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Electroactive organic electrode materials exhibit remarkable potential in aqueous zinc ion batteries (AZIBs) due to their abundant availability, customizable structures, sustainability, and high reversibility. However, the research on AZIBs has predominantly concentrated on unraveling the storage mechanism of zinc cations, often neglecting the significance of anions in this regard. Herein, bipolar poly(thionine) is synthesized by a simple and efficient polymerization reaction, and the kinetics of different anions are investigated using poly(thionine) as the cathode of AZIBs. Notably, poly(thionine) is a bipolar organic polymer electrode material and exhibits enhanced stability in aqueous solutions compared to thionine monomers. Kinetic analysis reveals that ClO4 - exhibits the fastest kinetics among SO4 2-, Cl-, and OTF-, demonstrating excellent rate performance (109 mAh g-1 @ 0.5 A g-1 and 92 mAh g-1 @ 20 A g-1). Mechanism studies reveal that the poly(thionine) cathode facilitates the co-storage of both anions and cations in Zn(ClO4)2. Furthermore, the lower electrostatic potential of ClO4 - influences the strength of hydrogen bonding with water molecules, thereby enhancing the overall kinetics in aqueous electrolytes. This work provides an effective strategy for synthesizing high-quality organic materials and offers new insights into the kinetic behavior of anions in AZIBs.
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BACKGROUND: Checkpoint inhibitor pneumonitis (CIP) is a potentially fatal adverse event characterized by new pulmonary infiltrates in cancer patients receiving immune checkpoint inhibitor therapy. This study aims to explore the interplay between lung microbiota, dysregulated metabolites, and host immunity in CIP. METHODS: We recruited thirteen hospitalized CIP patients, eleven idiopathic pulmonary fibrosis (IPF) patients, and ten new-onset non-small cell lung cancer patients. Bronchoalveolar lavage fluid samples were collected for 16S rRNA gene sequencing. The percentages of immune cells were determined using manual counting and flow cytometry. Interactions among microbiota, metabolites, and lymphocytes were analyzed using cultured mouse splenocytes and human T cells. FINDINGS: Proteobacteria emerged as the dominant phylum, notably abundant in both the CIP and IPF groups. Vibrio, Halomonas, Mangrovibacter, and Salinivibrio were the predominant microbiota because of their discriminative abundance patterns. Vibrio (r = 0.72, P-adj = 0.007) and Halomonas (r = 0.65, P-adj = 0.023) demonstrated strong correlations with lymphocytes. Vibrio metschnikovii and Mangrovibacter plantisponsors were more abundant in the CIP group than in the IPF group. Lauroylcarnitine, a key intermediary metabolite co-occurring with the predominant microbiota, exhibited a potent effect on cytokine secretion by mouse and human T cells, notably enhancing IFN-γ and TNF-α production from CD4 and CD8 cells in vitro. INTERPRETATION: Lauroylcarnitine, co-occurring with the predominant lung microbiota in CIP, could activate T cells in vitro. These findings suggest potential involvement of lung microbiota and acylcarnitine metabolism dysregulation in the pathogenesis of CIP. FUNDING: This work was supported by Peking University People's Hospital Scientific Research Development Funds (RDJ2022-15) and Provincial Key Clinical Specialty Capacity Building Project 2020 (Department of the Respiratory Medicine).
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The melanocortin 4 receptor (MC4R) gene plays a central role in regulating energy homeostasis and food intake in livestock, thereby affecting their economic worth and growth. In a previous study, the p.T117M mutation in the sheep MC4R gene, which leads to the transition of threonine to methionine, was found to affect the body weight at six months and the average daily gain in Hu sheep. However, there are still limited studies on the frequency of the sheep p.T117M missense mutation globally, and the underlying cellular mechanism remains elusive. Therefore, this study first used WGS to investigate the distribution of the MC4R gene p.T117M mutation in 652 individuals across 22 breeds worldwide. The results showed that the mutation frequency was higher in European breeds compared with Chinese sheep breeds, particularly in Poll Dorset sheep (mutation frequency > 0.5). The p.T117M mutation occurs in the first extracellular loop of MC4R. Mechanistically, the basal activity of the mutated receptor is significantly increased. Specifically, upon treatment with α-MSH and ACTH ligands, the cAMP and MAPK/ERK signaling activation of M117 MC4R is enhanced. These results indicate that the T117M mutation may change the function of the gene by increasing the constitutive activity and signaling activation of cAMP and MAPK/ERK, and, thus, may regulate the growth traits of sheep. In conclusion, this study delved into the global distribution and underlying cellular mechanisms of the T117M mutation of the MC4R gene, establishing a scientific foundation for breeding sheep with superior growth, thereby contributing to the advancement of the sheep industry.
