Hydroxyl-Bonded Co Single Atom Site on Boroncarbonitride Surface Realizes Nonsacrificial H2O2 Synthesis in the Near-Infrared Region.

Photocatalytic synthesis of hydrogen peroxide (H2O2) from O2 and H2O under near-infrared light is a sustainable renewable energy production strategy, but challenging reaction. The bottleneck of this reaction lies in the regulation of O2 reduction path by photocatalyst. Herein, the center of the one-step two-electron reduction (OSR) pathway of O2 for H2O2 evolution via the formation of the hydroxyl-bonded Co single-atom sites on boroncarbonitride surface (BCN-OH2/Co1) is constructed. The experimental and theoretical prediction results confirm that the hydroxyl group on the surface and the electronic band structure of BCN-OH2/Co1 are the key factor in regulating the O2 reduction pathway. In addition, the hydroxyl-bonded Co single-atom sites can further enrich O2 molecules with more electrons, which can avoid the one-electron reduction of O2 to •O2 -, thus promoting the direct two-electron activation hydrogenation of O2. Consequently, BCN-OH2/Co1 exhibits a high H2O2 evolution apparent quantum efficiency of 0.8% at 850 nm, better than most of the previously reported photocatalysts. This study reveals an important reaction pathway for the generation of H2O2, emphasizing that precise control of the active site structure of the photocatalyst is essential for achieving efficient conversion of solar-to-chemical.

A sensitive "turn-on" Schiff-base fluorescent probe for the selective detection of Fe3+ and bio-imaging.

A novel Schiff-base fluorescent probe, 4-(N-(2- hydroxyl-1-naphthalymethylimino)-ethylamino) -7-nitro-1,2,3-benzoxadiazole (HENB) was synthesized and utilized for spectral sensing of Fe3+ ions at neutral pH. The binding of Fe3+ to HENB in C2H5OH-HEPES buffer (1:1 v/ v, 25 mM, pH 7.2) resulted in a pronounced emission enhancement at 530 nm, which is possibly due to the inhibition of photo-induced electron transfer (PET) process as well as the chelation enhanced fluorescence (CHEF) effect. HENB shows good selectivity and sensitivity toward Fe3+ with the detection limit as low as 4.51 nM. Test strips made of HENB was used for rapid "naked-eye" detection of Fe3+ ions in aqueous medium. Moreover, HENB was successfully applied in fluorescence imaging of exogenous and endogenous Fe3+ in live Hela cells as well as zebrafish. Importantly, HENB is capable of effectively monitoring the variations of Fe3+ in living cells during ferroptosis process.

Endogenous FGF1 Deficiency Aggravates Doxorubicin-Induced Hepatotoxicity.

Doxorubicin (DOX) is a broad-spectrum antineoplastic agent that widely used in clinic. However, its application is largely limited by its toxicity in multiple organs. Fibroblast growth factor 1 (FGF1) showed protective potential in various liver diseases, but the role of endogenous FGF1 in DOX-induced liver damage is currently unknown. Both wild-type (WT) and FGF1 knockout (FGF1-KO) mice were treated with DOX. DOX induced loss of body weight and liver weight and elevation of ALT and AST in WT mice, which were aggravated by FGF1 deletion. FGF1 deletion exacerbated hepatic oxidative stress mirrored by further elevated 3-nitrosative modification of multiple proteins and malondialdehyde content. These were accompanied by blunted compensatively antioxidative responses indicated by impaired upregulation of nuclear factor erythroid 2-related factor 2 and its downstream antioxidant gene expression. The aggravated oxidative stress was coincided with exacerbated cell apoptosis in DOX-treated FGF1-KO mice reflected by further increased TUNEL positive cell staining and BCL-2-associated X expression and caspase 3 cleavage. These detrimental changes in DOX-treated FGF1-KO mice were associated with worsened intestinal fibrosis and increased upregulation fibrotic marker connective tissue growth factor and α-smooth muscle actin expression. However, DOX-induced hepatic inflammatory responses were not further affected by FGF1 deletion. These results demonstrate that endogenous FGF1 deficiency aggravates DOX-induced liver damage and FGF1 is a potential therapeutic target for treatment of DOX-associated hepatoxicity.

