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Geosmin is an environmental pollutant that causes off-flavor in water and aquatic products. The high occurrence of geosmin contamination in aquatic systems and aquaculture raises public awareness, however, few studies have investigated the response pathways of geosmin stress on freshwater fish. In this research, grass carp were exposed to 50 μg/L geosmin for 96 h, liver tissue was sequenced and validated using real-time qPCR. In total of 528 up-regulated genes and 488 down-regulated genes were observed, includes cytochrome P450 and uridine diphosphate (UDP)-glucuronosyltransferase related genes. KEGG analysis showed that chemical carcinogenesis-DNA adducts, metabolism of xenobiotics by cytochrome P450, drug metabolism-cytochrome P450 pathway was enriched. Common genes from the target genes of microRNAs and differential expression genes are enriched in metabolism of xenobiotics cytochrome P450 pathway. Two miRNAs (dre-miR-146a and miR-212–3p) down regulated their target genes (LOC127510138 and adh5, respectively) which are enriched cytochrome P450 related pathway. The results present that geosmin is genetoxic to grass carp and indicate that cytochrome P450 system and UDP-glucuronosyltransferase play essential roles in biotransformation of geosmin. MicroRNAs regulate the biotransformation of geosmin by targeting specific genes, which contributes to the development of strategies to manage its negative impacts in both natural and artificial environments.

Background The association between antipsychotics and cardiovascular diseases (CVDs) remains significant yet unestablished, especially in Chinese populations.Objective To investigate the risk of CVDs associated with antipsychotics among Chinese individuals with schizophrenia.Methods We conducted a nested case–control study on individuals diagnosed with schizophrenia in Shandong, China. The case group included individuals diagnosed with incident CVDs between 2012 and 2020. Each case was randomly matched with up to three controls. We used weighted logistic regression models to assess the risk of CVDs associated with antipsychotics and restricted cubic spline analysis to explore the dose–response relationship.Findings In total, 2493 cases and 7478 matched controls were included in the analysis. Compared with non-users, any antipsychotics use was associated with higher risk of any CVDs (weighted OR=1.54, 95% CI 1.32 to 1.79), with the risk mainly driven by ischaemic heart diseases (weighted OR=2.26, 95% CI 1.71 to 2.99). Treatments with haloperidol, aripiprazole, quetiapine, olanzapine, risperidone, sulpiride and chlorpromazine were associated with increased risk of CVDs. A non-linear dose–response relationship between dosage of antipsychotics and risk of CVDs was observed, with a sharp increase in risk in the beginning and then flattening out with higher doses.Conclusions Use of antipsychotics was associated with increased risk of incident CVDs among individuals with schizophrenia, and the risk varied substantially among different antipsychotics and specific CVDs.Clinical implications Clinicians should consider the cardiovascular risk of antipsychotics and choose the appropriate type and dose of drugs in the treatment of schizophrenia.

The harsh service environment of aeroengine hot-end components requires superalloys possessing excellent antioxidant properties. This study investigated the effect of pre-strain on the oxidation behavior of polycrystalline Ni3Al-based superalloys. The growth behaviors of oxidation products were analyzed by scanning electron microscope, transmission electron microscope, X-ray Photoelectron Spectroscopy and Raman spectroscopy. The results indicated that the 5% pre-strained alloys exhibited lower mass gain, shallower oxidation depth and more compact oxide film structures compared to the original alloy. This is mainly attributed to the formation of rapid diffusion paths for Al atoms diffusing to the surface under 5% pre-strain, which promotes the faster formation of protective Al2O3 film while continuing to increase the pre-strain to 25% results in less protective transient oxidation behavior being aggravated due to the increase in dislocation density within the alloy, which prevents the timely formation of the protective Al2O3 film, resulting in uneven oxidation behavior on the alloy.

Introduction: Numerous studies have found an association between autoimmune diseases of the nervous system (ADNS) and schizophrenia (SCZ), but the findings remain controversial. We conducted the first meta-analysis to summarize the current evidence from cohort studies that evaluated the association between ADNS and SCZ. Methods: PubMed, Web of Science, and Embase were comprehensively searched until May 30, 2022 for articles on the association between ADNS and SCZ. Every included study was reported effect size with 95% CIs for the association between ADNS and SCZ. Meta-regression and subgroup analysis were used to assess the heterogeneity. Results: A total of 8 cohort studies with 12 cohorts were included in the meta-analysis. We observed a significant association between ADNS and SCZ (RR = 1.42; 95%CI, 1.18–1.72). Subgroup analysis showed that the risk of SCZ was significantly increased when ADNS were used as exposure factors (RR = 1.48; 95%CI, 1.15–1.89), whereas with SCZ did not observe an increased risk of subsequent ADNS (RR = 1.33; 95%CI, 0.92–1.92); multiple sclerosis (MS) was positively associated with SCZ (RR = 1.36; 95%CI, 1.12–1.66), but no significant association was found between Guillain-Barre syndrome (GBS) and SCZ (RR = 1.90; 95%CI, 0.87–4.17). Meanwhile, we found location was the source of heterogeneity. Limitations: High heterogeneity was observed (I2 = 92.0%), and only English literature was included in the meta-analysis. Conclusions: We found a positive association between ADNS and SCZ, and the association was different across the different types of ADNS. The results of the study are helpful for clinicians to carry out targeted preventive measures for ADNS and SCZ.

