ABSTRACT
Ultrathin two-dimensional (2D) semiconducting layered materials offer great potential for extending Moore's law of the number of transistors in an integrated circuit1. One key challenge with 2D semiconductors is to avoid the formation of charge scattering and trap sites from adjacent dielectrics. An insulating van der Waals layer of hexagonal boron nitride (hBN) provides an excellent interface dielectric, efficiently reducing charge scattering2,3. Recent studies have shown the growth of single-crystal hBN films on molten gold surfaces4 or bulk copper foils5. However, the use of molten gold is not favoured by industry, owing to its high cost, cross-contamination and potential issues of process control and scalability. Copper foils might be suitable for roll-to-roll processes, but are unlikely to be compatible with advanced microelectronic fabrication on wafers. Thus, a reliable way of growing single-crystal hBN films directly on wafers would contribute to the broad adoption of 2D layered materials in industry. Previous attempts to grow hBN monolayers on Cu (111) metals have failed to achieve mono-orientation, resulting in unwanted grain boundaries when the layers merge into films6,7. Growing single-crystal hBN on such high-symmetry surface planes as Cu (111)5,8 is widely believed to be impossible, even in theory. Nonetheless, here we report the successful epitaxial growth of single-crystal hBN monolayers on a Cu (111) thin film across a two-inch c-plane sapphire wafer. This surprising result is corroborated by our first-principles calculations, suggesting that the epitaxial growth is enhanced by lateral docking of hBN to Cu (111) steps, ensuring the mono-orientation of hBN monolayers. The obtained single-crystal hBN, incorporated as an interface layer between molybdenum disulfide and hafnium dioxide in a bottom-gate configuration, enhanced the electrical performance of transistors. This reliable approach to producing wafer-scale single-crystal hBN paves the way to future 2D electronics.
ABSTRACT
In 1967, scientists used a simple climate model to predict that human-caused increases in atmospheric CO2 should warm Earth's troposphere and cool the stratosphere. This important signature of anthropogenic climate change has been documented in weather balloon and satellite temperature measurements extending from near-surface to the lower stratosphere. Stratospheric cooling has also been confirmed in the mid to upper stratosphere, a layer extending from roughly 25 to 50 km above the Earth's surface (S25â -â 50). To date, however, S25â -â 50 temperatures have not been used in pattern-based attribution studies of anthropogenic climate change. Here, we perform such a "fingerprint" study with satellite-derived patterns of temperature change that extend from the lower troposphere to the upper stratosphere. Including S25â -â 50 information increases signal-to-noise ratios by a factor of five, markedly enhancing fingerprint detectability. Key features of this global-scale human fingerprint include stratospheric cooling and tropospheric warming at all latitudes, with stratospheric cooling amplifying with height. In contrast, the dominant modes of internal variability in S25â -â 50 have smaller-scale temperature changes and lack uniform sign. These pronounced spatial differences between S25â -â 50 signal and noise patterns are accompanied by large cooling of S25â -â 50 (1 to 2[Formula: see text]C over 1986 to 2022) and low S25â -â 50 noise levels. Our results explain why extending "vertical fingerprinting" to the mid to upper stratosphere yields incontrovertible evidence of human effects on the thermal structure of Earth's atmosphere.
ABSTRACT
Single-cell RNA-seq has led to novel designations for mesenchymal cells associated with bone as well as multiple designations for what appear to be the same cell type. The main goals of this study were to increase the amount of single-cell RNA sequence data for osteoblasts and osteocytes, to compare cells from the periosteum to those inside bone, and to clarify the major categories of cell types associated with murine bone. We created an atlas of murine bone-associated cells by harmonizing published datasets with in-house data from cells targeted by Osx1-Cre and Dmp1-Cre driver strains. Cells from periosteal bone were analyzed separately from those isolated from the endosteum and trabecular bone. Over 100,000 mesenchymal cells were mapped to reveal 11 major clusters designated fibro-1, fibro-2, chondrocytes, articular chondrocytes, tenocytes, adipo-Cxcl12 abundant reticular (CAR), osteo-CAR, preosteoblasts, osteoblasts, osteocytes, and osteo-X, the latter defined in part by periostin expression. Osteo-X, osteo-CAR, and preosteoblasts were closely associated with osteoblasts at the trabecular bone surface. Wnt16 was expressed in multiple cell types from the periosteum but not in cells from endocortical or cancellous bone. Fibro-2 cells, which express markers of stem cells, localized to the periosteum but not trabecular bone in adult mice. Suppressing bone remodeling eliminated osteoblasts and altered gene expression in preosteoblasts but did not change the abundance or location of osteo-X or osteo-CAR cells. These results provide a framework for identifying bone cell types in murine single-cell RNA-seq datasets and suggest that osteoblast progenitors reside near the surface of remodeling bone.