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Background: Obstructive sleep apnea (OSA) syndrome and nonalcoholic fatty liver disease (NAFLD) have been shown to have a close association in previous studies, but their pathogeneses are unclear. This study explores the molecular mechanisms associated with the pathogenesis of OSA and NAFLD and identifies key predictive genes. Methods: Using the Gene Expression Omnibus (GEO) database, we obtained gene expression profiles GSE38792 for OSA and GSE89632 for NAFLD and related clinical characteristics. Mitochondrial unfolded protein response-related genes (UPRmtRGs) were acquired by collating and collecting UPRmtRGs from the GeneCards database and relevant literature from PubMed. The differentially expressed genes (DEGs) associated with OSA and NAFLD were identified using differential expression analysis. Gene Set Enrichment Analysis (GSEA) was conducted for signaling pathway enrichment analysis of related disease genes. Based on the STRING database, protein-protein interaction (PPI) analysis was performed on differentially co-expressed genes (Co-DEGs), and the Cytoscape software (version 3.9.1) was used to visualize the PPI network model. In addition, the GeneMANIA website was used to predict and construct the functional similar genes of the selected Co-DEGs. Key predictor genes were analyzed using the receiver operating characteristic (ROC) curve. Results: The intersection of differentially expressed genes shared between OSA and NAFLD-related gene expression profiles with UPRmtRGs yielded four Co-DEGs: ASS1, HDAC2, SIRT3, and VEGFA. GSEA obtained the relevant enrichment signaling pathways for OSA and NAFLD. PPI network results showed that all four Co-DEGs interacted (except for ASS1 and HDAC2). Ultimately, key predictor genes were selected in the ROC curve, including HDAC2 (OSA: AUC = 0.812; NAFLD: AUC = 0.729), SIRT3 (OSA: AUC = 0.775; NAFLD: AUC = 0.750), and VEGFA (OSA: AUC = 0.812; NAFLD: AUC = 0.861) (they have a high degree of accuracy in predicting whether a subject will develop two diseases). Conclusion: In this study, four co-expression differential genes for OSA and NAFLD were obtained, and they can predict the occurrence of both diseases. Transcriptional mechanisms involved in OSA and NAFLD interactions may be better understood by exploring these key genes. Simultaneously, this study provides potential diagnostic and therapeutic markers for patients with OSA and NAFLD.
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There has been interest in the connection between cardiovascular diseases and osteoporosis, both of which share hyperlipidemia as a common pathological basis. Osteoporosis is a progressive metabolic bone disease characterized by reduced bone mass, deteriorated bone microstructure, increased bone fragility and heightened risk of bone fractures. Dysfunction of osteoblastic cells, vital for bone formation, is induced by excessive internalization of lipids under hyperlipidemic conditions, forming the crux of hyperlipidemia-associated osteoporosis. Autophagy, a process fundamental to cell self-regulation, serves a critical role in osteoblastic cell function and bone formation. When activated by lipids, lipophagy inhibits osteoblastic cell differentiation in response to elevated lipid concentrations, resulting in reduced bone mass and osteoporosis. However, an in-depth understanding of the precise roles and mechanisms of lipophagy in the regulation of osteoblastic cell function is required. Study of the molecular mechanisms governing osteoblastic cell response to excessive lipids can result in a clearer understanding of osteoporosis; therefore, potential strategies for preventing hyperlipidemia-induced osteoporosis can be developed. The present review discusses recent progress in elucidating the molecular mechanisms of lipophagy in the regulation of osteoblastic cell function, offering insights into hyperlipidemia-induced osteoporosis.