Fgf21-Dubosiella axis mediates the protective effects of exercise against NAFLD development.

AIM: To explore the mechanism of gut microbiota mediates protective effects of exercise against non-alcoholic fatty liver disease (NAFLD) development. MAIN METHODS: The male C57BL/6 mice were fed with high fat food (HFD) or normal diet (CON) respectively, and the obese mice were randomly divided into sedentariness (HFD) and exercise groups (HFD + Exe). The total intervention period was 18 weeks. Antibiotic treatment and fecal microbiota transplantation were applied to evaluate gut microbiota mediates the protective effects of exercise against NAFLD development. 16S rDNA profiling of gut microbiota and extracorporeal rehydration of Dubosiella newyorkensis were performed to identify the crucial role of Dubosiella in NAFLD improvement during exercise training. FGF21 knock-out mice were used to reveal the potential mechanism of exercise increased the abundance of Dubosiella. RT-PCR, Western blot, Histopathological examinations and Biochemical testing were performed to evaluate the lipid deposition and function in the liver. KEY FINDINGS: Treadmill exercise significantly ameliorated hepatic function and mitigated lipid accumulation in NAFLD mice, and these hepatoprotective benefits were mostly mediated by the Dubosiella. In addition, the increased abundance of Dubosiella during exercise training was modulated by FGF21 specifically. SIGNIFICANCE: In short, Dubosiella, chiefly regulated by FGF21 signaling during exercise training, has been discovered to govern the protective impacts of exercising counter to the development of NAFLD and exhibits a promising treatment target for NAFLD.

BPDE-DNA adduct formation and alterations of mRNA, protein, and DNA methylation of CYP1A1, GSTP1, and GSTM1 induced by benzo[a]pyrene and the intervention of aspirin in mice.

Benzo[a]pyrene (B[a]P), one typical environmental pollutant, the toxicity mechanisms, and potential prevention remain perplexing. Available evidence suggests cytochrome P450 1A1 (CYP1A1) and glutathione S-transferases (GSTs) metabolize B[a]P, resulting in metabolic activation and detoxification of B[a]P. This study aimed to reveal the impact of B[a]P exposure on trans-7,8-diol-anti-9,10-epoxide DNA (BPDE-DNA) adduct formation, level of CYP1A1, glutathione S-transferase pi (GSTP1) and glutathione S-transferase mu1 (GSTM1) mRNA, protein and DNA methylation in mice, and the potential prevention of aspirin (ASP). This study firstly determined the BPDE-DNA adduct formation in an acute toxicity test of a large dose in mice induced by B[a]P, which subsequently detected CYP1A1, GSTP1, and GSTM1 at levels of mRNA, protein, and DNA methylation in the organs of mice in a subacute toxicity test at appropriate doses and the potential prevention of ASP, using the methods of real-time quantitative PCR (QPCR), western blotting, and real-time methylation-specific PCR (MSP), respectively. The results verified that B[a]P induced the formation of BPDE-DNA adduct in all the organs of mice in an acute toxicity test, and the order of concentration of which was lung > kidney > liver > brain. In a subacute toxicity test, following B[a]P treatment, mice showed a dose-dependent slowdown in body weight gain and abnormalities in behavioral and cognitive function and which were alleviated by ASP co-treatment. Compared to the controls, following B[a]P treatment, CYP1A1 was significantly induced in all organs in mice at mRNA level (P < 0.05), was suppressed in the lung and cerebrum of mice at protein level, and inhibited at DNA methylation level in the liver, lung, and cerebrum, whereas GSTP1 and GSTM1 at mRNA, protein, and DNA methylation levels showed organ-specific changes in mice following B[a]P treatment, which was generally alleviated by ASP intervention. In conclusion, B[a]P induced BPDE-DNA adduct formation in all organs in mice and altered the mRNA, protein, and DNA methylation levels in CYP1A1, GSTP1, and GSTM1 in an organ-dependent pattern, which could be related to the organ toxicity and mechanism of B[a]P. ASP intervention may be an effective measure to prevent B[a]P toxicity. The findings provide scientific evidence for further study on the organ toxicity and mechanisms of B[a]P.

