Palliative effect of rotating magnetic field on glucocorticoid-induced osteonecrosis of the femoral head in rats by regulating osteoblast differentiation.

With the substantial increase in the overuse of glucocorticoids (GCs) in clinical medicine, the prevalence of glucocorticoid-induced osteonecrosis of the femoral head (GC-ONFH) continues to rise in recent years. However, the optimal treatment for GC-ONFH remains elusive. Rotating magnetic field (RMF), considered as a non-invasive, safe and effective approach, has been proved to have multiple beneficial biological effects including improving bone diseases. To verify the effects of RMF on GC-ONFH, a lipopolysaccharide (LPS) and methylprednisolone (MPS)-induced invivo rat model, and an MPS-induced invitro cell model have been employed. The results demonstrate that RMF alleviated bone mineral loss and femoral head collapse in GC-ONFH rats. Meanwhile, RMF reduced serum lipid levels, attenuated cystic lesions, raised the expression of anti-apoptotic proteins and osteoprotegerin (OPG), while suppressed the expression of pro-apoptotic proteins and nuclear factor receptor activator-κB (RANK) in GC-ONFH rats. Besides, RMF also facilitated the generation of ALP, attenuated apoptosis and inhibits the expression of pro-apoptotic proteins, facilitated the expression of OPG, and inhibited the expression of RANK in MPS-stimulated MC3T3-E1 cells. Thus, this study indicates that RMF can improve GC-ONFH in rat and cell models, suggesting that RMF have the potential in the treatment of clinical GC-ONFH.

Construction of Poly(hydrophobic deep eutectic solvent)/Ethylcellulose Composite Films for Green Recyclable Tapes.

Constructing green recyclable cellulose-based tapes with high transparency, mechanical robustness, and strong wet adhesion using natural components is highly desirable but challenging. Herein, novel cellulose-based self-adhesive tapes were reported by coating a polymerizable hydrophobic deep eutectic solvent (DES) on ethylcellulose followed by photopolymerization. The prepared ethylcellulose-based self-adhesive tape (ECSAT) exhibited an optical transmittance of up to ∼88% and could provide strong adhesion by interfacial intermolecular interactions without obstructing information. Due to the hydrophobic nature of the overall structure, ECSAT does not exhibit significant adhesive strength and mechanical degradation under water, acid, and alkali environments. Notably, ECSAT can be completely dissolved in the resultant DES and furthermore reused as a self-adhesive coating. The recycled ECSAT still maintained good optical transparency, mechanical strength, and wet adhesion. We believe that ECSATs with all-around performances have a wide range of applications in packaging and other engineering fields.

The mtDNA-STING pathway plays an important role in both navitoclax- and S63845-induced autophagy and enhances cell death.

Targeting BCL2 family proteins to induce cancer cell death has been successful in the treatment of cancer. BH3 mimetics such as ABT-737 not only induce cell death, but also activate autophagy. The molecular mechanism by which the BH3 mimetics induce autophagy is still controversial. In this study, we show that the BCL2/BCLXL/BCLw inhibitor navitoclax and the MCL1 inhibitor S63845 induce both apoptosis and autophagy in mouse embryonic fibroblasts (MEFs) and leukemia cell lines, while autophagy induced by navticlax and S63845 in leukemia cell lines requires the inhibition of caspase activities. Further experiments demonstrate that the autophagy induced by navitoclax or S63845 does not depend on Beclin 1, but downstream of Bax/Bak. Moreover, both navitoclax and S63845 treatment induce mtDNA release in MEFs, which activates STING and thereby induces autophagy, while STING KO inhibits both navitoclax- and S63845-induced autophagy. Furthermore, STING KO diminishes navitoclax- or S63845-induced apoptosis, suggesting that STING activation enhances rather than inhibits apoptosis. Thus, our findings provide new insights into the regulations of navitoclax- or S63845-induced autophagy and cell death.

HIF in Gastric Cancer: Regulation and Therapeutic Target.

