Effects of climate warming on soil nitrogen cycles and bamboo growth in core giant panda habitat.

Climate change can pose a significant threat to terrestrial ecosystems by disrupting the circulation of soil nitrogen. However, experimental analyses on the effect of climate change on soil nitrogen cycles and the implications for the conservation of key wildlife species (i.e., the giant panda, Ailuropoda melanoleuca) remain understudied. We investigated the effects of a 1.5 °C, 3 °C, and 4.5 °C temperature increase on nitrogen distribution in different soil layers of bamboo forest via an in-situ experiment and assessed the implications for the growth and survival of arrow bamboo (Bashania faberi), a critical food resource for giant pandas. Our results showed that warming treatments generally increased soil N content, while effects differed between surface soil and subsurface soil and at different warming treatments. Particularly an increase of 1.5 °C raised the subsurface soil NO3-N content, as well as the content of N in bamboo leaves. We found a significant positive correlation between the subsurface soil NO3-N content and the N content of arrow bamboo. An increase of 3-4.5 °C raised the content of total N and NO3-N in the surface soil and led to a reduction in the total aboveground biomass and survival rate of arrow bamboo. Limited warming (e.g., the increase of 0-1.5 °C) may promote the soil N cycle, raise the N-acetylglucosaminidase (NAG) enzyme activity, increase NO3-N in subsurface soil, increase the N content of bamboo, and boost the biomass of bamboo - all of which could be beneficial to giant panda survival. However, higher warming (e.g., an increase of 3-4.5 °C) resulted in mass death of bamboo and a large reduction in aboveground biomass. Our findings provide a cautiously optimistic scenario for bamboo forest ecosystems under low levels of warming over a short period of time, but risks from higher levels of warming may be serious, especially considering the unpredictability of global climatic change.

What Determines the Low-Friction Mechanism of the Silicon-Doped Diamond-like Carbon Film in a Water Environment: An Atomic-Level Understanding.

It is widely acknowledged that doping silicon can significantly enhance the friction performance of diamond-like carbon (DLC) films in a water environment. However, the mechanism of low friction caused by doped silicon is still highly controversial. Therefore, this article compares the interface interaction between DLC and Si-DLC films in a water environment through first-principles calculations of physisorption and chemisorption effects. The results indicate that water molecules are predominantly chemically adsorbed rather than physically adsorbed on the Si-DLC surface. Further study reveals that when OH-termination is formed on the Si-DLC surface, water molecules are predominantly physically adsorbed rather than chemically adsorbed on the Si-DLC hydroxylation surface. Consequently, a more stable hydration layer is formed on the surface through the hydrogen bond network formed by Si-OH groups, ultimately leading to lower friction. Moreover, molecular dynamics simulations further suggest that the lower friction coefficient of Si-DLC films in a water environment may be due to more water molecules at the friction interface and fewer interface covalent bonds. In short, the low-friction coefficient of the Si-DLC film in a water environment may be caused not only by the chemisorption of water molecules on its surface but also by the physisorption of water molecules on the Si-DLC film after surface hydroxylation.

Ring-Opening Coupling of Cyclopropanol with 1,2,3-Triazole for the Synthesis of Fused Triazoles.

A radical ring-opening arylation of cyclopropanol with 1,2,3-triazole has been achieved. This synthetic protocol provides straightforward access to a wide range of structurally diverse and chiral 4,5,6,7-tetrahydro[1,2,3]triazolo[1,5-a]pyridines with high efficiency from readily available chiral cyclopropanols.

Assessment of medical information on irritable bowel syndrome information in Wikipedia and Baidu Encyclopedia: comparative study.

