Search

The Cygnus region, which contains massive molecular and atomic clouds and young stars, is a promising Galactic neutrino source candidate. Cosmic-ray transport in the region can produce neutrinos and γ -rays. Recently, the Large High Altitude Air Shower Observatory (LHAASO) detected an ultrahigh-energy γ -ray bubble (Cygnus Bubble) in this region. Using publicly available track events detected by the IceCube Neutrino Observatory in 7 yr of full detector operation, we conduct searches for correlated neutrino signals from the Cygnus Bubble with neutrino emission templates based on LHAASO γ -ray observations. No significant signals were found for any employed templates. With the 7 TeV γ -ray flux template, we set a flux upper limit of 90% confidence level for the neutrino emission from the Cygnus Bubble to be 5.7 × 10−13 TeV−1 cm−2 s−1 at 5 TeV. [ABSTRACT FROM AUTHOR]

Resourceful and inexpensive seawater direct splitting omits the desalination process and effectively increases the efficiency of hydrogen energy generation. However, the development of seawater splitting is hampered by the competing selectivity challenges from anodic oxygen evolution reaction (OER) and chlorine evolution reaction and the issues of electrode corrosion. Herein, the borate anion‐intercalated NiV‐LDH nanoflakes/NiCoP nanowires heterostructures supported on Ni foam (2D/1D NiV‐BLDH/NiCoP/NF) is synthesized. Theoretical calculations show that a small amount of V atom doping in Ni(OH)2 is favorable for changing the electronic environment around Ni atoms via bridging Ni─O, which can construct Ni─O─V to accelerate electron transfer and promote catalytic activity. The borate anions (B(OH)4−) intercalation not only results in the good hydrophilicity and high OH− selectivity but also weakens the adsorption of chlorine (Cl−), which effectively restrains the chlorine evolution reaction. Thus, the component optimized NiV0.1‐BLDH/NiCoP/NF electrocatalyst only requires 268 mV overpotential to reach 100 mA cm−2 for OER in an alkaline environment. Particularly, the NiCoP/NF||NiV0.1‐BLDH/NiCoP/NF cell exhibits attractive overall water splitting performance with a low voltage of 1.46 and 1.53 V at 10 mA cm−2 in alkaline freshwater and alkaline seawater, respectively. The design strategy of this electrocatalyst provides a new avenue for seawater splitting. [ABSTRACT FROM AUTHOR]

Objectives: Interleukin 33 (IL-33) is a crucial inflammatory factor that functions as an alarm signal in endometriosis (EMs). Epithelial-mesenchymal transition (EMT), a process related to inflammatory signals, intracellular reactive oxygen species (ROS) production, and lipid peroxidation, have been proposed as potential mechanisms that contribute to the development and progression of EMs. IL-33 is highly upregulated in the ectopic milieu. Moreover, ectopic endometrial cells constitutively express interleukin-33 receptor ST2 (IL-33R). However, the role of IL-33/ST2 in the EMT of EMs remains largely unknown. In this study, we aimed to mechanistically determine the role of IL-33/ST2 in EMs-associated fibrosis. Materials and methods: We established a non-lethal oxidative stress model to explore the conditions that trigger IL-33 induction. We performed α-smooth muscle actin (α-SMA) protein detection, cell counting kit-8 (CCK-8) assays, and scratch assays to analyze the impact of IL-33 on primary endometrial stromal cells (ESCs) proliferation and invasion. Clinical samples from patients with or without EMs were subjected to immunohistochemical (IHC) and and immunofluorescence(IF) staining to assess the clinical relevance of IL-33 receptor ST2 and EMT-related proteins. Furthermore, we used the ectopic human endometrial epithelial cell line 12Z and normal human epithelial cell line EEC to evaluate the effects of IL-33 on Wnt/β-catenin signaling. The effect of IL-33 on EMT-associated fibrosis was validated in vivo by intraperitoneal injections of IL-33 and antiST2. Results: We observed that ectopic milieu, characterized by ROS, TGF-β1, and high level of estrogen, triggers the secretion of IL-33 from ectopic ESCs. Ectopic endometrial lesions exhibited higher level of fibrotic characteristics and ST2 expression than that in the normal endometrium. Exogenous recombinant human (rhIL-33) enhanced ESC migration and survival. Similarly, 12Z cells displayed a higher degree of EMT characteristics with elevated expression of CCN4 and Fra-1, downstream target genes of the WNT/β-catenin pathway, than that observed in EECs. Conversely, blocking IL-33 with neutralizing antibodies, knocking down ST2 or β-catenin with siRNA, and β-catenin dephosphorylation abolished its effects on EMT promotion. In vivo validation demonstrated that IL-33 significantly promotes EMs-related fibrosis through the activation of Wnt/β-catenin signaling. Conclusion: Our data strongly support the vital role of the IL-33/ST2 pathway in EMs-associated fibrosis and emphasize the importance of the EMT in the pathophysiology of fibrosis. Targeting the IL-33/ST2/Wnt/β-catenin axis may hold promise as a feasible therapeutic approach for controlling fibrosis in EMs. [ABSTRACT FROM AUTHOR]

PurposeMethodsResultsConclusionPROSPERO registration numberEvidence shows diet promotes brain health. Combining foods and nutrients may have beneficial synergistic effects, but the effects on cognitive function interventions are inconsistent. So, a meta-analysis of RCTs was conducted to examine the specific effects on cognitive function.We searched four databases from creation to April 2023. Eligible randomized controlled trials were identified. A random-effects meta-analysis was used to combine standardized mean differences (SMD) (95% confidence intervals [CI]), and homogeneity tests for a variance were calculated.A total of 19 studies involving 12,119 participants were included in this systematic review. The dietary intervention group had a positive effect on overall cognitive functioning compared to the control group (SMD = 0.14, 95% CI [0.08, 0.20], P < 0.00001). The dietary intervention improved executive function, processing speed and language skills (SMD = −0.10, 95% CI [−0.17,−0.04], P = 0.002, I2 = 0%), (SMD = −0.16, 95% CI [−0.23,−0.09], P < 0.00001, I2 = 0%), (SMD = 0.10, 95% CI [0.01, 0.20], P = 0.03, I2 = 0%). The dietary intervention had no effect on delayed memory and spatial ability (SMD = 0.04, 95% CI [−0.02, 0.09], P = 0.20, I2 = 0%), (SMD = 0.08, 95% CI [−0.01, 0.16], P = 0.08, I2 = 0%).The Mediterranean diet, a diet with restricted caloric intake, a diet incorporating aerobic exercise, a low-carbohydrate diet, and a healthy lifestyle diet (increased intake of fruits and vegetables, and weight and blood pressure management) appear to have positive effects on cognitively healthy adults, as reflected in their overall cognitive, processing speed, executive, and language functions.CRD42023414704. [ABSTRACT FROM AUTHOR]