Tunable Optical Activity in Twisted Anisotropic Two-Dimensional Materials.

Twisted van der Waals structures exhibit a variety of unusual electrical and optical phenomena and could provide a powerful means for designing nanodevices with tunable chiral properties. However, programming intrinsic chiral properties of the film on the atomic scale remains a great challenge due to the limitations of fabrication and measurement techniques. Here, we report a highly tunable large optical activity of twisted anisotropic two-dimensional (2D) materials, including black phosphorus (BP), ReS2, PdSe2, and α-MoO3, by varying the twist angle between the stacked layers. The chirality can be deliberately tailored through the engineering of the symmetry, band structure, and anisotropy of 2D materials, demonstrating the high tunability of the chirality. The results show the highest thickness-normalized ellipticity value (13.8 deg µm-1, twisted ReS2) and ellipticity value (1581 mdeg, twisted BP) among the systems based on 2D materials. It is also shown that the chiroptical response exists in an extremely large spectral range from the visible to the infrared. Furthermore, the twisted ReS2 enabled spin-selective control of the information transformation. These results show that highly controllable chirality in twisted 2D anisotropic materials has considerable potential in on-chip polarization optics, nano-optoelectronics, and biology.

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies.

Several models have been developed to investigate angiogenesis in vivo. However, most of these models are complex and expensive, require specialized equipment, or are hard to perform for subsequent quantitative analysis. Here we present a modified matrix gel plug assay to evaluate angiogenesis in vivo. In this protocol, vascular cells were mixed with matrix gel in the presence or absence of pro-angiogenic or anti-angiogenic reagents, and then subcutaneously injected into the back of recipient mice. After 7 days, phosphate buffer saline containing dextran-FITC is injected via the tail vein and circulated in vessels for 30 min. Matrix gel plugs are collected and embedded with tissue embedding gel, then 12 µm sections are cut for fluorescence detection without staining. In this assay, dextran-FITC with high molecular weight (~150,000 Da) can be used to indicate functional vessels for detecting their length, while dextran-FITC with low molecular weight (~4,400 Da) can be used to indicate the permeability of neo-vessels. In conclusion, this protocol can provide a reliable and convenient method for the quantitative study of angiogenesis in vivo.

Nonlinear and Anisotropic Ion Transport in Black Phosphorus Nanochannels.

Two-dimensional material nanochannels with molecular-scale confinement can be constructed by Van der Waals assembly and show unexpected fluid transport phenomena. The crystal structure of the channel surface plays a key role in controlling fluid transportation, and many strange properties are explored in these confined channels. Here, we use black phosphorus as the channel surface to enable ion transport along a specific crystal orientation. We observed a significant nonlinear and anisotropic ion transport phenomenon in the black phosphorus nanochannels. Theoretical results revealed an anisotropy of ion transport energy barrier on the black phosphorus surface, with the minimum energy barrier along the armchair direction approximately ten times larger than that along the zigzag direction. This difference in energy barrier affects the electrophoretic and electroosmotic transport of ions in the channel. This anisotropic transport, which depends on the orientation of the crystal, may provide new approaches to controlling the transport of fluids.

Lewis Acid-Induced Reversible Disproportionation of TEMPO Enables Aqueous Aluminum Radical Batteries.

