Texture of cooked germinated brown rice subjected to freeze-thaw treatment and its improvement by magnetic field treatment.

This study aimed to investigate the textural changes of cooked germinated brown rice (GBR) during freeze-thaw treatment and propose a strategy for enhancing its texture using magnetic field (MF). Seven freeze-thaw cycles exhibited more pronounced effects compared to 7 days of freezing, resulting in increases in GBR hardness by 85.59 %-164.36 % and decreases in stickiness by 10.34 %-43.55 %. Water loss, structural damage of GBR flour, and starch retrogradation contributed to the deterioration of texture. MF mitigated these effects by inhibiting the transformation of bound water into free water, reducing water loss by 0.39 %-0.57 %, and shortening the phase transition period by 2.0-21.5 min, thereby diminishing structural damage to GBR flour and hindering starch retrogradation. Following MF treatment (5 mT), GBR hardness decreased by 21.00 %, while stickiness increased by 45.71 %. This study elucidates the mechanisms through which MF enhances the texture, offering theoretical insights for the industrial production of high-quality frozen rice products.

Black phosphorus nanosheets induce autophagy dysfunction by a size- and surface modification-related impairment of lysosomes in macrophages.

The widespread application of black phosphorus nanosheets (BPNSs) raises concerns about their potential impact on human health. Although that the autophagy-inducing properties of BPNSs in cancer cells are documented, their effects on macrophages-key components of the immune system and the mechanisms involved remain obscure, especially in terms of the influences of BPNS the size and surface modifications on the autophagic process. This study investigated the effects of bare BPNSs and PEGylated BPNSs (BP-PEG) on macrophage autophagy and its underlying mechanisms by comprehensive biochemical analyses. The results indicated that both BPNSs and BP-PEG are internalized by RAW264.7 cells through phagocytosis and caveolin-dependent endocytosis, leading to lysosomal accumulation. The internalized BPNSs induced mitochondrial dysfunction, which subsequently elevated the NAD+/NADH ratio and activated the SIRT-1 pathway, initiating autophagy. However, BPNSs disrupted the autophagic flux by impairing autolysosome formation, leading to apoptosis in a size-dependent manner. In contrast, BP-PEG preserved lysosomal integrity, maintaining autophagic activity and cell viability. These findings deepen our understanding of the influence of nanosheet size and surface modifications on macrophage autophagy, contributing to the formulation of regulatory guidelines to minimize the potential adverse effects and health risks associated with BPNS utilization in various applications.

Disruption of branched-chain amino acid homeostasis promotes the progression of DKD via enhancing inflammation and fibrosis-associated epithelial-mesenchymal transition.

BACKGROUND AND AIMS: The disrupted homeostasis of branched-chain amino acids (BCAAs, including leucine, isoleucine, and valine) has been strongly correlated with diabetes with a potential causal role. However, the relationship between BCAAs and diabetic kidney disease (DKD) remains to be established. Here, we show that the elevated BCAAs from BCAAs homeostatic disruption promote DKD progression unexpectedly as an independent risk factor. METHODS AND RESULTS: Similar to other tissues, the suppressed BCAAs catabolic gene expression and elevated BCAAs abundance were detected in the kidneys of type 2 diabetic mice and individuals with DKD. Genetic and nutritional studies demonstrated that the elevated BCAAs from systemic disruption of BCAAs homeostasis promoted the progression of DKD. Of note, the elevated BCAAs promoted DKD progression without exacerbating diabetes in the animal models of type 2 DKD. Mechanistic studies demonstrated that the elevated BCAAs promoted fibrosis-associated epithelial-mesenchymal transition (EMT) by enhancing the activation of proinflammatory macrophages through mTOR signaling. Furthermore, pharmacological enhancement of systemic BCAAs catabolism using small molecule inhibitor attenuated type 2 DKD. Finally, the elevated BCAAs also promoted DKD progression in type 1 diabetic mice without exacerbating diabetes. CONCLUSION: BCAA homeostatic disruption serves as an independent risk factor for DKD and restoring BCAA homeostasis pharmacologically or dietarily represents a promising therapeutic strategy to ameliorate the progression of DKD.

Layer-by-layer self-assembly coatings on strontium titanate nanotubes with antimicrobial and anti-inflammatory properties to prevent implant-related infections.