Abstract Background Influenza A virus (IAV) triggers acute exacerbation of chronic obstructive pulmonary disease (AECOPD), but the molecular mechanisms remain unclear. In this study, we investigated the role of IAV induced NLRP3 inflammasome activation to increase airway inflammation response in the progression of AECOPD. Methods Human bronchial epithelial cells were isolated and cultured from normal and COPD bronchial tissues and co-cultured with IAV. The NLRP3 inflammasome associated genes were identified using RNA sequencing, and the expressions of NLRP3 inflammasome components were measured using qRT-PCR and western blot after cells were transfected with siRNA and treated with MCC950. Moreover, IAV-induced COPD rat models were established to confirm the results; 37 AECOPD patients were included to measure the serum and bronchoalveolar lavage fluid (BALF) of interleukin (IL)-18 and IL-1β. Results Increased levels of NLRP3 inflammasome components were not seen until 6 h post-inoculation in normal cells. However, both cell groups reached peak NLRP3 level at 12 h post-inoculation and maintained it for up to 24 h. ASC, Caspase-1, IL-1β and IL-18 were also elevated in a similar time-dependent pattern in both cell groups. The mRNA and protein expression of the NLRP3 inflammasome components were decreased when COPD cells treated with siRNA and MCC950. In COPD rats, the NLRP3 inflammasome components were elevated by IAV. MCC950 alleviated lung damage, improved survival time, and reduced NLRP3 inflammasome components expression in COPD rats. Additionally, the serum and BALF levels of IL-1β and IL-18 were increased in AECOPD patients. Conclusions NLRP3 inflammasome is activated in COPD patients as a pre-existing condition that is further exacerbated by IAV infection.

ObjectivePrevious studies have demonstrated an association between anxiety and metabolic syndrome (MetS). However, the association is still controversial. This updated meta-analysis aimed to reanalyze the association between anxiety and MetS.MethodsWe comprehensively searched PubMed, Embase and Web of Science for all related studies published before January 23, 2023. Observational studies that informed effect size with 95% confidence interval (CI) for the association between anxiety and MetS were included. According to heterogeneity between studies, fixed or random effects models were applied to calculate the pooled effect size. Publication bias was examined by funnel plots.ResultsThe research included 24 cross-sectional studies: 20 studies used MetS as the dependent variable with a pooled OR of 1.07 (95% CI: 1.01–1.13) and four studies used anxiety as the dependent variable with a pooled OR of 1.14 (95% CI: 1.07–1.23). Three cohort studies were found: two studies detected the association of baseline anxiety with the risk of MetS, one of the studies demonstrated a significant association, but a similar result was not found in another study; one study showed no significant association between baseline MetS and the risk of anxiety.ConclusionCross-sectional studies indicated an association between anxiety and MetS. The results from cohort studies are still inconsistent and limited. More large-scale prospective studies are needed to further reveal the causal relationship of anxiety with MetS.

ABSTRACT Bradyrhizobium guangxiense CCBAU53363 efficiently nodulates peanut but exhibits incompatible interaction with mung bean. By comparing the common nod region with those of other peanut bradyrhizobia efficiently nodulating these two hosts, distinctive characteristics with a single nodD isoform (nodD1) and a truncated nolA were identified. However, the regulatory roles of NodD1 and NolA and their coordination in legume-bradyrhizobial interactions remain largely unknown in terms of explaining the contrasting symbiotic compatibility. Here, we report that nolA was important for CCBAU53363 symbiosis with peanut but restricted nodulation on mung bean, while nodD1 was dispensable for CCBAU53363 symbiosis with peanut but essential for nodulation on mung bean. Moreover, nolA exerted a cumulative contribution with nodD1 to efficient symbiosis with peanut. Additionally, mutants lacking nolA delayed nodulation on peanut, and both nolA and nodD1 were required for competitive nodule colonization. It is noteworth that most of the nodulation genes and type III secretion system (T3SS)-related genes were significantly downregulated in a strain 53ΔnodD1nolA mutant compared to wild-type strain CCBAU53363, and the downregulated nodulation genes also had a greater impact than T3SS-related genes on the symbiotic defect of 53ΔnodD1nolA on peanut, which was supported by a more severe symbiotic defect induced by 53ΔnodC than that with the 53ΔnodD1nopP, 53ΔnodD1rhcJ, and 53ΔnodD1ttsI mutants. NolA did not regulate nod gene expression but did regulate the T3SS effector gene nopP in an indirect way. Meanwhile, nolA, nodW, and some T3SS-related genes besides nopP were also demonstrated as new “repressors” that seriously impaired CCBAU53363 symbiosis with mung bean. Taken together, the roles and essentiality of nolA and nodD1 in modulating symbiotic compatibility are sophisticated and host dependent. IMPORTANCE The main findings of this study were that we clarified that the roles and essentiality of nodD1 and nolA are host dependent. Importantly, for the first time, NolA was found to positively regulate T3SS effector gene nopP to mediate incompatibility on mung bean. Additionally, NolA does not regulate nod genes, which are activated by NodD1. nolA exerts a cumulative effect with nodD1 on CCBAU53363 symbiosis with peanut. These findings shed new light on our understanding of coordinated regulation of NodD1 and NolA in peanut bradyrhizobia with different hosts.