Subject(s)
Mesenchymal Stem Cells , Osteoblasts , Osteocytes , Periosteum , Animals , Mice , Chondrocytes/metabolism , Chondrocytes/cytology , Mesenchymal Stem Cells/metabolism , Mesenchymal Stem Cells/cytology , Osteoblasts/metabolism , Osteoblasts/cytology , Osteocytes/metabolism , Osteocytes/cytology , Periosteum/cytology , Periosteum/metabolism , Single-Cell Analysis , Mice, Inbred C57BLABSTRACT
Salicylic acid (SA) plays a crucial role in plant defense against biotrophic and semi-biotrophic pathogens. In Arabidopsis (Arabidopsis thaliana), isochorismate synthase 1 (AtICS1) is a key enzyme for the pathogen-induced biosynthesis of SA via catalytic conversion of chorismate into isochorismate, an essential precursor for SA synthesis. Despite the extensive knowledge of ICS1-related menaquinone, siderophore, tryptophan (MST) enzymes in bacteria, the structural mechanisms for substrate binding and catalysis in plant isochorismate synthase (ICS) enzymes are unknown. This study reveals that plant ICS enzymes catalyze the isomerization of chorismate through a magnesium-dependent mechanism, with AtICS1 exhibiting the most substantial catalytic activity. Additionally, we present high-resolution crystal structures of apo AtICS1 and its complex with chorismate, offering detailed insights into the mechanisms of substrate recognition and catalysis. Importantly, our investigation indicates the existence of a potential substrate entrance channel and a gating mechanism regulating substrate into the catalytic site. Structural comparisons of AtICS1 with MST enzymes suggest a shared structural framework with conserved gating and catalytic mechanisms. This work provides valuable insights into the structural and regulatory mechanisms governing substrate delivery and catalysis in AtICS1, as well as other plant ICS enzymes.
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BACKGROUND: Hyperglycemia-a symptom that characterizes diabetes-is highly associated with atherothrombotic complications. However, the underlying mechanism by which hyperglycemia fuels platelet activation and arterial thrombus formation is still not fully understood. METHODS: The profiles of polyunsaturated fatty acid metabolites in the plasma of patients with diabetes and healthy controls were determined with targeted metabolomics. FeCl3-induced carotid injury model was used to assess arterial thrombus formation in mice with endothelial cell (EC)-specific YAP (yes-associated protein) deletion or overexpression. Flow cytometry and clot retraction assay were used to evaluate platelet activation. RNA sequencing and multiple biochemical analyses were conducted to unravel the underlying mechanism. RESULTS: The plasma PGE2 (prostaglandin E2) concentration was elevated in patients with diabetes with thrombotic complications and positively correlated with platelet activation. The PGE2 synthetases COX-2 (cyclooxygenase-2) and mPGES-1 (microsomal prostaglandin E synthase-1) were found to be highly expressed in ECs but not in other type of vessel cells in arteries from both patients with diabetes and hyperglycemic mice, compared with nondiabetic individuals and control mice, respectively. A combination of RNA sequencing and ingenuity pathway analyses indicated the involvement of YAP signaling. EC-specific deletion of YAP limited platelet activation and arterial thrombosis in hyperglycemic mice, whereas EC-specific overexpression of YAP in mice mimicked the prothrombotic state of diabetes, without affecting hemostasis. Mechanistically, we found that hyperglycemia/high glucose-induced endothelial YAP nuclear translocation and subsequently transcriptional expression of COX-2 and mPGES-1 contributed to the elevation of PGE2 and platelet activation. Blockade of EP3 (prostaglandin E receptor 3) activation by oral administration of DG-041 reversed the hyperactivity of platelets and delayed thrombus formation in both EC-specific YAP-overexpressing and hyperglycemic mice. CONCLUSIONS: Collectively, our data suggest that hyperglycemia-induced endothelial YAP activation aggravates platelet activation and arterial thrombus formation via PGE2/EP3 signaling. Targeting EP3 with DG-041 might be therapeutic for diabetes-related thrombosis.