One way to effectively address endophyte infection and loosening is the creation of multifunctional coatings that combine anti-inflammatory, antibacterial, and vascularized osteogenesis. This study started with the preparation of strontium-doped titanium dioxide nanotubes (STN) on the titanium surface. Next, tannic acid (TA), gentamicin sulfate (GS), and pluronic F127 (PF127) were successfully loaded into the STN via layer-by-layer self-assembly, resulting in the STN@TA-GS/PF composite coatings. The findings demonstrated the excellent hydrophilicity and bioactivity of the STN@TA-GS/PF coating. STN@TA-GS/PF inhibited E. coli and S. aureus in vitro to a degree of roughly 80.95 % and 92.45 %, respectively. Cellular investigations revealed that on the STN@TA-GS/PF surface, the immune-system-related RAW264.7, the vasculogenic HUVEC, and the osteogenic MC3T3-E1 showed good adhesion and proliferation activities. STN@TA-GS/PF may influence RAW264.7 polarization toward the M2-type and encourage MC3T3-E1 differentiation toward osteogenesis at the molecular level. Meanwhile, the STN@TA-GS/PF coating achieved effective removal of ROS within HUVEC and significantly promoted angiogenesis. In both infected and non-infected bone defect models, the STN@TA-GS/PF material demonstrated strong anti-inflammatory, antibacterial, and vascularization-promoting osteogenesis properties. In addition, STN@TA-GS/PF had good hemocompatibility and biosafety. The three-step process used in this study to modify the titanium surface for several purposes gave rise to a novel concept for the clinical design of antimicrobial coatings with immunomodulatory properties.

Genome-wide identification of metal tolerance protein genes in Quercus dentata and their roles in response to various heavy metal stresses.

Metal tolerance protein (MTP) is a cation transporter that plays an important role in tolerance to heavy metal stress. However, thus far, there has been no genome-wide investigation of the MTP gene family in Quercus plants. Quercus dentata is one of the main constructive species of forest in northern China. It has strong tolerance to a variety of heavy metal stresses. In this study, 25 MTPs were identified from the Q. dentata genome and classified into three subfamilies and seven groups according to their sequence characteristics and phylogenetic relationships. Both tandem and segmental duplication events contributed to the expansion of the QdMTP gene family. Interestingly, all 10 tandem duplication events contributed to the expansion of the Mn-CDF subfamily. The expression of Mn-CDF subfamily members in different organs and tissues of Q. dentata was different, and they responded differently to manganese, iron, zinc and cadmium stress treatments. QdMTP10.7, a member of the Mn-CDF subfamily, enhanced yeast growth under manganese, zinc and iron stresses. The subcellular localization in tobacco leaf epidermis cells showed that QdMTP10.7 was located in vacuoles. These data generated from this study provide an important foundation to elucidate the biological roles of QdMTP genes related to heavy metal tolerance in Q. dentata.

Associations between insomnia and cardiovascular diseases: a meta-review and meta-analysis of observational and Mendelian randomization studies.

STUDY OBJECTIVES: Observational studies suggest associations between insomnia and cardiovascular diseases (CVDs), but the causal mechanism remains unclear. We investigated the potential causal associations between insomnia and CVDs by a combined systematic meta-review and meta-analysis of observational and Mendelian randomization (MR) studies. METHODS: We searched PubMed, Web of Science, and Embase for English-language articles from inception to 7/11/2023. Two reviewers independently screened the articles to minimize potential bias. We summarized the current evidence on the associations of insomnia with coronary artery disease (CAD), atrial fibrillation (AF), heart failure (HF), myocardial infarction (MI), hypertension (HTN), and stroke risk by combining meta-analyses of observational and MR studies. RESULTS: Four meta-analyses of observational studies and 9 MR studies were included in the final data analysis. A systematic meta-review of observational studies provided strong evidence that insomnia is an independent risk factor for many CVDs, including AF, MI, and HTN. A meta-analysis of MR studies revealed that insomnia may be potentially causally related to CAD (odds ratio (OR)=1.14, 95% confidence interval (CI)=1.10-1.19, I2=97%), AF (OR=1.02, 95% CI=1.01-1.04, I2=94%), HF (OR=1.04, 95% CI=1.03-1.06, I2 =97%), HTN (OR=1.16, 95% CI=1.13-1.18, I2=28%), large artery stroke (OR=1.14, 95% CI=1.05-1.24, I2=0%), any ischemic stroke (OR=1.09, 95% CI=1.03-1.14, I2=60%), and primary intracranial hemorrhage (OR=1.16, 95% CI=1.05-1.27, I2=0%). No evidence suggested that insomnia is causally associated with cardioembolic or small vessel stroke. CONCLUSIONS: Our results provide strong evidence supporting a possible causal association between insomnia and CVD risk. Strategies to treat insomnia may be promising targets for preventing CVDs.

