An optimized impedance matching construction strategy: carbon nanofibers inlaid with Ni nanocrystals by electrospinning for high-performance microwave absorber.

With the widespread use of electronic goods, solving electromagnetic pollution has become one of the new challenges. Higher requirements for microwave-absorbing materials (MAM) have emerged to address this issue. The composite of carbon nanofiber (CNF) and magnetic nanoparticles is the material that effectively absorbs microwaves. This paper fabricated Ni/C nanofibers using a combination of electrospinning and high-temperature carbonization. With 50 wt% paraffin wax, Ni/C nanofibers demonstrated optimal microwave absorption capabilities. With a thickness of 3 mm, the minimum RL value can reach -30.6 dB, and the effective absorption bandwidth is 5.96 GHz. By encapsulating Ni nanoparticles in carbon nanofibers, the synergic interaction of dielectric and magnetic losses effectively meets the need for constant attenuation and impedance matching, and effectively improves microwave-absorbing properties. Hence, Ni/C nanofibers are promising for MAM application with excellent MA performance.

CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway.

BACKGROUND: White matter injury (WMI) represents a significant etiological factor contributing to neurological impairment subsequent to Traumatic Brain Injury (TBI). CD36 receptors are recognized as pivotal participants in the pathogenesis of neurological disorders, including stroke and spinal cord injury. Furthermore, dynamic fluctuations in the phenotypic polarization of microglial cells have been intimately associated with the regenerative processes within the injured tissue following TBI. Nevertheless, there is a paucity of research addressing the impact of CD36 receptors on WMI and microglial polarization. This investigation aims to elucidate the functional role and mechanistic underpinnings of CD36 in modulating microglial polarization and WMI following TBI. METHODS: TBI models were induced in murine subjects via controlled cortical impact (CCI). The spatiotemporal patterns of CD36 expression were examined through quantitative polymerase chain reaction (qPCR), Western blot analysis, and immunofluorescence staining. The extent of white matter injury was assessed via transmission electron microscopy, Luxol Fast Blue (LFB) staining, and immunofluorescence staining. Transcriptome sequencing was employed to dissect the molecular mechanisms underlying CD36 down-regulation and its influence on white matter damage. Microglial polarization status was ascertained using qPCR, Western blot analysis, and immunofluorescence staining. In vitro, a Transwell co-culture system was employed to investigate the impact of CD36-dependent microglial polarization on oligodendrocytes subjected to oxygen-glucose deprivation (OGD). RESULTS: Western blot and qPCR analyses revealed that CD36 expression reached its zenith at 7 days post-TBI and remained sustained at this level thereafter. Immunofluorescence staining exhibited robust CD36 expression in astrocytes and microglia following TBI. Genetic deletion of CD36 ameliorated TBI-induced white matter injury, as evidenced by a reduced SMI-32/MBP ratio and G-ratio. Transcriptome sequencing unveiled differentially expressed genes enriched in processes linked to microglial activation, regulation of neuroinflammation, and the TNF signaling pathway. Additionally, bioinformatics analysis pinpointed the Traf5-p38 axis as a critical signaling pathway. In vivo and in vitro experiments indicated that inhibition of the CD36-Traf5-MAPK axis curtailed microglial polarization toward the pro-inflammatory phenotype. In a Transwell co-culture system, BV2 cells treated with LPS + IFN-γ exacerbated the damage of post-OGD oligodendrocytes, which could be rectified through CD36 knockdown in BV2 cells. CONCLUSIONS: This study illuminates that the suppression of CD36 mitigates WMI by constraining microglial polarization towards the pro-inflammatory phenotype through the down-regulation of the Traf5-MAPK signaling pathway. Our findings present a potential therapeutic strategy for averting neuroinflammatory responses and ensuing WMI damage resulting from TBI.

The potential of antifungal peptides derived from Lactiplantibacillus plantarum WYH for biocontrol of Aspergillus flavus contamination.