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INTRODUCTION: Esophageal-Squamous Cell Carcinoma (ESCC) is often diagnosed at the middle or late stage, thus requiring more effective therapeutic strategies. Pharmacologically, the anti-tumor activity of the principal active constituent of Sophora flavescens, matrine (MA), has been explored widely. Notwithstanding, it is significant to nanotechnologically enhance the anti-tumor activity of MA in view of its potential to distribute non-tumor cells. METHODS: Herein, MA-loaded Nano-Liposomes (MNLs) were prepared to enhance the effect of anti-ESCC. The MNL showed a smaller sized particle (25.95 ± 1.02 nm) with a low polydispersed index (PDI = 0.130 ± 0.054), uniform spherical morphology, good solution stability, and encapsulated efficiency (65.55% ± 2.47). Furthermore, we determined the characteristics of KYSE-150 cells by cell viability assay, IC50, Mitochondrial Membrane Potential (MMP), Western blot, and apoptotic analysis, which indicated that MNLs down-regulated the cell viability and IC50 in a concentration-dependent manner and induced a significant change in JC-1 fluorescence from red to green. RESULTS: The above observations resulted in increased Bax and Caspase-3 levels, coupled with a substantial decrease in Bcl-2 and apoptotic promotion at the advanced stage compared with MA. CONCLUSION: Based on these results, MNLs may serve as a more effective and promising therapeutic option for ESCC.
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Objective: To investigate the effect of Sanshentongmai (SSTM) mixture on the regulation of oxidative damage to rat cardiomyocytes (H9C2) through microRNA-146a and its mechanism. Methods: H9C2 were cultured in vitro, H2O2 was used as an oxidant to create an oxidative damage model in H9C2 cells. SSTM intervention was administered to the H9C2 cells. Then, the changes in H2O2-induced oxidative damage in H9C2 cells and the expression of microRNA-146a were observed to explore the protective effect of SSTM on H9C2 and its mechanism. H9C2 cells cultured i n vitro were divided into 3 groups, including a control group, a model group of H2O2-induced oxidative damage (referred to hereafter as the model group), and a group given H2O2 modeling plus SSTM intervention at 500 µg/L for 72 h (referred to hereafter as the treatment group). The cell viability was measured by CCK8 assay. In addition, the levels of N-terminal pro-brain natriuretic peptide (Nt-proBNP), nitric oxide (NO), high-sensitivity C-reactive protein (Hs-CRP), and angiotensin were determined by enzyme-linked immunosorbent assay (ELISA). The expression level of microRNA-146a was determined by real-time PCR (RT-PCR). Result: H9C2 cells were pretreated with SSTM at mass concentrations ranging from 200 to 1500 µg/L. Then, CCK8 assay was performed to measure cell viability and the findings showed that the improvement in cell proliferation reached its peak when the mass concentration of SSTM was 500 µg/L, which was subsequently used as the intervention concentration. ELISA was performed to measure the indicators related to heart failure, including Nt-proBNP, NO, Hs-CRP, and angiotensin â ¡. Compared with those of the control group, the expressions of Nt-proBNP and angiotensin â ¡ in the treatment group were up-regulated (P<0.05), while the expression of NO was down-regulated (P<0.05). There was no significant difference in the expression of Hs-CRP between the treatment group and the control group. These findings indicate that SSTM could effectively ameliorate oxidative damage in H9C2 rat cardiomyocytes. Finally, according to the RT-PCR findings for the expression of microRNA-146a in each group, H2O2 treatment at 15 µmol/L could significantly reduce the expression of microRNA-146a, and the expression of microRNA-146a in the treatment group was nearly doubled compared with that in the model group. There was no significant difference between the treatment group and the control group. Conclusion: SSTM can significantly resist the H2O2-induced oxidative damage of H9C2 cells and may play a myocardial protective role by upregulating microRNA-146a.