An all-metallic multi-layered parallel-plate slot array antenna operated in the 60-GHz band with wide impedance bandwidth and high-gain characteristics is proposed. The $16\,{\times }\,16$ -slot antenna is composed of $2\,{\times }\,2$ -slot subarrays perpendicularly-fed by a hollow waveguide corporate feeding network. The subarray is partitioned into three functional layers including a bottom one for feeding, a mediate one for radiating and a parasitic one atop for bandwidth enhancement. An undesired resonance of a high-order mode introduced with the parasitic layer is eliminated by loading metal grids between the slotted plates. The contribution of the parasitic layer on bandwidth improvement is verified by a measured 19.2% bandwidth of the antenna with reflection below −10 dB. The removal of the dielectric plate loaded in the conventional double-layered counterpart also contributes to the better performance of the array. The all-metallic feature exempts the design from dielectric loss and beneficial for realizing a higher gain. A high aperture efficiency over 90% is realized over a 19.3% bandwidth and an antenna efficiency over 70% is obtained over a 18.5% bandwidth for the fabricated prototype antennas. The measured realized gain is up to 33.2 dB and the antenna efficiency is 87.2% at 62.0 GHz.

Abstract Background Previous epidemiological studies have indicated the seasonal variability of serum lipid levels. However, little research has explicitly examined the separate secular and seasonal trends of dyslipidemia. The present study aimed to identify secular and seasonal trends for the prevalence of dyslipidemia and the 4 clinical classifications among the urban Chinese population by time series decomposition. Methods A total of 306,335 participants with metabolic-related indicators from January 2011 to December 2017 were recruited based on routine health check-up systems. Multivariate direct standardization was used to eliminate uneven distributions of the age, sex, and BMI of participants over time. Seasonal and trend decomposition using LOESS (STL decomposition) was performed to break dyslipidemia prevalence down into trend component, seasonal component and remainder component. Results A total of 21.52 % of participants were diagnosed with dyslipidemia, and significant differences in dyslipidemia and the 4 clinical classifications were observed by sex (P 23.9). Conclusions There were significant secular and seasonal features for dyslipidemia prevalence among the urban Chinese population. Different seasonal trends were found in the 4 clinical classifications of dyslipidemia. Precautionary measures should be implemented to control elevated dyslipidemia prevalence in specific seasons, especially in the winter and during traditional holidays.

Airway mucus hypersecretion is a vital pathophysiologic feature in chronic obstructive pulmonary disease (COPD) patients in which airflow limitation result, and it is key to strategizing in the management of COPD. To investigate the mechanisms underlying the action of interleukin-6 neutralizing antibody (IL-6 Ab) in attenuating airway mucus hypersecretion in COPD, human and mouse primary bronchial epithelial cells from COPD patients and mice were isolated, human organoid model of trachea was established and all treated with IL-6 and/or IL-6 Ab. The differential expression of Muc5ac and Nrf2 were determined in pDHBE compared to pNHBE cells via high-throughput sequencing of transcriptome. The serum concentration of Muc5ac was significantly elevated and positively correlated with IL-6 in COPD patients using ELISA, and the excessive mucus secretion was observed in the trachea of COPD patients using HE, AB-PAS and IHC staining. The levels of Muc5ac were significantly elevated in the IL-6-treated group, and diminished with IL-6 Ab treatment, both in vitro and in the organoid model using qRT-PCR, WB and IF. The expression levels of protein Muc5ac were significantly reduced in cells transfected with the IL-6 small interfering RNA (siRNA-IL-6), which was in contrast to the levels of protein Nrf2, and the protective effects of IL-6 Ab were inhibited in cells transfected with Nrf2 short hairpin RNA (shRNA-Nrf2). IL-6 Ab significantly attenuated hypersecretion of airway mucus by inducing nuclear translocation of Nrf2 in COPD. These findings indicated that IL-6 Ab may constitute a novel therapeutic agent for IL-6-induced airway mucus hypersecretion by improving airflow limitation in COPD patients.