HIF means hypoxia-inducible factor gene family, and it could regulate various biological processes, including tumor development. In 2021, the FDA approved the new drug Welireg for targeting HIF-2a, and it is mainly used to treat von Hippel-Lindau syndrome, which demonstrated its good prospects in tumor therapy. As the fourth deadliest cancer worldwide, gastric cancer endangers the health of people all across the world. Currently, there are various treatment methods for patients with gastric cancer, but the five-year survival rate of patients with advanced gastric cancer is still not high. Therefore, here we reviewed the regulatory role and target role of HIF in gastric cancer, and provided some references for the treatment of gastric cancer.

Angiotensin II promotes EMT of hepatocellular carcinoma cells through high mobility group protein B1 mediated by E4F1.

To screen for specific transcription factors (TFs) that induce expression of the HMGB1 promoter in response to stimulation by Ang-II. A HMGB1 overexpressing vector and small interfering (si)RNA were constructed and used to transfect the three HCC cell lines used in scratched monolayer wound healing and Transwell assays. Chromatin immunoprecipitation (ChIP) assays were used to confirm the relationship between a specific TF and the HMGB1 promoter. Invasion and migration by HMGB1 overexpressing HCC cells after treatment with Ang-II were significantly increased compared to negative controls (NC); E-cadherin was down-regulated while vimentin was up-regulated. However, compared with NC, invasion and migration by HMGB1 siRNA HCC cells stimulated by Ang-II were not altered; the expression of E-cadherin and vimentin was also unaltered. Nineteen TFs were predicted by Promoter 2.0 Prediction Server and TFsitescan. Real-time qPCR was used to evaluate TF expression levels. E4F1 was the only TF abnormally elevated in all three HCC cell lines when stimulated by Ang-II. WB and ChIP assays revealed high expression of E4F1 compared to other TFs in cells stimulated by Ang-II. E4F1 is activated by Ang-II and binds to the HMGB1 promoter region to promote HMGB1 expression; it then enhances Ang-II to induce HCC cell invasion and migration, and EMT.

Extension of Spectral Shift Controls from Equivalent Substitution to an Energy Migration Model Based on Eu2+/Tb3+-Activated Ba4-xSrxGd3-xLuxNa3(PO4)6F2 Phosphors.

Single-phase phosphors with tunable emission colors are crucial to develop high-performance white light-emitting diodes since they are valuable to improve the energy efficiency, color rendering index, and correlated color temperature. Most of the studies have been conducted to control the spectral shifts via a polyhedral distortion or chemical unit cosubstitution strategy. The combination of host optimization and dopant activator design in a single-phase phosphor system is very rare. Herein, a partial substitution strategy of [Ba2+-Gd3+] by [Sr2+-Lu3+] has been employed in Ba4-xSrxGd3-x-yLuxNa3(PO4)6F2/5% Eu2+ (x = 0-0.40) phosphors. Also, the energy migration from Eu2+ to Tb3+ ions has been investigated in as-prepared samples. Consequently, the emitted signal is observed to shift from 470 to 575 nm derived from equivalent substitutions, which is attributed to specific performance by the emission profile of Eu2+, and such results are closely related to splitting of the crystal field and energy transfer among various luminescent centers. Moreover, the tunable yellowish-green emitting material has been assembled by incorporating ion pairs (Eu2+ → Tb3+) into the Ba3.85Sr0.15Gd2.85Lu0.15Na3(PO4)6F2, and their relative ratios are varied. The corresponding Eu2+ → Tb3+ energy migration process is assigned to be the dipole-quadrupole interaction by the Inokuti-Hirayama model. This work provides rational guidance for the design and discovery of new products with tunable emission colors, originating from the cosubstitution strategy and energy conversion model.

Selective binding of mitophagy receptor protein Bcl-rambo to LC3/GABARAP family proteins.