Subject(s)
Drugs, Chinese Herbal , Hydrogen Peroxide , MicroRNAs , Myocytes, Cardiac , Oxidative Stress , Up-Regulation , Myocytes, Cardiac/metabolism , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/cytology , Animals , MicroRNAs/metabolism , MicroRNAs/genetics , Rats , Oxidative Stress/drug effects , Hydrogen Peroxide/toxicity , Drugs, Chinese Herbal/pharmacology , Up-Regulation/drug effects , Cell Survival/drug effects , Cell Line , Drug CombinationsABSTRACT
Retardation induced by media can be used as an image contrast to depict the cumulative birefringent features and local variations of the sample, respectively. It is commonly assumed that the retardation is induced by the light propagation; however, the light scattering would generate the retardation as well. In our work, the scattering-induced retardation as a high-sensitivity image contrast for revealing collagen fibers is presented. First, it is shown that the retardation induced by fiber scattering is equal to π when modeled as cylinders. Using the data for the chicken breast and the palm measured by the polarization-sensitive optical coherence tomography system as an example, the scattering-induced retardation is calculated. The measured value of π is in complete agreement with the theory, and the corresponding retardation per unit distance is two orders of magnitude greater than the light-propagation-induced retardation, demonstrating its predominant role on the overall retardation and providing a possibility for highly sensitive displays. Compared with the accumulated retardation image and the differential retardation image, the scattering-induced retardation images could exhibit sharper fiber structures even in deeper regions. This work might be helpful for the early diagnosis of collagen-related diseases.
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BACKGROUND: Sows commonly experience insulin resistance in late gestation and lactation, causing lower feed intake and milk production, which can lead to higher mortality rates in newborn piglets. The probiotic Lactobacillus rhamnosus GG (LGG) is known to improve insulin resistance. However, whether supplementing LGG can improve insulin sensitivity in sows and enhance lactation performance, particularly the early survival of offspring remains unclear. Hence, we explored the effects and mechanisms of supplementing LGG during late gestation and lactation on sow insulin sensitivity, lactation performance, and offspring survival. In total, 20 sows were randomly allocated to an LGG (n = 10) and control group (n = 10). RESULTS: In sows, LGG supplementation significantly improved insulin sensitivity during late gestation and lactation, increased feed intake, milk production and colostrum lactose levels in early lactation, and enhanced newborn piglet survival. Moreover, LGG treatment significantly reshaped the gut microbiota in sows, notably increasing microbiota diversity and enriching the relative abundance of insulin sensitivity-associated probiotics such as Lactobacillus, Bifidobacterium, and Bacteroides. Serum metabolite and amino acid profiling in late-gestation sows also revealed decreased branched-chain amino acid and kynurenine serum levels following LGG supplementation. Further analyses highlighted a correlation between mitigated insulin resistance in late pregnancy and lactation by LGG and gut microbiota reshaping and changes in serum amino acid metabolism. Furthermore, maternal LGG enhanced immunity in newborn piglets, reduced inflammation, and facilitated the establishment of a gut microbiota. CONCLUSIONS: We provide the first evidence that LGG mitigates insulin resistance in sows and enhances offspring survival by modulating the gut microbiota and amino acid metabolism.
