Exosomes loaded a smart bilayer-hydrogel scaffold with ROS-scavenging and macrophage-reprogramming properties for repairing cartilage defect.

Enhancing the regeneration of cartilage defects remains challenging owing to limited innate self-healing as well as acute inflammation arising from the overexpression of reactive oxygen species (ROS) in post-traumatic microenvironments. Recently, stem cell-derived exosomes (Exos) have been developed as potential cell-free therapy for cartilage regeneration. Although this approach promotes chondrogenesis, it neglects the emerging inflammatory microenvironment. In this study, a smart bilayer-hydrogel dual-loaded with sodium diclofenac (DC), an anti-inflammatory drug, and Exos from bone marrow-derived mesenchymal stem cells was developed to mitigate initial-stage inflammation and promote late-stage stem-cell recruitment and chondrogenic differentiation. First, the upper-hydrogel composed of phenylboronic-acid-crosslinked polyvinyl alcohol degrades in response to elevated levels of ROS to release DC, which mitigates oxidative stress, thus reprogramming macrophages to the pro-healing state. Subsequently, Exos are slowly released from the lower-hydrogel composed of hyaluronic acid into an optimal microenvironment for the stimulation of chondrogenesis. Both in vitro and in vivo assays confirmed that the dual-loaded bilayer-hydrogel reduced post-traumatic inflammation and enhanced cartilage regeneration by effectively scavenging ROS and reprogramming macrophages. The proposed platform provides multi-staged therapy, which allows for the optimal harnessing of Exos as a therapeutic for cartilage regeneration.

N-glycosylation of SCAP exacerbates hepatocellular inflammation and lipid accumulation via ACSS2-mediated histone H3K27 acetylation.

Sterol regulatory element binding protein (SREBP) cleavage-activating protein (SCAP) is a widely expressed membrane glycoprotein that acts as an important modulator of lipid metabolism and inflammatory stress. N-glycosylation of SCAP has been suggested to modulate cancer development, but its role in NASH is poorly understood. In this study, the N-glycosylation of SCAP was analyzed by using sequential trypsin proteolysis and glycosidase treatment. The liver cell lines expressing wild-type and N-glycosylation sites mutated SCAP were constructed to investigate the N-glycosylation role of SCAP in regulating inflammation and lipid accumulation as well as the underlying mechanisms. The hepatic SCAP protein levels were significantly increased in C57BL/6J mice fed with western diet and sweet water (WD+SW) and diabetic db/db mice, which exhibited typical liver steatosis and inflammation. In vitro, the enhanced N-glycosylation increased the protein stability of SCAP and hence increased its total protein levels, while the ablation of N-glycosylation significantly decreased SCAP protein stability and alleviated lipid accumulation and inflammation in hepatic cell lines. Mechanistically, the presence of SCAP N-glycosylation increased not only the SREBP1-mediated acetyl-CoA synthetase 2 (ACSS2) transcription but also the AMPK-mediated S659 phosphorylation of ACCS2 protein, causing the enhanced ACSS2 levels in nucleus and hence increasing the histone H3K27 acetylation (H3K27ac), which is a key epigenetic modification associated with NASH. Modulating ACSS2 expression or its location in cytoplasm abolished the effects of SCAP N-glycosylation on H3K27ac and lipid accumulation and inflammation. In conclusion, SCAP N-glycosylation aggravates inflammation and lipid accumulation through enhancing ACSS2-mediated H3K27ac in hepatocytes.

Poly(butylene adipate-co-terephthalate)/Polylactic Acid/Tetrapod-Zinc Oxide Whisker Composite Films with Antibacterial Properties.