Background: Mixed-lineage leukemia (MLL) fusion gene caused by chromosomal rearrangement is a dominant oncogenic driver in leukemia. Due to having diverse MLL rearrangements and complex characteristics, MLL leukemia treated by currently available strategies is frequently associated with a poor outcome. Therefore, there is an urgent need to identify novel therapeutic targets for hematological malignancies with MLL rearrangements. Methods: qRT-PCR, western blot, and spearman correction analysis were used to validate the regulation of LAMP5-AS1 on LAMP5 expression. In vitro and in vivo experiments were conducted to assess the functional relevance of LAMP5-AS1 in MLL leukemia cell survival. We utilized chromatin isolation by RNA purification (ChIRP) assay, RNA pull-down assay, chromatin immunoprecipitation (ChIP), RNA fluorescence in situ hybridization (FISH), and immunofluorescence to elucidate the relationship among LAMP5-AS1, DOT1L, and the LAMP5 locus. Autophagy regulation by LAMP5-AS1 was evaluated through LC3B puncta, autolysosome observation via transmission electron microscopy (TEM), and mRFP-GFP-LC3 puncta in autophagic flux. Results: The study shows the crucial role of LAMP5-AS1 in promoting MLL leukemia cell survival. LAMP5-AS1 acts as a novel autophagic suppressor, safeguarding MLL fusion proteins from autophagic degradation. Knocking down LAMP5-AS1 significantly induced apoptosis in MLL leukemia cell lines and primary cells and extended the survival of mice in vivo. Mechanistically, LAMP5-AS1 recruits the H3K79 histone methyltransferase DOT1L to LAMP5 locus, directly activating LAMP5 expression. Importantly, blockade of LAMP5-AS1-LAMP5 axis can represses MLL fusion proteins by enhancing their degradation. Conclusions: The findings underscore the significance of LAMP5-AS1 in MLL leukemia progression through the regulation of the autophagy pathway. Additionally, this study unveils the novel lncRNA-DOT1L-LAMP5 axis as promising therapeutic targets for degrading MLL fusion proteins. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD), mainly comprising ulcerative colitis and Crohn's disease, is a group of gradually progressive diseases bringing significant mental anguish and imposes serious economic burdens. Interplay of genetic, environmental, and immunological factors have been implicated in its pathogenesis. Nutrients, as crucial environmental determinants, mainly encompassing carbohydrates, fats, proteins, and micronutrients, are closely related to the pathogenesis and development of IBD. Nutrition is essential for maintaining the dynamic balance of intestinal eco‐environments to ensure intestinal barrier and immune homeostasis, while this balance can be disrupted easily by maladjusted nutrition. Research has firmly established that nutrition has the potential to shape the composition and function of gut microbiota to affect the disease course. Unhealthy diet and eating disorders lead to gut microbiota dysbiosis and further destroy the function of intestinal barrier such as the disruption of membrane integrity and increased permeability, thereby triggering intestinal inflammation. Notably, appropriate nutritional interventions, such as the Mediterranean diet, can positively modulate intestinal microecology, which may provide a promising strategy for future IBD prevention. In this review, we provide insights into the interplay between nutrition and gut microbiota and its effects on IBD and present some previously overlooked lines of evidence regarding the role of derived metabolites in IBD processes, such as trimethylamine N‐oxide and imidazole propionate. Furthermore, we provide some insights into reducing the risk of onset and exacerbation of IBD by modifying nutrition and discuss several outstanding challenges and opportunities for future study. [ABSTRACT FROM AUTHOR]

Background: As a dual-function metabolite, succinate has emerged in cell function and plays a key signaling role in linking mitochondrial function to other cellular functions. Succinate accumulation in the cytoplasm is commonly associated with hypoxia in the microenvironment and immune cell activation. Extracellular succinate released into the microenvironment is considered an inflammatory alarm that can be sensed by its membrane receptor SUCNR1, which boosts proinflammatory responses and acts akin to classical hormones and cytokines. Succinate plays an important role in the development of inflammatory diseases. Whether succinate facilitates the progression of endometriosis (EMs), characterized by chronic inflammation and peritoneal adhesion, is worth exploring. Objective: We mimicked the ectopic milieu in vitro and in vivo to evaluate the main source and potential role of succinate in endometriosis. We assessed the molecular and functional effects of succinate on macrophages and peritoneal mesothelial cells in peritoneal cavity. The effect of succinate/SUCNR1 signaling on ectopic endometrial stromal cells (ESCs) was further explored in this study. Methods: In this study, we used targeted organic acid metabolomics analysis and in vitro assays to assess the potential accumulation of succinate in the peritoneal fluid of EMs patients. We examined its correlation with disease severity, Visual Analogue Scale, and the Endometriosis Fertility Index. Flow cytometry, enzyme linked immunosorbent assay, western blot assay, quantitative real-time PCR, and other molecular biology techniques were used to explore the potential mechanisms. Results: By mimicking the ectopic milieu, we constructed an in vitro co-culture system and found that M1 polarized macrophages and that the peritoneal mesothelial cell line (HMrSV5) mainly released succinate into their microenvironment and activated the succinate receptor (SUCNR1) signal, which further polarized the macrophages and significantly enhanced the invasive survival of ESCs, and the adhesion to the peritoneum. We further investigated the pathological effects of extracellular succinate in vivo using a xenograft mouse models of endometriosis. Conclusions: Succinate-SUCNR1 signaling facilitates the creation of inflammatory cells and plays a vital role in EMs progression and peritoneal adhesion. Our work on the molecular mechanisms underlying succinate accumulation and function will help elucidate the phenotypic mysteries of pain and infertility in EMs. BkiB34NQBDvkGHWZYD1GB2 Video Abstract [ABSTRACT FROM AUTHOR]