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BACKGROUND: Limited data exist for global prevalence of claudin 18 isoform 2 (CLDN18.2) positivity and association of CLDN18.2 status with clinical and tumor characteristics in patients with locally advanced (LA) unresectable or metastatic gastric or gastroesophageal junction (mG/GEJ) adenocarcinoma. We report prevalence of CLDN18.2 positivity (phase 3; SPOTLIGHT, NCT03504397; GLOW, NCT03653507) and concordance of CLDN18.2 status between a subset of pair-matched tumor samples (phase 2, ILUSTRO, NCT03505320; phase 1, NCT03528629) from clinical studies of zolbetuximab. METHODS: Tumor samples from patients with LA unresectable or mG/GEJ adenocarcinoma were tested for CLDN18.2 status by immunohistochemistry. Human epidermal growth factor receptor 2 (HER2) expression was tested per central or local assessment. RESULTS: Across SPOTLIGHT and GLOW, the prevalence of CLDN18.2 positivity (≥ 75% of tumor cells demonstrating moderate-to-strong membranous CLDN18 staining) was 38.4%. Prevalence was similar in gastric versus GEJ adenocarcinoma samples and regardless of collection method (biopsy versus resection) or collection site (primary versus metastatic). CLDN18.2 positivity was most prevalent in patients with diffuse-type tumors. In ILUSTRO and the phase 1 study, concordance of CLDN18.2 positivity was 61.1% between archival (i.e., any time before treatment) and baseline (i.e., ≤ 3 months before first treatment) samples, and concordance of any CLDN18 staining (≥ 1% of tumor cells demonstrating moderate-to-strong membranous CLDN18 staining) was 88.9%. CONCLUSIONS: CLDN18.2 was a highly prevalent biomarker in patients with HER2-negative, LA unresectable or mG/GEJ adenocarcinoma. CLDN18.2 positivity remained relatively stable over time in many patients. Biomarker testing for CLDN18.2 should be considered in standard clinical practice in these patients.
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The adult mammalian cardiomyocyte has a limited capacity for self-renewal, which leads to the irreversible heart dysfunction and poses a significant threat to myocardial infarction patients. In the past decades, research efforts have been predominantly concentrated on the cardiomyocyte proliferation and heart regeneration. However, the heart is a complex organ that comprises not only cardiomyocytes but also numerous noncardiomyocyte cells, all playing integral roles in maintaining cardiac function. In addition, cardiomyocytes are exposed to a dynamically changing physical environment that includes oxygen saturation and mechanical forces. Recently, a growing number of studies on myocardial microenvironment in cardiomyocyte proliferation and heart regeneration is ongoing. In this review, we provide an overview of recent advances in myocardial microenvironment, which plays an important role in cardiomyocyte proliferation and heart regeneration.
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BACKGROUND: More and more evidence has shown the process of Parkinson's disease (PD). Probably, inflammation exerts a crucial role between them. Therefore, the aim of this study was to analyze the impact of interleukin-6 receptor (IL-6R) expression on the IL-6/signal transducer and activator of transcription 3 (STAT3)/hypoxia-inducible factor-1α (HIF-1α) inflammatory signaling pathway within a mouse model of PD with type 2 diabetes mellitus (T2DM) as co-morbidity. METHODS: We chose healthy wild-type C57BL/6J male mice at the age of 10 weeks to prepare a mouse model of PD with T2DM co-morbidity. Adeno-associated virus (AAV) overexpressing IL-6R or AAV IL-6R-shRNA genes were injected into the substantia nigra (SN) of the mice. The behavioral indices of the pole test were used for examining the motor function of the mice. Using immunofluorescence analysis, the impacts of IL-6R on the level of tyrosine hydroxylase (TH) and anti-ionized calcium-binding adaptor molecule 1 (IBA-1) on dopaminergic neurons and microglia were examined. Additionally, enzyme-linked immunosorbent assay (ELISA) was adopted for determining the expressions of HIF-1α and inflammatory cytokines like tumor necrosis factor-α (TNF-α), IL-1ß, IL-6, and IL-4 in the serum. In this study, the protein expression levels of TH, α-Synuclein (α-Syn), IBA-1, IL-6, IL-6R, phosphorylated and total signal transducer and activator of transcription 3 (p-STAT3 (Tyr705) and STAT3) and HIF-1α in the SN were tested via western blotting. To ascertain the mRNA expressions of TNF-α, IL-1ß, IL-6, IL-4, and HIF-1α, we used quantitative Real-Time Polymerase Chain Reaction (RT-qPCR). RESULTS: IL-6R-shRNA treatment could markedly shorten the total time of PD in the T2DM co-morbidity mouse model based on the pole test results, reverse the decrease in TH-positive neurons stimulated by 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP), and lower the activation of microglia (all p < 0.05). Further, IL-6R-shRNA treatment hindered the expression of IL-6, p-STAT3 (Tyr705), and HIF-1α in the SN, lowered the levels of TNF-α, IL-1ß, IL-6, IL-4, and HIF-1α in the serum, and mRNA expressions of TNF-α, IL-1ß, IL-6, and HIF-1α in the SN (all p < 0.05). In contrast, IL-6R overexpression reduced TH levels, upregulated the level of IBA-1, IL-6, p-STAT3 (Tyr705), and HIF-1α, increased the level of IL-1ß, TNF-α, IL-6, IL-4, and HIF-1α (all p < 0.05) in the serum and SN in the PD mouse model with T2DM as a co-morbidity. CONCLUSIONS: PD progression with T2DM as a co-morbidity can be boosted by AAV IL-6R-overexpression through upregulation of the IL-6/STAT3/HIF-1α axis. Conversely, AAV IL-6R-shRNA treatment suppressed the IL-6/STAT3/HIF-1α pathway and alleviated neuroinflammation, thus weakening the development of PD with T2DM as a co-morbidity.