Abstract Background Airway remodeling is a major pathological characteristic of chronic obstructive pulmonary disease (COPD), and has been shown to be associated with oxidative stress. Sestrin2 has recently drawn attention as an important antioxidant protein. However, the underlying correlation between sestrin2 and airway remodeling in COPD has yet to be clarified. Methods A total of 124 subjects were enrolled in this study, including 62 control subjects and 62 COPD patients. The pathological changes in airway tissues were assessed by different staining methods. The expression of sestrin2 and matrix metalloproteinase 9 (MMP9) in airway tissues was monitored by immunohistochemistry. Enzyme-linked immunosorbent assays (ELISAs) were used to detect the serum concentrations of sestrin2 and MMP9. The airway parameters on computed tomography (CT) from all participants were measured for evaluating airway remodeling. The relationship between serum sestrin2 and MMP9 concentration and airway parameters in chest CT was also analyzed. Results In patients with COPD, staining of airway structures showed distinct pathological changes of remodeling, including cilia cluttered, subepithelial fibrosis, and reticular basement membrane (Rbm) fragmentation. Compared with control subjects, the expression of sestrin2 and MMP9 was significantly increased in both human airway tissues and serum. Typical imaging characteristics of airway remodeling and increased airway parameters were also found by chest CT. Additionally, serum sestrin2 concentration was positively correlated with serum MMP9 concentration and airway parameters in chest CT. Conclusion Increased expression of sestrin2 is related to airway remodeling in COPD. We demonstrated for the first time that sestrin2 may be a novel biomarker for airway remodeling in patients with COPD.

NADPH oxidase 4 (Nox4) is an important source of reactive oxygen species (ROS) production, and its expression is increased in lipopolysaccharide- (LPS-) stimulated lung epithelial cells. Polymerase δ-interacting protein 2 (Poldip2) has been proved to bind Nox4 and participates in oxidative stress and inflammation. However, the role of Poldip2/Nox4 in LPS-induced oxidative stress and inflammation in lung epithelial cells remains unclear. Cell viability was measured via MTT assays. The expression of Poldip2, Nox4, heme oxygenase-1 (HO-1), cyclooxygenase-2 (COX-2), AKT, and p-AKT was detected by Western blotting and/or immunofluorescence. Poldip2 and Nox4 interaction was analyzed via coimmunoprecipitation (Co-IP) assay. NADPH enzymatic activity and production of ROS, prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were assessed simultaneously. The small interfering RNA (siRNA) or plasmid targeting Nox4 was used to downregulate or upregulate Nox4, and the lentiviral vector encoding Poldip2 was used to downregulate or upregulate Poldip2. The present study demonstrated that LPS stimulation significantly increased the protein levels of Poldip2 and Nox4 and proved that Poldip2 interacted with Nox4 proved by Co-IP. Importantly, Poldip2 acted as an upstream regulator of Nox4. The increased expression of Nox4 and COX-2; NADPH enzymatic activity; production of ROS, PGE2, TNF-α, and IL-1β; and decreased HO-1 expression were significantly suppressed by lentiviral Poldip2 shRNA downregulation but were increased by lentiviral upregulation of Poldip2. Furthermore, inhibiting of PI3K-AKT signaling notably attenuated LPS-induced Poldip2/Nox4 activation. Our study demonstrated that Poldip2 mediates LPS-induced oxidative stress and inflammation via interaction with Nox4 and was regulated by the PI3K-AKT signaling. Targeting Poldip2 could be a beneficial therapeutic strategy for the treatment of ALI.

Airway barrier damage and excessive inflammation induced by influenza A virus (IAV) are associated with disease progression and prognosis. ResolvinD1 (RvD1) is a promising lipid mediator with critical protection against infection in the lung. However, whether RvD1 protects against IAV-induced injury and the underlying mechanisms remain elusive. In this study, primary normal human bronchial epithelial (pNHBE) cells were isolated and co-cultured with IAV and/or RvD1. Then, the expressions of E-cadherin, Zonula occludins-1, inflammatory mediators and proteins in Nrf2-dependent pathway were detected. To further explore the mechanisms, Nrf2 short hairpin RNA (Nrf2 shRNA) was applied in pNHBE cells. Furthermore, mice were infected with IAV, and were subsequently treated with RvD1. We found that IAV downregulated expressions of E-cadherin, Zonula occludins-1, Nrf2 and HO-1, upregulated the phosphorylation of NF κ B p65 and IKBα, levels of IL-8 and TNF-α, as well as ROS production. RvD1 reversed these damaging effects induced by IAV. However, when Nrf2 expression was suppressed with shRNA in pNHBE cells, the protective effects of RvD1 on IAV-induced injury were inhibited. In vivo studies further demonstrated that RvD1 could alleviate barrier protein breakdown and reduce airway inflammatory reactions. Collectively, the study demonstrated that RvD1 could play dual beneficial roles in protecting airway epithelium barrier function and reducing inflammation via the Nrf2 pathway, which may provide a better treatment option for influenza A virus infection.