Cell division cycle-associated (CDCA) gene family members are essential cell proliferation regulators and play critical roles in various cancers. However, the function of the CDCA family genes in gliomas remains unclear. This study aims to elucidate the role of CDCA family members in gliomas using in vitro and in vivo experiments and bioinformatic analyses. We included eight glioma cohorts in this study. An unsupervised clustering algorithm was used to identify novel CDCA gene family clusters. Then, we utilized multi-omics data to elucidate the prognostic disparities, biological functionalities, genomic alterations, and immune microenvironment among glioma patients. Subsequently, the scRNA-seq analysis and spatial transcriptomic sequencing analysis were carried out to explore the expression distribution of CDCA2 in glioma samples. In vivo and in vitro experiments were used to investigate the effects of CDCA2 on the viability, migration, and invasion of glioma cells. Finally, based on ten machine-learning algorithms, we constructed an artificial intelligence-driven CDCA gene family signature called the machine learning-based CDCA gene family score (MLCS). Our results suggested that patients with the higher expression levels of CDCA family genes had a worse prognosis, more activated RAS signaling pathways, and more activated immunosuppressive microenvironments. CDCA2 knockdown inhibited the proliferation, migration, and invasion of glioma cells. In addition, the MLCS had robust and favorable prognostic predictive ability and could predict the response to immunotherapy and chemotherapy drug sensitivity. • An integration analysis of CDCA gene family in gliomas by multiple omics data. • Novel CDCA family clusters with distinct signaling, genomic features, TIME, and prognosis. • Experiments showed CDCA2 acted as an oncogene in gliomas by RAS signaling. • An artificial intelligence-driven CDCA family signature was developed. • The MLCS was a stable and robust biomarker for prognosis and immunotherapy. [ABSTRACT FROM AUTHOR]

• Highlights the critical role of the CXCR6/CXCL16 axis in fibrosis across various organs, including liver, kidney, lungs, cardiovascular system, skin, and intestines. • Discusses the mechanisms by which the CXCR6/CXCL16 axis modulates immune cell communication and fibroblast activity in fibrotic diseases. • Highlights the potential of targeting the CXCR6/CXCL16 axis as a therapeutic approach for treating fibrotic diseases. CXC chemokine receptor 6 (CXCR6), a seven-transmembrane domain G-protein-coupled receptor, plays a pivotal regulatory role in inflammation and tissue damage through its interaction with CXC chemokine ligand 16 (CXCL16). This axis is implicated in the pathogenesis of various fibrotic diseases and correlates with clinical parameters that indicate disease severity, activity, and prognosis in organ fibrosis, including afflictions of the liver, kidney, lung, cardiovascular system, skin, and intestines. Soluble CXCL16 (sCXCL16) serves as a chemokine, facilitating the migration and recruitment of CXCR6-expressing cells, while membrane-bound CXCL16 (mCXCL16) functions as a transmembrane protein with adhesion properties, facilitating intercellular interactions by binding to CXCR6. The CXCR6/CXCL16 axis is established to regulate the cycle of damage and repair during chronic inflammation, either through modulating immune cell-mediated intercellular communication or by independently influencing fibroblast homing, proliferation, and activation, with each pathway potentially culminating in the onset and progression of fibrotic diseases. However, clinically exploiting the targeting of the CXCR6/CXCL16 axis requires further elucidation of the intricate chemokine interactions within fibrosis pathogenesis. This review explores the biology of CXCR6/CXCL16, its multifaceted effects contributing to fibrosis in various organs, and the prospective clinical implications of these insights. [ABSTRACT FROM AUTHOR]

In the present study, the synergetic gelation of curdlan gum (CG) and gellan gum (CG) at different biopolymer ratios were investigated. The optimal gelation of CG and GG was determined at total biopolymer concentration of 0.6% and a mass ratio of 1:1 according to visual observation and viscoelastic properties. The gelation behavior of the CG/GG binary composite gel exhibited ratio-dependent behavior at different biopolymer mixing ratios (2:8–8:2). With the increase in the CG/GG ratio from 2:8 to 8:2, the gel strength and transition temperature of the CG/GG gel showed an increasing trend followed by a decrease, reaching a peak at 5:5, with corresponding G′ , melting and gelling temperatures of 335.8 Pa, 82.5 °C and 33.7 °C, respectively. The improved gel properties could be ascribed to hydrogen bonds between CG and GG, as reflected by the blueshift of the O–H vibration peaks and water associated regional variation. Moreover, the CG/GG binary composite gel exhibited a significantly increasing water holding capacity (WHC) as the ratio of CG/GG decreased from 8:2 to 4:6, while the excess involvement of GG had no effect on the WHC improvement. Furthermore, the CG/GG binary composite gel exhibited denser and more homogeneous microstructures in comparison to individual CG and GG and performed the most compact gel network at ratio of 5:5, supporting the stronger gel rigidity and WHC. Therefore, these novel CG/GG hydrogels showed considerable gel strength and microstructures, which would provide a better mechanistic understanding of the polysaccharide complex in practical applications as a hydrogel base material. [Display omitted] • The addition ratio between CG and GG exhibited a significant effect on the synergy. • CG/GG binary composite gels exhibited good water holding capacity. • The CG/GG binary composite gels mainly driven by hydrogen bonding forces. • The CG/GG binary composite gels exhibited dense and homogeneous microstructures. [ABSTRACT FROM AUTHOR]

