress targets,cytokine modulation,endothelial cell modulation,etc.,that are being conceptualized for the management of sepsis and septic shock.

Mechanism, modification and stability of tungsten oxide-based electrocatalysts for water splitting: A review

Electrocatalysis plays a crucial role in the field of clean energy conversion and provides essential support for the development of eco-friendly technology. There is a pressing need for electrocatalysts in renewable energy systems that exhibit exceptional activity, selectivity, stability, and economic viability. The utilization of metal oxides as electrocatalysts for the process of water splitting has made substantial progress in both theoretical and practical aspects and has emerged as a widely explored field of research. Tungsten oxides(WO_(x)) have attracted much attention and are regarded as a highly promising electrocatalytic material due to their exceptional electrocatalytic activity, cost-effectiveness, and ability to withstand extreme conditions. This review introduces the fundamental mechanism of WOx-based electrocatalysts for the hydrogen evolution reaction and the oxygen evolution reaction, providing a comprehensive overview of recent research advancements in their modification. Factors contributing to the catalytic activity and stability of WOxare explored, highlighting their potential for industrial applications. The aim herein is to provide guidelines for the design and fabrication of WOx-based electrocatalysts, thereby facilitating further research on their mechanistic properties and stability improvements in water splitting.

Enhancing m^(6)A modification in the motor cortex facilitates corticospinal tract remodeling after spinal cord injury

Spinal cord injury typically causes corticospinal tract disruption. Although the disrupted corticospinal tract can self-regenerate to a certain degree, the underlying mechanism of this process is still unclear. N6-methyladenosine(m^(6)A) modifications are the most common form of epigenetic regulation at the RNA level and play an essential role in biological processes. However, whether m^(6)A modifications participate in corticospinal tract regeneration after spinal cord injury remains unknown. We found that expression of methyltransferase 14 protein(METTL14) in the locomotor cortex was high after spinal cord injury and accompanied by elevated m^(6)A levels. Knockdown of Mettl14 in the locomotor cortex was not favorable for corticospinal tract regeneration and neurological recovery after spinal cord injury. Through bioinformatics analysis and methylated RNA immunoprecipitation-quantitative polymerase chain reaction, we found that METTL14 regulated Trib2 expression in an m^(6)A-regulated manner, thereby activating the mitogen-activated protein kinase pathway and promoting corticospinal tract regeneration. Finally, we administered syringin, a stabilizer of METTL14, using molecular docking. Results confirmed that syringin can promote corticospinal tract regeneration and facilitate neurological recovery by stabilizing METTL14. Findings from this study reveal that m^(6)A modification is involved in the regulation of corticospinal tract regeneration after spinal cord injury.

New perspectives on DNA methylation modifications in ocular diseases

The methylation of DNA is a prevalent epigenetic modification that plays a crucial role in the pathological progression of ocular diseases.DNA methylation can regulate gene expression,thereby affecting cell function and signal transduction.Ophthalmic diseases are a kind of complex diseases,and their pathogenesis involves many factors such as genetic,environmental and individual differences.In addition,inflammation,oxidative stress and lipid metabolism,which abnormal DNA methylation is closely related to,are also considered to be major factors in eye diseases.The current understanding of DNA methylation in eye diseases is becoming more complex and comprehensive.In addition to the simple suppression of gene expression by hypermethylation,factors such as hypomethylation or demethylation,DNA methylation in non-promoter regions,interactions with other epigenetic modifications,and dynamic changes in DNA methylation must also be considered.Interestingly,although some genes are at abnormal methylation levels,their expression is not significantly changed,which indirectly reflects the complexity of gene regulation.This review aims to summarize and compare some relevant studies,and provide with new ideas and methods for the prevention and treatment of different eye diseases,such as glaucoma,retinoblastoma,and diabetic retinopathy.