Subject(s)
Diabetes Mellitus , Hyperglycemia , Thrombosis , Animals , Humans , Mice , Blood Platelets/metabolism , Cyclooxygenase 2/metabolism , Diabetes Mellitus/metabolism , Dinoprostone/metabolism , Hyperglycemia/complications , Hyperglycemia/metabolism , Mice, Obese , Thrombosis/genetics , Thrombosis/metabolismABSTRACT
In recent years, the simple synthesis of artificial humic substances (A-HS) by alkaline hydrothermal processing of waste biomass was described. This A-HS was shown to support water and mineral binding, to change soil structure, to avoid fertilizer mineralization, and to support plant growth. Many of the observed macroscopic effects could, however, not be directly related to the minute amounts of A-HS which have been added, and an A-HS stimulated microbiome was found to be the key for understanding. In this review, we describe such anthropogenic soil in the language of the modern concept of living engineered materials and identify natural and artificial HS as the enabler to set up the interactive microbial system along the interfaces of the mineral grains. In that, old chemical concepts as surface activity, redox mediation, and pH buffering are the base of the system structure build-up and the complex self-adaptability of biological systems. The resulting chemical/biological hybrid system has the potential to address world problems as soil fertility, nutrition of a growing world population, and climate change.
Subject(s)
Humic Substances , Soil , Biomass , Carbon , WaterABSTRACT
SignificanceFor oxide catalysts, it is important to elucidate and further control their atomic structures. In this work, well-defined CrO2 bilayer islands and Cr2O7 dinuclear clusters have been grown on Au(111) and unambiguously identified by scanning tunneling microscopy and theoretical calculations. Upon cycled redox treatments, the two kinds of oxide nanostructures can be reversibly transformed. It is interesting to note that both Cr oxides do not exist in bulk but need to be stabilized by the metal surface and the specific environment. Our results suggest that both redox atmosphere and interface confinement effects can be used to construct an oxide nanostructure with the specific chemical state and structure.
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BACKGROUND: Hypertrophic scar (HTS) is a prevalent chronic inflammatory skin disorder characterized by abnormal proliferation and extracellular matrix deposition and the precise mechanisms underlying HTS remain elusive. This study aimed to identify and validate potential immune-related genes associated with hypertrophic scar formation. METHODS: Skin samples from normal (n = 12) and hypertrophic scar tissues (n = 12) were subjected to RNA-seq analysis. Differentially expressed genes (DEGs) and significant modular genes in Weighted gene Co-expression Network Analysis (WGCNA) were identified. Subsequently, functional enrichment analysis was performed on the intersecting genes. Additionally, eight immune-related genes were matched from the ImmPort database. Validation of NRG1 and CRLF1 was carried out using an external cohort (GSE136906). Furthermore, the association between these two genes and immune cells was assessed by Spearman correlation analysis. Finally, RNA was extracted from normal and hypertrophic scar samples, and RT-qPCR, Immunohistochemistry staining and Western Blot were employed to validate the expression of characteristic genes. RESULTS: A total of 940 DEGs were identified between HTS and normal samples, and 288 key module genes were uncovered via WGCNA. Enrichment analysis in key module revealed involvement in many immune-related pathways, such as Th17 cell differentiation, antigen processing and presentation and B cell receptor signaling pathway. The eight immune-related genes (IFI30, NR2F2, NRG1, ESM1, NFATC2, CRLF1, COLEC12 and IL6) were identified by matching from the ImmPort database. Notably, we observed that activated mast cell positively correlated with CRLF1 expression, while CD8 T cells exhibited a positive correlation with NRG1. The expression of NRG1 and CRLF1 was further validated in clinical samples. CONCLUSION: In this study, two key immune-related genes (CRLF1 and NRG1) were identified as characteristic genes associated with HTS. These findings provide valuable insights into the immune-related mechanisms underlying hypertrophic scar formation.