Nitroxide radicals, such as 2,2,6,6-tetramethylpiperidyl-1-oxy (TEMPO), are typical organic electrode materials featuring high redox potentials and fast electrochemical kinetics and have been widely used as cathode materials in multivalent metal-ion batteries. However, TEMPO and its derivatives have not been used in emerging rechargeable aluminum-ion batteries (AIBs) due to the known disproportionation and possible degradation of nitroxide radicals in acidic conditions. In this study, the (electro)chemical behavior of TEMPO is examined in organic and aqueous Lewis acid electrolytes. Through in situ (electro)chemical characterizations and theoretical computation, we reveal for the first time an irreversible disproportionation of TEMPO in organic Al(OTf)3 electrolytes that can be steered to a reversible process when switching to an aqueous media. In the latter case, a fast hydrolysis and ligand exchange between [Al(OTf)3TEMPO]- anion and water enable the overall reversible electrochemical redox reaction of TEMPO. These findings lead to the first design of radical polymer aqueous AIBs that are fire-retardant and air-stable, delivering a stable voltage output of 1.25 V and a capacity of 110 mAh g-1 over 800 cycles with 0.028% loss per cycle. This work demonstrates the promise of using nonconjugated organic electroactive materials for cost-effective and safe AIBs that currently rely on conjugated organic molecules.

An electron-hole rich dual-site nickel catalyst for efficient photocatalytic overall water splitting.

Photocatalysis offers an attractive strategy to upgrade H2O to renewable fuel H2. However, current photocatalytic hydrogen production technology often relies on additional sacrificial agents and noble metal cocatalysts, and there are limited photocatalysts possessing overall water splitting performance on their own. Here, we successfully construct an efficient catalytic system to realize overall water splitting, where hole-rich nickel phosphides (Ni2P) with polymeric carbon-oxygen semiconductor (PCOS) is the site for oxygen generation and electron-rich Ni2P with nickel sulfide (NiS) serves as the other site for producing H2. The electron-hole rich Ni2P based photocatalyst exhibits fast kinetics and a low thermodynamic energy barrier for overall water splitting with stoichiometric 2:1 hydrogen to oxygen ratio (150.7 µmol h-1 H2 and 70.2 µmol h-1 O2 produced per 100 mg photocatalyst) in a neutral solution. Density functional theory calculations show that the co-loading in Ni2P and its hybridization with PCOS or NiS can effectively regulate the electronic structures of the surface active sites, alter the reaction pathway, reduce the reaction energy barrier, boost the overall water splitting activity. In comparison with reported literatures, such photocatalyst represents the excellent performance among all reported transition-metal oxides and/or transition-metal sulfides and is even superior to noble metal catalyst.

Construction of a mineralized collagen nerve conduit for peripheral nerve injury repair.

A new nerve guidance conduits (NGCs) named MC@Col containing Type I collagen (Col) and mineralized collagen (MC) was developed, enhancing mechanical and degradation behavior. The physicochemical properties, the mechanical properties and in vitro degradation behavior were all evaluated. The adhesion and proliferation of Schwann cells (SCs) were observed. In the in vivo experiment, MC@Col NGC and other conduits including Col, chitosan (CST) and polycaprolactone (PCL) conduit were implanted to repair a 10-mm-long Sprague-Dawley rat's sciatic nerve defect. Histological analyses, morphological analyses, electrophysiological analyses and further gait analyses were all evaluated after implantation in 12 weeks. The strength and degradation performance of the MC@Col NGC were improved by the addition of MC in comparison with pure Col NGC. In vitro cytocompatibility evaluation revealed that the SCs had good viability, attachment and proliferation in the MC@Col. In in vivo results, the regenerative outcomes of MC@Col NGC were close to those by an autologous nerve graft in some respects, but superior to those by Col, CST and PCL conduits. The MC@Col NGC exhibited good mechanical performance as well as biocompatibility to bridge nerve gap and guide nerve regeneration, thus showing great promising potential as a new type of conduit in clinical applications.