Mitophagy regulates the metabolic level and cell fates by specifically degrading damaged or redundant mitochondria in these cells. During the formation of autophagosomes, autophagy receptors and adaptors, which usually contain a LC3-interacting region (LIR) domain, are recruited through their interactions with LC3/GABARAP family of proteins. Bcl-rambo is one of the mitophagy receptors that interact with LC3s/GABARAPs. In this study, we first measured the binding of Bcl-rambo to LC3s/GABARAPs in vitro and found Bcl-rambo has a selectivity to LC3C/GABARP/GABARAPL1. Further investigations with bioinformatics analyses and mutagenesis suggested that the interactions with the HP1 and HP2 sites of LC3s/GABARAPs and the residues at the X2 site of the LIR domain of Bcl-rambo are both critical for the selectivity. Moreover, assays in vivo showed that manipulating the selective binding of Bcl-rambo resulted in the changes of mitophagy inductions in the cells. Overall, our data revealed the selective binding between Bcl-rambo and LC3s/GABARAPs and its molecular mechanisms and biological significances, which will be helpful for future studies of mitophagy mediated by Bcl-rambo.

Membrane Metalloendopeptidase (MME) Suppresses Metastasis of Esophageal Squamous Cell Carcinoma (ESCC) by Inhibiting FAK-RhoA Signaling Axis.

Esophageal squamous cell carcinoma (ESCC) is a typical neoplastic disease and a frequent cause of death in China. Although great achievements have been made in diagnostic strategies and combination therapies in recent years, the prognosis of ESCC is still poor. Metastasis/recurrence has been the major factor responsible for poor prognosis. However, the underlying mechanism of ESCC dissemination remains elusive. Membrane metalloendopeptidase (MME) is a transmembrane glycoprotein that degrades a number of substrates. This study's results indicated that the down-regulation of MME is significantly associated with advanced clinical stage (P < 0.05) and lymph node metastasis (P < 0.05). The down-regulation of MME in ESCC tumor tissues is correlated to poorer prognosis of the patients. Functional studies demonstrated that MME could significantly inhibit ESCC tumor cell metastasis in vitro and in vivo. MME overexpression could also interrupt ESCC tumor cell adhesion. Mechanistically, MME inhibits the phosphorylation of FAK thus interrupting the FAK-RhoA axis, which is important in cell movement. Taken together, these data show that MME regulates ESCC via FAK-RhoA axis. High expression of MME may indicate a beneficial outcome for patients.

A New Co-Substitution Strategy as a Model to Study a Rare-Earth-Free Spinel-Type Phosphor with Red Emissions and Its Application in Light-Emitting Diodes.

The substitution of metal sites in Mg2TiO4 substrate leads to charge imbalance that will be closely related to a variety of changes including lattice structure, cell distortion, and photophysical properties. Herein, the co-substitution strategy of [Ga3+-Ga3+] for [Mg2+-Ti4+] and Sn4+ for Ti4+ achieves for the first time the novel Mg3Ga2SnO8 (MGS):xMn4+ (x = 0-3%) phosphors with efficient red emissions. In terms of X-ray powder diffraction (XRD) and Rietveld refinement analysis, MGS:Mn4+ possesses a structure isotypic of Mg2TiO4 in the cubic space group Fd3̅m (227). There are two types of octahedra for Mn4+ ions in this structure, where Ga3+ ions completely occupy a group of octahedral sites and Mg2+/Sn4+ has been randomly distributed over another group of octahedral sites. A strong excitation band in the broad spectral range (220-550 nm) has been identified, thus facilitating the commercial uses for blue LED chips excitation. An intense red emission band at 680 nm has been observed due to the characteristic 2Eg-4A2g transition of Mn4+ ions. A concentration quenching effect occurs when the Mn4+ content exceeds 1.5%, and the quenching mechanism is demonstrated to be dipole-quadrupole interactions. Temperature-dependent luminescence measurements support its good thermal stability, and the corresponding activation energy Ea is determined to be 0.2552 eV. The possible luminous mechanism of the Mn4+ ion is explained by the Tanabe-Sugano energy level diagram. The crystal field strength and the Racah parameters together with the nephelauxetic ratio are also determined for Mn4+ in the MGS lattice. High color rendition warm white-light-emitting diodes (WLEDs) based on the optimal phosphor MGS:1.5%Mn4+,1.5%Li+ possess a color rendering index and color temperature of 85.6 and 3658 K, respectively. Its feasibility for application in solid-state white lighting has been verified.