Background: Patients with chronic obstructive pulmonary disease (COPD) are more susceptible to influenza A virus (IAV) with more severe symptoms, yet the underlying molecular mechanisms of the hypersusceptibility of airway inflammatory response remain unclear.Methods: The primary human bronchial epithelial cells (pHBECs) were isolated from normal and COPD bronchial tissues (NHBE and DHBE) and cultured with/without IAV infection in vitro. DHBE cells were exposed to IAV for 24 h after knockdown of lncRNA TUG1 with short hairpin RNA (shRNA). Gain-of-function assays were performed with the miR-145-5p inhibitor and NF-κBp65 transfection. The expressions of lncRNA TUG1, miR-145-5p, phospho-NF-κBp65, NF-κBp65, TNF-α, and (Interleukin) IL-1β were examined with qRT-PCR, Western blotting, and ELISA. The interactions of lncRNA TUG1, miR-145-5p, and NF-κB were verified with luciferase reporter assay.Results: The expressions of lncRNA TUG1, phospho-NF-κBp65, TNF-α, and IL-1β were increased significantly in pHBECs after being infected with IAV for 24 h (all p

Background: Oxidative stress plays a critical role in pulmonary fibrosis after acute lung injury (ALI), and epithelial-mesenchymal transition (EMT) events are involved in this process. The purpose of this study was to investigate the protective effects of melatonin, a natural antioxidant, on lipopolysaccharide (LPS)-induced EMT in human alveolar epithelial cells. Methods: Human type II alveolar epithelial cell-derived A549 cells were incubated with LPS and melatonin alone or in combination for up to 24 h. The morphological changes of the treated cells were evaluated as well as indexes of oxidative stress. EMT-related proteins and the Nrf2 signaling pathway were detected by western blot analysis and immunofluorescence staining, respectively. To further investigate the underlying mechanisms, the effects of melatonin on cells transfected Nrf2 short hairpin RNA (shRNA) and the PI3K / GSK-3β signaling pathway were evaluated. Results: Treatment with melatonin upregulated Nrf2 expression, inhibited LPS-induced cell morphological change, reversed the expressions of EMT-related proteins, and reduced reactive oxygen species (ROS) production in A549 cells, as well as the levels of malondialdehyde (MDA) and anti-oxidative enzymes. Yet, the effects of melatonin were almost completely abolished in cells transfected Nrf2 shRNA. Furthermore, the data demonstrated that melatonin could activate the PI3K/AKT signaling pathway, resulting in phosphorylation of GSK-3β (Ser9) and upregulation of the Nrf2 protein in A549 cells, which ultimately attenuated LPS-induced EMT. Conclusion: The present study is the first to demonstrate that melatonin can protect human alveolar epithelial cells against oxidative stress by effectively inhibiting LPS-induced EMT, which was mostly dependent on upregulation of the Nrf2 pathway via the PI3K/GSK-3β axis. Further studies are warranted to investigate the role of melatonin for the treatment of oxidative stress-associated diseases, as well as pulmonary fibrosis after ALI.

Background: The aim of the present study was to investigate the synergistic effects and interactive mechanisms of Shufeng Jiedu Capsule (SFJDC) combined with oseltamivir in the treatment of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) induced by the influenza A virus (IAV). Methods: The extraction of SFJDC was analyzed by UHPLC/ESI Q-Orbitrap Mass Spectrometry. Human bronchial epithelial cells were isolated from COPD (DHBE) bronchial tissues, co-cultured with IAV for 24 h, and were subsequently treated with SFJDC and/or oseltamivir. Cell viability was detected by MTT assay. A rat model of COPD with IAV infection was established and treated with SFJDC and/or oseltamivir. Interleukin (IL)-1β and IL-18 in serum and bronchoalveolar lavage fluid (BALF) were measured by ELISA. Additionally, mRNA and protein levels of NLRP3 inflammasome pathway were measured by quantitative real-time PCR and Western blotting, respectively. Results: SFJDC and/or oseltamivir, at their optimal concentrations, had no significant cytotoxicity against DHBEs. The levels of NLRP3-inflammasome-associated components were significantly elevated after cells were inoculated with IAV, whereas the mRNA and protein levels of these components were significantly decreased after treatment with SFJDC and/or oseltamivir in vitro. Moreover, in vivo, the combination of SFJDC and oseltamivir improved survival rates, attenuated clinical symptoms, induced weight gain, alleviated lung damage, and significantly reduced IL-1β and IL-18 levels in serum and BALF, as well as reduced the expression levels of NLRP3-associated components and viral titers in lung homogenates. Conclusion: SFJDC combined with oseltamivir treatment significantly attenuated IAV-induced airway inflammation and lung viral titers. Hence, our findings may provide a novel therapeutic strategy for IAV-induced respiratory infection.