Biodegradable composite films comprising of poly(butylene adipate-co-terephthalate) (PBAT), polylactic acid (PLA), and tetrapod-zinc oxide (T-ZnO) whisker were prepared by a melt-extrusion and blow molding process. The effect of the incorporation of the T-ZnO whisker (1 to 7 wt.%) in the PBAT/PLA blend film was studied systematically. The composite films with an optimal T-ZnO whisker concentration of 3 wt.% exhibited the highest mechanical (tensile strength ~32 MPa), rheological (complex viscosity~1200 Pa.s at 1 rad/s angular frequency), and gas barrier (oxygen permeability~20 cc/m2·day) properties, whereas the composite films with 7 wt.% T-ZnO whiskers exhibited the highest antibacterial properties. The developed composite films can find potential application as antibacterial food packaging materials.

Blockade of BTLA alone or in combination with PD-1 restores the activation and proliferation of CD8+ T cells during in vitro infection with NCP BVDV.

Bovine viral diarrhea virus (BVDV) infection can result in typical peripheral blood lymphopenia and immune dysfunction. However, the molecular mechanism underlying the onset of lymphopenia remains unclear. B and T lymphocyte attenuator (BTLA) is a novel immune checkpoint molecule that primarily inhibits activation and proliferation of T cells. Blockade of BTLA with antibodies can boost the proliferation and anti-viral immune functions of T cells. Nonetheless, the immunomodulatory effects of BTLA in CD8+ T cells during BVDV infection remain unknown. Therefore, BTLA expression was measured in bovine peripheral blood CD8+ T cells infected with BVDV in vitro. Furthermore, the effects of BTLA or PD-1 blockade on CD8+ T cell activation, proliferation, and anti-viral immunological activities were investigated, as well as expression of signaling molecules downstream of BTLA, both alone and in combination. The results demonstrated that BTLA and PD-1 mRNA and protein levels were considerably increased in CD8+ T cells infected with cytopathic and non-cytopathic (NCP) BVDV. Surprisingly, as compared to blockade of either BTLA or PD-1, blockade of both dramatically increased proliferation and expression of CD25 and p-EKR of CD8+ T cells infected with NCP BVDV. Furthermore, blockade of BTLA, but not PD-1, had no effect on BVDV replication or IFN-γ expression. These findings confirmed the immunomodulatory roles of BTLA during BVDV infection, as well as the synergistic role of BTLA and PD-1 in NCP BVDV infection, thereby providing new insights to promote activation and the anti-viral immunological activities of CD8+ T cells.

Inhibiting cholesterol de novo synthesis promotes hepatocellular carcinoma progression by upregulating prostaglandin E synthase 2-mediated arachidonic acid metabolism under high fatty acid conditions.

Inhibition of cholesterol de novo synthesis (DNS) by statins has controversial effects on the treatment of hepatocellular carcinoma (HCC). High fatty acid conditions have been reported to limit the effect of statins on metabolism diseases. Whether high fatty acid conditions interfere with the effect of statins on HCC remains unclear. Here, we reported that inhibiting cholesterol DNS with atorvastatin promoted the oncogenic capabilities of diethylnitrosamine (DEN) in mice fed high fatty acid diets (HFD). The combined analysis of metabolomics and transcriptomics revealed that arachidonic acid (AA) metabolism was the most significant changed pathway between mice with and without atorvastatin treatment. In vitro, in the presence of AA precursor linoleic acid (LA), atorvastatin promoted the proliferation and migration ability of HCC cell lines. However, in the absence of LA, these phenomena disappeared. TCGA and tissue microarray examination revealed that prostaglandin e synthase 2 (PTGES2), a key enzyme in AA metabolism, was associated with the poor outcome of HCC patients. Overexpression of PTGES2 promoted the proliferation and migration of HCC cell lines, and knockdown of PTGES2 inhibited the proliferation and migration of cells. Additionally, atorvastatin upregulated PTGES2 expression by enhancing Sterol-regulatory element binding protein 2 (SREBP2)-mediated transcription. Knockdown of PTGES2 reversed the proliferation and migration ability enhanced by atorvastatin. Overall, our study reveals that a high fatty acid background is one of the possible conditions limiting the application of statins in HCC, under which statins promote the progression of HCC by enhancing SREBP2-mediated PTGES2 transcription.