Background: Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder (FGID) with heterogeneous clinical presentations. There are no clear testing parameters for its diagnosis, and the complex pathophysiology of IBS and the limited time that doctors have to spend with patients makes it difficult to adequately educate patients in the outpatient setting. An increased awareness of IBS means that patients are more likely to self-diagnose and self-manage IBS based on their own symptoms. These factors may make patients more likely to turn to Internet resources. Wikipedia is the most popular online encyclopedia among English-speaking users, with numerous validations. However, in Mandarin-speaking regions, the Baidu Encyclopedia is most commonly used. There have been no studies on the reliability, readability, and objectivity of IBS information on the two sites. This is an urgent issue as these platforms are accessed by approximately 1.45 billion people. Objective: We compared the IBS content on Wikipedia (in English) and Baidu Baike (in Chinese), two online encyclopedias, in terms of reliability, readability, and objectivity. Methods: The Baidu Encyclopedia (in Chinese) and Wikipedia (in English) were evaluated based on the Rome IV IBS definitions and diagnoses. All possible synonyms and derivatives for IBS and IBS-related FGIDs were screened and identified. Two gastroenterology experts evaluated the scores of articles for both sites using the DISCERN instrument, the Journal of the American Medical Association scoring system (JAMA), and the Global Quality Score (GQS). Results: Wikipedia scored higher overall with DISCERN (p < .0001), JAMA (p < .0001) and GQS (p < .05) than the Baidu Encyclopedia. Specifically, Wikipedia scored higher in DISCERN Section 1 (p < .0001), DISCERN Section 2 (p < .01), DISCERN Section 3 (p < .001), and the General DISCERN score (p < .0001) than the Baidu Encyclopedia. Both sites had low DISCERN Section 2 scores (p = .18). Wikipedia also had a larger percentage of high quality scores in total DISCERN, DISCERN Section 1, and DISCERN Section 3 (p < .0001, P < .0001, P < .0004, respectively, based on the above 3 (60%) rule). Conclusions: Wikipedia provides more reliable, higher quality, and more objective IBS-related health information than the Baidu Encyclopedia. However, there should be improvements in the information quality for both sites. Medical professionals and institutions should collaborate with these online platforms to offer better health information for IBS.

SIRT1 Stabilizes ß-TrCP1 to Inhibit Snail1 Expression in Maintaining Intestinal Epithelial Integrity to Alleviate Colitis.

BACKGROUND & AIMS: Dysfunction of the intestinal epithelial barrier comprising the junctional complex of tight junctions and adherent junctions leads to increased intestinal permeability, which is a major cause of uncontrolled inflammation related to inflammatory bowel disease (IBD). The NAD+-dependent deacetylase SIRT1 is implicated in inflammation and the pathologic process of IBD. We aimed to elucidate the protective role and underlying mechanism of SIRT1 in cell-cell junction and intestinal epithelial integrity. METHODS: The correlation of SIRT1 expression and human IBD was analyzed by GEO or immunohistochemical analyses. BK5.mSIRT1 transgenic mice and wild-type mice were given dextran sodium sulfate (DSS) and the manifestation of colitis-related phenotypes was analyzed. Intestinal permeability was measured by FITC-dextran and cytokines expression was analyzed by quantitative polymerase chain reaction. The expression of the cell junction-related proteins in DSS-treated or SIRT1-knockdown Caco2 or HCT116 cells was analyzed by Western blotting. The effects of nicotinamide mononucleotide in DSS-induced mice colitis were investigated. Correlations of the SIRT1-ß-TrCP1-Snail1-Occludin/Claudin-1/E-cadherin pathway with human IBD samples were analyzed. RESULTS: Reduced SIRT1 expression is associated with human IBD specimens. SIRT1 transgenic mice exhibit much-reduced manifestations of DSS-induced colitis. The activation of SIRT1 by nicotinamide mononucleotide bolsters intestinal epithelial barrier function and ameliorates DSS-induced colitis in mice. Mechanistically, DSS downregulates SiRT1 expression, leading to destabilization of ß-TrCP1 and upregulation of Snail1, accompanied by reduced expression of E-cadherin, Occludin, and Claudin-1, consequently resulting in increased epithelial permeability and inflammation. The deregulated SIRT1-ß-TrCP1-Snail1-Occludin/Claudin-1/E-cadherin pathway correlates with human IBD. CONCLUSIONS: SIRT1 is pivotal in maintaining the intestinal epithelial barrier integrity via modulation of the ß-TrCP1-Snail1-E-cadhein/Occludin/Claudin-1 pathway.

Potential molecular mechanism of exercise reversing insulin resistance and improving neurodegenerative diseases.

Neurodegenerative diseases are debilitating nervous system disorders attributed to various conditions such as body aging, gene mutations, genetic factors, and immune system disorders. Prominent neurodegenerative diseases include Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis. Insulin resistance refers to the inability of the peripheral and central tissues of the body to respond to insulin and effectively regulate blood sugar levels. Insulin resistance has been observed in various neurodegenerative diseases and has been suggested to induce the occurrence, development, and exacerbation of neurodegenerative diseases. Furthermore, an increasing number of studies have suggested that reversing insulin resistance may be a critical intervention for the treatment of neurodegenerative diseases. Among the numerous measures available to improve insulin sensitivity, exercise is a widely accepted strategy due to its convenience, affordability, and significant impact on increasing insulin sensitivity. This review examines the association between neurodegenerative diseases and insulin resistance and highlights the molecular mechanisms by which exercise can reverse insulin resistance under these conditions. The focus was on regulating insulin resistance through exercise and providing practical ideas and suggestions for future research focused on exercise-induced insulin sensitivity in the context of neurodegenerative diseases.