Subject(s)
Cicatrix, Hypertrophic , Neuregulin-1 , Receptors, Cytokine , Humans , Cell Differentiation , Cicatrix, Hypertrophic/genetics , Databases, Factual , Extracellular Matrix , Skin , Receptors, Cytokine/geneticsABSTRACT
Amorphous strategies have been extensively used in improving the dissolution of insoluble drugs for decades due to their high free energy. However, the formation of amorphous small-molecule gels (ASMGs) presents a counter-intuitive discovery that significantly limits their practical application. Recently, ASMGs have garnered attention because of their noncovalent structures, excellent biodegradability, and significant potential in various drug delivery systems in the pharmaceutical field. Hence, a comprehensive review is necessary to contribute to a better understanding of recent advances in ASMGs. This review aimed to introduce the main formation mechanisms, summarize possible influencing factors, generalize unique properties, outline elimination strategies, and discuss clinical application potential with preclinical cases of ASMGs. Moreover, few ASMGs are advanced to clinical stages. Intensive clinical research is needed for further development. We hope that this review can provide more efficient and rational guidance for exploring further clinical applications of ASMGs.
ABSTRACT
In the context of improving the efficacy of autologous fat grafts (AFG) in reconstructive surgery, this study delineates the novel use of adipose-derived mesenchymal stem cells (ADSCs) and their extracellular vesicles (EVs) as vehicles for delivering DLL4 siRNA. The aim was to inhibit DLL4, a gene identified through transcriptome analysis as a critical player in the vascular endothelial cells of AFG tissues, thereby negatively affecting endothelial cell functions and graft survival through the Notch signaling pathway. By engineering ADSC EVs to carry DLL4 siRNA (ADSC EVs-siDLL4), the research demonstrated a marked improvement in endothelial cell proliferation, migration, and lumen formation, as well as enhanced angiogenesis in vivo, leading to a significant increase in the survival rate of AFGs. This approach presents a significant advancement in the field of tissue engineering and regenerative medicine, offering a potential method to overcome the limitations of current fat grafting techniques.
ABSTRACT
Senile osteoporosis increases fracture risks. Bone marrow stromal cells (BMSCs) are sensitive to aging. Deep insights into BMSCs aging are vital to elucidate the mechanisms underlying age-related bone loss. Recent advances showed that osteoporosis is associated with aberrant DNA methylation of many susceptible genes. Galectin-1 (Gal-1) has been proposed as a mediator of BMSCs functions. In our previous study, we showed that Gal-1 was downregulated in aged BMSCs and global deletion of Gal-1 in mice caused bone loss via impaired osteogenesis potential of BMSCs. Gal-1 promoter is featured by CpG islands. However, there are no reports concerning the DNA methylation status in Gal-1 promoter during osteoporosis. In the current study, we sought to investigate the role of DNA methylation in Gal-1 downregulation in aged BMSCs. The potential for anti-bone loss therapy based on modulating DNA methylation is explored. Our results showed that Dnmt3b-mediated Gal-1 promoter DNA hypermethylation plays an important role in Gal-1 downregulation in aged BMSCs, which inhibited ß-catenin binding on Gal-1 promoter. Bone loss of aged mice was alleviated in response to in vivo deletion of Dnmt3b from BMSCs. Finally, when bone marrow of young wild-type (WT) mice or young Dnmt3bPrx1-Cre mice was transplanted into aged WT mice, Gal-1 level in serum and trabecular bone mass were elevated in recipient aged WT mice. Our study will benefit for deeper insights into the regulation mechanisms of Gal-1 expression in BMSCs during osteoporosis development, and for the discovery of new therapeutic targets for osteoporosis via modulating DNA methylation status.NEW & NOTEWORTHY There is Dnmt3b-mediated DNA methylation in Gal-1 promoter in aged bone marrow stromal cell (BMSC). DNA methylation causes Gal-1 downregulation and osteogenesis attenuation of aged BMSC. DNA methylation blocks ß-catenin binding on Gal-1 promoter. Bone loss of aged mice is alleviated by in vivo deletion of Dnmt3b from BMSC.