A dataset of low-carbon energy transition index for Chinese cities 2003-2019.

Cities are at the heart of climate change mitigation as they account for over 70% of global carbon emissions. However, cities vary in their energy systems and socioeconomic capacities to transition to renewable energy. To address this heterogeneity, this study proposes an Energy Transition Index (ETI) specifically designed for cities, and applies it to track the progress of energy transition in Chinese cities. The city-level ETI framework is based on the national ETI developed by the World Economic Forum (WEF) and comprises two sub-indexes: the Energy System Performance sub-index, which evaluates the current status of cities' energy systems in terms of energy transition, and the Transition Readiness sub-index, which assesses their socioeconomic capacity for future energy transition. The initial version of the dataset includes ETI and its sub-indexes for 282 Chinese cities from 2003 to 2019, with annual updates planned. The spatiotemporal data provided by the dataset facilitates research into the energy transition roadmap for different cities, which can help China achieve its energy transition goals.

Correction: Chen et al. Identification of the Causal Agent of Brown Leaf Spot on Kiwifruit and Its Sensitivity to Different Active Ingredients of Biological Fungicides. Pathogens 2022, 11, 673.

In the original publication [...].

Protein Kinase C Is Involved in Vegetative Development, Stress Response and Pathogenicity in Verticillium dahliae.

Potato Verticillium wilt, caused by Verticillium dahliae, is a serious soil-borne vascular disease, which restricts the sustainable development of the potato industry, and the pathogenic mechanism of the fungus is complex. Therefore, it is of great significance to explore the important pathogenic factors of V. dahliae to expand the understanding of its pathology. Protein kinase C (PKC) gene is located in the Ca2+ signaling pathway, which is highly conserved in filamentous fungi and involved in the regulation of a variety of biological processes. In the current study, the PKC gene in V. dahliae (VdPKC) was characterized, and its effects on the fungal pathogenicity and tolerance to fungicide stress were further studied. The results showed that the VdPKC positively regulated the growth and development, conidial germination, and production of V. dahliae, which was necessary for the fungus to achieve pathogenicity. It also affected the formation of melanin and microsclerotia and changed the adaptability of V. dahliae to different environmental stresses. In addition, VdPKC altered the tolerance of V. dahliae to different fungicides, which may be a potential target for polyoxin. Therefore, our results strongly suggest that VdPKC gene is necessary for the vegetative growth, stress response, and pathogenicity of V. dahliae.

Strain-Driven Bidirectional Spin Orientation Control in Epitaxial High Entropy Oxide Films.

High entropy oxides (HEOs), based on the incorporation of multiple-principal cations into the crystal lattice, offer the possibility to explore previously inaccessible oxide compositions and unconventional properties. Here it is demonstrated that despite the chemical complexity of HEOs external stimuli, such as epitaxial strain, can selectively stabilize certain magneto-electronic states. Epitaxial (Co0.2 Cr0.2 Fe0.2 Mn0.2 Ni0.2 )3 O4 -HEO thin films are grown in three different strain states: tensile, compressive, and relaxed. A unique coexistence of rocksalt and spinel-HEO phases, which are fully coherent with no detectable chemical segregation, is revealed by transmission electron microscopy. This dual-phase coexistence appears as a universal phenomenon in (Co0.2 Cr0.2 Fe0.2 Mn0.2 Ni0.2 )3 O4 epitaxial films. Prominent changes in the magnetic anisotropy and domain structure highlight the strain-induced bidirectional control of magnetic properties in HEOs. When the films are relaxed, their magnetization behavior is isotropic, similar to that of bulk materials. However, under tensile strain, the hardness of the out-of-plane (OOP) axis increases significantly. On the other hand, compressive straining results in an easy OOP magnetization and a maze-like magnetic domain structure, indicating the perpendicular magnetic anisotropy. Generally, this study emphasizes the adaptability of the high entropy design strategy, which, when combined with coherent strain engineering, opens additional prospects for fine-tuning properties in oxides.