EH domain-containing protein 2 (EHD2): Overview, biological function, and therapeutic potential.

EH domain-containing protein 2 (EHD2) is a member of the EHD protein family and is mainly located in the plasma membrane, but can also be found in the cytoplasm and endosomes. EHD2 is also a nuclear-cytoplasmic shuttle protein. After entering the cell nuclear, EHD2 acts as a corepressor of transcription to inhibit gene transcription. EHD2 regulates a series of biological processes. As a key regulator of endocytic transport, EHD2 is involved in the formation and maintenance of endosomal tubules and vesicles, which are critical for the intracellular transport of proteins and other substances. The N-terminal of EHD2 is attached to the cell membrane, while its C-terminal binds to the actin-binding protein. After binding, EHD2 connects with the actin cytoskeleton, forming the curvature of the membrane and promoting cell endocytosis. EHD2 is also associated with membrane protein trafficking and receptor signaling, as well as in glucose metabolism and lipid metabolism. In this review, we highlight the recent advances in the function of EHD2 in various cellular processes and its potential implications in human diseases such as cancer and metabolic disease. We also discussed the prospects for the future of EHD2. EHD2 has a broad prospect as a therapeutic target for a variety of diseases. Further research is needed to explore its mechanism, which could pave the way for the development of targeted treatments.

Excellent thermomagnetic power generation for harvesting waste heat via a second-order ferromagnetic transition.

Thermomagnetic generation (TMG), a promising technology to convert low-grade waste heat to electricity, utilizes high performance TMG materials. However, the drawbacks of large hysteresis, poor mechanical properties and inadequate service life hinder the practical applications. For the first time, we evaluated the effect of different phase transitions on the TMG performance by systematically comparing the TMG performance of three typical Heusler alloys with similar composition but different phase transitions. Ni2Mn1.4In0.6 exhibits second-order magnetic transition (SOMT) from the ferromagnetic (FM) to paramagnetic (PM) state around TC = 316 K without thermal hysteresis. It presents highly comprehensive TMG performance, which is not only better than those of other two Heusler alloys with different phase transitions, but also better than those of most typical TMG materials. The maximum power density (1752.3 mW m-3), cost index (2.78 µW per €), and power generation index PGI (8.91 × 10-4) of Ni2Mn1.4In0.6 are 1-5, 1-4, and 1-7 orders of magnitude higher than those of most typical reported materials, respectively. In addition, Ni2Mn1.4In0.6 with SOMT also shows some advantages that first-order magnetic transition (FOMT) materials do not have, such as zero hysteresis and a long-term service life. In contrast to the short lifetime of a few minutes for the materials with FOMT, Ni2Mn1.4In0.6 with SOMT can serve for one month or even longer with excellent cycling stability. Consequently, we conclude that the SOMT Ni2Mn1.4In0.6 Heusler alloy with good TMG performance as well as zero hysteresis and long service life can be a better candidate than FOMT materials for practical applications of TMG.

[Xixin Decoction regulates Th17/Treg balance and transcription factor expression in senescence-accelerated mouse-prone].