Subject(s)
Benzamides , Mesenchymal Stem Cells , Osteoporosis , Tyrosine/analogs & derivatives , Animals , Mice , DNA Methylation/genetics , beta Catenin/metabolism , Galectin 1/genetics , Galectin 1/metabolism , Osteogenesis/genetics , Osteoporosis/genetics , Osteoporosis/metabolism , Mesenchymal Stem Cells/metabolism , Promoter Regions, Genetic/genetics , Cell Differentiation , Bone Marrow Cells/metabolismABSTRACT
Integrin-based focal adhesion is one of the major mechanosensory in osteocytes. The aim of this study was to mine the hub genes associated with focal adhesion and investigate their roles in osteoporosis based on the data of single-cell RNA sequencing and RNA-sequencing. Two hub genes (FAM129A and RNF24) with the same expression trend and AUC values greater than 0.7 in both GSE56815 and GSE56116 cohorts were uncovered. The nomogram was created to predict the risk of OP based on two hub genes. Subsequently, the competing endogenous RNA network was established based on two hub genes, 14 microRNAs and five long noncoding RNAs. Meanwhile, transcription factors-hub gene network was established based on two hub genes and 14 TFs. Finally, 73 drugs were predicted, of which there were 13 drugs targeting FAM129A and 66 drugs targeting RNF24. In both mouse and human blood samples, FAM129A expression was decreased in granulocytes and RNF24 expression was increased in monocytes. In the mouse experiment, FAM129A and anti-RNF24 were found to partially alleviate the progression of osteoporosis. In conclusion, two hub genes related to focal adhesion were identified by combined scRNA-seq and RNA-seq analyses, which might supply a new insight for the treatment and evaluation of OP.
Subject(s)
MicroRNAs , Osteoporosis , Humans , Animals , Mice , RNA-Seq , Focal Adhesions , Sequence Analysis, RNAABSTRACT
Constructing low-dimensional/three-dimensional (LD/3D) perovskite solar cells can improve efficiency and stability. However, the design and selection of LD perovskite capping materials are incredibly scarce for inverted perovskite solar cells (PSCs) because LD perovskite capping layers often favor hole extraction and impede electron extraction. Here, we develop a facile and effective strategy to modify the perovskite surface by passivating the surface defects and modulating surface electrical properties by incorporating morpholine hydriodide (MORI) and thiomorpholine hydriodide (SMORI) on the perovskite surface. Compared with the PI treatment that we previously developed, the one-dimensional (1D) perovskite capping layer derived from PI is transformed into a two-dimensional (2D) perovskite capping layer (with MORI or SMORI), achieving dimension regulation. It is shown that the 2D SMORI perovskite capping layer induces more robust surface passivation and stronger n-N homotype 2D/3D heterojunctions, achieving a p-i-n inverted solar cell with an efficiency of 24.55%, which retains 87.6% of its initial efficiency after 1500 h of operation at the maximum power point (MPP). Furthermore, 5 × 5 cm2 perovskite mini-modules are presented, achieving an active-area efficiency of 22.28%. In addition, the quantum well structure in the 2D perovskite capping layer increases the moisture resistance, suppresses ion migration, and improves PSCs' structural and environmental stability.
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An enclosed nanospace often shows a significant confinement effect on chemistry within its inner cavity, while whether an open space can have this effect remains elusive. Here, we show that the open surface of TiO2 creates a confined environment for In2O3 which drives spontaneous transformation of free In2O3 nanoparticles in physical contact with TiO2 nanoparticles into In oxide (InOx) nanolayers covering onto the TiO2 surface during CO2 hydrogenation to CO. The formed InOx nanolayers are easy to create surface oxygen vacancies but are against over-reduction to metallic In in the H2-rich atmospheres, which thus show significantly enhanced activity and stability in comparison with the pure In2O3 catalyst. The formation of interfacial In-O-Ti bonding is identified to drive the In2O3 dispersion and stabilize the metastable InOx layers. The InOx overlayers with distinct chemistry from their free counterpart can be confined on various oxide surfaces, demonstrating the important confinement effect at oxide/oxide interfaces.