In this paper, an adaptive dynamic surface integral sliding mode fault-tolerant controller is designed for the multimachine power system with static var compensator (SVC) to overcome the problem of actuator failure. The main features of the proposed method are as follows: (1) By combining the dynamic surface control (DSC) method with integral sliding mode (ISM), the tracking errors of the system converge to the neighborhood of zero within a finite time, and the convergence speed, tracking accuracy, and anti-interference ability of the system are also significantly improved. (2) By introducing the failure factors, an adaptive fault-tolerant controller is designed to ensure the stability of the entire system after partial failure of the actuator. (3) By estimating the norm of the ideal weight vector of the radial basis function neural networks (RBFNNs), the computational burden of the controller is reduced. Finally, the simulation results show the effectiveness of the proposed control scheme.

The objective of this study was to investigate the correlation between cattle breeds and deposit of adipose tissues in different positions and the gene expressions of peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid synthase (FASN), and Acyl-CoA dehydrogenase (ACADM), which are associated with lipid metabolism and are valuable for understanding the physiology in fat depot and meat quality. Yanbian yellow cattle and Yan yellow cattle reared under the same conditions display different fat proportions in the carcass. To understand this difference, the expression of PPARγ, FASN, and ACADM in different adipose tissues and longissimus dorsi muscle (LD) in these two breeds were analyzed using the Real-time quantitative polymerase chain reaction method (qRT-PCR). The result showed that PPARγ gene expression was significantly higher in adipose tissue than in LD in both breeds. PPARγ expression was also higher in abdominal fat, in perirenal fat than in the subcutaneous fat (p

High nitrogen austenitic stainless steels (HNASSs) have received widespread attention owing to their outstanding corrosion resistance, excellent weldability and workability. However, these materials usually exhibit insufficient yield strength to satisfy the requirement in service because of their face-centered cubic (fcc) structure. Here, we report a novel material design strategy of constructing both grain-scaled and atomic-scaled heterostructure through applying appropriate thermo-mechanical treatment to improve the comprehensive mechanical properties of HNASS. The optimal comprehensive mechanical properties with a yield strength of 1361 MPa and a uniform elongation of 10.6% are achieved. The results show that the ultrahigh yield strength mainly originates from the lath structure consisting of local chemical order domains (∼490 MPa), and the satisfactory ductility benefits from both deformation twinning and dislocation slip. This work proposes for the first time the strategy to improve mechanical properties of HNASS by introducing the multi-scaled heterostructure, and guides the development of high-performance steels and many other advanced fcc materials.

Abstract In van der Waals heterostructures (vdWHs), the manipulation of interlayer stacking/coupling allows for the construction of customizable quantum systems exhibiting exotic physics. An illustrative example is the diverse range of states of matter achieved through varying the proximity coupling between two-dimensional (2D) quantum spin liquid (QSL) and superconductors within the TaS2 family. This study presents a demonstration of the intertwined physics of spontaneous rotational symmetry breaking, hidden magnetism, and Ising superconductivity (SC) in the three-fold rotationally symmetric, non-magnetic natural vdWHs 6R-TaS2. A distinctive phase emerges in 6R-TaS2 below a characteristic temperature (T *) of approximately 30 K, which is characterized by a remarkable set of features, including a giant extrinsic anomalous Hall effect (AHE), Kondo screening, magnetic field-tunable thermal hysteresis, and nematic magneto-resistance. At lower temperatures, a coexistence of nematicity and Kondo screening with Ising superconductivity is observed, providing compelling evidence of hidden magnetism within a superconductor. This research not only sheds light on unexpected emergent physics resulting from the coupling of itinerant electrons and localized/correlated electrons in natural vdWHs but also emphasizes the potential for tailoring exotic quantum states through the manipulation of interlayer interactions.

Abstract The interplay of topology, magnetism, and correlations gives rise to intriguing phases of matter. In this study, through state-of-the-art angle-resolved photoemission spectroscopy, density functional theory, and dynamical mean-field theory calculations, we visualize a fourfold degenerate Dirac nodal line at the boundary of the bulk Brillouin zone in the antiferromagnet YMn2Ge2. We further demonstrate that this gapless, antiferromagnetic Dirac nodal line is enforced by the combination of magnetism, space-time inversion symmetry, and nonsymmorphic lattice symmetry. The corresponding drumhead surface states traverse the whole surface Brillouin zone. YMn2Ge2 thus serves as a platform to exhibit the interplay of multiple degenerate nodal physics and antiferromagnetism. Interestingly, the magnetic nodal line displays a d-orbital dependent renormalization along its trajectory in momentum space, thereby manifesting Hund’s coupling. Our findings offer insights into the effect of electronic correlations on magnetic Dirac nodal lines, leading to an antiferromagnetic Hund nodal line.