Subject(s)
Diabetes Mellitus, Type 2 , Disease Models, Animal , Hypoxia-Inducible Factor 1, alpha Subunit , Interleukin-6 , Mice, Inbred C57BL , Parkinson Disease , Receptors, Interleukin-6 , STAT3 Transcription Factor , Signal Transduction , Animals , Hypoxia-Inducible Factor 1, alpha Subunit/metabolism , Hypoxia-Inducible Factor 1, alpha Subunit/genetics , Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/complications , STAT3 Transcription Factor/metabolism , STAT3 Transcription Factor/genetics , Interleukin-6/metabolism , Male , Mice , Receptors, Interleukin-6/metabolism , Receptors, Interleukin-6/genetics , Parkinson Disease/metabolism , Parkinson Disease/geneticsABSTRACT
The performance of perovskite solar cells has been continuously improving. However, humidity stability has become a key problem that hinders its promotion in the process of commercialization. A buffer layer deposited by atomic layer deposition is a very helpful method to solve this problem. In this work, MgO film is deposited between Spiro-OMeTAD and electrode by low-temperature atomic layer deposition at 80 °C, which resists the erosion of water vapor, inhibits the migration of electrode metal ions and the decomposition products of perovskite, then finally improves the stability of the device. At the same time, the MgO buffer layer can passivate the defects of porous Spiro, thus enhancing carrier transport efficiency and device performance. The Cs0.05(FAPbI3)0.85(MAPbBr3)0.15 perovskite device with a MgO buffer layer has displayed PCE of 22.74%, also with a high Voc of 1.223 V which is an excellent performance in devices with same perovskite component. Moreover, the device with a MgO buffer layer can maintain 80% of the initial efficiency after 7200 h of storage at 35% relative humidity under room temperature. This is a major achievement for humidity stability in the world, providing more ideas for further improving the stability of perovskite devices.
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The total organic carbon (OC) from plant litter in riparian zones is an important nutrient source for aquatic organisms and plays a crucial role in the nutrient cycling of river ecosystems. Nevertheless, the total amount of OC in dammed rivers gradually decreases, and the restoration methods are rarely researched. A hypothesis was proposed that the periodic inundation altered the process of OC release from plant litter. To explore the impact of periodic inundation on OC release from litter in the riparian zone, litter bags in situ tests were conducted in the Yalong River. Three inundation treatments were conducted for the test samples, which were NS (never submerged by water), PIS (periodic submerged), and PMS (permanent submerged). Results indicated that the amount of OC released from litters in PIS treatment was about 1.1 times that in PMS treatment, and about 2.1 times that in NS treatment. The average release rate coefficient k of PIS treatment (at mean water level) was the highest (12.8 × 10-4 d-1), followed by PMS treatment (11.0 × 10-4 d-1), and NS treatment (5.6 × 10-4 d-1), which demonstrated that the periodic inundation was critical for OC release. The mean water level was a demarcation line where there was a significant difference in the release of OC in the riparian zone (p < 0.05). Flow velocity alone could account for 84% of the variation in OC release rate, while the flow velocity and inundation duration together could achieve an explanatory degree of 86%. This research can provide a valuable scientific basis for the protection and restoration of river ecosystems, especially for the recovery of OC concentration in dammed rivers.