Aspergillus flavus is a notorious fungus that contaminates food crops with toxic aflatoxins, posing a serious threat to human health and the agricultural economy. To overcome the inadequacy of traditional control methods and meet consumer preferences for natural-sources additives, there is an urgent demand for novel biocontrol agents that are safe and efficient. This study aims to investigate the antifungal properties of a novel antifungal agent derived from the biologically safe Lactiplantibacillus plantarum WYH. Firstly, antifungal peptides (AFPs) with a molecular weight of less than 3kD, exhibiting remarkable temperature stability and effectively retarding fungal growth in a dose-dependent manner specifically against A. flavus, were concentrated from the fermentation supernatant of L. plantarum WYH and were named as AFPs-WYH. Further analysis demonstrated that AFPs-WYH might exert antifungal effects through the induction of oxidative stress, disruption of mitochondrial function, alteration of membrane permeability, and cell apoptosis in A. flavus. To further validate our findings, a transcriptomics analysis was conducted on A. flavus treated with 2 and 5 mg/mL of AFPs-WYH, which elucidated the potential effect of AFPs-WYH administration on the regulation of genes involved in impairing fungal development and preventing aflatoxin biosynthesis pathways. Overall, AFPs-WYH reduced the A. flavus proliferation and affected the AFB1 biosynthesis, exhibiting a promising potential for food industry applications as a biopreservative and biocontrol agent.

An Automated Video Analysis System for Retrospective Assessment and Real-Time Monitoring of Endoscopic Procedures (with Video).

BACKGROUND AND AIMS: Accurate recognition of endoscopic instruments facilitates quantitative evaluation and quality control of endoscopic procedures. However, no relevant research has been reported. In this study, we aimed to develop a computer-assisted system, EndoAdd, for automated endoscopic surgical video analysis based on our dataset of endoscopic instrument images. METHODS: Large training and validation datasets containing 45,143 images of 10 different endoscopic instruments and a test dataset of 18,375 images collected from several medical centers were used in this research. Annotated image frames were used to train the state-of-the-art object detection model, YOLO-v5, to identify the instruments. Based on the frame-level prediction results, we further developed a hidden Markov model to perform video analysis and generate heatmaps to summarize the videos. RESULTS: EndoAdd achieved high accuracy (>97%) on the test dataset for all 10 endoscopic instrument types. The mean average accuracy, precision, recall, and F1-score were 99.1%, 92.0%, 88.8%, and 89.3%, respectively. The area under the curve values exceeded 0.94 for all instrument types. Heatmaps of endoscopic procedures were generated for both retrospective and real-time analyses. CONCLUSIONS: We successfully developed an automated endoscopic video analysis system, EndoAdd, which supports retrospective assessment and real-time monitoring. It can be used for data analysis and quality control of endoscopic procedures in clinical practice.

Weak-Interaction Environment in a Composite Electrolyte Enabling Ultralong-Cycling High-Voltage Solid-State Lithium Batteries.

Poly(vinylidene fluoride) (PVDF)-based solid electrolytes with a Li salt-polymer-little residual solvent configuration are promising candidates for solid-state batteries. Herein, we clarify the microstructure of PVDF-based composite electrolyte at the atomic level and demonstrate that the Li+-interaction environment determines both interfacial stability and ion-transport capability. The polymer works as a "solid diluent" and the filler realizes a uniform solvent distribution. We propose a universal strategy of constructing a weak-interaction environment by replacing the conventional N,N-dimethylformamide (DMF) solvent with the designed 2,2,2-trifluoroacetamide (TFA). The lower Li+ binding energy of TFA forms abundant aggregates to generate inorganic-rich interphases for interfacial compatibility. The weaker interactions of TFA with PVDF and filler achieve high ionic conductivity (7.0 × 10-4 S cm-1) of the electrolyte. The solid-state Li||LiNi0.8Co0.1Mn0.1O2 cells stably cycle 4900 and 3000 times with cutoff voltages of 4.3 and 4.5 V, respectively, as well as deliver superior stability at -20 to 45 °C and a high energy density of 300 Wh kg-1 in pouch cells.

Hydrogen Peroxide Promotes Tomato Leaf Senescence by Regulating Antioxidant System and Hydrogen Sulfide Metabolism.