Heterostructured metals and alloys are a new class of materials in which mechanical behaviors between the heterogeneous regions are significantly different, and the mechanical properties of bulk materials are superior to the superposition of individual regions. In this paper, three distinct types of heterostructures were constructed in Mg-2.77Y (wt.%) alloy by applying simple thermomechanical processing. Namely, Type I: the non-recrystallized grains of several tens of microns were embedded in the micron-scaled recrystallized grains that were distributed along shear bands and dispersed near grain boundaries; Type II: the aggregations of micron-scaled recrystallized grains were surrounded by the non-recrystallized grains; Type II: the micron-scaled recrystallized grains dominated the microstructure, and the non-recrystallized regions with diameters of tens of micrometers were surrounded by those fine recrystallized grains. Mechanical tests showed that the material with type III heterostructure had the optimal combination of yield strength and uniform elongation. This is attributed to its remarkable hetero-deformation induced (HDI) strengthening and dislocation strengthening. At the initial stage of plastic deformation (engineering strain below 4%), the rapid accumulation of geometrically necessary dislocations (GNDs) at the interfaces between recrystallized and non-recrystallized regions and between neighboring recrystallized grains lead to the significant HDI strengthening. As deformation proceeded, the HDI strengthening effect gradually decreased, and the traditional dislocation strengthening that was caused by GNDs accumulation at grain boundaries became significant. In-situ electron back-scattered diffraction (EBSD) testing revealed that the non-basal slip in the non-recrystallized regions became more remarkable in the late stage of deformation, which improved ductility and strain hardening of the alloy. These findings provide new insight into the design of high-performance hexagonal close-packed structural materials by using the concept of HDI strengthening.

Abstract The van der Waals antiferromagnetic topological insulator MnBi2Te4 represents a promising platform for exploring the layer-dependent magnetism and topological states of matter. Recently observed discrepancies between magnetic and transport properties have aroused controversies concerning the topological nature of MnBi2Te4 in the ground state. In this article, we demonstrate that fabrication can induce mismatched even-odd layer dependent magnetotransport in few-layer MnBi2Te4. We perform a comprehensive study of the magnetotransport properties in 6- and 7-septuple-layer MnBi2Te4, and reveal that both even- and odd-number-layer device can show zero Hall plateau phenomena in zero magnetic field. Importantly, a statistical survey of the optical contrast in more than 200 MnBi2Te4 flakes reveals that the zero Hall plateau in odd-number-layer devices arises from the reduction of the effective thickness during the fabrication, a factor that was rarely noticed in previous studies of 2D materials. Our finding not only provides an explanation to the controversies regarding the discrepancy of the even-odd layer dependent magnetotransport in MnBi2Te4, but also highlights the critical issues concerning the fabrication and characterization of 2D material devices.

BackgroundGrass coverage (GC) under no-tillage systems in orchards signifcantly infuences underground carbon (C) and nitrogen (N) sequestration, primarily through promoting mineral nutrient utilization by rhizospheric microorganisms. However, the comprehensive impact of GC on microbial communities and plant responses using soil metabolomics remains inadequately recognized.MethodsWe investigated two rhizosphere types established since 2002: bristlegrass (Setaria viridis (L.) P. Beauv.) coverage (SC) and clean cultivation (CC) to assess their efects on soil parameters, enzyme activities, and key pear agronomic traits, including yield (single fruit weight (SFW)) and qualities (soluble solids content (SSC), and total soluble sugar (TSS)). We combined microbiological analysis (16S rRNA sequencing) and non-targeted metabolomics (UPLC-MS/MS and GC–MS) to explore how microbial communities infuence fruit agronomic traits and soil nutrient dynamics in pear orchards under SC conditions.ResultsOur fndings indicate that SC signifcantly enhances soil organic carbon (SOC), soil organic nitrogen (SON), the C:N ratio, and available nitrogen (AN). Moreover, SC leads to pronounced increases in soil enzyme activities involved in the C cycle and storage, including soil sucrase, β-glucosidase, polyphenol oxidase and cellulase. Microbiome analysis revealed substantial diferences in microbial community composition and diversity indices between SC and CC rhizosphere soils within the 0–40 cm depth. Metabolomic analysis demonstrated significant alterations in metabolite profiles across both the 0-20 cm and 20-40 cm layers under SC conditions. The identifed metabolites primarily involve sugar and amino acid-related metabolic pathways, refecting perturbations in C and N metabolism consistent with shifts in bacterial community structure. Several plant growth-promoting rhizobacteria (PGPRs) taxa (e.g., Haliangium, Bacteroides, mle1-7, Subgroup_22, Ellin6067, MND1, Flavobacterium, and Cellvibrio) were enriched under SC, associated with metabolites such as sucrose, N-acetyl-D-glucosamine, N-acetyl-L-glutamic acid, rhamnose, UDP-GlcNAc and D-maltose. These fndings suggest their roles in promoting C and N sequestration processes through sucrose synthesis and glycolytic pathways in the soil, which was signifcantly correlated with the formation of agronomic traits such as fruit yield, SFW SSC and TSS (p