Heavy metal ions and organic pollutants discharged into various water bodies have caused serious water pollution, and the efficient removal of these contaminants remains a challenge. Here, we report a novel MXene/poly-melamine-formaldehyde (PMF) composite membrane, in which the PMF particles serve as spacers, and the –NH 2 groups of PMF and the hydroxyl groups of MXene nanosheets have a synergistic effect on the adsorption of pollutants, and the crosslinking of glutaraldehyde inhibits the swelling of the composite membrane. The MXene/PMF composite membrane with 83.7% PMF particle loading displays a water permeability of 381.2 L m−2 h−1 bar−1 (405% that of MXene membrane) and excellent adsorption ability. In static adsorption, the removal rates of Zn2+, Pb2+, phenol, and crystal violet reach 96.2%, 91.7%, 99.1%, and 96.4% respectively, 20∼100% higher than those of MXene membranes. In dynamic adsorption, the breakthrough volumes of the membrane for 2 ppm p-nitrophenol solution and methyl blue solution reach 75 mL (about 8500 times membrane volume) and 350 mL (about 39800 times membrane volume), and the saturation volumes are 1500 mL and 5000 mL, respectively. After cyclic adsorption/desorption for four times, the removal rate of the membranes still maintains above 90%. This work provides an efficient composite membrane for removing pollutants from wastewater. [Display omitted] • A novel MXene/poly-melamine-formaldehyde (PMF) composite membrane are prepared. • The introduction of PMF particles widens the transmission channel and increases water permeance. • PMF and MXene nanosheets have a synergistic effect on the adsorption of pollutants. • Removal rates of Zn2+, Pb2+, phenol and crystal violet by MXene composite membranes are above 90%. • After 4 times of use, the removal rate of pollutant of composite membrane is above 90%. [ABSTRACT FROM AUTHOR]

• A multiphysics simulation model of LU inspection is established. • Propagation characteristics of excited ultrasonic waves in different LPBF alloys is studied. • Interaction between ultrasonic waves and submillimeter artificial defects is investigated. • Four typical LPBF alloys are fabricated and measured by the LU through-transmission inspection. In the development of additive manufacturing (AM) technology, laser powder bed fusion (LPBF) is one of the important processing methods. However, the hole defects in the fabricated samples limit the development. Laser ultrasonic (LU) technology plays a major role in the detection of LPBF parts with tiny defects, which has the advantages of non-contact and non-destructive. In this work, the detection of submillimeter internal defects in four typical LPBF alloys by LU technology is studied numerically and experimentally. A multiphysics simulation model of LU detection is established to investigate the propagation characteristics of excited ultrasonic waves in different LPBF alloys and their interaction with submillimeter artificial defects. Simulation results show that the amplitude of longitudinal (L) wave at the defect is the largest in AlSi10Mg alloy, and the amplitude of L wave in the 316L alloy, Ti6Al4V alloy and In718 alloy are very close, but their phases are slightly different. The amplitude of L wave tends to decrease nearly linearly with the increase in defect diameter. Then, four typical LPBF alloys are fabricated and measured by the LU through-transmission detection. The geometric information of artificial holes with a diameter larger than 0.2 mm are clearly characterized by the LU C-scan results, indicating the prominent applicability and feasibility of LU detection on different materials fabricated by LPBF. [ABSTRACT FROM AUTHOR]

An excess of osteoclastogenesis significantly contributes to the development of rheumatoid arthritis (RA). Activation of the nuclear factor erythroid-2 related factor 2 (Nrf2) and nuclear factor kappa B (NF-κB) ligand (RANKL)-induced reactive oxygen species (ROS)-to-NF-κB signaling cascade are important mechanisms regulating osteoclastogenesis; however, whether Nrf2 is involved in RANKL-induced NF-κB activation is controversial. Isoquercitrin, a natural flavonoid compound, has been shown to have Nrf2-dependent antioxidant effects inprevious studies. We sought to verify whether isoquercitrin could modulate RANKL-induced NF-κB activation by activating Nrf2, thereby affecting osteoclastogenesis. Tartrate-resistant acid phosphatase staining, F-actin ring staining and resorption pit assay suggested that isoquercitrin significantly inhibited osteoclastogenesis and osteolytic function. Mitosox staining showed that RANKL-induced ROS generation was significantly inhibited by isoquercitrin from day 3 of the osteoclast differentiation cycle. Quantitative real-time PCR, Western blot, and immunofluorescence indicated that isoquercitrin activated the Nrf2 signaling pathway and inhibited NF-κB expression. And when we used the Nrf2-specific inhibitor ML385, the inhibition of NF-κB by isoquercitrin disappeared. Moreover, we found that Nrf2 is not uninvolved in RANKL-induced NF-κB activation and may be related to the timing of ROS regulation. When we limited isoquercitrin administration to 2 days, Nrf2 remained activated and the inhibition of NF-κB disappeared. In vivo experiments suggested that isoquercitrin attenuated RA modeling-induced bone loss. Overall, isoquercitrin-activated Nrf2 blocked the RANKL-induced ROS-to-NF-κB signaling cascade response, thereby inhibiting osteoclastogenesis and bone loss. These findings provide new ideas for the treatment of RA. [Display omitted] • Isoquercitrin inhibits osteoclast differentiation and osteolytic function by increasing Nrf2-dependent antioxidant capacity. • Activation of Nrf2 by isoquercitrin blocks the RANKL-induced ROS signaling cascade, thereby inhibiting NF-κB activation. • Isoquercitrin reduces osteoclastogenesis and bone loss in the model of rheumatoid arthritis. • Isoquercitrin might be a promising candidate for treatment of RA in the future. [ABSTRACT FROM AUTHOR]