Hydrogen peroxide (H2O2) is relatively stable among ROS (reactive oxygen species) and could act as a signal in plant cells. In the present work, detached tomato leaves were treated with exogenous H2O2 at 10 mmol/L for 8 h to study the mechanism of how H2O2 regulates leaf senescence. The data indicated that H2O2 treatment significantly accelerated the degradation of chlorophyll and led to the upregulation of the expression of leaf senescence-related genes (NYC1, PAO, PPH, SGR1, SAG12 and SAG15) during leaf senescence. H2O2 treatment also induced the accumulation of H2O2 and malondialdehyde (MDA), decreased POD and SOD enzyme activities and inhibited H2S production by reducing the expression of LCD1/2 and DCD1/2. A correlation analysis indicated that H2O2 was significantly and negatively correlated with chlorophyll, the expression of leaf senescence-related genes, and LCD1/2 and DCD1/2. The principal component analysis (PCA) results show that H2S showed the highest load value followed by O2•-, H2O2, DCD1, SAG15, etc. Therefore, these findings provide a basis for studying the role of H2O2 in regulating detached tomato leaf senescence and demonstrated that H2O2 plays a positive role in the senescence of detached leaves by repressing antioxidant enzymes and H2S production.

Associations of Whole Blood Zinc Levels with Coronary Artery Calcification and Future Cardiovascular Events in CKD Patients.

This study was conducted to compare the differences of the whole blood zinc concentration in patients with chronic kidney disease (CKD) as compared to healthy controls, and to explore the correlations of the whole blood zinc level with coronary artery calcification (CAC) and cardiovascular event (CVE) in CKD patients. A total of 170 CKD patients and 62 healthy controls were recruited. The whole blood zinc concentration was determined in using atomic absorption spectroscopy (AAS) method. The degrees of CAC were evaluated by Agatston score based on computed tomography (CT). Regular follow-up visits were performed to record the incidence of CVE, and risk factors were analyzed by COX proportional hazard model and Kaplan-Meier survival curve. There were statistically significant lower zinc levels in CKD patients than in healthy population. The prevalence of CAC was 58.82% in CKD patients. Correlation analysis showed that dialysis duration, intact parathyroid hormone (iPTH), alkaline phosphatase (ALP), 25-hydroxyvitamin D3 (25(OH)D3), neutrophil-lymphocyte ratio (NLR), total cholesterol (TC), and high-sensitive C-reactive protein (Hs-CRP) were positively correlated with CAC, while albumin (ALB), hemoglobin (Hb), and zinc levels were negatively associated with CAC. Further COX proportional hazard model demonstrated that moderate to severe CAC, NLR, phosphate, 25(OH)D3, iPTH, and high-density lipoprotein (HDL) were associated with an increased risk for CVE, while zinc levels, Hb, and ALB were inversely associated with a reduced risk for CVE. Kaplan-Meier curve showed that low zinc (zinc < 86.62 µmol/L) patients and moderate to severe CAC patients had lower survival respectively. Our study found the lower levels of zinc and higher prevalence of CAC in CKD patients; the low zinc is involved in the high incidence rate of moderate to severe CAC and CVE in CKD patients.

Pre-optimization and one-step preparation of cascade enzymes system with broad substrates by model guidance: Application of chiral L-norvaline and L-phenylglycine biosynthesis.

Cascade biocatalyst systems with catalytic promiscuity can be used for synthesis of a class of chiral chemicals but the optimization of these systems by model guidance is poorly explored. In this study, a cascade system with broad substrate spectrum was characterized and simulated by kinetic model with substrates of DL-Norvaline (DL-Nor) and DL-Phenylglycine (DL-Phg) as examples. To evaluate the optimal cascade system, maximum accumulation of intermediate products and conversion rate in the process were investigated by simultaneous solution of the rate equations for varying enzyme quantities. According to the simulation results, the cascade system was optimized by regulating the expression of D-amino acid oxidase and formate dehydrogenase and was prepared by one-step. The conversion efficiency of DL-Nor and DL-Phg have been significantly improved compared with that of before optimization. Moreover, the total of L-Nor and L-Phg were reached 498.2 mM and 79.5 mM through a gradient fed-batch conversion strategy, respectively.