Risk factors of bloodstream infection in erythroderma from atopic dermatitis, psoriasis, and drug reactions: a retrospective observational cohort study.

Background: Atopic dermatitis (AD), psoriasis, and drug reactions associated with erythroderma are frequently complicated by infections. However, bloodstream infection (BSI) have received less research attention. Objectives: This study aimed to investigate the clinical characteristics and risk factors associated with BSI in patients with erythroderma. Methods: A retrospective analysis was conducted on 141 erythroderma cases. Eleven cases were identified as having BSI. Clinical records of both BSI and non-BSI groups were reviewed and compared. Results: BSI was diagnosed in 7.80% (11/141) of erythroderma cases, with a breakdown of 7.14% in AD, 2.00% in psoriasis, and 17.14% in drug reactions. Notably, all positive skin cultures (7/7) showed bacterial isolates concordant with blood cultures. Univariate logistic regression analysis revealed several significant associations with BSI, including temperature (≤36.0 or ≥38.5 °C; odds ratio (OR) = 28.06; p < 0.001), chilling (OR = 22.10; p < 0.001), kidney disease (OR = 14.64; p < 0.001), etiology of drug reactions (OR = 4.18; p = 0.03), albumin (ALB) (OR = 0.86; p < 0.01), C-reaction protein (CRP) (OR = 1.01; p = 0.02), interleukin 6 (IL-6) (OR = 1.02; p = 0.02), and procalcitonin (PCT) (OR = 1.07; p = 0.03). Receiver operating characteristic (ROC) curves demonstrated significant associations with ALB (p < 0.001; the area under curve (AUC) = 0.80), PCT (p = 0.009; AUC = 0.74), and CRP (p = 0.02; AUC = 0.71). Conclusions: Increased awareness of BSI risk is essential in erythroderma management. Patients with specific risk factors, such as abnormal body temperature (≤36.0 or ≥38.5 °C), chilling sensations, kidney disease, a history of drug reactions, elevated CRP (≥32 mg/L), elevated PCT (≥1.00 ng/ml), and low albumin (≤31.0 g/L), require close monitoring for BSI development.

Intermittent protein restriction before but not after the onset of diabetic kidney disease attenuates disease progression in mice.

Background: High dietary protein intake exacerbates proteinuria in individuals with diabetic kidney disease (DKD). However, studies on the impacts of low protein diet (LPD) on DKD have yielded conflicting results. Furthermore, patient compliance to continuous protein restriction is challenging. Objective: The current study aims to investigate the effects of intermittent protein restriction (IPR) on disease progression of DKD. Methods: Diabetic KK-Ay mice were used in this study. For the IPR treatment, three consecutive days of LPD were followed by four consecutive days of normal protein diet (NPD) within each week. For early intervention, mice received IPR before DKD onset. For late intervention, mice received IPR after DKD onset. In both experiments, age-matched mice fed continuous NPD served as the control group. Kidney morphology, structure and function of mice in different groups were examined. Results: Intermittent protein restriction before DKD onset ameliorated pathological changes in kidney, including nephromegaly, glomerular hyperfiltration, tubular injuries and proteinuria, without improving glycemic control. Meanwhile, IPR initiated after DKD onset showed no renoprotective effects despite improved glucose homeostasis. Conclusion: Intermittent protein restriction before rather than after DKD onset protects kidneys, and the impacts of IPR on the kidneys are independent of glycemic control. IPR shows promise as an effective strategy for managing DKD and improving patient compliance.

Correlation between newborn weight and serum BCAAs in pregnant women with diabetes.