Konjac Glucomannan: An Emerging Specialty Medical Food to Aid in the Treatment of Type 2 Diabetes Mellitus.

There are many factors causing T2DM; thus, it is difficult to prevent and cure it with conventional treatment. In order to realize the continuous intervention of T2DM, the treatment strategy of combining diet therapy and traditional medication came into being. As a natural product with the concept of being healthy, konjac flour and its derivatives are popular with the public. Its main component, Konjac glucomannan (KGM), can not only be applied as a food additive, which greatly improves the taste and flavor of food and extends the shelf life of food but also occupies an important role in T2DM. KGM can extend gastric emptying time, increase satiety, and promote liver glycogen synthesis, and also has the potential to improve intestinal flora and the metabolic system through a variety of molecular pathways in order to positively regulate oxidative stress and immune inflammation, and protect the liver and kidneys. In order to establish the theoretical justification for the adjunctive treatment of T2DM, we have outlined the physicochemical features of KGM in this article, emphasizing the advantages of KGM as a meal for special medical purposes of T2DM.

CXCR7 Agonist TC14012 Improves Angiogenic Function of Endothelial Progenitor Cells via Activating Akt/eNOS Pathway and Promotes Ischemic Angiogenesis in Diabetic Limb Ischemia.

PURPOSE: Endothelial progenitor cells (EPCs) play a critical role in repairing damaged vessels and triggering ischemic angiogenesis, but their number is reduced and function is impaired under diabetic conditions. Improving EPC function has been considered a promising strategy to ameliorate diabetic vascular complications. In the present study, we aim to investigate whether and how CXCR7 agonist TC14012 promotes the angiogenic function of diabetic EPCs. METHODS: High glucose (HG) treatment was used to mimic the hyperglycemia in diabetes. Tube formation, cell scratch recovery and transwell assay, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and cleaved-caspase3 expression were used to evaluate the angiogenic capability, cell migration, and apoptosis of EPCs, respectively. Hind limb ischemia (HLI) model was used to appraise the ability of TC14012 in promoting diabetic ischemic angiogenesis in vivo. RESULTS: HG treatment impaired EPC tube formation and migration, and induced EPC apoptosis and oxidative damage, while TC14012 rescued tube formation and migration, and prevented HG-induced apoptosis and oxidative damage of EPCs. Furthermore, these beneficial effects of TC14012 on EPCs were attenuated by specific siRNAs against CXCR7, validating that CXCR7 is a functional target of TC14012 in EPCs. Mechanistic studies demonstrated that HG treatment reduced CXCR7 expression in EPCs, and impaired Akt and endothelial nitric oxide synthase (eNOS) phosphorylation and nitric oxide (NO) production; similarly, these signal impairments in HG-exposed EPCs could be rescued by TC14012. However, the protective effects of TC14012 on tube formation and migration, Akt and eNOS phosphorylation, and NO production in HG-treated EPCs were almost completely abolished by siRNAs against CXCR7 or Akt specific inhibitor wortmannin. More importantly, in vivo study showed that TC14012 administration enhanced blood perfusion recovery and angiogenesis in the ischemic hind limb and increased the EPC number in peripheral circulation of db/db mice, demonstrating the capability of TC14012 in promoting EPC mobilization and ischemia angiogenic function. CONCLUSION: TC14012 can prevent EPCs from HG-induced dysfunction and apoptosis, improve eNOS activity and NO production via CXCR7/Akt signal pathway, and promote EPC mobilization and diabetic ischemia angiogenesis.

Liraglutide Improves the Angiogenic Capability of EPC and Promotes Ischemic Angiogenesis in Mice under Diabetic Conditions through an Nrf2-Dependent Mechanism.