Diabetes mellitus and glymphatic dysfunction:Roles for oxidative stress,mitochondria,circadian rhythm,artificial intelligence,and imaging

Diabetes mellitus(DM)is a debilitating disorder that impacts all systems of the body and has been increasing in prevalence throughout the globe.DM represents a significant clinical challenge to care for individuals and prevent the onset of chronic disability and ultimately death.Underlying cellular mechanisms for the onset and development of DM are multi-factorial in origin and involve pathways associated with the production of reactive oxygen species and the generation of oxidative stress as well as the dysfunction of mitochondrial cellular organelles,programmed cell death,and circadian rhythm impairments.These pathways can ultimately involve failure in the glymphatic pathway of the brain that is linked to circadian rhythms disorders during the loss of metabolic homeostasis.New studies incorporate a number of promising techniques to examine patients with metabolic disorders that can include machine learning and artificial intelligence pathways to potentially predict the onset of metabolic dysfunction.

Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2

The pathophysiology of Huntington's disease involves high levels of the neurotoxin quinolinic acid. Quinolinic acid accumulation results in oxidative stress, which leads to neurotoxicity. However, the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington's disease pathology remain unknown. In this study, we established in vitro and in vivo models of Huntington's disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice, respectively. We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum, which was accompanied by down-regulation of cystathionine β-synthase, an enzyme responsible for hydrogen sulfide production. However, treatment with NaHS(a hydrogen sulfide donor) increased hydrogen sulfide levels in the neurons and in mouse serum, as well as cystathionine β-synthase expression in the neurons and the mouse striatum, while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum. These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression. Finally, treatment with the nuclear factor erythroid 2-related factor 2inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress. Taken together, our findings show that hydrogen sulfide reduces oxidative stress in Huntington's disease by activating nuclear factor erythroid 2-related factor 2,suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington's disease.

KEAP1 inhibitor-scutellarin-based liposomes serve as an antioxidant switch foroxidative stress induced by ischemic stroke injury

Background:Ischemic stroke is a disease characterized by the damage of brain tissue due to insufficient blood supply.The neuronal necrosis caused by oxidative stress during the acute phase of ischemic stroke leads to serious consequences,including blood-brain barrier disruption and vascular aging.The Kelch-like ECH-associated protein 1(KEAP1),is a key switch of antioxidative system in human body.Until now,there is still a lack of effective treatment to ischemic stroke.Methods:We developed scutellarin-based liposomes for treating ischemic stroke injury caused neuronal damage.Results:The results showed that scutellarin could directly bind to KEAP1 protein,and the Kd was 26.1μM.The scutellarin-based liposomes significantly reduced cellular reactive oxygen species(ROS)levels.It could also upregulate the protein expression level of nuclear factor E2-related factor 2(NRF2),which is the substrate protein of KEAP1.Next,both the mRNA and protein expression level of the NRF2 downstream anti-oxidative element,heme oxygenase 1(HO-1)and NAD(P)H quinone dehydrogenase 1(NQO1)were promoted.Furthermore,the coimmunoprecipitation(Co-IP)and hydrogen-deuterium exchange mass spectrometry(HDX-MS)revealed that scutellarin directly bound to KEAP1’s Kelch domain,interrupting the interaction between KEAP1 and NRF2.Conclusion:Our work indicates that the scutellarin-based liposomes might be a promising therapeutic approach for ischemic stroke induced neuronal necrosis.

Surface modification of fabrics using dielectric barrier discharge plasma for improved antifouling performance