BACKGROUND: Branched-chain amino acids (BCAAs), including leucine, isoleucine, and valine, are essential amino acids for mammals. Maternal BCAAs during pregnancy have been associated with newborn development. Meanwhile, BCAAs have been tightly linked with insulin resistance and diabetes in recent years. Diabetes in pregnancy is a common metabolic disorder. The current study aims to assess the circulating BCAA levels in pregnant women with diabetes and their relationship with neonatal development. METHODS: The serum concentrations of BCAAs and their corresponding branched-chain α-keto acids (BCKAs) catabolites in 33 pregnant women with normal glucose tolerance, 16 pregnant women with type 2 diabetes before pregnancy (PDGM), and 15 pregnant women with gestational diabetes mellitus (GDM) were determined using a liquid chromatography system coupled to a mass spectrometer. The data were tested for normal distribution and homogeneity of variance before statistical analysis. Correlations were computed with the Pearson correlation coefficient. RESULTS: The maternal serum BCAAs and BCKAs levels during late pregnancy were higher in women with PGDM than those in healthy women. Meanwhile, the circulating BCAAs and BCKAs showed no significant changes in women with GDM compared with those in healthy pregnant women. Furthermore, the circulating BCAA and BCKA levels in women with PGDM were positively correlated with the weight of the newborn. The circulating leucine level in women with GDM was positively correlated with the weight of the newborn. BCAA and BCKA levels in healthy pregnant women showed no correlation with newborn weight. CONCLUSIONS: The serum BCAAs in pregnant women with diabetes, which was elevated in PGDM but not GDM, were positively correlated with newborn weight. These findings highlight potential approaches for early identification of high-risk individuals and interventions to reduce the risk of adverse pregnancy outcomes.

Spinal myeloid sarcoma presenting as initial symptom in acute promyelocytic leukemia with a rare cryptic PLZF::RARα fusion gene: a case report and literature review.

Background: Acute promyelocytic leukemia (APL) is rarely caused by the PLZF::RARα fusion gene. While APL patients with PLZF::RARα fusion commonly exhibit diverse hematologic symptoms, the presentation of myeloid sarcoma (MS) as an initial manifestation is infrequent. Case presentation: A 61-year-old patient was referred to our hospital with 6-month history of low back pain and difficulty walking. Before this admission, spine magnetic resonance imaging (MRI) conducted at another hospital revealed multiple abnormal signals in the left iliac bone and vertebral bodies spanning the thoracic (T11-T12), lumbar (L1-L4), and sacral (S1/S3) regions. This led to a provisional diagnosis of bone tumors with an unknown cause. On admission, complete blood count (CBC) test and peripheral blood smear revealed a slightly increased counts of monocytes. Immunohistochemical staining of both spinal and bone marrow (BM) biopsy revealed positive expression for CD117, myeloperoxidase (MPO), and lysozyme. BM aspirate showed a significant elevation in the percentage of promyelocytes (21%), which were morphologically characterized by round nuclei and hypergranular cytoplasm. Multiparameter flow cytometry of BM aspirate revealed that blasts were positive for CD13, CD33, CD117, and MPO. Through the integrated application of chromosome analysis, fluorescence in situ hybridization (FISH), reverse transcriptase polymerase chain reaction (RT-PCR), and Sanger sequencing, it was determined that the patient possessed a normal karyotype and a rare cryptic PLZF::RARα fusion gene, confirming the diagnosis of APL. Conclusion: In the present study, we report the clinical features and outcome of a rare APL patient characterized by a cryptic PLZF::RARα fusion and spinal myeloid sarcoma (MS) as the initial presenting symptom. Our study not only offers valuable insights into the heterogeneity of APL clinical manifestations but also emphasizes the crucial need to promptly consider the potential link between APL and MS for ensuring a timely diagnosis and personalized treatments.

Essential role of ABA signaling and related transcription factors in phenolic acid and lignin synthesis during muskmelon wound healing.