Hepatocyte CD36 protects mice from NASH diet-induced liver injury and fibrosis via blocking N1ICD production.

BACKGROUND & AIMS: Fatty acid translocase CD36 (CD36/FAT) is a widely expressed membrane protein with multiple immuno-metabolic functions. Genetic CD36 deficiency is associated with increased risk of metabolic dysfunction-associated fatty liver disease (MAFLD) in patients. Liver fibrosis severity mainly affects the prognosis in patients with MAFLD, but the role of hepatocyte CD36 in liver fibrosis of MAFLD remains unclear. METHODS: A high-fat high-cholesterol diet and a high-fat diet with high-fructose drinking water were used to induce nonalcoholic steatohepatitis (NASH) in hepatocyte-specific CD36 knockout (CD36LKO) and CD36flox/flox (LWT) mice. Human hepG2 cell line was used to investigate the role of CD36 in regulating Notch pathway in vitro. RESULTS: Compared to LWT mice, CD36LKO mice were susceptible to NASH diet-induced liver injury and fibrosis. The analysis of RNA-sequencing data revealed that Notch pathway was activated in CD36LKO mice. LY3039478, an inhibitor of γ-secretase, inhibited Notch1 protein S3 cleavage and Notch1 intracellular domain (N1ICD) production, alleviating liver injury and fibrosis in CD36LKO mice livers. Likewise, both LY3039478 and knockdown of Notch1 inhibited the CD36KO-induced increase of N1ICD production, causing the decrease of fibrogenic markers in CD36KO HepG2 cells. Mechanistically, CD36 formed a complex with Notch1 and γ-secretase in lipid rafts, and hence CD36 anchored Notch1 in lipid rafts domains and blocked Notch1/γ-secretase interaction, inhibiting γ-secretase-mediated cleavage of Notch1 and the production of N1ICD. CONCLUSIONS: Hepatocyte CD36 plays a key role in protecting mice from diet-induced liver injury and fibrosis, which may provide a potential therapeutic strategy for preventing liver fibrogenesis in MAFLD.

The impact of urban population spatial distribution on CO2 emissions in China from the perspective of individual and interactive effects.

As China's rapid urbanization continues, uneven urban population spatial distribution (UPSD) has a profound impact on its CO2 emissions. To understand how UPSD shapes CO2 emissions in China, this study employs geographic detectors to analyze the spatial stratified heterogeneity patterns of urban CO2 emissions and explore the spatial individual and interactive effects of UPSD in 2005 and 2015. Results show that CO2 emissions increased significantly from 2005 to 2015, especially in developed cities and resource-based cities. The spatial individual effect of UPSD on spatial stratified heterogeneity pattern of CO2 emissions has gradually increased in the North Coast, South Coast, the Middle Yellow River, and the Middle Yangtze River. The interaction of UPSD and urban transportation infrastructure, urban economic development, and urban industrial structure plays a more important role on the North Coast and East Coast than in other city groups in 2005. In 2015, the interaction between UPSD and urban research and development was the traction of mitigating CO2 emissions in developed city groups, especially on the North Coast and East Coast. Moreover, the spatial interaction between the UPSD and urban industrial structure has gradually weakened in developed city groups, which means UPSD drives the prosperity of the service industry, thus contributing to the low-carbon development of Chinese cities.

Mitochondrial folate metabolism-mediated α-linolenic acid exhaustion masks liver fibrosis resolution.