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In current clinical practice, radiotherapy (RT) is prescribed as a pre-determined total dose divided over daily doses (fractions) given over several weeks. The treatment response is typically assessed months after the end of RT. However, the conventional one-dose-fits-all strategy may not achieve the desired outcome, owing to patient and tumor heterogeneity. Therefore, a treatment strategy that allows for RT dose personalization based on each individual response is preferred. Multiple strategies have been adopted to address this challenge. As an alternative to current known strategies, artificial intelligence (AI)-derived mechanism-independent small data phenotypic medicine (PM) platforms may be utilized for N-of-1 RT personalization. Unlike existing big data approaches, PM does not engage in model refining, training, and validation, and guides treatment by utilizing prospectively collected patient's own small datasets. With PM, clinicians may guide patients' RT dose recommendations using their responses in real-time and potentially avoid over-treatment in good responders and under-treatment in poor responders. In this paper, we discuss the potential of engaging PM to guide clinicians on upfront dose selections and ongoing adaptations during RT, as well as considerations and limitations for implementation. For practicing oncologists, clinical trialists, and researchers, PM can either be implemented as a standalone strategy or in complement with other existing RT personalizations. In addition, PM can either be used for monotherapeutic RT personalization, or in combination with other therapeutics (e.g. chemotherapy, targeted therapy). The potential of N-of-1 RT personalization with drugs will also be presented.
Subject(s)
Neoplasms , Precision Medicine , Humans , Precision Medicine/methods , Neoplasms/radiotherapy , Artificial Intelligence , Phenotype , Radiotherapy DosageABSTRACT
Unraveling bacterial identity through Raman scattering techniques has been persistently challenging due to homogeneously amplified Raman signals across a wide variety of bacterial molecules, predominantly protein- or nucleic acid-mediated. In this study, we present an approach involving the use of silver nanoparticles to completely and uniformly "mask" adsorption on the surface of bacterial molecules through sodium borohydride and sodium chloride. This approach enables the acquisition of enhanced surface-enhanced Raman scattering (SERS) signals from all components on the bacterial surface, facilitating rapid, specific, and label-free bacterial identification. For the first time, we have characterized the identity of a bacterium, including its DNA, metabolites, and cell walls, enabling the accurate differentiation of various bacterial strains, even within the same species. In addition, we embarked on an exploration of the origin and variability patterns of the main characteristic peaks of Gram-positive and Gram-negative bacteria. Significantly, the SERS peak ratio was found to determine the inflection point of accelerated bacterial death upon treatment with antimicrobials. We further applied this platform to identify 15 unique clinical antibiotic-resistant bacterial strains, including five Escherichia coli strains in human urine, a first for Raman technology. This work has profound implications for prompt and accurate identification of bacteria, particularly antibiotic-resistant strains, thereby significantly enhancing clinical diagnostics and antimicrobial treatment strategies.
Subject(s)
Metal Nanoparticles , Silver , Spectrum Analysis, Raman , Spectrum Analysis, Raman/methods , Silver/chemistry , Silver/pharmacology , Metal Nanoparticles/chemistry , Anti-Bacterial Agents/pharmacology , Anti-Bacterial Agents/chemistry , Anti-Bacterial Agents/analysis , Bacteria/drug effects , Bacteria/isolation & purification , Drug Resistance, Bacterial , Escherichia coli/drug effects , Escherichia coli/isolation & purification , Escherichia coli/chemistry , HumansABSTRACT
Polydimethylsiloxane (PDMS)-based transparent and superhydrophobic coatings have important applications, such as anti-icing, corrosion resistance, self-cleaning, etc. However, their applications are limited by the inevitable introduction of nanoparticles/high-temperature/segmented PDMS to facilitate a raspy surface. In this study, a self-roughed, neat PDMS superhydrophobic coating with high transparency is developed via a one-step spray-coating technique. PDMS suspensions with various droplet sizes are synthesized and used as building blocks for raspy surface formation by controlled curing on the warm substrate. The optimal coating exhibits a large water contact angle of 155.4° and transparency (T550 = 82.3%). Meanwhile, the employed spray-coating technique is applicable to modify a plethora of substrates. For proof-of-concept demonstrations, the use of the PDMS hydrophobic coating for anti-liquid-interference electrothermal devices and further transparent observation window for long-term operation in a sub-zero environment is shown successful. The proposed facile synthesis method of hydrophobic PDMS coating is expected to have great potential for a broad range of applications in the large-scale fabrication of fluorine-free, eco-friendly superhydrophobic surfaces.