Down-regulation of POTEG predicts poor prognosis in esophageal squamous cell carcinoma patients.

POTE ankyrin domain family, member G (poteg) belongs to POTE family. The POTE family is composed of many proteins which are very closely related and expressed in prostate, ovary, testis, and placenta. Some POTE paralogs are related with some cancers. Here we showed that down-regulation of POTEG was detected in about 60% primary esophageal squamous cell carcinoma (ESCC) tumor tissues. Clinical association studies determined that POTEG down-regulation was significantly correlated with tumor differentiation, lymph nodes metastasis and TNM staging. Kaplan-Meier analysis determined that POTEG down-regulation was associated with poorer clinical outcomes of ESCC patients (P = 0.026). Functional studies showed that POTEG overexpression could suppress tumor cell growth and metastasis capacity in vitro and in vivo. Molecular analyses revealed that POTEG downregulated CDKs, leading to subsequent inhibition of Rb phosphorylation, and consequently arrested Cell Cycle at G1/S Checkpoint. POTEG overexpression induced apoptosis by activating caspases and PARP, and regulating canonical mitochondrial apoptotic pathways. On the other side, POTEG inhibited epithelial-mesenchymal transition and suppressed tumor cell metastasis. In conclusion, our study reveals a functionally important control mechanism of POTEG in esophageal cancer pathogenesis, suggesting potential use in the ESCC intervention and therapeutic strategies.

Expression of EIF5A2 associates with poor survival of nasopharyngeal carcinoma patients treated with induction chemotherapy.

BACKGROUND: Nasopharyngeal carcinoma (NPC) is a type of head-neck cancer with a distinguishable geographic and racial distribution worldwide. Increasing evidence supports that the accumulation of additional genetic and epigenetic abnormalities is important in driving the NPC tumorigenic process. In this study, we aim to investigate the association between EIF5A2 (Eukaryotic translation initiation factor 5A2) expression status and NPC clinical outcomes. METHODS: The expression status of EIF5A2 was investigated in the NPC tissue microarray. Tissues were from 166 NPC patients staging II-IV, collected between 1999 and 2005. All patients were administered 2-3 cycles of DDP (cisplatin) + 5-Fu (5-fluorouracil) induction therapy and then treated with a uniform conventional two-dimensional radiotherapy. Cell motility assay, tumor growth assay and cytotoxicity assay were performed on the EIF5A2 overexpressed cells and control cells. siRNA was also used in the in vitro studies. RESULTS: Positive staining of EIF5A2 was observed in 85.4 % (105/123) informative tumor cases. Multivariate analyses demonstrated that EIF5A2 was an independent prognostic marker of poor overall survival (OS) (P = 0.041), failure-free survival (FFS) (P = 0.029), and distant failure-free survival (D-FFS) (P = 0.043) in patients with locoregionally advanced NPC patients treated with cisplatin + 5-Fu chemoradiotherapy. The forced expression of EIF5A2 in NPC cells enhanced the cells' motility and growth ability. Knock-down of EIF5A2 in NPC cells decreased the cell's motility and growth ability. Our results also demonstrated that EIF5A2 overexpression induced chemoresistance of NPC cells to 5-Fu. CONCLUSIONS: Our findings suggested that EIF5A2 expression, as examined by immunohistochemistry, could function as an independent prognostic factor of outcomes in NPC patients with cisplatin + 5-Fu chemoradiotherapy. EIF5A2 might be a novel therapeutic target for the inhibition of NPC progress.

Expression of Aurora-B and FOXM1 predict poor survival in patients with nasopharyngeal carcinoma.