• Epoxypropyl dimethydodecyl ammonium chloride (EPDDMAC) were grafted on γ-Al 2 O 3 particles. • α-Al 2 O 3 were coated with EVOH and modified with EPDDMAC. • Using the TIPS method, the alumina particles can be completely encapsulated with less polymer. • γ-Al 2 O 3 /EPDDMAC particles and α-Al 2 O 3 @EVOH/EPDDMAC particles showed great antimicrobial performance. Antimicrobial particles can inhibit or kill microorganisms, and have been widely used as antimicrobial filler in coatings and polymers. Herein, we present a facile method to prepare antimicrobial alumina particles by grafting epoxypropyl dimethydodecyl ammonium chloride (EPDDMAC) on γ-Al 2 O 3 or ethylene–vinyl alcohol copolymer (EVOH) coated α-Al 2 O 3.The results show that EPDDMAC can be grafted on γ-Al 2 O 3 or EVOH-coated α-Al 2 O 3 particles effectively, and the grafting rate rises with the increased EPDDMAC amount. The grafted composite particles exhibit excellent antibacterial properties against Escherichia coli and display great potential in antibacterial applications. [ABSTRACT FROM AUTHOR]

The phytohormone cytokinin has various roles in plant development, including meristem maintenance, vascular differentiation, leaf senescence, and regeneration. Prior investigations have revealed that cytokinin acts via a phosphorelay similar to the two-component system by which bacteria sense and respond to external stimuli. The eventual targets of this phosphorelay are type-B ARABIDOPSIS RESPONSE REGULATORS (B-ARRs), containing the conserved N-terminal receiver domain (RD), middle DNA binding domain (DBD), and C-terminal transactivation domain. While it has been established for two decades that the phosphoryl transfer from a specific histidyl residue in ARABIDOPSIS HIS PHOSPHOTRANSFER PROTEINS (AHPs) to an aspartyl residue in the RD of B-ARRs results in a rapid transcriptional response to cytokinin, the underlying molecular basis remains unclear. In this work, we determine the crystal structures of the RD-DBD of ARR1 (ARR1RD-DBD) as well as the ARR1DBD-DNA complex from Arabidopsis. Analyses of the ARR1DBD-DNA complex have revealed the structural basis for sequence-specific recognition of the GAT trinucleotide by ARR1. In particular, comparing the ARR1RD-DBD and ARR1DBD-DNA structures reveals that unphosphorylated ARR1RD-DBD exists in a closed conformation with extensive contacts between the RD and DBD. In vitro and vivo functional assays have further suggested that phosphorylation of the RD weakens its interaction with DBD, subsequently permits the DNA binding capacity of DBD, and promotes the transcriptional activity of ARR1. Our findings thus provide mechanistic insights into phosphorelay activation of gene transcription in response to cytokinin. [ABSTRACT FROM AUTHOR]

Objective Methods Results Conclusions We aimed to investigate the prevalence of vascular complications in acute pancreatitis (AP), to compare patient outcomes using various treatments, and to explore the related risk factors.Consecutive AP patients admitted from January 2010 to July 2017 were retrospectively included. Demographics, vascular complications, laboratory indices, and imaging findings were collected. Univariate and multivariate analyses were used to explore potential risk factors of vascular complications.Of 3048 AP patients, 808 (26.5%) had vascular complications, including visceral vein thrombosis, sinistral portal hypertension, and arterial complications. And 38 (4.7%) patients received anticoagulant therapy and had a higher rate of recanalization (P < 0.001). Bleeding occurred in 95 (11.8%) patients, who received further treatment. Multivariate analysis identified male gender (odds ratio [OR] 1.650, 95% confidence interval [CI] 1.101–2.472), hyperlipidemia (OR 1.714, 95% CI 1.356–2.165), disease recurrence (OR 3.727, 95% CI 2.713–5.118), smoking (OR 1.519, 95% CI 1.011–2.283), hemoglobin level (OR 0.987, 95% CI 0.981–0.993), white blood cell (WBC) count (OR 1.094, 95% CI 1.068–1.122), non‐vascular local complications (OR 3.018, 95% CI 1.992–4.573), computed tomography severity index (CTSI) (OR 1.425, 95% CI 1.273–1.596), and acute physiology and chronic health evaluation (APACHE) II score (OR 1.057, 95% CI 1.025–1.090) were related to vascular complications.Vascular complications in AP is prevalent and their treatment is challenging. Further investigations are warranted to determine the optimal treatment strategy. Independent risk factors included male gender, hyperlipidemia, disease recurrence, smoking, WBC count, non‐vascular local complications, CTSI, and APACHE II score. [ABSTRACT FROM AUTHOR]

The field of spintronics has seen a surge of interest in altermagnetism due to novel predictions and many possible applications. MnTe is a leading altermagnetic candidate that is of significant interest across spintronics due to its layered antiferromagnetic structure, high Neel temperature (TN ≈ 310 K) and semiconducting properties. The results on molecular beam epitaxy (MBE) grown MnTe/InP(111) films are presented. Here, it is found that the electronic and magnetic properties are driven by the natural stoichiometry of MnTe. Electronic transport and in situ angle‐resolved photoemission spectroscopy show the films are natively metallic with the Fermi level in the valence band and the band structure is in good agreement with first‐principles calculations for altermagnetic spin‐splitting. Neutron diffraction confirms that the film is antiferromagnetic with planar anisotropy and polarized neutron reflectometry indicates weak ferromagnetism, which is linked to a slight Mn‐richness that is intrinsic to the MBE‐grown samples. When combined with the anomalous Hall effect, this work shows that the electronic response is strongly affected by the ferromagnetic moment. Altogether, this highlights potential mechanisms for controlling altermagnetic ordering for diverse spintronic applications. [ABSTRACT FROM AUTHOR]