Surface modification of fabrics is an effective way to endow them with antifouling properties while still maintaining their key advantages such as comfort,softness and stretchability.Herein,an atmospheric pressure dielectric barrier discharge(DBD)plasma method is demonstrated for the processing of silk fabrics using 1H,1H,2H,2H-perfluorodecyltriethoxysilane(PFDS)as the precursor.The results showed the successful grafting of PFDS groups onto the surface of silk fabrics without causing damage.Meanwhile,the gas temperature is rather low during the whole processing procedure,suggesting the non-equilibrium characteristics of DBD plasma.The influence on fabrics of the processing parameters(PFDS concentration,plasma treatment time and plasma discharge power)was systematically investigated.An optimum processing condition was determined to be a PFDS concentration of 8wt%,a plasma processing time of 40 s and a plasma power of 11.87 W.However,with prolonged plasma processing time or enhanced plasma power,the plasma-grafted PFDS films could be degraded.Further study revealed that plasma processing of silk fabrics with PFDS would lead to a change in their chemical composition and surface roughness.As a result,the surface energy of the fabrics was reduced,accompanied by improved water and oil repellency as well as enhanced antifouling performance.Besides,the plasma-grafted PFDS films also had good durability and stability.By extending the method to polyester and wool against different oil-/water-based stains,the DBD plasma surface modification technique demonstrated good versatility in improving the antifouling properties of fabrics.This work provides guidance for the surface modification of fabrics using DBD plasma to confer them with desirable functionalities.

Review of rare earth oxide doping-modified laser cladding of Fe-based alloy coatings

Conventional Fe-C alloy parts used in mechanical transmission and braking systems exposed to the external environment often suffer from wear and corrosion failures.Surface coating strengthening technologies have been explored to improve the surface performance and prolong service life of these parts.Among these technologies,laser cladding has shown promise in producing Fe-based alloy coatings with superior interfacial bonding properties to the Fe-C alloy substrate.Additionally,the microstructure of the Fe-based alloy coating is more uniform and the grain size is finer than that of surfacing welding,thermal spraying,and plasma cladding,and the oxide film of alloying elements on the coating surface can improve the coating performance.However,Fe-based alloy coatings produced by laser cladding typically exhibit lower hardness,lower wear resistance,corrosion resistance,and oxidation resistance compared to coatings based on Co and Ni alloys.Moreover,these coatings are susceptible to defects such as pores and cracks.To address these limitations,the incorporation of rare-earth oxides through doping in the laser cladding process has garnered significant attention.This approach has demonstrated substantial improvements in the microstructure and properties of Fe-based alloy coatings.This paper reviewed recent research on the structure and properties of laser-cladded Fe-based alloy coatings doped with various rare earth oxides,including La_(2)O_(3),CeO_(2),and Y_(2)O_(3).Specifically,it discussed the effects of rare earth oxides and their concentrations on the structure,hardness,friction,wear,corrosion,and oxidation characteristics of these coatings.Furthermore,the mechanisms by which rare earth oxides influence the coating’s structure and properties were summarized.This review aimed to serve as a valuable reference for the application and advancement of laser cladding technology for rare earth modified Fe-based alloy coatings.

Nogo-A Protein Mediates Oxidative Stress and Synaptic Damage Induced by High-Altitude Hypoxia in the Rat Hippocampus

Objective High-altitude hypoxia exposure often damages hippocampus-dependent learning and memory.Nogo-A is an important axonal growth inhibitory factor.However,its function in high-altitude hypoxia and its mechanism of action remain unclear.Methods In an in vivo study,a low-pressure oxygen chamber was used to simulate high-altitude hypoxia,and genetic or pharmacological intervention was used to block the Nogo-A/NgR1 signaling pathway.Contextual fear conditioning and Morris water maze behavioral tests were used to assess learning and memory in rats,and synaptic damage in the hippocampus and changes in oxidative stress levels were observed.In vitro,SH-SY5Y cells were used to assess oxidative stress and mitochondrial function with or without Nogo-A knockdown in Oxygen Glucose-Deprivation/Reperfusion(OGD/R)models.Results Exposure to acute high-altitude hypoxia for 3 or 7 days impaired learning and memory in rats,triggered oxidative stress in the hippocampal tissue,and reduced the dendritic spine density of hippocampal neurons.Blocking the Nogo-A/NgR1 pathway ameliorated oxidative stress,synaptic damage,and the learning and memory impairment induced by high-altitude exposure.Conclusion Our results demonstrate the detrimental role of Nogo-A protein in mediating learning and memory impairment under high-altitude hypoxia and suggest the potential of the Nogo-A/NgR1 signaling pathway as a crucial therapeutic target for alleviating learning and memory dysfunction induced by high-altitude exposure.