PURPOSE: The purpose of this work was to investigate the relationship between Aurora-B, FOXM1, and clinical outcomes in patients with nasopharyngeal carcinoma (NPC) who were treated with a combination of induction chemotherapy and radiotherapy. PATIENTS AND METHODS: The expression of Aurora-B and FOXM1 were investigated by immunohistochemistry using a tissue microarray (TMA) containing samples from 166 NPC patients who were treated with cisplatin (DDP) + fluorouracil (5-FU) induction chemotherapy and radiotherapy between 1999 and 2005. The relationship of Aurora-B, FOXM1, and survival of these NPC patients was analyzed. RESULTS: Informative TMA results were obtained in 91 tumor cases for Aurora-B and 93 tumor cases for FOXM1. The 8-year failure-free survival rate (FFS) for the Aurora-B-negative and Aurora-B-positive group was 65.6 and 37.3%, respectively (p = 0.024), and the 8-year distant FFS (D-FFS) rate was 65.6 and 41.5%, respectively (p = 0.047). The 8-year overall survival (OS) in the FOXM1-negative group was moderately higher than in the FOXM1-positive group (58.4 vs 39.1%, p = 0.081). Cox regression analysis revealed that for FFS, Aurora-B expression was a significant prognostic factor (p = 0.025), while for D-FFS, Aurora-B expression was a marginally significant prognostic factor (p = 0.056). When FOXM1 expression was analyzed, the Cox regression analyses showed that FOXM1 expression was a marginally significant prognostic factor (p = 0.056) for OS. Correlation analysis showed that Aurora-B and FOXM1 expression had no significant correlation. CONCLUSION: Aurora-B and FOXM1 were both adverse prognostic markers for NPC patients treated with chemoradiotherapy. However, the two markers had no significant correlation.

S-scheme homojunction of 0D cubic/2D hexagonal ZnIn2S4 for efficient photocatalytic reduction of nitroarenes.

The targeted conversion of toxic nitroarenes to corresponding aminoarenes presents significant promise in simultaneously addressing environmental pollution concerns and producing value-added fine chemicals. In this study, we synthesize a 0D/2D ZnIn2S4 homojunction (CH-ZnIn2S4) by in situ growth of cubic ZnIn2S4 (C-ZnIn2S4) quantum dots onto the surface of ultrathin hexagonal ZnIn2S4 (H-ZnIn2S4) nanosheets for photocatalytic reduction of nitroarenes to aminoarenes using water as a hydrogen donor. The optimal performance of photocatalytic nitro reduction over the 0D/2D CH-ZnIn2S4 homojunction reaches 96.1% within 20 min of visible light irradiation, which is 2.45 and 1.52 times than that of C-ZnIn2S4 (39.3%) and H-ZnIn2S4 (63.3%), respectively. The improved photocatalytic performance can be attributed to the formation of a step-type S-scheme homojunction, characterized by identity chemical composition and natural lattice matching. The configuration enables continuous band bending and a low energy barrier of charge transportation, benefiting the charge transfer across the interface while maximizing their redox capabilities. Furthermore, the 2D structure of H-ZnIn2S4 nanosheets offers abundant surface sites to immobilize the 0D C-ZnIn2S4 that provides ample exposed active sites with low overpotential for HER, thereby ensuring high hydrogenation reduction activity of nitroarenes. The study is expected to inspire further interest in the reasonable design of homojunction structures for efficient and sustainable photocatalytic redox reactions.

Heat-sealable, transparent, and degradable arabinogalactan/polyvinyl alcohol films with UV-shielding, antibacterial, and antioxidant properties.

Petroleum-based packaging materials are nondegradable and unsustainable and thus are harmful to the environment. Renewable packaging films prepared from bio-based raw materials are promising alternatives to petroleum-based packaging materials. In this study, colorless and transparent bio-based films were successfully cast using a solution containing a mixture of arabinogalactan (AG) and poly (vinyl alcohol) (PVA). Vanillin was incorporated into the mixture to endow the films with UV-shielding, antioxidant, and antibacterial properties. The morphological, physical, antioxidant, and antibacterial properties of the blend films were then characterized. At an AG:PVA weight ratio of 1:3, and the vanillin content was 0.15 %, the tensile strength of the AG/PVA/Vanillin (APV) films reached ~28 MPa, while their elongation at break reached ~475 %. The addition of vanillin significantly affected the antioxidant and antibacterial properties of the blend films, which exhibited superb UV barrier capacity. The APV films exhibited extremely low oxygen transmittance, delaying the onset of mold/rot in strawberries and reducing their weight loss. Because of the heat sealability of the blend films, they can be used for encapsulating various substances, such as concentrated laundry liquid. Moreover, the blend films were recyclable and biodegradable. Thus, these films have great potential for applications that require sustainable packaging.

Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarization.

Neuroinflammation, triggered by aberrantly activated microglia, is widely recognized as a key contributor to the initiation and progression of Alzheimer's disease (AD). Microglial activation in the central nervous system (CNS) can be classified into two distinct phenotypes: the pro-inflammatory M1 phenotype and the anti-inflammatory M2 phenotype. In this study, we investigated the effects of a non-invasive rotating magnetic field (RMF) (0.2T, 4Hz) on cognitive and memory impairments in a sporadic AD model of female Kunming mice induced by AlCl3 and D-gal. Our findings revealed significant improvements in cognitive and memory impairments following RMF treatment. Furthermore, RMF treatment led to reduced amyloid-beta (Aß) deposition, mitigated damage to hippocampal morphology, prevented synaptic and neuronal loss, and alleviated cell apoptosis in the hippocampus and cortex of AD mice. Notably, RMF treatment ameliorated neuroinflammation, facilitated the transition of microglial polarization from M1 to M2, and inhibited the NF-кB/MAPK pathway. Additionally, RMF treatment resulted in reduced aluminum deposition in the brains of AD mice. In cellular experiments, RMF promoted the M1-M2 polarization transition and enhanced amyloid phagocytosis in cultured BV2 cells while inhibiting the TLR4/NF-кB/MAPK pathway. Collectively, these results demonstrate that RMF improves memory and cognitive impairments in a sporadic AD model, potentially by promoting the M1 to M2 transition of microglial polarization through inhibition of the NF-кB/MAPK signaling pathway. These findings suggest the promising therapeutic applications of RMF in the clinical treatment of AD.

Anti-ulcerative colitis effect of rotating magnetic field on DSS-induced mice by modulating colonic inflammatory deterioration.

Ulcerative colitis (UC) is a prevalent inflammatory disorder that emerges in the colon and rectum, exhibiting a rising global prevalence and seriously impacting the physical and mental health of patients. Significant challenges remain in UC treatment, highlighting the need for safe and effective long-term therapeutic approaches. Heralded as a promising physical treatment, the rotating magnetic field (RMF) demonstrates safety, stability, manageability, and efficiency. This study delves into RMF's potential in mitigating DSS-induced UC in mice, assessing disease activity indices (DAI) and pathological alterations such as daily body weight, fecal occult blood, colon length, and morphological changes. Besides, several indexes have been detected, including serum concentrations of pro-inflammatory cytokines (IL6, IL-17A, TNF-α, IFN-γ) and anti-inflammatory cytokines (TGF-ß, IL-4, IL-10), the ratio of splenic CD3+, CD4+, and CD8+ T cells, the rate of apoptotic colonic cells, the expression of colonic inflammatory and tight junction-associated proteins. The results showed that RMF had beneficial effects on the decrease of intestinal permeability, the restoration of tight junctions, and the mitigation of mitochondrial respiratory complexes (MRCs) by attenuating inflammatory dysfunction in colons of DSS-induced UC model of mice. In conclusion, this study demonstrates that RMF attenuates colonic inflammation, enhances colonic tight junction, and alleviates MRCs impairment by regulating the equilibrium of pro-inflammatory and anti-inflammatory cytokines in UC mice, suggesting the potential application of RMF in the clinical treatment of UC.

Structural elucidation and immunomodulatory activities in vitro of type I and II arabinogalactans from different origins of Astragalus membranaceus.