Abscisic acid (ABA) is a key phytohormone involved in wound healing in fruits and vegetables, while fluridone (FLD) is its synthetic inhibitor. However, it is unknown whether ABA signaling and downstream transcription factors are involved in the synthesis of phenolic acids and lignin monomers in muskmelon wounds, and the underlying mechanisms. In our study, exogenous ABA promoted endogenous ABA synthesis by increasing the levels of ß-carotenoid and zeaxanthin, activating 9-cis-epoxycarotenoid dioxygenase (NCED) and zeaxanthin epoxidase (ZEP), facilitated ABA signaling by increasing the expression levels of protein phosphatases type 2C (CmPP2C) and ABA-responsive element binding factors (CmABF), upregulated the expression levels of CmMYB1 and CmWRKY1, and ABA induced phenylpropanoid metabolism by activating phenylalanine ammonia-lyase (PAL), 4-coenzyme A ligase (4CL), and cinnamyl alcohol dehydrogenase (CAD), which further increased the synthesis of phenolic acids and lignin monomers in muskmelon wounds during healing. Taken together, exogenous ABA induced phenylpropanoid metabolism and increased the synthesis of phenolic acid and lignin monomer in muskmelon wounds during healing, and may be involved in endogenous ABA synthesis and signaling and related transcription factors.

Machine learning and experimentally exploring the controversial role of nitrogen in CO2 uptake by waste-derived nitrogen-containing porous carbons.

Waste-derived nitrogen-containing porous carbons were widely accepted as promising carbon capture materials. However, roles of nitrogen in CO2 uptake were highly controversial, posing a challenge in designing high CO2 uptake porous carbons. Herein, nitrogen-containing species was firstly introduced into machine learning (ML) models to uncover the complex relationship of nitrogen, micropore and CO2 uptake by combining ML models, DFT computations and experiments. The results revealed that micropore volume (Vmicro) was the most important property influencing CO2 uptake, but was not the only determinant factor. Nitrogen-containing species (pyrrolic/pyridonic-N (N5) and pyridinic-N (N6)) rather than total nitrogen content, also played an essential role. On the one hand, they can enhanced CO2 adsorption by Lewis acid-base and hydrogen bonding. On the other hand, they promoted development of micropores by participating in activation reactions. The model further indicated that excessive N5 (>1.5 wt%) or N6 (>1.7 wt%) led to restriction on developments of micropores, which was attributed to enlargement of pore size, collapses or blockage of micropores. The double edged-sword effect of N5 and N6 on changes of microporous structures was responsible for the long-standing controversy over nitrogen. The result was further verified by synthesizing eight porous carbons with different textural and chemical properties. This study provided not only a new perspective for resolving the controversy of nitrogen in CO2 uptake, but also a graphical user interface prediction software meaningful for designing porous carbons.

Effect of magnetic field pretreatment on germination characteristics, phenolic biosynthesis, and antioxidant capacity of quinoa.

The development of quinoa-based functional foods with cost-effective methods has gained considerable attention. In this study, the effects of magnetic field pretreatment on the germination characteristics, phenolic synthesis, and antioxidant system of quinoa (Chenopodium quinoa Willd.) were investigated. The results showed that the parameters of magnetic field pretreatment had different effects on the germination properties of five quinoa varieties, in which Sanjiang-1 (SJ-1) was more sensitive to magnetic field pretreatment. The content of total phenolics and phenolic acids in 24-h germinated seeds increased by 20.48% and 26.54%, respectively, under the pretreatment of 10 mT magnetic fields for 10 min compared with the control. This was closely related to the activation of the phenylpropanoid pathway by increasing enzyme activities and gene expression. In addition, magnetic field improved 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2'-Azinobis-(3-ethylbenzthiazoline-6-sulphonate) (ABTS) free radicals scavenging capacities and increased peroxidase (POD), catalase (CAT), superoxide dismutase (SOD), ascorbate peroxidase (APX) and glutathione peroxidase (GSH-Px) activities. This study suggests that magnetic field pretreatment enhanced gene expression of phenylalanine ammonia lyase (PAL), 4-coumarate-CoA ligase (4CL), chalcone synthase (CHS) and chalcone isomerase (CHI), increased antioxidant enzyme activity and phenolics content. Thereby lead to an increase in the antioxidative capacity of quinoa.

MYB24, MYB144, and MYB168 positively regulate suberin biosynthesis at potato tuber wounds during healing.