Sustainable TGF-ß1 signaling drives organ fibrogenesis. However, the cellular adaptation to maintain TGF-ß1 signaling remains unclear. In this study, we revealed that dietary folate restriction promoted the resolution of liver fibrosis in mice with nonalcoholic steatohepatitis. In activated hepatic stellate cells, folate shifted toward mitochondrial metabolism to sustain TGF-ß1 signaling. Mechanistically, nontargeted metabolomics screening identified that α-linolenic acid (ALA) is exhausted by mitochondrial folate metabolism in activated hepatic stellate cells. Knocking down serine hydroxymethyltransferase 2 increases the bioconversion of ALA to docosahexaenoic acid, which inhibits TGF-ß1 signaling. Finally, blocking mitochondrial folate metabolism promoted liver fibrosis resolution in nonalcoholic steatohepatitis mice. In conclusion, mitochondrial folate metabolism/ALA exhaustion/TGF-ßR1 reproduction is a feedforward signaling to sustain profibrotic TGF-ß1 signaling, and targeting mitochondrial folate metabolism is a promising strategy to enforce liver fibrosis resolution.

Can ocean carbon sink trading achieve economic and environmental benefits? Simulation based on DICE-DSGE model.

Low-carbon development requires joint efforts in terms of "carbon reduction" and "carbon sink increase." This study thus proposes a DICE-DSGE model for exploring the environmental and economic benefits of ocean carbon sinks and provides policy suggestions for marine economic development and carbon emission policy choices. The results are as follows: (1) while the economic benefits of heterogeneous technological shocks are apparent, the environmental benefits of carbon tax and carbon quota shocks are significant; (2) increasing the efficiency of ocean carbon sinks improves the environmental benefits of technological shocks as well as the output benefits of emission reduction tools, while increasing the share of marine output can improve both the economic benefits of technological shocks and the environmental benefits of emission reduction tools; and (3) ocean output proportion has the most considerable positive effect on social welfare, followed by marine total factor productivity (TFP). The correlation effect of ocean carbon sink efficiency is negative.

Hepatocyte CD36 modulates UBQLN1-mediated proteasomal degradation of autophagic SNARE proteins contributing to septic liver injury.

Macroautophagy/autophagy plays a protective role in sepsis-induced liver injury. As a member of class B scavenger receptors, CD36 plays important roles in various disorders, such as atherosclerosis and fatty liver disease. Here we found that the expression of CD36 in hepatocytes was increased in patients and a mouse model with sepsis, accompanied by impaired autophagy flux. Furthermore, hepatocyte cd36 knockout (cd36-HKO) markedly improved liver injury and the impairment of autophagosome-lysosome fusion in lipopolysaccharide (LPS)-induced septic mice. Ubqln1 (ubiquilin 1) overexpression (OE) in hepatocyte blocked the protective effect of cd36-HKO on LPS-induced liver injury in mice. Mechanistically, with LPS stimulation, CD36 on the plasma membrane was depalmitoylated and distributed to the lysosome, where CD36 acted as a bridge molecule linking UBQLN1 to soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins and hence promoting the proteasomal degradation of SNARE proteins, resulting in fusion impairment. Overall, our data reveal that CD36 is essential for modulating the proteasomal degradation of autophagic SNARE proteins in a UBQLN1-dependent manner. Targeting CD36 in hepatocytes is effective for improving autophagic flux in sepsis and therefore represents a promising therapeutic strategy for clinical treatment of septic liver injury.Abbreviations: AAV8: adeno-associated virus 8; AOSC: acute obstructive suppurative cholangitis; ATP1A1: ATPase, Na+/K+ transporting, alpha 1 polypeptide; CASP3: caspase 3; CASP8: caspase 8; CCL2: chemokine (C-C motif) ligand 2; cd36-HKO: hepatocyte-specific cd36 knockout; Co-IP: co-immunoprecipitation; CQ: chloroquine; Cys: cysteine; GOT1: glutamic-oxaloacetic transaminase 1, soluble; GPT: glutamic-pyruvic transaminase, soluble; IL1B: interleukin 1 beta; IL6: interleukin 6; KO: knockout; LAMP1: lysosomal associated membrane protein 1; LDH, lactate dehydrogenase; LPS: lipopolysaccharide; LYPLA1: lysophospholipase 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; OE: overexpression; qPCR: quantitative polymerase chain reaction; SNAP29: synaptosome associated protein 29; SNARE: soluble N-ethylmaleimide-sensitive factor attachment protein receptor; SQSTM1/p62: sequestosome 1; STX17: syntaxin 17; TNF: tumor necrosis factor; TRIM: tripartite motif-containing; UBA: ubiquitin-associated; UBL: ubiquitin-like; UBQLN: ubiquilin; VAMP8: vesicle associated membrane protein 8; WT: wild-type.