This study aims to investigate the effect of Xixin Decoction on the T helper 17 cell(Th17)/regulatory T cell(Treg) ba-lance of intestinal mucosa and the expression of related transcription factors in the senescence-accelerated mouse-prone 8(SAMP8) model. Fifty 14-week male mice of SAMP8 were randomized by the random number table method into model group, probiotics group, and high-, medium-, and low-dose Xixin Decoction groups, with 10 mice in each group. Ten 14-week male mice of senescence-acce-lerated mouse-resistant 1(SAMR1) served as control group. After 10 weeks of feeding, the mice were administrated with correspon-ding drugs for 10 weeks. Morris water maze test was carried out to examine the learning and memory abilities of mice. Enzyme-linked immunosorbent assay(ELISA) was employed to determine the content of secretory immunoglobulin A(SIgA) in the intestinal mucosa, and flow cytometry to detect the percentage content of Th17 and Treg in the intestinal mucosa. Western blot was performed to determine the protein levels of retinoid-related orphan receptor gamma t(RORγt) and forkhead box p3(Foxp3) in the mouse colon tissue. Compared with control group, the escape latency of mice in model group was significantly prolonged(P<0.01), and the number of times of crossing the platform and the residence time in the target quadrant were significantly reduced within 60 s(P<0.01), intestinal mucosal SIgA content was significantly decreased(P<0.01), Th17 content was increased(P<0.05), Treg content was decreased(P<0.01), the expression of RORγt protein was increased and Foxp3 protein was decreased in colon(P<0.01). Compared with the model group, high-dose Xixin Decoction group improved the learning and memory ability(P<0.05 or P<0.01). Probiotics group and high-and medium-dose Xixin Decoction group increased the content of SIgA in intestinal mucosa(P<0.05 or P<0.01), decreased percentage content of Th17 and increased the percentage content of Treg in intestinal mucosa(P<0.05 or P<0.01). Furthermore, they down-regulated the protein level of RORγt and up-regulated the protein level of Foxp3 in the intestinal mucosa(P<0.01). In conclusion, Xixin Decoction may act on intestinal mucosal immune barrier, affect gut-brain information exchange, and improve the learning and memory ability of SAMP8 by promoting SIgA secretion and regulating the Th17/Treg balance and the expression of RORγt and Foxp3.

Reevaluating Adiponectin's impact on obesity hypertension: a Chinese case-control study.

BACKGROUND: Obesity and hypertension are major risk factors for cardiovascular diseases that affect millions of people worldwide. Both conditions are associated with chronic low-grade inflammation, which is mediated by adipokines such as adiponectin. Adiponectin is the most abundant adipokine that has a beneficial impact on metabolic and vascular biology, while high serum concentrations are associated with some syndromes. This "adiponectin paradox" still needs to be clarified in obesity-associated hypertension. The aim of this study was to investigate how adiponectin affects blood pressure, inflammation, and metabolic function in obesity hypertension using a Chinese adult case-control study. METHODS: A case-control study that had finished recruiting 153 subjects divided as four characteristic groups. Adiponectin serum levels were tested by ELISA in these subjects among these four characteristic Chinese adult physical examination groups. Waist circumference (WC), body mass index (BMI), systolic blood pressure (SB), diastolic blood pressure (DB), and other clinical laboratory data were collected. Analyzation of correlations between the research index and differences between groups was done by SPSS. RESULTS: Serum adiponectin levels in the| normal healthy group (NH group) were significantly higher than those in the newly diagnosed untreated just-obesity group (JO group), and negatively correlated with the visceral adiposity index. With multiple linear egression analysis, it was found that, for serum adiponectin, gender, serum albumin (ALB), alanine aminotransferase (ALT) and high-density lipoprotein cholesterol (HDLC) were the significant independent correlates, and for SB, age and HDLC were the significant independent correlates, and for DB, alkaline phosphatase (ALP) was the significant independent correlate. The other variables did not reach significance in the model. CONCLUSIONS: Our study reveals that adiponectin's role in obesity-hypertension is multifaceted and is influenced by the systemic metabolic homeostasis signaling axis. In obesity-related hypertension, compensatory effects, adiponectin resistance, and reduced adiponectin clearance from impaired kidneys and liver all contribute to the "adiponectin paradox".

Bioinspired Bottlebrush Polymers Effectively Alleviate Frictional Damage Both In Vitro and In Vivo.

Bottlebrush polymers (BB) have emerged as compelling candidates for biosystems to face tribological challenges, including friction and wear. This study provides a comprehensive assessment of an engineered triblock BB polymer's affinity, cell toxicity, lubrication, and wear protection in both in vitro and in vivo settings, focusing on applications for conditions like osteoarthritis and dry eye syndrome. Results show that the designed polymer rapidly adheres to various surfaces (e.g., cartilage, eye, and contact lens), forming a robust, biocompatible layer for surface lubrication and protection. The tribological performance and biocompatibility are further enhanced in the presence of hyaluronic acid (HA) both in vitro and in vivo. The exceptional lubrication performance and favorable interaction with HA position the synthesized triblock polymer as a promising candidate for innovative treatments addressing deficiencies in bio-lubricant systems.

Causal effect of interleukin (IL)-6 on blood pressure and hypertension: A mendelian randomization study.