Astragalus membranaceus polysaccharide (APS) possesses excellent immunomodulatory activity. However, there are several studies on the structural characterization of APS. Here, we aimed to elucidate the repeating units of polysaccharides (APS1, 106.5 kDa; APS2, 114.5 kDa) obtained from different Astragalus membranaceus origins and further investigated their immunomodulatory activities. Based on structural analysis, types of the two polysaccharides were identified as arabinogalactan-I (AG-I) and arabinogalactan-II (AG-II), and co-elution of arabinogalactans (AGs) and α-glucan was observed. The backbone of AG-I was 1,4-linked ß-Galp occasionally substituted by α-Araf at O-2 and/or O-3. AG-II was a highly branched polysaccharide with long branches of α-Araf, which were attached to the O-3 of 1,6-linked ß-Galp of the backbone. The presence of AGs in A. membranaceus was confirmed for the first time. The two polysaccharides could promote the expression of IL-6, IL-1ß and TNF-α in RAW264.7 cells via MAPKs and NF-κB signaling pathways. The constants for APS1 and APS2 binding to Toll-like receptor 4 (TLR4) were 1.83 × 10-5 and 2.08 × 10-6, respectively. Notably, APS2 showed better immunomodulatory activity than APS1, possibly because APS2 contained more AGs. Hence, the results suggested that AGs were the vital components of APS in the immunomodulatory effect.

Corrigendum to "SOX8 promotes tumor growth and metastasis through FZD6-dependent Wnt/ß-catenin signaling in colorectal carcinoma" [Heliyon 9(12) (December 2023) e22586].

[This corrects the article DOI: 10.1016/j.heliyon.2023.e22586.].

Green, recyclable, mechanically robust, wet-adhesive and ionically conductive cellulose-based bioplastics enabled by supramolecular covalent hydrophobic eutectic networks.

The development of novel cellulose-based bioplastics (CBPs) is highly desirable because CBPs are green, rationally use resources, and lead to a reduction in environmental pollution compared to alternative materials. However, incorporating high transparency, water resistance, mechanical robustness, wet-adhesion, ionic conductivity and recyclability into CBP remains a challenge. In this paper, novel CBPs with supramolecular covalent networks are fabricated by introducing polymerizable hydrophobic deep eutectic solvents (HDES) into ethylcellulose (EC) networks through in situ plasticization followed by a rapid photopolymerization process. The excellent molecular interfacial compatibility enables EC to be loaded with a high content of poly(HDES), while allowing high transparency (more than 90 %) of the prepared CBPs. Multiple intermolecular interactions provide CBPs with mechanical robustness, water resistance, and underwater adhesion, and CBPs can be readily recovered by the solvent in a closed loop. Moreover, CBPs possess inherent ionic conductivities, and using them as green substrates, personalized electroluminescent devices can be successfully constructed. The method proposed in this paper provides a new strategy for the preparation of multifunctional CBPs, which will greatly enrich their applications in self-adhesive materials, green flexible electronics and other package materials.

Twin boundary defect engineering in Au cocatalyst to promote alcohol splitting for coproduction of H2 and fine chemicals.

The microstructure of Au metal cocatalyst has been shown to significantly influence its optical and electronic properties. However, the impact of Au defect engineering on photocatalytic activity remains underexplored. In this study, we synthesize different Au-TiO2 composites by in-situ hybridizing face-centered cubic (F-Au) and twin boundary defect Au (T-Au) nanoparticles (NPs) onto the surface of TiO2. We find that T-Au NPs with twin defects serve as highly efficient cocatalysts for converting alcohols into their corresponding aldehydes while also generating H2. The optimized T-Au/TiO2 composite yields an H2 evolution rate of 6850 µmol h-1 g-1 and a BAD formation rate of 6830 µmol h-1 g-1, about 38 times higher than that of blank TiO2. Compared to F-Au/TiO2, the T-Au/TiO2 composite enhances charge separation, extends the lifetime of electrons, and provides more active sites for H2 reduction. The twin defect also improves alcohol reactant adsorption, boosting overall photocatalytic performance. This research paves the way for more studies on defect engineering in metal cocatalysts for enhanced catalytic activities in organic synthesis and H2 evolution.