Hypothetical Protein VDAG_07742 Is Required for Verticillium dahliae Pathogenicity in Potato.

Verticillium dahliae is a soil-borne pathogenic fungus that causes Verticillium wilt in host plants, a particularly serious problem in potato cultivation. Several pathogenicity-related proteins play important roles in the host infection process, hence, identifying such proteins, especially those with unknown functions, will surely aid in understanding the mechanism responsible for the pathogenesis of the fungus. Here, tandem mass tag (TMT) was used to quantitatively analyze the differentially expressed proteins in V. dahliae during the infection of the susceptible potato cultivar "Favorita". Potato seedlings were infected with V. dahliae and incubated for 36 h, after which 181 proteins were found to be significantly upregulated. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses showed that most of these proteins were involved in early growth and cell wall degradation. The hypothetical, secretory protein with an unknown function, VDAG_07742, was significantly upregulated during infection. The functional analysis with knockout and complementation mutants revealed that the associated gene was not involved in mycelial growth, conidial production, or germination; however, the penetration ability and pathogenicity of VDAG_07742 deletion mutants were significantly reduced. Therefore, our results strongly indicate that VDAG_07742 is essential in the early stage of potato infection by V. dahliae.

Natural variation in the hrpL promoter renders the phytopathogen Pseudomonas syringae pv. actinidiae nonpathogenic.

The genetic basis underlying loss-of-virulence mutations that arise among natural phytopathogen populations is not well documented. In this study, we examined the virulence of 377 isolates of Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) that were isolated from 76 kiwifruit orchards suffering from bacterial canker disease. Eighty-four nonpathogenic isolates were identified in 40 orchards. A nonpathogenic isolate G166 was found to be defective in hrpL transcription and the downstream type III secretion system (T3SS)-dependent phenotypes. Comparative genomics and complementary expression assay revealed that a single-base "G" insertion in the hrpL promoter blocks gene transcription by reducing promoter activity. The electrophoretic mobility shift assay showed that the genetic variation impairs σ54 /promoter binding during gene transcription under hrp-inducing conditions, resulting in lower expression of hrpL. A PCR-restriction fragment length polymorphism assay was performed to trace the evolutionary history of this mutation, which revealed the independent onset of genetic variations in natural Psa3 populations. We also found that nonpathogenic variants outperformed virulent Psa3 bacteria for both epiphytic and apoplast colonization of kiwifruit leaves in mixed inoculations. Our study highlights a novel mechanism for loss of virulence in Psa3 and provides insight into bacterial adaptive evolution under natural settings.

An Adhesive Bioink toward Biofabrication under Wet Conditions.

Three-dimensional (3D) bioprinting is driving significant innovations in biomedicine over recent years. Under certain scenarios such as in intraoperative bioprinting, the bioinks used should exhibit not only cyto/biocompatibility but also adhesiveness in wet conditions. Herein, an adhesive bioink composed of gelatin methacryloyl, gelatin, methacrylated hyaluronic acid, and skin secretion of Andrias davidianus is designed. The bioink exhibits favorable cohesion to allow faithful extrusion bioprinting in wet conditions, while simultaneously showing good adhesion to a variety of surfaces of different chemical properties, possibly achieved through the diverse bonds presented in the bioink formulation. As such, this bioink is able to fabricate sophisticated planar and volumetric constructs using extrusion bioprinting, where the dexterity is further enhanced using ergonomic handheld bioprinters to realize in situ bioprinting. In vitro experiments reveal that cells maintain high viability; further in vivo studies demonstrate good integration and immediate injury sealing. The characteristics of the bioink indicate its potential widespread utility in extrusion bioprinting and will likely broaden the applications of bioprinting toward situations such as in situ dressing and minimally invasive tissue regeneration.