To examine whether circulating interleukin-6 (IL-6) levels (CirIL6) have a causal effect on blood pressure using Mendelian randomization (MR) methods. We used data from genome-wide association studies (GWAS) of European ancestry to obtain genetic instruments for circulating IL-6 levels and blood pressure measurements. We applied several robust MR methods to estimate the causal effects and to test for heterogeneity and pleiotropy. We found that circulating IL-6 had a significant positive causal effect on systolic blood pressure (SBP) and pulmonary arterial hypertension (PAH), but not on diastolic blood pressure (DBP) or hypertension. We found that as CirIL6 genetically increased, SBP increased using Inverse Variance Weighted (IVW) method (for ukb-b-20175, ß = 0.082 with SE = 0.032, P = 0.011; for ukb-a-360, ß = 0.075 with SE = 0.031, P = 0.014) and weighted median (WM) method (for ukb-b-20175, ß = 0.061 with SE = 0.022, P = 0.006; for ukb-a-360, ß = 0.065 with SE = 0.027, P = 0.014). Moreover, CirIL6 may be associated with an increased risk of PAH using WM method (odds ratio (OR) = 15.503, 95% CI, 1.025-234.525, P = 0.048), but not with IVW method. Our study provides novel evidence that circulating IL-6 has a causal role in the development of SBP and PAH, but not DBP or hypertension. These findings suggest that IL-6 may be a potential therapeutic target for preventing or treating cardiovascular diseases and metabolic disorders. However, more studies are needed to confirm the causal effects of IL-6 on blood pressure and to elucidate the underlying mechanisms and pathways.

Integrated genomic and proteomic analyses identify PYGL as a novel experimental therapeutic target for clear cell renal cell carcinoma.

Sunitinib, the first-line targeted therapy for metastatic clear cell renal cell carcinoma (ccRCC), faces a significant challenge as most patients develop acquired resistance. Integrated genomic and proteomic analyses identified PYGL as a novel therapeutic target for ccRCC. PYGL knockdown inhibited cell proliferation, cloning capacity, migration, invasion, and tumorigenesis in ccRCC cell lines. PYGL expression was increased in sunitinib-resistant ccRCC cell lines, and CP-91149 targeting the PYGL could restore drug sensitivity in these cell lines. Moreover, chromatin immune-precipitation assays revealed that PYGL upregulation is induced by the transcription factor, hypoxia-inducible factor 1α. Overall, PYGL was identified as a novel diagnostic biomarker by combining genomic and proteomic approaches in ccRCC, and sunitinib resistance to ccRCC may be overcome by targeting PYGL.

Combined association of urinary volatile organic compounds with chronic bronchitis and emphysema among adults in NHANES 2011-2014: The mediating role of inflammation.

Evidence on the association of volatile organic compounds (VOCs) with chronic bronchitis (CB) and emphysema is spare and defective. To evaluate the relationship between urinary metabolites of VOCs (mVOCs) with CB and emphysema, and to identify the potential mVOC of paramount importance, data from NHANES 2011-2014 waves were utilized. Logistic regression was conducted to estimate the independent association of mVOCs with respiratory outcomes. Least absolute shrinkage and selection operator (LASSO) regression was performed to screen a parsimonious set of CB- and emphysema-relevant mVOCs that were used for further co-exposure analyses of weighted quantile sum (WQS) regression and Bayesian kernel machine regression (BKMR). Mediation analysis was employed to detect the mediating role of inflammatory makers in such associations. In single exposure analytic model, nine mVOCs were individually and positively associated with CB, while four mVOCs were with emphysema. In WQS regression, positive association between LASSO selected mVOCs and CB was identified (OR = 1.82, 95% CI: 1.25 to 2.69), and N-acetyl-S-(4-hydroxy-2-butenyl)-l-cysteine (MHBMA3) weighted the highest. Results from BKMR further validated such combined association and the significance of MHBMA3. As for emphysema, significantly positive overall trend of mVOCs was only observed in BKMR model and N-acetyl-S-(N-methylcarbamoyl)-l-cysteine (AMCC) contributed most to the mixed effect. White blood cell count (WBC) and lymphocyte number (LYM) were mediators in the positive pattern of mVOCs mixture with CB, while association between mVOCs mixture and emphysema was significantly mediated by LYM and segmented neutrophils num (NEO). This study demonstrated that exposure to VOCs was associated with CB and emphysema independently and combinedly, which might be partly speculated that VOCs were linked to activated inflammations. Our findings shed novel light on VOCs related respiratory illness, and provide a new basis for the contribution of certain VOCs to the risk of CB and emphysema, which has potential public health implications.