Oxidative modification of caspase-9 facilitates its activation via disulfide-mediated interaction with Apaf-1

Intracellular reactive oxygen species （ROS） are known to regulate apoptosis. Activation of caspase-9, the initial caspase in the mitochondrial apoptotic cascade, is closely associated with ROS, but it is unclear whether ROS regulate caspase-9 via direct oxidative modification. The present study aims to elucidate the molecular mechanisms by which ROS mediate caspase-9 activation. Our results show that the cellular oxidative state facilitates caspase-9 activation. Hydrogen peroxide treatment causes the activation of caspase-9 and apoptosis, and promotes an interac- tion between easpase-9 and apoptotic protease-activating factor 1 （Apaf-1） via disulfide formation. In addition, in an in vitro mitochondria-free system, the thiol-oxidant diamide promotes auto-cleavage of caspase-9 and the caspase-9/ Apaf-1 interaction by facilitating the formation of disulfide-linked complexes. Finally, a point mutation at C403 of caspase-9 impairs both H2O2-promoted caspase-9 activation and interaction with Apaf-1 through the abolition of disulfide formation. The association between cytochrome c and the C403S mutant is significantly weaker than that between cytochrome c and wild-type caspase-9, indicating that oxidative modification of caspase-9 contributes to apoptosome formation under oxidative stress. Taken together, oxidative modification of caspase-9 by ROS can medi- ate its interaction with Apaf-1, and can thus promote its auto-cleavage and activation. This mechanism may facilitate apoptosome formation and caspase-9 activation under oxidative stress.

Improved Efficiency and Stability of Organic Solar Cells by Interface Modification Using Atomic Layer Deposition of Ultrathin Aluminum Oxide

The interfacial contacts between the electron transporting layers(ETLs)and the photoactive layers are crucial to device performance and stability for OSCs with inverted architecture.Herein,atomic layer deposition(ALD)fabricated ultrathin Al_(2)O_(3)layers are applied to modify the ETLs/active blends(PM6:BTP-BO-4F)interfaces of OSCs,thus improving device performance.The ALD-Al_(2)O_(3)thin layers on ZnO significantly improved its surface morphology,which led to the decreased work function of ZnO and reduced recombination losses in devices.The simultaneous increase in open-circuit voltage(V_(OC)),short-circuit current density(J_(SC))and fill factor(FF)were achieved for the OSCs incorporated with ALD-Al_(2)O_(3)interlayers of a certain thickness,which produced a maximum PCE of 16.61%.Moreover,the ALD-Al_(2)O_(3)interlayers had significantly enhanced device stability by suppressing degradation of the photoactive layers induced by the photocatalytic activity of ZnO and passivating surface defects of ZnO that may play the role of active sites for the adsorption of oxygen and moisture.

Ultrahydrophobic melamine sponge via interfacial modification with reduced graphene oxide/titanium dioxide nanocomposite and polydimethylsiloxane for oily wastewater treatment

Three-dimensional(3D)porous absorbents have attracted significant attention in the oily wastewater treatment technology due to their high porosity and elasticity.Given their amphiphilic surface,they have a propensity to simultaneously absorb water and oil,which restricts their range of applications.In this study,a reduced graphene oxide and titanium dioxide nanocomposite(rGO/TiO_(2))was used to fabricate an ultra-hydrophobic melamine sponge(MS)through interfacial modification using a solution immersion technique.To further modify it,poly-dimethylsiloxane(PDMS)was grafted onto its surface to establish stronger covalent bonds with the composite.The water contact angle of the sponge(rGO/TiO_(2)/PDMS/MS)was 164.2°,which satisfies the condition for ultrahydrophobicity.The evidence of its water repellency was demonstrated by the Cassie-Baxter theory and the lotus leaf effect.As a result of the increased density of rGO/TiO_(2)/PDMS/MS,it recorded an initial capacity that was 2 g/g lower than the raw MS for crude oil absorption.The raw MS retained 53% of its initial absorption capacity after 20 cycles of absorption,while rGO/TiO_(2)/PDMS/MS retained 97%,suggesting good recyclability.Excellent oil and organic solvent recovery(90%-96%)was demonstrated by rGO/TiO_(2)/PDMS/MS in oil-water combinations.In a continuous separation system,it achieved a remarkable separation efficiency of 2.4×10^(6)L/(m^(3)·h),and in turbulent emulsion separation,it achieved a demulsification efficiency of 90%-91%.This study provides a practical substitute for massive oil spill cleaning.