Measuring the low-carbon energy transition in Chinese cities.

Cities' transition from fossil-based systems of energy production and consumption to renewable energy sources-the energy transition-is critical to mitigating climate change impact as cities' energy consumption and CO2 emissions account for two-thirds and over 70% of the world's total, respectively. Given cities' heterogeneity, they need specific low-carbon roadmaps instead of one-size-fits-all approaches. Here, we used an Energy Transition Index (ETI) to characterize the city-level energy transitions from energy system performance and transition readiness dimensions. The ETI scores for 282 cities in China revealed a significant heterogeneity across cities and over time, and the gap between the cities in the top and bottom quartiles was persistent. We estimated that China's energy and carbon intensity could decrease by 34% and 32%, respectively, and that carbon per capita could fall by 17% if each city modestly follows the sustainable development path forged by the best performing cities with similar economic structures.

High Entropy Approach to Engineer Strongly Correlated Functionalities in Manganites.

Technologically relevant strongly correlated phenomena such as colossal magnetoresistance (CMR) and metal-insulator transitions (MIT) exhibited by perovskite manganites are driven and enhanced by the coexistence of multiple competing magneto-electronic phases. Such magneto-electronic inhomogeneity is governed by the intrinsic lattice-charge-spin-orbital correlations, which, in turn, are conventionally tailored in manganites via chemical substitution, charge doping, or strain engineering. Alternately, the recently discovered high entropy oxides (HEOs), owing to the presence of multiple-principal cations on a given sub-lattice, exhibit indications of an inherent magneto-electronic phase separation encapsulated in a single crystallographic phase. Here, the high entropy (HE) concept is combined with standard property control by hole doping in a series of single-phase orthorhombic HE-manganites (HE-Mn), (Gd0.25 La0.25 Nd0.25 Sm0.25 )1- x Srx MnO3 (x = 0-0.5). High-resolution transmission microscopy reveals hitherto-unknown lattice imperfections in HEOs: twins, stacking faults, and missing planes. Magnetometry and electrical measurements infer three distinct ground states-insulating antiferromagnetic, unpercolated metallic ferromagnetic, and long-range metallic ferromagnetic-coexisting or/and competing as a result of hole doping and multi-cation complexity. Consequently, CMR ≈1550% stemming from an MIT is observed in polycrystalline pellets, matching the best-known values for bulk conventional manganites. Hence, this initial case study highlights the potential for a synergetic development of strongly correlated oxides offered by the high entropy design approach.

In situ synthesis of magnesium-doped hydroxyapatite aerogel for highly efficient U(VI) separation with ultra high adsorption capacity and excellent recyclability.

Mg-doped HAP aerogel (MHAPA) was firstly in situ prepared via freeze-drying-calcination technology to capture U(VI). The U(VI) removal capacity by MHAPA even arrived 2685.6 mg g-1, which was about 2 times over purchased HAP, illustrating that the incorporation of Mg ions could greatly enhance the U(VI) removal capacity. Compared with HAP, MHAPA also showed better anti-ion interference ability and dynamic removal performances. In comparison with other HAP-based adsorbents, MHAPA possessed good recyclability and its desorption rate was up to 93.4% in the first cycle. The excellent U(VI) removal performances of MHAPA might be owing to its low crystallinity and grain size, fast ion exchange rate and partial ionization under acidic conditions, which would accelerate the process of electrostatic attraction, ion-exchange, and complexation to immobilize U(VI). To sum up, the prepared MHAPA was expected to be an environmentally friendly, recyclable and effective adsorbent to immobilize U(VI) in actual wastewater.