Dielectric Filler-Induced Hybrid Interphase Enabling Robust Solid-State Li Metal Batteries at High Areal Capacity.

The fillers in composite solid-state electrolyte are mainly responsible for the enhancement of the conduction of Li ions but barely regulate the formation of solid electrolyte interphase (SEI). Herein, a unique filler of dielectric NaNbO3 for the poly(vinylidene fluoride) (PVDF)-based polymer electrolyte, which is subjected to the exchange of Li+ and Na+ during cycling, is reported and the substituted Na+ is engaged in the construction of a fluorinated Li/Na hybrid SEI with high Young's modulus, facilitating the fast transport of Li+ at the interface at a high areal capacity and suppressing the Li dendrite growth. The dielectric NaNbO3 also induces the generation of high-dielectric ß phase of PVDF to promote the dissociation of Li salt. The Li/Li symmetrical cell exhibits a long-term dendrite-free cycling over 600 h at a high areal capacity of 3 mA h cm-2. The LiNi0.8Mn0.1Co0.1O2/Li solid-state cells with NaNbO3 stably cycle 2200 times at 2 C and that paired with high-loading cathode (10 mg cm-2) can stably cycle for 150 times and exhibit excellent performances at -20 °C. This work provides a novel design principle of fillers undertaking interfacial engineering in composite solid-state electrolytes for developing the safe and stable solid-state lithium metal battery.

Molecular basis of methyl-salicylate-mediated plant airborne defence.

Aphids transmit viruses and are destructive crop pests1. Plants that have been attacked by aphids release volatile compounds to elicit airborne defence (AD) in neighbouring plants2-5. However, the mechanism underlying AD is unclear. Here we reveal that methyl-salicylate (MeSA), salicylic acid-binding protein-2 (SABP2), the transcription factor NAC2 and salicylic acid-carboxylmethyltransferase-1 (SAMT1) form a signalling circuit to mediate AD against aphids and viruses. Airborne MeSA is perceived and converted into salicylic acid by SABP2 in neighbouring plants. Salicylic acid then causes a signal transduction cascade to activate the NAC2-SAMT1 module for MeSA biosynthesis to induce plant anti-aphid immunity and reduce virus transmission. To counteract this, some aphid-transmitted viruses encode helicase-containing proteins to suppress AD by interacting with NAC2 to subcellularly relocalize and destabilize NAC2. As a consequence, plants become less repellent to aphids, and more suitable for aphid survival, infestation and viral transmission. Our findings uncover the mechanistic basis of AD and an aphid-virus co-evolutionary mutualism, demonstrating AD as a potential bioinspired strategy to control aphids and viruses.

The macrophage polarization by miRNAs and its potential role in the treatment of tumor and inflammation (Review).

The characteristics of monocyte/macrophage lineage are diversity and plasticity, mainly manifested by M1 and M2 subtypes in the body tissues, and playing different roles in the immunity. In the polarization process of macrophages, the classic molecular mechanism is related to sequential transcription factors. Whether in tumor or inflammatory local microenvironment, the pathological factors of the local microenvironment often affect the polarization of M1 and M2 macrophages, and participate in the occurrence and development of these pathological processes. In recent years, a growing number of research results demonstrated that non­coding RNA (ncRNA) also participates in the polarization process of macrophages, in addition to traditional cytokines and transcriptional regulation signal pathway molecules. Among numerous ncRNAs, microRNAs (miRNAs) have attracted more attention from scholars both domestically and internationally, and significant progress has been made in basic and clinical research. Therefore, for improved understanding of the molecular mechanism of miRNAs in macrophage polarization and analysis of the potential value of this regulatory pathway in tumor and inflammatory intervention therapy, a comprehensive review of the progress of relevant literature research was conducted and some viewpoints and perspectives were proposed.

GLS as a diagnostic biomarker in breast cancer: in-silico, in-situ, and in-vitro insights.