Oxidative coupling of methane:MO_x-modified (M=Ti,Mg,Ga,Zr) Mn_2O_3-Na_2WO_4/SiO_2 catalysts and effect of MO_x modification

Mn_2O_3-Na_2WO_4/SiO_2 is considered as the most promising catalyst for the oxidative coupling of methane（OCM） process; however, it only has a better catalytic performance over 800 °C. To improve its low-temperature performance, an attempt has been made to modify the Mn_2O_3-Na_2WO_4/SiO_2 catalyst using TiO_2, MgO, Ga_2O_3, and ZrO_2. Among the synthesized catalysts, the TiO_2-modified Mn_2O_3-Na_2WO_4/SiO_2 catalyst shows markedly improved low-temperature OCM performance,achieving a high CH_4 conversion of ~23% and a good C_2-C_3 selectivity of ~73% at 700 °C（the catalyst bed temperature）, along with promising stability for at least 300 h without signs of deactivation.In comparison with the unmodified Mn_2O_3-Na_2WO_4/SiO_2 catalyst, the TiO_2 modification results in significant improvement in the low-temperature activity/selectivity, whereas the MgO modification has almost no impact and the Ga_2O_3 and ZrO_2 modifications have a negative effect. The X-ray diffraction（XRD） and Raman results reveal that the formation of a MnTiO_3 phase and a MnTiO_3-dominated catalyst surface is crucial for the improvement of the low-temperature activity/selectivity in the OCM process.

Optimized Electronic Modification of S-Doped CuO Induced by Oxidative Reconstruction for Coupling Glycerol Electrooxidation with Hydrogen Evolution

Glycerol(electrochemical) oxidation reaction(GOR) producing organic small molecule acid and coupling with hydrogen evolution reaction is a critical aspect of ensuring balanced glycerol capacity and promoting hydrogen generation on a large scale. However, the development of highly efficient and selective non-noble metal-based GOR electrocatalysts is still a key problem. Here, an S-doped CuO nanorod array catalyst(S-CuO/CF) constructed by sulfur leaching and oxidative remodeling is used to drive GOR at low potentials: It requires potentials of only 1.23 and 1.33 V versus RHE to provide currents of 100 and 500 mA cm^(-2), respectively. Moreover, it shows satisfactory comprehensive performance(at 100 mA cm^(-2), V_(cell) = 1.37 V) when assembled as the anode in asymmetric coupled electrolytic cell. Furthermore, we propose a detailed cycle reaction pathway(in alkaline environment) of S-doped CuO surface promoting GOR to produce formic acid and glycolic acid. Among them, the C–C bond breaking and lattice oxygen deintercalation steps frequently involved in the reaction pathway are the key factors to determine the catalytic performance and product selectivity. This research provides valuable guidance for the development of transition metal-based electrocatalysts for GOR and valuable insights into the glycerol oxidation cycle reaction pathway.