The essence of wound healing is the accumulation of suberin at wounds, which is formed by suberin polyphenolic (SPP) and suberin polyaliphatic (SPA). The biosynthesis of SPP and SPA monomers is catalyzed by several enzyme classes related to phenylpropanoid metabolism and fatty acid metabolism, respectively. However, how suberin biosynthesis is regulated at the transcriptional level during potato (Solanum tuberosum) tuber wound healing remains largely unknown. Here, 6 target genes and 15 transcription factors related to suberin biosynthesis in tuber wound healing were identified by RNA-seq technology and qRT-PCR. Dual luciferase and yeast one-hybrid assays showed that StMYB168 activated the target genes StPAL, StOMT, and St4CL in phenylpropanoid metabolism. Meanwhile, StMYB24 and StMYB144 activated the target genes StLTP, StLACS, and StCYP in fatty acid metabolism, and StFHT involved in the assembly of SPP and SPA domains in both native and wound periderms. More importantly, virus-induced gene silencing in S. tuberosum and transient overexpression in Nicotiana benthamiana assays confirmed that StMYB168 regulates the biosynthesis of free phenolic acids, such as ferulic acid. Furthermore, StMYB24/144 regulated the accumulation of suberin monomers, such as ferulates, α, ω-diacids, and ω-hydroxy acids. In conclusion, StMYB24, StMYB144, and StMYB168 have an elaborate division of labor in regulating the synthesis of suberin during tuber wound healing.

Inhibitory effects of black phosphorus nanosheets on tumor cell proliferation through downregulation of ADIPOQ and downstream signaling pathways.

Exposure to environmental pollutants, including nanomaterials, has a significant impact on tumor progression. The increased demand for black phosphorus nanosheets (BPNSs), driven by their exceptional properties, raises concerns about potential environmental contamination. Assessing their toxicity on tumor growth is essential. Herein, we employed a range of biological techniques, including cytotoxicity measurement, bioinformatics tools, proteomics, target gene overexpression, Western blot analysis, and apoptosis detection, to investigate the toxicity of BPNSs across A549, HepG-2, MCF-7, and Caco-2 cell lines. Our results demonstrated that BPNSs downregulated the expression of ADIPOQ and its associated downstream pathways, such as AMP-activated protein kinase (AMPK), nuclear factor erythroid 2-related factor 2 (Nrf2), and other unidentified pathways. These downregulated pathways ultimately led to mitochondria-dependent apoptosis. Notably, the specific downstream pathways involved varied depending on the type of tumors. These insightful findings not only confirm the consistent inhibitory effects of BPNSs across different tumor cells, but also elucidate the cytotoxicity mechanisms of BPNSs in different tumors, providing valuable information for their safe application and health risk assessment.

USP7 promotes cervical cancer progression by stabilizing MTDH expression through deubiquitination.

BACKGROUND: Metadherin (MTDH) and ubiquitin specific protease 7 (USP7) have been identified to involve in the tumorigenesis of cervical cancer (CC). USP7 is one of the deubiquitinating enzymes. Here, this study aimed to explore whether USP7 affected CC progression via interacting with MTDH and regulating its stability via deubiquitination. METHODS: qRT-PCR and western blotting assays detected the levels of genes and proteins. Functional analysis was conducted using 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, transwell, and tube formation assays, respectively. Proteins between USP7 and MTDH were identified by co-immunoprecipitation assay. A mouse xenograft model was established for in vivo analysis. RESULTS: MTDH was highly expressed in CC tissues and cells, silencing of MTDH suppressed CC cell proliferation, migration, invasion, angiogenesis, and macrophage M2 polarization. Mechanistically, USP7 directly bound to MTDH, and maintained its stability by removing ubiquitination on MTDH. CC tissues and cells showed high USP7 expression, and USP7 knockdown also inhibited CC cell proliferation, migration, invasion, angiogenesis and macrophage M2 polarization, and these effects mediated by USP7 knockdown were reversed by MTDH overexpression. Moreover, USP7 knockdown impeded CC growth in vivo by regulating MTDH. CONCLUSION: Collectively, USP7 promoted CC cell proliferation, migration, invasion, angiogenesis, and macrophage M2 polarization in vitro, as well as tumor growth in vivo by regulating MTDH.

Crystal phase and nanoscale size regulation utilizing the in-situ catalytic pyrolysis of bamboo sawdust in the recycling of spent lithium batteries.