The impairment in endothelial progenitor cell (EPC) functions results in dysregulation of vascular homeostasis and dysfunction of the endothelium under diabetic conditions. Improving EPC function has been considered as a promising strategy for ameliorating diabetic vascular complications. Liraglutide has been widely used as a therapeutic agent for diabetes. However, the effects and mechanisms of liraglutide on EPC dysfunction remain unclear. The capability of liraglutide in promoting blood perfusion and angiogenesis under diabetic conditions was evaluated in the hind limb ischemia model of diabetic mice. The effect of liraglutide on the angiogenic function of EPC was evaluated by cell scratch recovery assay, tube formation assay, and nitric oxide production. RNA sequencing was performed to assess the underlying mechanisms. Liraglutide enhanced blood perfusion and angiogenesis in the ischemic hindlimb of db/db mice and streptozotocin-induced type 1 diabetic mice. Additionally, liraglutide improved tube formation, cell migration, and nitric oxide production of high glucose (HG)-treated EPC. Assessment of liraglutide target pathways revealed a network of genes involved in antioxidant activity. Further mechanism study showed that liraglutide decreased the production of reactive oxygen species and increased the activity of nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 deficiency attenuated the beneficial effects of liraglutide on improving EPC function and promoting ischemic angiogenesis under diabetic conditions. Moreover, liraglutide activates Nrf2 through an AKT/GSK3ß/Fyn pathway, and inhibiting this pathway abolished liraglutide-induced Nrf2 activation and EPC function improvement. Overall, these results suggest that Liraglutide represents therapeutic potential in promoting EPC function and ameliorating ischemic angiogenesis under diabetic conditions, and these beneficial effects relied on Nrf2 activation.

Advances in Biomedical Functions of Natural Whitening Substances in the Treatment of Skin Pigmentation Diseases.

Pigmentation diseases can lead to significant color differences between the affected part and the normal part, resulting in severe psychological and emotional distress among patients. The treatment of pigmentation diseases with good patient compliance is mainly in the form of topical drugs. However, conventional hydroquinone therapy contributes to several pathological conditions, such as erythema, dryness, and skin desquamation, and requires a longer treatment time to show significant results. To address these shortcomings, natural whitening substances represented by kojic acid and arbutin have gradually become the candidate ingredients of traditional local preparations due to their excellent biological safety. This review focuses on several natural whitening substances with potential therapeutic effects in pigmentation disease and their mechanisms, and a thorough discussion has been conducted into the solution methods for the challenges involved in the practical application of natural whitening substances.

Nrf2 transcriptional upregulation of IDH2 to tune mitochondrial dynamics and rescue angiogenic function of diabetic EPCs.

Endothelial progenitor cells (EPCs) are reduced in number and impaired in function in diabetic patients. Whether and how Nrf2 regulates the function of diabetic EPCs remains unclear. In this study, we found that the expression of Nrf2 and its downstream genes were decreased in EPCs from both diabetic patients and db/db mice. Survival ability and angiogenic function of EPCs from diabetic patients and db/db mice also were impaired. Gain- and loss-of-function studies, respectively, showed that knockdown of Nrf2 increased apoptosis and impaired tube formation in EPCs from healthy donors and wild-type mice, while Nrf2 overexpression decreased apoptosis and rescued tube formation in EPCs from diabetic patients and db/db mice. Additionally, proangiogenic function of Nrf2-manipulated mouse EPCs was validated in db/db mice with hind limb ischemia. Mechanistic studies demonstrated that diabetes induced mitochondrial fragmentation and dysfunction of EPCs by dysregulating the abundance of proteins controlling mitochondrial dynamics; upregulating Nrf2 expression attenuated diabetes-induced mitochondrial fragmentation and dysfunction and rectified the abundance of proteins controlling mitochondrial dynamics. Further RNA-sequencing analysis demonstrated that Nrf2 specifically upregulated the transcription of isocitrate dehydrogenase 2 (IDH2), a key enzyme regulating tricarboxylic acid cycle and mitochondrial function. Overexpression of IDH2 rectified Nrf2 knockdown- or diabetes-induced mitochondrial fragmentation and EPC dysfunction. In a therapeutic approach, supplementation of an Nrf2 activator sulforaphane enhanced angiogenesis and blood perfusion recovery in db/db mice with hind limb ischemia. Collectively, these findings indicate that Nrf2 is a potential therapeutic target for improving diabetic EPC function. Thus, elevating Nrf2 expression enhances EPC resistance to diabetes-induced oxidative damage and improves therapeutic efficacy of EPCs in treating diabetic limb ischemia likely via transcriptional upregulating IDH2 expression and improving mitochondrial function of diabetic EPCs.