Surface engineering of TeO_(x) modification on MoVTeNbO creates a high-performance catalyst for oxidation of toluene homologues to aldehydes

The heterogeneous catalytic oxidation of toluene by O_(2)is an inherently safe and green route for production of benzaldehyde,but after more than fifty years of effort,it remains a great challenge.Here,we report the best heterogeneous catalyst,TeO_(x)/MoVTeNbO,up to now for the green oxidation of toluene by O_(2)to benzaldehyde,balancing the catalyst activity,selectivity,and stability.The deposition of TeO_(x) endows the MoVTeNbO composite oxide with entirely new property for toluene oxidation and the surface engineering mechanism has been fully explained.The discrete TeO_(x) clusters on the surface,shielding the nonselective oxidation sites that interact strongly with the benzene ring of toluene molecule,allows toluene molecule to chemically adsorb to the surface perpendicularly and the methyl is then prone to oxidation to aldehyde on the reshaped selective oxidation sites,where V=O is the main active species responsible for continuously extracting hydrogen from methyl and implanting oxygen to form benzaldehyde.The TeO_(x) clusters participate in this reaction through variable valences and stabilize benzaldehyde by couple interaction with the–CHO group of benzaldehyde,thereby achieving high selectivity to benzaldehyde(>95%).The extended works indicate that the catalytic mechanism is effective in a series of selective oxidation of toluene homologues to corresponding aldehydes.

Advancements in cobalt-based oxide catalysts for soot oxidation: Enhancing catalytic performance through modification and morphology control

The widespread use of diesel engines results in significant environmental contamination due to emitted pollutants,particularly soot particles.These pollut-ants are detrimental to public health.At present,one of the most effective ways to remove soot particles is the catalytic diesel particulate filter after-treatment tech-nology,which requires the catalyst to have superior low temperature activity.Compared with cerium oxide which is widely used,cobalt oxide in transition metal oxides has been widely studied in recent years because of its high redox ability and easy to control morphology.This paper elaborates on the influence of modification techniques such as doping,loading,and solid solution on the catalytic performance of cobalt-based catalysts in soot oxidation.Along the same lines,it further reviews the research progress on cobalt-based oxide catalysts with specific dimensional structures and morphologies in soot oxidation.Finally,it provides an outlook on the challenges faced by the theoretical basis and applied research of cobalt-based catalysts in soot oxidation.

Electroacupuncture alleviates diabetic peripheral neuropathy through modulating mitochondrial biogenesis and suppressing oxidative stress

BACKGROUND Peripheral neuropathy caused by diabetes is closely related to the vicious cycle of oxidative stress and mitochondrial dysfunction resulting from metabolic abnormalities.The effects mediated by the silent information regulator type 2 homolog-1(SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator-1α(PGC-1α)axis present new opportunities for the treatment of type 2 diabetic peripheral neuropathy(T2DPN),potentially breaking this harmful cycle.AIM To validate the effectiveness of electroacupuncture(EA)in the treatment of T2DPN and investigate its potential mechanism based on the SIRT1/PGC-1αaxis.METHODS The effects of EA were evaluated through assessments of metabolic changes,morphological observations,and functional examinations of the sciatic nerve,along with measurements of inflammation and oxidative stress.Proteins related to the SIRT1/PGC-1αaxis,involved in the regulation of mitochondrial biogenesis and antioxidative stress,were detected in the sciatic nerve using Western blotting to explain the underlying mechanism.A counterevidence group was created by injecting a SIRT1 inhibitor during EA intervention to support the hypothesis.RESULTS In addition to diabetes-related metabolic changes,T2DPN rats showed significant reductions in pain threshold after 9 weeks,suggesting abnormal peripheral nerve function.EA treatment partially restored metabolic control and reduced nerve damage in T2DPN rats.The SIRT1/PGC-1αaxis,which was downregulated in the model group,was upregulated by EA intervention.The endogenous antioxidant system related to the SIRT1/PGC-1αaxis,previously inhibited in diabetic rats,was reactivated.A similar trend was observed in inflammatory markers.When SIRT1 was inhibited in diabetic rats,these beneficial effects were abolished.CONCLUSION EA can alleviate the symptoms of T2DNP in experimental rats,and its effects may be related to the mitochondrial biogenesis and endogenous antioxidant system mediated by the SIRT1/PGC-1αaxis.