Background: Recently, a novel programmed cell death mechanism, Cuproptosis, has been discovered and found to play an important role in the development and progression of diverse tumors. In the present study, we comprehensively investigated the core gene of this mechanism, GLS, in breast cancer. Materials and methods: Bulk RNA sequencing data were curated from the TCGA repository to investigate the aberrant expression of GLS over diverse cancer types. Then, we examined its efficacy as a diagnostic biomarker in breast cancer by Area Under Curve (AUC) of the Receiver Operative Characteristic (ROC) curve. Furthermore, by applying siRNA technique, we knocked down the GLS expression level in cancerous cell lines, measuring the corresponding effects on cell proliferation and metastasis. Afterward, we explored the potential implications of GLS expression in the tumor immune microenvironment quantitatively by using several R packages and algorithms, including ESTIMATE, CIBERSORT, etc. Results: Pan-cancer analysis suggested that GLS was aberrantly over-expressed in many cancer types, with breast cancer being typical. More in-depth analyses revealed the expression of GLS exerted a high ROC-AUC value in breast cancer diagnosis. Through the knock-down of GLS expression, it was found that GLS expression was strongly relevant to the growth and metastasis of tumor. Furthermore, it was also found to be correlated with the immune tumor microenvironment. Conclusion: We highlighted that GLS expression might be applicable as a diagnostic biomarker in breast cancer and possess significant implications in the growth and metastasis of tumor and the immune tumor microenvironment, sharing new insights into ontological and personalized medicine.

Neutrophil extracellular traps facilitate sympathetic hyperactivity by polarizing microglia toward M1 phenotype after traumatic brain injury.

Traumatic brain injury (TBI), particularly diffuse axonal injury (DAI), often results in sympathetic hyperactivity, which can exacerbate the prognosis of TBI patients. A key component of this process is the role of neutrophils in causing neuroinflammation after TBI by forming neutrophil extracellular traps (NETs), but the connection between NETs and sympathetic excitation following TBI remains unclear. Utilizing a DAI rat model, the current investigation examined the role of NETs and the HMGB1/JNK/AP1 signaling pathway in this process. The findings revealed that sympathetic excitability intensifies and peaks 3 days post-injury, a pattern mirrored by the activation of microglia, and the escalated NETs and HMGB1 levels. Subsequent in vitro exploration validated that HMGB1 fosters microglial activation via the JNK/AP1 pathway. Moreover, in vivo experimentation revealed that the application of anti-HMGB1 and AP1 inhibitors can mitigate microglial M1 polarization post-DAI, effectively curtailing sympathetic hyperactivity. Therefore, this research elucidates that post-TBI, NETs within the PVN may precipitate sympathetic hyperactivity by stimulating M1 microglial polarization through the HMGB1/JNK/AP1 pathway.

AFB1 Microbial Degradation by Bacillus subtilis WJ6 and Its Degradation Mechanism Exploration Based on the Comparative Transcriptomics Approach.

Aflatoxin pollution poses great harm to human and animal health and causes huge economic losses. The biological detoxification method that utilizes microorganisms and their secreted enzymes to degrade aflatoxin has the advantages of strong specificity, high efficiency, and no pollution inflicted onto the environment. In this study, Bacillus subtilis WJ6 with a high efficiency in aflatoxin B1 degradation was screened and identified through molecular identification, physiological, and biochemical methods. The fermentation broth, cell-free supernatant, and cell suspension degraded 81.57%, 73.27%, and 8.39% of AFB1, respectively. The comparative transcriptomics analysis indicated that AFB1 led to 60 up-regulated genes and 31 down-regulated genes in B. subtilis WJ6. A gene ontology (GO) analysis showed that the function classifications of cell aggregation, the organizational aspect, and the structural molecule activity were all of large proportions among the up-regulated genes. The down-regulated gene expression was mainly related to the multi-organism process function under the fermentation condition. Therefore, B. subtilis WJ6 degraded AFB1 through secreted extracellular enzymes with the up-regulated genes of structural molecule activity and down-regulated genes of multi-organism process function.

ZmMS1/ZmLBD30-orchestrated transcriptional regulatory networks precisely control pollen exine development.