ABSTRACT
Alkali metal-sulfur batteries (particularly, lithium/sodium- sulfur (Li/Na-S)) have attracted much attention because of their high energy density, the natural abundance of sulfur, and environmental friendliness. However, Li/Na-S batteries still face big challenges, such as limited cycle life, poor conductivity, large volume changes, and the "shuttle effect" caused by the high solubility of Li/Na-polysulfides. Herein, novel organosulfur-containing materials, i.e., bis(4-hydroxy-2,2,6,6-tetramethylpiperidin-1-yl)disulfide (BiTEMPS-OH) and 2,4-thiophene/arene copolymer (TAC) are proposed as cathode materials for Li and Na batteries. BiTEMPS-OH shows an initial discharge/charge capacity of 353/192 mAh g-1 and a capacity of 62 mAh g-1 after 200 cycles at 100 mA g-1 in ether-based Li-ion electrolyte. Meanwhile, TAC has an initial discharge/charge capacity of 270/248 mAh g-1 and better cycling performance (106 mAh g-1 after 200 cycles) than BiTEMPS-OH in the same electrolyte. However, the rate capability of TAC is limited by the slow diffusion of Li-ions. Both materials show inferior electrochemical performances in Na battery cells compared to the Li analogs. X-ray powder diffraction reveals that BiTEMPS-OH loses its crystalline structure permanently upon cycling in Li battery cells. X-ray photoelectron spectroscopy demonstrates the cleavage and partially reversible formation of S-S bonds in BiTEMPS-OH and the formation/decomposition of thick solid electrolyte interphase on the electrode surface of TAC.
ABSTRACT
CCAAT/enhancer-binding protein beta (CEBPB) has been associated with sepsis. However, its role in sepsis-induced myocardial injury (SIMI) remains ill-defined. This research was designed to illustrate the involvement of CEBPB in SIMI and its upstream modifier. The transcriptomic changes in heart biopsies of mice that had undergone polymicrobial sepsis were downloaded from the GEO dataset for KEGG enrichment analysis. CEBPB, on the TNF signaling pathway, was significantly enhanced in the myocardial tissues of mice with SIMI. Downregulation of CEBPB alleviated SIMI, as evidenced by minor myocardial injury and inflammatory manifestations. Moreover, ubiquitination modification of CEBPB by constitutive photomorphogenesis protein 1 homolog (COP1) led to the degradation of CEBPB and inhibited inflammatory responses in macrophages. Upregulation of COP1 protected against SIMI in mice overexpressing CEBPB. Collectively, our findings demonstrated that COP1 protected the heart against SIMI through the ubiquitination modification of CEBPB, which might be a novel therapeutic approach in the future.
Subject(s)
Arabidopsis Proteins , Sepsis , Mice , Animals , Arabidopsis Proteins/genetics , Arabidopsis Proteins/metabolism , Ubiquitin-Protein Ligases/genetics , Ubiquitin-Protein Ligases/metabolism , Ubiquitination , Macrophages/metabolism , Sepsis/complications , Sepsis/geneticsABSTRACT
Salmonella constitutes a prevalent alimentary pathogen, instigating zoonotic afflictions. Consequently, the prompt discernment of Salmonella in sustenance is of cardinal significance. Lateral flow assays utilizing colorimetric methodologies adequately fulfill the prerequisites of point-of-care diagnostics, however, their detection threshold remains elevated, generally permitting only qualitative discernment, an impediment to the preliminary screening of nascent pathogens. In response to this conundrum, we propose a lateral flow diagnostic predicated upon a streptavidin-biotin amplification system with recombinase polymerase amplification engineered for the expeditious and quantitative discernment of Salmonella enteritidis. Trace nucleic acids within a sample undergo exponential amplification via recombinase polymerase amplification to a level discernable, constituting the initial signal amplification. Subsequently, along the test line (T-line) of the lateral flow strip, the chromatic signal undergoes augmentation by securing a greater quantity of AuNPs through the magnification capacity of the streptavidin-biotin mechanism, affecting the second signal amplification. Quantitative results are procured via smartphone capture and transferred to computer software for precise calculation of the targeted quantity. The lateral flow strip exhibits a LOD at 19.41â CFU/mL for cultured S. enteritidis. The RSD of three varying concentrations were respectively 3.74 %, 5.96 %, and 4.25 %.