Optimization of a DNA-launched SARS-CoV-2 replicon with RNA splicing inhibitor Isoginkgetin.

We have previously developed a bacterial artificial chromosome (BAC)-vectored SARS-CoV-2 replicon, namely BAC-CoV2-Rep, which, upon transfection into host cells, serves as a transcription template for SARS-CoV-2 replicon mRNA to initiate replicon replication and produce nanoluciferase (Nluc) reporter from the subgenomic viral mRNA. However, an inherent issue of such DNA-launched replicon system is that the nascent full-length replicon transcript undergoes process by host RNA splicing machinery, which reduces replicon replication and generates spliced mRNA species expressing NLuc reporter independent of replicon replication. To mitigate this problem, we employed Isoginkgetin, a universal eukaryotic host splicing inhibitor, to treat cells transfected with BAC-CoV2-Rep. Isoginkgetin effectively increased the level of full-length replicon transcripts while concurrently reducing the level of Nluc signal derived from spliced replicon mRNA, making the Nluc reporter signal more correlated with replicon replication, as evidenced by treatment with known SARS-CoV-2 replication inhibitors including Remdesivir, GC376, and EIDD-1931. Thus, our study emphasizes that host RNA splicing is a confounding factor for DNA-launched SARS-CoV-2 replicon systems, which can be mitigated by Isoginkgetin treatment.

Fasting, a Potential Intervention in Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the onset of symptoms, typically occurring later in life, and significant deficits in cognitive functions including learning, memory, speech, and behavior. Ongoing research endeavors seek to explore methods for preventing and treating AD, as well as delving into the molecular mechanisms underlying existing and novel therapeutic approaches encompassing exercise, diet, and drug regimens for individuals with AD or those at risk of developing AD. Among these interventions, dietary interventions have garnered increasing attention due to their potential in addressing the disease. Eating is among the most fundamental of human daily activities, and controlled dietary practices, such as fasting, have gained prominence as essential clinical methods for disease prevention and treatment. Research findings indicate that fasting holds promise in effectively alleviating and improving the cognitive decline associated with age or as consequence of disease. The clinical efficacy of fasting in addressing AD and related disorders might be grounded in its influence on various molecular mechanisms, including neuroinflammation, glial cell activation, insulin resistance, autophagy regulation, nerve regeneration, the gut microbiome, and accumulations of amyloid-ß and tau proteins. The present study reviews possible molecular mechanisms underpinning the therapeutic effects of fasting in patients with AD, as well as in models of the disorder, to establish a theoretical basis for using fasting as a viable approach to treat AD.

Preparation and Performance of Micro-Arc Oxidation Coatings for Corrosion Protection of LaFe11.6Si1.4 Alloy.

The microstructure, corrosion resistance, and phase-transition process of micro-arc oxidation (MAO) coatings prepared on LaFe11.6Si1.4 alloy surfaces in different electrolyte systems were systematically investigated. Research has demonstrated that various electrolyte systems do not alter the main components of the coatings. However, the synergistic action of Na2CO3 and Na2B4O7 more effectively modulated the ionization and chemical reactions of the MAO process and accelerated the formation of α-Al2O3. Moreover, the addition of Na2CO3 and Na2B4O7 improved the micromorphology of the coating, resulting in a uniform coating thickness and good bonding with the LaFe11.6Si1.4 substrate. The dynamic potential polarization analysis was performed in a three-electrode system consisting of a LaFe11.6Si1.4 working electrode, a saturated calomel reference electrode, and a platinum auxiliary electrode. The results showed that the self-corrosion potential of the LaFe11.6Si1.4 alloy without surface treatment was -0.68 V, with a current density of 8.96 × 10-6 A/cm2. In contrast, the presence of a micro-arc electrolytic oxidation coating significantly improved the corrosion resistance of the LaFe11.6Si1.4 substrate, where the minimum corrosion current density was 1.32 × 10-7 A/cm2 and the corrosion potential was -0.50 V. Similarly, after optimizing the MAO electrolyte with Na2CO3 and Na2B4O7, the corrosion resistance of the material further improved. Simultaneously, the effect of the coatings on the order of the phase transition, latent heat, and temperature is negligible. Therefore, micro-arc oxidation technology based on the in situ growth coating of the material surface effectively improves the working life and stability of La(Fe, Si)13 materials in the refrigeration cycle, which is an excellent alternative as a protection technology to promote the practical process of magnetic refrigeration technology.