Because of its significance for plant male fertility and, hence, direct impact on crop yield, pollen exine development has inspired decades of scientific inquiry. However, the molecular mechanism underlying exine formation and thickness remains elusive. In this study, we identified that a previously unrecognized repressor, ZmMS1/ZmLBD30, controls proper pollen exine development in maize. Using an ms1 mutant with aberrantly thickened exine, we cloned a male-sterility gene, ZmMs1, which encodes a tapetum-specific lateral organ boundary domain transcription factor, ZmLBD30. We showed that ZmMs1/ZmLBD30 is initially turned on by a transcriptional activation cascade of ZmbHLH51-ZmMYB84-ZmMS7, and then it serves as a repressor to shut down this cascade via feedback repression to ensure timely tapetal degeneration and proper level of exine. This activation-feedback repression loop regulating male fertility is conserved in maize and sorghum, and similar regulatory mechanism may also exist in other flowering plants such as rice and Arabidopsis. Collectively, these findings reveal a novel regulatory mechanism of pollen exine development by which a long-sought master repressor of upstream activators prevents excessive exine formation.

Probiotic Potential, Antibacterial, and Antioxidant Capacity of Aspergillus luchuensis YZ-1 Isolated From Liubao Tea.

Aspergillus fungi are widely used in the traditional fermentation of food products, so their safety risks and functions are worthy of investigation. In this study, one Aspergillus luchuensis YZ-1 isolated from Liubao tea was identified based on phylogenetic analyses of sequences of three genes coding for internal transcribed spacer 1 (ITS1), ß-tubulin (benA), and calmodulin (CaM). The results of hemolytic activity, DNase activity, cytotoxicity assay, and antibiotic resistance assay indicated that the strain is potentially safe. The excellent gastrointestinal fluid tolerance, acid tolerance, bile tolerance, auto-aggregation, co-aggregation, cell surface hydrophobicity, and adhesion to human colon adenocarcinoma (HT29) cell line were observed on analysis of the probiotic properties. Furthermore, the results of the antibacterial activity of A. luchuensis YZ-1 indicated that the strain had strong antagonistic effects against Gram-negative and Gram-positive bacteria as well as fungi. Simultaneously, the water extracts and 80% ethanolic extracts of A. luchuensis YZ-1 cells also showed strong ABTS, DPPH, and OH- scavenging ability. Taken together, our results suggest that A. luchuensis YZ-1 has desirable functional probiotic properties and can be proposed as a biocontrol agent in the food industry.

DTL is a Novel Downstream Gene of E2F1 that Promotes the Progression of Hepatocellular Carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC), one of the world's most prevalent malignancies, accounts for 90% of primary liver cancer cases. Recent studies have shown an increased expression of denticles E3 ubiquitin protein ligase homolog (DTL) in several different tumor types, but its function and regulatory mechanisms remain unclear. AIMS: This study aimed to investigate the expressions of the Cullin4 (CUL4) complex in HCC and elucidate the roles of DTL in HCC cells. METHODS: The relative expression of the CUL4 complex and its clinical significance were analyzed with The Cancer Genome Atlas (TCGA) data, and the level of DTL was confirmed by immunohistochemistry. The functions of DTL1 and upstream E2F1 were evaluated by a Western blot, MTT, transwell, and xenograft in HCC cell lines. RESULTS: The elevated mRNA expression of the CUL4 complex, including CUL4B, DDB1 (Damage Specific DNA Binding Protein 1), and DTL, was associated with the overall survival of HCC patients. We also found that the DTL protein was elevated in HCC tissues, and patients with highly expressed DTL and nucleus-located DTL had a poorer survival time. DTL knockdown significantly inhibited cancer proliferation, migration, and invasion. Further experiments showed that E2F1 was an upstream regulatory molecule of DTL, which was bound to the promoter of DTL, promoting the expression of DTL. CONCLUSION: The study results demonstrate that E2F1-DTL signaling promotes the growth, migration, and invasion of HCC cells, which provides new insights and a potential biological target for future HCC therapies.

Analysis of Mean Corpuscular Volume and Red Cell Distribution Width in Patients with Aplastic Anemia.