Carbon structures have been shown to be potentially efficient hydrogen storage media, but the micro adsorption/diffusion kinetic properties of hydrogen storage are still unclear. We investigated the adsorption of H 2 in carbonaceous nanoporous by molecular dynamics simulations. It was found that the hydrogen molecules were completely adsorbed when the pore size was 1 nm, and existed in both adsorbed and free forms when the pore size was 2–6 nm, and the adsorption was in a saturated state, with the absolute adsorption amount keeping constant. Modification of functional groups on the inner side of graphene pores reduces the hydrogen storage capacity, and this effect becomes more and more obvious with decreasing pore size, especially for 1 nm pores. The total adsorption amount of H 2 in 1 nm graphene pores was 0.01315 × 10−3 mol/m2, which was 3.8846 times that of graphene oxide pore. The hydrogen adsorption effect on different surfaces is: G > GO (-O-) > GO (-OH) > GO (-O-/OH). The results of this study are helpful to further understand the physical adsorption mechanism of molecular hydrogen on carbonaceous materials. The graphical abstract are summarized below:. [Display omitted] • The total adsorption increases almost linearly with pressure at the same pore size. • The 2 nm pore is the critical pore for absolute and excess hydrogen adsorption. • Hydrogen adsorption on different surfaces: G > GO (-O-) > GO (-OH) > GO (-O-/OH). [ABSTRACT FROM AUTHOR]

This study aimed to elucidate the mechanism by which wall shear stress (WSS) influences vascular walls, accounting for the susceptibility of intracranial aneurysms (IAs) to rupture. We collected blood samples from the sacs of 24 ruptured and 28 unruptured IAs and analyzed the expression of chemokine CCL7 using enzyme-linked immunosorbent assay (ELISA). Univariate and multivariate logistic regression analyses were employed to assess clinical data, aneurysm morphology, and hemodynamics in both groups. Pearson correlation analysis investigated the relationship between CCL7 expression in aneurysm sac blood and WSS. Additionally, we established a bionic cell parallel plate co-culture shear stress model and a mouse low shear stress (LSS) model. The model was modulated using CCL7 recombinant protein, CCR1 inhibitor, and TAK1 inhibitor. We further evaluated CCL7 expression in endothelial cells and the levels of TAK1, NF-κB, IL-1β, and TNF-α in macrophages. Subsequently, the intergroup differences in expression were calculated. CCL7 expression was significantly higher in the ruptured group compared to the unruptured group. Hemodynamic analysis indicated that WSS was an independent predictor of the risk of aneurysm rupture. A negative linear correlation was observed between CCL7 expression and WSS. Upon addition of CCL7 recombinant protein, upregulation of CCR1 expression and increased levels of p-TAK1 and p-p65 were observed. Treatment with CCR1 and TAK1 inhibitors reduced inflammatory cytokine expression in macrophages under LSS conditions. Overexpression of TAK1 significantly alleviated the inhibitory effects of CCR1 inhibitors on p-p65 and inflammatory cytokines. LSS prompts endothelial cells to secrete CCL7, which, upon binding to the macrophage surface receptor CCR1, stimulates the release of macrophage inflammatory factors via the TAK1/NF-κB signaling pathway. This process exacerbates aneurysm wall inflammation and increases the risk of aneurysm rupture. Schematic diagram of LSS inducing an inflammatory response in the vascular wall via the CCL7/CCR1/TAK1/NF-κB pathway. Vascular endothelial cells secrete CCL7 under LSS, and CCR1 receptors on infiltrating macrophages in the vascular wall bind to CCL7 and further stimulate the phosphorylation of NF-κB into the nucleus through phosphorylation of TAK1, inducing the production of inflammatory factors and aggravating the inflammation of the vascular wall, thereby increasing the rupture risk of IAs. [Display omitted] • CCL7 chemokine level was found to be a risk factor for intracranial aneurysm rupture. • Low shear stress can increase CCL7 expression in endothelial cells and induce a pro-inflammatory phenotype of macrophages. • CCL7 can regulate arterial wall inflammation through CCR1/TAK1/ NF-κB axis. [ABSTRACT FROM AUTHOR]

In order to enhance the heat transfer effect and improve the energy utilization efficiency of the circular tube under turbulent flow, rhombic and triangular winglet vortex generators are proposed on the basis of rectangular winglet vortex generator. The effects of three vortex generators on flow and heat transfer in the tube are investigated by numerical simulations. The results indicate that, the rectangular and triangular winglets generate two pairs of longitudinal vortices and the triangular winglets generate four pairs of longitudinal vortices due to additional shrinkage regions. The multiple longitudinal vortices increase the mixing between the fluids, raise the temperature in the central region of the tube, and enhance the heat transfer effect. Furthermore, the triangular winglet enhanced tube has the largest direct flow area and the least effect on resistance. The triangular winglet enhanced tube had the best comprehensive performance, followed by the rhombic winglet enhanced tube, and finally, the rectangular winglet enhanced tube. The performance evaluation criterion reached 1.04-1.13, 1.05-1.15, and 1.08-1.21 for the three enhanced tubes in the given flow rate interval. In addition, the effect of inclination angle on the triangular winglet enhanced tube was further investigated, and the results show that the best comprehensive performance of enhanced heat transfer is achieved at an inclination angle of 45°, with a maximum performance evaluation criterion of 1.25. [ABSTRACT FROM AUTHOR]

To explore the influence of extracellular matrix protein ABI-interactor 3-binding protein (ABI3BP) on vesicular stomatitis virus (VSV) genome replication and innate immune signaling pathway. The small interfering RNA (siRNA) was transfected to knock down ABI3BP gene in human skin fibroblast BJ-Sta cells. VSV-green fluorescent protein (VSV-GFP)-infected cell model was established. The morphological changes and F-actin stress fiber formation were detected on ABI3BP knockdown cells by phalloidin immunofluorescence staining. The mRNA level of virus replication was detected by RT-qPCR in BJ-Sta cells after VSV-GFP infection; western blotting was performed to detect the changes in interferon regulatory factor 3 (IRF3) and TANK-binding kinase 1 (TBK1) phosphorylation levels. The VSV-GFP-infected BJ-Sta cell model was successfully established. Efficient knockdown of ABI3BP in BJ-Sta cells was achieved. Phalloidin immunofluorescence staining revealed structural rearrangement of intracellular F-actin after ABI3BP gene knockdown. Compared with the control group, the gene copy number of VSV-GFP in ABI3BP knockdown cells increased by 2.2 – 3.5 times (P <0.01) and 2.2 – 4.0 times (P <0.01) respectively when infected with VSV of multiplicity of infection 0.1 and 1. The expression of viral protein significantly increased in ABI3BP knockdown cells after virus infection. The activation of type-I interferon pathway, as determined by phosphorylated IRF3 and phosphorylated TBK1, was significantly decreased in ABI3BP knockdown cells after VSV-GFP infection. Extracellular matrix protein ABI3BP plays an important role in maintaining the formation and rearrangement of actin structure. ABI3BP gene deletion promotes RNA virus replication, and ABI3BP is an important molecule that maintains the integrity of type I interferon pathway. [ABSTRACT FROM AUTHOR]