Summary: Cartilage maintains the structure and function of joints, with disturbances leading to potential osteoarthritis. N6-methyladenosine (m6A), the most widespread post-transcriptional modification in eukaryotes, plays a crucial role in regulating biological processes. While current research has indicated that m6A affects the progression of osteoarthritis, its function in the development and homeostasis of articular cartilage remains unclear. Here we report that Mettl3 deficiency in chondrocytes leads to mandibular condylar cartilage morphological alterations, early temporomandibular joint osteoarthritis, and diminished adaptive response to abnormal mechanical stimuli. Mechanistically, METTL3 modulates Lats1 mRNA methylation and facilitates its degradation in an m6A-YTHDF2-dependent manner, which subsequently influences the degradation and nuclear translocation of YAP1. Intervention with the Hippo pathway inhibitor XMU-MP-1 alleviates condylar abnormality caused by Mettl3 knockout. Our findings demonstrate the role of METTL3 in cartilage development and homeostasis, offering insights into potential treatment strategies for osteoarthritis.

The investigate of novel cementitious system suitable for negative temperature concreting was the key way to solve the high energy consumption of traditional winter construction. In this study, the matching effects of anti-freezing agents (CaCl2, NaNO2 and Li2CO3) on the Portland cement-calcium sulphoaluminate cement blended system (PC-CSA system) based on Taguchi-Grey Relational Analysis (Taguchi-GRA method) were studied. The setting time, compressive strength and freezing point were tested, and the hydration products, pore structure and morphology were also analyzed to reveal the mechanism. The results showed that CaCl2 was the main parameter influencing the initial and final setting time. Whether at the early stage of continuous negative temperature curing, or from negative to positive temperature curing, CaCl2 had a dominant influence on the compressive strength of PC-CSA system, which promoted the increase of the early hydration products, resulting in the rapid formation of a network structure. At the later stage of continuous negative temperature curing, the influential parameter changed to NaNO2. The basic condition for hydration was provided due to the lowering of the freezing point of the liquid phase by NaNO2. The presence of Li2CO3 enhanced the promoting effect of CaCl2 on early strength. The optimal parameter combination for PC-CSA system was 1.0 % CaCl2, 2.0 % NaNO2 and 0.4 % Li2CO3 based on Taguchi-GRA method.

Background Myocardial ischemia is a prevalent cardiovascular disorder associated with significant morbidity and mortality. While prompt restoration of blood flow is essential for improving patient outcomes, the subsequent reperfusion process can result in myocardial ischemia–reperfusion injury (MIRI). Mitophagy, a specialized autophagic mechanism, has consistently been implicated in various cardiovascular disorders. However, the specific connection between ischemia–reperfusion and mitophagy remains elusive. This study aims to elucidate and validate central mitophagy-related genes associated with MIRI through comprehensive bioinformatics analysis. Methods We acquired the microarray expression profile dataset (GSE108940) from the Gene Expression Omnibus (GEO) and identified differentially expressed genes (DEGs) using GEO2R. Subsequently, these DEGs were cross-referenced with the mitophagy database, and differential nucleotide sequence analysis was performed through enrichment analysis. Protein–protein interaction (PPI) network analysis was employed to identify hub genes, followed by clustering of these hub genes using cytoHubba and MCODE within Cytoscape software. Gene set enrichment analysis (GSEA) was conducted on central genes. Additionally, Western blotting, immunofluorescence, and quantitative polymerase chain reaction (qPCR) analyses were conducted to validate the expression patterns of pivotal genes in MIRI rat model and H9C2 cardiomyocytes. Results A total of 2719 DEGs and 61 mitophagy-DEGs were identified, followed by enrichment analyses and the construction of a PPI network. HSP90AA1, RPS27A, EEF2, EIF4A1, EIF2S1, HIF-1α, and BNIP3 emerged as the seven hub genes identified by cytoHubba and MCODE of Cytoscape software. Functional clustering analysis of HIF-1α and BNIP3 yielded a score of 9.647, as determined by Cytoscape (MCODE). In our MIRI rat model, Western blot and immunofluorescence analyses confirmed a significant elevation in the expression of HIF-1α and BNIP3, accompanied by a notable increase in the ratio of LC3II to LC3I. Subsequently, qPCR confirmed a significant upregulation of HIF-1α, BNIP3, and LC3 mRNA in the MIRI group. Activation of the HIF-1α/BNIP3 pathway mediates the regulation of the degree of Mitophagy, thereby effectively reducing apoptosis in rat H9C2 cardiomyocytes. Conclusions This study has identified seven central genes among mitophagy-related DEGs that may play a pivotal role in MIRI, suggesting a correlation between the HIF-1α/BNIP3 pathway of mitophagy and the pathogenesis of MIRI. The findings highlight the potential importance of mitophagy in MIRI and provide valuable insights into underlying mechanisms and potential therapeutic targets for further exploration in future studies.