To explore the characteristics of hemogram in patients with aplastic anemia (AA), especially mean corpuscular volume (MCV) and red cell distribution width (RDW). We examined the blood routine of 180 new-onset AA patients and used 166 patients with myelodysplastic syndrome (MDS) as controls. Among the 180 AA patients, 105 (58.3%) were diagnosed with severe AA (SAA), while 75 (41.7%) were diagnosed with non-severe AA (NSAA). Compared to MDS, patients with SAA generally had unfavorable hemogram, including significantly lower white blood cell (WBC), absolute neutrophil count (ANC), hemoglobin (Hb), platelet (PLT) and reticulocyte counts (RET). However, WBC, ANC and lymphocyte counts were higher in the NSAA group than in the MDS group; Hb and Ret were comparable between the two groups. 8.5% of SAA patients and 58.1% of NSAA patients presented with macrocytic anemia, whereas 25.7% of SAA and 64.0% of NSAA had a high RDW. In the MDS group, 54.7% of patients presented with macrocytic anemia, and 84.7% had increased RDW. WBC, ANC, PLT, and Ret in a high-RDW group (25.7% of SAA) were significantly higher than in a normal-RDW group (74.3% of SAA). Overall, most SAA patients exhibited normocytic-normochromic anemia, and their hemograms decreased more significantly; more than half of NSAA patients showed macrocytic-heterogeneous anemia, and their hemograms were similar to those of MDS. Patients with elevated RDW may have better residual bone marrow hematopoietic function than those with normal RDW but with more severe anemia.

Ultrarapid Nanomanufacturing of High-Quality Bimetallic Anode Library toward Stable Potassium-Ion Storage.

Bimetallic alloy nanomaterials are promising anode materials for potassium-ion batteries (KIBs) due to their high electrochemical performance. The most well-adopted fabrication method for bimetallic alloy nanomaterials is tube furnace annealing (TFA) synthesis, which can hardly satisfy the trade-off among granularity, dispersity and grain coarsening due to mutual constraints. Herein, we report a facile, scalable and ultrafast high-temperature radiation (HTR) method for the fabrication of a library of ultrafine bimetallic alloys with narrow size distribution (≈10-20 nm), uniform dispersion and high loading. The metal-anchor containing heteroatoms (i.e., O and N), ultrarapid heating/cooling rate (≈103  K s-1 ) and super-short heating duration (several seconds) synergistically contribute to the successful synthesis of small-sized alloy anodes. As a proof-of-concept demonstration, the as-prepared BiSb-HTR anode shows ultrahigh stability indicated by negligible degradation after 800 cycles. The in situ X-ray diffraction reveals the K+ storage mechanism of BiSb-HTR. This study can shed light on the new, rapid and scalable nanomanufacturing of high-quality bimetallic alloys toward extended applications of energy storage, energy conversion and electrocatalysis.

Understanding and eliminating the reductant interference on Chromium VI measurement with USEPA method 3060A.

Excessive reductants are used in engineering to ensure a reliable remediation effect of chromite ore processing residue (COPR), however, re-yellowing phenomenon of remediated COPR occurs after some time though the Cr(VI) content meets regulatory requirements after curing period. This problem is due to a negative bias on Cr(VI) determination using USEPA method 3060A. To address this issue, this study tried to reveal the interference mechanisms and proposed two methods to amend the bias. Results of ion concentrations, UV-Vis spectrum, XRD, and XPS together showed that Cr(VI) was reduced by ions (Fe2+, S52-) in the digestion stage of USEPA method 3060A, and as a result, method 7196A would not reflect the true Cr(VI) concentration. The interference on Cr(VI) determination generated by excess reductants mainly occurs during the curing period of remediated COPR, but it decreases over time as reductants being oxidized gradually by the air. Compared with the thermal oxidation, the chemical oxidation with K2S2O8 prior to alkaline digestion performs better to eliminate the masking effect brought by excess reductants. This study provides an approach on how to accurately determine the Cr(VI) concentration in the remediated COPR. It might be helpful to reduce the occurrence possibility of re-yellowing phenomenon.