Objectives Materials and Methods Results Conclusions To search for pathogenic gene of a family with non‐syndromic tooth agenesis, and explore the possible pathogenesis.A Chinese family with non‐syndromic tooth agenesis was recruited and screened for the pathogenic variants by whole exome sequencing technology and co‐segregation analysis. The subcellular localization of wild‐type and mutant protein was detected by immunofluorescence assay. Cycloheximide chase assay was performed to examine the difference in degradation rate between mutant protein and wild‐type one. Dual‐luciferase reporter assays were conducted to explore the alterations of mutant protein in the regulation of downstream target genes.A novel missense variant of PAX9 (c.296C>A:p.A99D) was found in this family. Bioinformatics software showed β‐return and the random coil were shortened in the p.A99D. The variant did not affect the subcellular localization of PAX9, but the degradation rate of p.A99D was accelerated (p < 0.05). p.A99D inhibited the activation of downstream target gene BMP4 (p < 0.05).This novel variant expands the pathogenic gene spectrum. The variant impaired the protein structure, accelerated the degradation of protein, and inhibited the activation of the downstream target gene BMP4, an upstream molecule in the TGF‐β/BMP pathway, which may contribute to tooth agenesis in this family. [ABSTRACT FROM AUTHOR]

The farming–pastoral zone in northern China is one of the most ecologically sensitive areas globally, having experienced extensive cropland abandonment and land reclamation over decades, primarily influenced by policy adjustment and global warming. However, the spatiotemporal patterns and suitability of long-term cropland change remain poorly understood. Using the annual China land cover dataset (CLCD), we provide a cropland abandonment and land reclamation mapping approach based on actual land use processes (rather than land cover conditions) to investigate spatiotemporal features of abandonment and reclamation and evaluate the rationality. Our findings show that: (1) Returning farmland to forest and grassland has been a clear trend in the study area over the past 30 years. Specifically, cropland use has undergone three phases of change, i.e., cropland contraction and expansion alternately (before 2000), followed by substantial abandonment (after 2000), and low-intensity reclamation (after 2010). (2) In the last decade, the intensity of the abandonment of cropland with high and moderate suitability is low. The rate of abandonment decreased, while the intensity of land reclamation was relatively high. The rate of the reclamation increased, and the spatial distribution of cropland tended to be reasonable. Our study emphasizes the importance of monitoring actual cropland changes based on land use processes, and this method can be effectively extended to regional or global long-term cropland monitoring. [ABSTRACT FROM AUTHOR]

The Von Hippel–Lindau (VHL) protein, which is frequently mutated in clear-cell renal cell carcinoma (ccRCC), is a master regulator of hypoxia-inducible factor (HIF) that is involved in oxidative stresses. However, whether VHL possesses HIF-independent tumor-suppressing activity remains largely unclear. Here, we demonstrate that VHL suppresses nutrient stress-induced autophagy, and its deficiency in sporadic ccRCC specimens is linked to substantially elevated levels of autophagy and correlates with poorer patient prognosis. Mechanistically, VHL directly binds to the autophagy regulator Beclin1, after its PHD1-mediated hydroxylation on Pro54. This binding inhibits the association of Beclin1-VPS34 complexes with ATG14L, thereby inhibiting autophagy initiation in response to nutrient deficiency. Expression of non-hydroxylatable Beclin1 P54A abrogates VHL-mediated autophagy inhibition and significantly reduces the tumor-suppressing effect of VHL. In addition, Beclin1 P54-OH levels are inversely correlated with autophagy levels in wild-type VHL-expressing human ccRCC specimens, and with poor patient prognosis. Furthermore, combined treatment of VHL-deficient mouse tumors with autophagy inhibitors and HIF2α inhibitors suppresses tumor growth. These findings reveal an unexpected mechanism by which VHL suppresses tumor growth, and suggest a potential treatment for ccRCC through combined inhibition of both autophagy and HIF2α. Synopsis: PHD1-mediated prolyl hydroxylation targets HIF-1α for VHL-dependent ubiquitination and is a key step in the cell's oxygen sensing machinery. This work shows that PHD1 and VHL also inhibit Beclin1 and autophagy initiation, with dysregulation leading to clear-cell renal cell carcinoma progression. PHD1 mediates Beclin1 Pro54 hydroxylation on pre-autophagosomal structures in clear-cell renal cell carcinoma cells. VHL binds to Pro54-hydroxylated Beclin1 and prevents the association between ATG14L and Beclin1/VPS34. VHL inhibits VPS34-dependent PI(3)P production, autophagy initiation, and kidney tumor growth. The Von Hippel-Lindau (VHL) E3 ligase binds to proline-hydroxylated Beclin1, inhibiting the initiation of autophagy and blocking kidney tumor growth. [ABSTRACT FROM AUTHOR]