Current Li-ion battery (LIB) recycling methods exhibit the disadvantages of low metal recovery efficiencies and high levels of pollution and energy consumption. Here, products generated via the in-situ catalytic pyrolysis of bamboo sawdust (BS) were utilized to regulate the crystal phase and nanoscale size of the NCM cathode to enhance the selective Li extraction and leaching efficiencies of other valuable metals from spent LIBs. The catalytic effect of the NCM cathode significantly promoted the release of gases from BS pyrolysis. These gases (H2, CO, and CH4) finally transformed the crystal phase of the NCM cathode from LiNixCoyMnzO2 into (Ni-Co/MnO/Li2CO3)/C. The size of the spent NCM cathode material was reduced approximately 31.7-fold (from 4.1 µm to 129.2 nm) after roasting. This could be ascribed to the in-situ catalytic decomposition of aromatic compounds generated via the primary pyrolysis of BS into C and H2 on the surface of the cathode material, resulting in the formation of the nanoscale composite (Ni-Co/MnO/Li2CO3)/C. This process enabled the targeted control of the crystal phase and nanoscale size of the material. Water leaching studies revealed a remarkable selective Li extraction efficiency of 99.27 %, and sulfuric acid leaching experiments with a concentration of 2 M revealed high extraction efficiencies of 99.15 % (Ni), 93.87 % (Co), and 99.46 % (Mn). Finally, a novel mechanism involving synergistic thermo-reduction and carbon modification for crystal phase regulation and nanoscale control was proposed. This study provides a novel concept for use in enhancing the recycling of valuable metals from spent LIBs utilizing biomass waste and practices the concept of "treating waste with waste".

Corrigendum: Integrated analysis of transcriptome and metabolome reveals the mechanism of chlorine dioxide repressed potato (Solanum tuberosum L.) tuber sprouting.

[This corrects the article DOI: 10.3389/fpls.2022.887179.].

Controlled Formation of Nanoribbons and Their Heterostructures via Assembly of Mass-Selected Inorganic Ions.

Control of nanomaterial dimensions with atomic precision through synthetic methods is essential to understanding and engineering of nanomaterials. For single-layer inorganic materials, size and shape controls have been achieved by self-assembly and surface-catalyzed reactions of building blocks deposited at a surface. However, the scope of nanostructures accessible by such approach is restricted by the limited choice of building blocks that can be thermally evaporated onto surfaces, such as atoms or thermostable molecules. Herein this limitation is bypassed by using mass-selected molecular ions obtained via electrospray ionization as building blocks to synthesize nanostructures that are inaccessible by conventional evaporation methods. As the first example, micron-scale production of MoS2 and WS2 nanoribbons and their heterostructures on graphene are shown by the self-assembly of asymmetrically shaped building blocks obtained from the electrospray. It is expected that judicious use of electrospray-generated building blocks would unlock access to previously inaccessible inorganic nanostructures.

Immunomodulation of nutritional formula containing epigallocatechin-3-gallate, ginseng extract, and polydextrose on inflammation and macrophage polarization.

Single nutrient likes polyphenol or dietary fiber have been exhaustively investigated to validate their positive intervention in health or disease. Meanwhile, the common interaction of inner systems with the nutrient complex has not been well elucidated, which raises the scientific issue of the modulatory effect of the nutrient complex on immunity. The representative prebiotics of epigallocatechin-3-gallate (EGCG), ginseng extract, and polydextrose (PDX) were selected on behalf of the classification of polyphenol, flavone or polysaccharides, and dietary fiber to generally cover the daily food intake in this study to explore their intervention in inflammation and macrophage polarization. The intervention of selected nutrients on inflammation and macrophage polarization has been evaluated against macrophages to unveil their comprehensive effects. The synergistic effect of selected nutrients was demonstrated by inhibiting M1 macrophage polarization and the promotion of M2 macrophage polarization. Then, the nutrient formula was set up to verify the intervention effect, and the results revealed the significant inhibition of cell inflammation and the effect on cell proliferation through promoting the cell cycle in the G2 phase. The nutrient complex could inhibit M1 macrophage polarization to inhibit M1-mediated inflammation and promote M2 macrophages for anti-inflammatory effect and enhance cell phagocytosis. Moreover, the varied intervention effects of the nutrient complex with different formulas could be summarized. In general, the formula containing EGCG, ginseng extract, and PDX was demonstrated to possess an enhanced immunomodulatory effect on cell inflammation and macrophage polarization, which could potentially inspire the investigation of complex nutrients in health and diseases.