Advances in lncRNAs from stem cell-derived exosome for the treatment of cardiovascular diseases.

Cardiovascular diseases (CVDs) are the leading cause of mortality globally. Benefiting from the advantages of early diagnosis and precision medicine, stem cell-based therapies have emerged as promising treatment options for CVDs. However, autologous or allogeneic stem cell transplantation imposes a potential risk of immunological rejection, infusion toxicity, and oncogenesis. Fortunately, exosome can override these limitations. Increasing evidence has demonstrated that long non-coding RNAs (lncRNAs) in exosome from stem cell paracrine factors play critical roles in stem cell therapy and participate in numerous regulatory processes, including transcriptional silencing, transcriptional activation, chromosome modification, and intranuclear transport. Accordingly, lncRNAs can treat CVDs by directly acting on specific signaling pathways. This mini review systematically summarizes the key regulatory actions of lncRNAs from different stem cells on myocardial aging and apoptosis, ischemia-reperfusion injury, retinopathy, atherosclerosis, and hypertension. In addition, the current challenges and future prospects of lncRNAs treatment for CVDs are discussed.

High performance polypyrrole coated carbon-based electrocatalytic membrane for organic contaminants removal from aqueous solution.

Electrocatalytic filtration process adopting the electrocatalytic membrane as both filtration membrane and active electrode showed great prospect on the organic pollutant removal from water. In this work, a high-performance metal-free polypyrrole (PPy) coated carbon-based electrocatalytic membrane (PPy@CCM) was developed through the facile and controllable electro-polymerization deposition method. Structural properties and electrochemical performance of the prepared PPy@CCM were characterized systematically. The influences of preparation parameters and operational parameters on water treatment performance of PPy@CCM were also investigated. Results indicates that the spherical PPy particles uniformly distributed on the surface of PPy@CCM. Coating with PPy particles can significantly improve the hydrophilicity and electrochemical activity of CCM, therefore PPy@CCM has lower hydraulic resistance and higher water treatment performance than CCM. The phenol and chemical oxygen demand (COD) removal rates obtained by PPy@CCM are up to 99.51% and 89.90%, respectively, under the optimal condition of 2.0 V cell potential, 2.50 g·L-1 Na2SO4, 1.5 ml·min-1 flow rate and 50 mg·L-1 phenol, and only 0.5 kWh·kgCOD-1 energy consumption is consumed. In addition, PPy@CCM also exhibits good treatment performance in different water matrixes. Moreover, PPy@CCM has good stability for several cycle operation and considerable applicability for different types of organic pollutants removal. The oxidation mechanism study reveals that PPy@CCM has both direct and indirect oxidation activity during the electrocatalytic filtration treatment, and the coating of PPy can improve the direct oxidation ability and ·OH yield of CCM.

[The research progress of PD-1/L1 inhibitors application in the treatment of head and neck squamous cell carcinoma].

Over the past few years, the FDA has approved PD-1/L1 inhibitor for the treatment of advanced head and neck squamous cell carcinoma, involving PD-1/L1 inhibitor monotherapy, PD-1/L1 inhibitor combined with chemoradiotherapy, combined with targeted therapy, combined with neoadjuvant immunotherapy and duplex-block of immune checkpoints and so on. Herein, we briefly review the latest research results in this field, and summarize the application and efficacy of immunotherapy in the treatment of head and neck squamous cell carcinoma， which will benefits such patients to develop more precise and individualized treatment plans.