Dual-Emission Single Sensing Element-Assembled Fluorescent Sensor Arrays for the Rapid Discrimination of Multiple Surfactants in Environments.

Surfactants are considered as typical emerging pollutants, their extensive use of in disinfectants has hugely threatened the ecosystem and human health, particularly during the pandemic of coronavirus disease-19 (COVID-19), whereas the rapid discrimination of multiple surfactants in environments is still a great challenge. Herein, we designed a fluorescent sensor array based on luminescent metal-organic frameworks (UiO-66-NH2@Au NCs) for the specific discrimination of six surfactants (AOS, SDS, SDSO, MES, SDBS, and Tween-20). Wherein, UiO-66-NH2@Au NCs were fabricated by integrating UiO-66-NH2 (2-aminoterephthalic acid-anchored-MOFs based on zirconium ions) with gold nanoclusters (Au NCs), which exhibited a dual-emission features, showing good luminescence. Interestingly, due to the interactions of surfactants and UiO-66-NH2@Au NCs, the surfactants can differentially regulate the fluorescence property of UiO-66-NH2@Au NCs, producing diverse fluorescent "fingerprints", which were further identified by pattern recognition methods. The proposed fluorescence sensor array achieved 100% accuracy in identifying various surfactants and multicomponent mixtures, with the detection limit in the range of 0.0032 to 0.0315 mM for six pollutants, which was successfully employed in the discrimination of surfactants in real environmental waters. More importantly, our findings provided a new avenue in rapid detection of surfactants, rendering a promising technique for environmental monitoring against trace multicontaminants.

Restoration of the Mucosal IgA Response by Improving CD4+ T Pyroptosis Fails to Attenuate Gut Bacterial Translocation and Organ Damage After LPS Attack.

BACKGROUND: Currently, the mechanisms of impaired gut mucosal immunity in sepsis remain unclear. Gut immunoglobulin A (IgA) is an important defense mechanism against invasive pathogens, and CD4+ T cells regulate the IgA response. AIM: We aimed to verify the hypothesis indicating that CD4+ T pyroptosis induced by lipopolysaccharide (LPS) leads to an impaired gut IgA response and subsequent bacterial translocation and organ damage. METHODS: Cultured CD4+ T cells and mice were manipulated with LPS, and pyroptosis was improved by A438079 or adoptive CD4+ T cell transfer. The changes demonstrated in pyroptosis-related molecules, cytotoxicity and CD4+ T cells were examined to determine CD4+ T pyroptosis. The changes demonstrated in IgA+ B cells, AID (key enzyme for immunoglobulins) and IgA production and function were examined to evaluate the IgA response. Serum biomarkers, bacterial colonies and survival analysis were detected for bacterial translocation and organ damage. RESULTS: LPS attack induced CD4+ T pyroptosis, as evidenced by increased expression of P2X7, Caspase-11 and cleaved GSDMD, which elevated cytotoxicity and decreased CD4+ T cells. Decreased CD4+ T subsets (Foxp3+ T and Tfh cells) influenced the IgA response, as evidenced by lower AID expression, which decreased IgA+ B cells and IgA production and function. A438079 or cell transfer improved the IgA response but failed to reduce the translocation of gut pathogens, damage to the liver and kidney, and mortality of mice. CONCLUSION: LPS attack results in CD4+ T pyroptosis. Improvement of pyroptosis restores the mucosal IgA response but fails to ameliorate bacterial translocation and organ damage.

Stereoselective bioaccumulation and degradation of chiral pesticide hexythiazox in earthworm-soil microcosm.

The chiral pesticide hexythiazox was extensively employed in agricultural activities and has garnered growing concern for its harmful impact on the ecosystem. This study investigates the toxicodynamic earthworm at the enantiomeric level of hexythiazox. Earthworms exhibited notable enantioselectivity during the accumulation stage. Furthermore, the presence of earthworms can impact the rate of degradation and enantioselectivity of hexythiazox in soil. The accumulation of the two hexythiazox enantiomers in the earthworm adhered to the one-compartment model, whereas the elimination phase was governed by the first-order kinetics equation. Furthermore, it was discovered that there was no notable enantioselectivity observed during the elimination phase.