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Carbon , Rivers , Rivers/chemistry , Plants , EcosystemABSTRACT
Background: Acute respiratory failure is the main clinical manifestation and a major cause of death in patients with COVID-19. However, few reports on its prevention and control have been published because of the need for laboratory predictive indicators. This study aimed to evaluate the predictive value of hematocrit level, serum albumin level difference, and fibrinogen-to-albumin ratio for COVID-19-associated acute respiratory failure. Material and methods: A total of 120 patients with COVID-19 from the First Affiliated Hospital of Anhui Medical University were selected between December 2022 and March 2023. Patients were divided into acute respiratory failure and non-acute respiratory failure groups and compared patient-related indicators between them using univariate and multivariate logistic regression analyses. Receiver operating characteristic analysis was performed to determine the discrimination accuracy. Results: In total, 48 and 72 patients were enrolled in the acute respiratory failure and non-acute respiratory failure groups, respectively. The Quick COVID-19 Severity Index scores, fibrinogen-to-albumin ratio, hematocrit and serum albumin level difference, fibrinogen, and hematocrit levels were significantly higher in the acute respiratory failure group than in the non-acute respiratory failure group. A Quick COVID-19 Severity Index >7, fibrinogen-to-albumin ratio >0.265, and hematocrit and serum albumin level difference >12.792 had a 96.14 % positive predictive rate and a 94.06 % negative predictive rate. Conclusion: Both fibrinogen-to-albumin ratio and hematocrit and serum albumin level difference are risk factors for COVID-19-associated acute respiratory failure. The Quick COVID-19 Severity Index score combined with fibrinogen-to-albumin ratio, and hematocrit and serum albumin level difference predict high and low risks with better efficacy and sensitivity than those of the Quick COVID-19 Severity Index score alone; therefore, these parameters can be used collectively as a risk stratification method for assessing patients with COVID-19.
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Developing high-efficiency durable electrocatalysts in wide pH range for water splitting is significant for environmentally-friendly synthesis of renewable hydrogen energy. Herein, a facile method by dealloying designable multicomponent metallic glass precursors is reported to synthesize amorphous-crystalline heterostructured nanoporous high-entropy alloys (AC-HEAs) of CuAgAuPtPd, CuAgAuIrRu, and CuAgAuPtPdIrRu, heaped up by nanocrystalline particles with an average size of 2-3 nm and the amorphous glued phase. The synthesized AC-HEA-CuAgAuPtPd owns highly catalytic performances for hydrogen evolution reaction (HER), with 9.5 and 20 mV to reach 10 mA·cm-2 in 0.5 m H2SO4 and 1.0 m KOH, and AC-HEA-CuAgAuIrRu delivers 208 and 200 mV for oxygen evolution reaction (OER). Moreover, a two-electrode electrolyzer made of the AC-HEA-CuAgAuIrRu bifunctional electrodes exhibit a low cell voltage of 1.48 and 1.49 V in the acidic and alkaline conditions at 10 mA·cm-2 for overall water splitting. Combining the enhanced catalytic activities from nanoscale amorphous structure and atom-level synergistic catalyst in AC-HEAs provides an effective pathway for pH-universal electrocatalysts of water splitting.
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Neonatal respiratory distress syndrome (NRDS) is one of the most severe respiratory disorders in preterm infants (PTIs) due to immature lung development. To delineate the serum metabolic alterations and gut microbiota variations in NRDS and assess their implications on neonatal development, we enrolled 13 NRDS neonates and 12 PTIs and collected fecal and serum specimens after birth. Longitudinal fecal sampling was conducted weekly for a month in NRDS neonates. NRDS neonates were characterized by notably reduced gestational ages and birth weights and a higher rate of asphyxia at birth relative to PTIs. Early postnatal disturbances in tryptophan metabolism were evident in the NRDS group, concomitant with elevated relative abundance of Haemophilus, Fusicatenibacter, and Vibrio. Integrative multiomics analyses revealed an inverse relationship between tryptophan concentrations and Blautia abundance. At one-week old, NRDS neonates exhibited cortisol regulation anomalies and augmented hepatic catabolism. Sequential microbial profiling revealed distinct gut microbiota evolution in NRDS subjects, characterized by a general reduction in potentially pathogenic bacteria. The acute perinatal stress of NRDS leads to mitochondrial compromise, hormonal imbalance, and delayed gut microbiota evolution. Despite the short duration of NRDS, its impact on neonatal development is significant and requires extended attention.
Subject(s)
Feces , Gastrointestinal Microbiome , Infant, Premature , Respiratory Distress Syndrome, Newborn , Humans , Infant, Newborn , Respiratory Distress Syndrome, Newborn/microbiology , Respiratory Distress Syndrome, Newborn/metabolism , Feces/microbiology , Female , Male , Gestational Age , Tryptophan/metabolism , Tryptophan/blood , Hydrocortisone/bloodABSTRACT
PURPOSE: Ultrasound shear wave elastography has potential use in assessing tendon tissue; however, reducing measurement variability remains challenging. The primary purpose of this study was to identify the amount of variability accounted for by ultrasound parameter (frequency, harmonics and CrossXBeam) settings on shear wave speed at two testing sites. METHODS: Shear wave elastography images of the Achilles tendon were obtained from individuals with healthy tendons (n = 28) at two testing sites with standardised image acquisition/postprocessing protocols. Images were acquired at a range of frequencies (7-15 MHz) with CrossXBeam (a filtering technique) and harmonics settings toggled on and off. Variance decomposition analysis was performed to identify the amount of variability in shear wave speed accounted for by scan acquisition settings and testing sites. RESULTS: Shear wave speed variance was primarily attributed to participants (56.87% of variance; residual error: 35%). All scanning parameters, testing site and interaction terms each accounted for less than 2.5% of the variance. A statistically significant, negative relationship was observed between shear wave speed and image quality (p = 0.001) suggesting poor image quality yields higher shear wave speed estimates. CONCLUSION: The findings of this study suggest that natural variation in Achilles tendon mechanics between individuals without tendon pathology accounts for most of the shear wave speed variability. Optimising image quality, which may be observed in higher frequencies, should be considered to improve shear wave speed estimation. Clinically, this study highlights the need to take multiple images, maintain consistent ultrasound settings when tracking patient progress over time and use caution when comparing raw values from tendon scans performed in different clinics with shear wave elastography. LEVEL OF EVIDENCE: Level III.
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Plant-mediated interactions between herbivores play an important role in regulating the composition of herbivore community. The fall armyworm (FAW), Spodoptera frugiperda, which has become one of the most serious pests on corn in China since it invaded in 2018, has been found feeding rice in the field. However, how FAW interacts with native rice insect pests remains largely unknown. Here, we investigated the interaction between FAW and a resident herbivore, striped stem borer (SSB, Chilo suppressalis) on rice. The infestation of rice leaf sheaths (LSs) by SSB larvae systemically enhanced the level of jasmonic acid (JA), abscisic acid (ABA), and trypsin proteinase inhibitors (TPIs), reduced relative water content (RWC) in leaf blades (LBs), and suppressed the growth of FAW larvae. In contrast, because FAW larvae infested LBs and did not affect defence responses in LSs, they did not influence the performance of SSB larvae. Using different mutants, together with bioassays and chemical analysis, we revealed that SSB-induced suppression of FAW larvae growth depended on both the SSB-activated JA pathway and RWC in LBs, whereas the ABA pathway activated by SSB larvae promoted the growth of FAW larvae by impeding water loss. These results provide new insights into mechanisms underlying plant-mediated interactions between herbivores.