Background: Transcription factor 7-like 2 (TCF7L2) rs7903146 polymorphism has been shown to display a significant association with gestational diabetes mellitus (GDM). But the effects of TCF7L2 rs7903146 on glucose and lipid metabolism are not clear. Objective: The purpose of this study was to assess the role of TCF7L2 rs7903146 genotypes on glycolipid metabolism in GDM. Methods: In total, 484 individuals (239 in GDM group and 245 in control group) were included in the final analysis from January 2015 to February 2022. Their baseline demographics, plasma lipid concentration in the first trimester and third trimester, blood glucose values of the OGTT during gestational 24–28 weeks, glycosylated hemoglobin, fasting plasma glucose and fasting insulin in third trimester, 1 min Apgar scores, 5 min Apgar scores, glucose values of cord blood, and umbilical artery pH were collected. TCF7L2 rs7903146 genotypes were analyzed by polymerase chain reaction-Sanger sequencing. Results: The frequencies of TCF7L2 rs7903146 genotype were found to have no significant differences between the two groups; however, the plasma lipid concentrations during the first trimester were higher in GDM group than control group. In GDM group, women carried the risk allele (T) in TCF7L2 rs7903146 displayed the significantly higher glucose values at 1-h during OGTT, and the higher TG and lower fasting insulin levels than those in non-carriers. Conclusion: Our results indicate that the risk allele (T) in TCF7L2 rs7903146 plays an important role in the abnormality of glucose and lipid metabolism in GDM women. For the risk allele(T) carriers of TCF7L2 rs7903146, low-fat and low-sugar diets, exercise interventions can be carried out at an early stage, and insulin therapy should be considered when their blood glucose were inadequately controlled. [ABSTRACT FROM AUTHOR]

A numerical modeling method to reproduce the structures of needle-punched nonwoven geotextile based on the actual manufacturing process (web formation and web bonding) was developed. The geotextile model was built based on the statistical characteristics of the computed tomography (CT) observations, physical and mechanical properties of fibers, and physical parameters of the geotextile. A combination of the finite element model and pore network model method was proposed to obtain the pore size characteristics. The appearance and pore size characteristics before and under uniaxial tensile strains were investigated. It is shown that the method can simulate the geotextile manufacturing process satisfactorily. The pore size distribution (PSD) curves obtained from the model show good agreement with the CT-based results. Moreover, the method can reasonably simulate the tensile behaviors of geotextile under uniaxial tensile strain. The specimen necking phenomenon during the uniaxial tensile test was well reproduced. The PSD curves moved towards the direction of larger pore size with increasing uniaxial strain, and characteristic pore sizes (O 98 , O 95 , O 50 , O 30 , O 10) all show a relatively steady increasing trend. • The structures of nonwoven geotextiles are reproduced by numerical simulation of the actual preparing process (web formation and web bonding). • A FEM-PNM method was proposed to obtain the pore size characteristics of the geotextile model. • The PSD curves obtained from the numerical model show a good agreement with the experimental results based on CT. • The specimen necking phenomenon during the uniaxial tensile test was well reproduced. • The PSD curves moved towards the direction of larger pore size with uniaxial strain, and characteristic pore sizes all show an increasing trend. [ABSTRACT FROM AUTHOR]

Background: Stickler syndrome is a multisystemic disorder characterized by ophthalmological and non‐ophthalmological abnormalities, frequently misdiagnosed due to high clinical heterogeneity. Stickler syndrome type I (STL1) is predominantly caused by mutations in the COL2A1 gene. Methods: Exome sequencing and co‐segregation analysis were utilized to scrutinize 35 families with high myopia, and pathogenic mutations were identified. Mutant COL2A1 was overexpressed in cells for mechanistic study. A retrospective genotype–phenotype correlation analysis was further conducted. Results: Two novel pathogenic mutations (c.2895+1G>C and c.3505G>A (p.Val1169Ile)) and two reported mutations (c.1597C>T (p.Arg533*) and c.1693C>T (p.Arg565Cys)) in COL2A1 were identified causing STL1. These mutations are all in the G‐X‐Y triplet, and c.2895+1G>C contributed to aberrant RNA splicing. COL2A1 mutants tended to form large aggregates in the endoplasmic reticulum (ER) and elevated ER stress. Additionally, mutations c.550G>A (p.Ala184Thr) and c.2806G>A (p.Gly936Ser) in COL2A1 were found in high myopia families, but were likely benign, although c.2806G>A (p.Gly936Ser) is on G‐X‐Y triplet. Moreover, genotype–phenotype correlation analysis revealed that mutations in exon 2 mainly contribute to retinal detachment, whereas mutations in the collagen alpha‐1 chain region of COL2A1 tend to cause non‐ophthalmologic symptoms. Conclusion: This study broadens the COL2A1 gene mutation spectrum, provides evidence for ER stress caused by pathogenic COL2A1 mutations and highlights the importance of non‐ophthalmological examination in clinical diagnosis of high myopia. [ABSTRACT FROM AUTHOR]

Fine-grained object recognition (FGOR) aims to learn discriminative features that can identify the subtle distinctions between visually similar objects. However, less effort has been devoted to overcoming the impact of object's personalized differences, e.g., varying posture or perspective. We argue that the personalized differences could decline the network's perception of discriminative features, thus discarding some discriminative clues and degrading the FGOR performance accordingly. This motivates us to explore the intrinsic structure knowledge: the fixed spatial correlation between object parts, and thus apply this knowledge to associate diverse semantic parts and recover the missing discriminative details caused by the personalized differences accordingly. In this paper, we propose an end-to-end Structure-driven Relation Graph Network (SRGN) for fine-grained object recognition, and target at exploring and exploiting the object structure information without any additional annotations to associate diverse semantic parts, making the network sensitive to discriminative details influenced by personalized differences. Specifically, the core of SRGN is a Structure-aware Axial Graph (SAG) module, which first infers the structure embedding by establishing the correlation between position information and visual features along the axial direction, and then applies this embedding as aggregation weights to emphasize each discriminative representation by weighted reassembling all relevant features to it. Additionally, our SAG can be readily extensible to a multi-graph schema, that leverages the complementary advantages of different structure embeddings between the position information and visual content, further improving SAG. In this way, our SRGN can demonstrate remarkable robustness in scenarios characterized by extreme distribution perturbations, ultimately leading to superior performance. Extensive experiments and explainable visualizations validate the efficacy of the proposed approach on widely-used fine-grained benchmarks. [ABSTRACT FROM AUTHOR]

Opioids are used for pain relief in patients suffering from acute myocardial ischemia or infarction. Clinical and laboratory studies demonstrate that morphine treated patients or the experimental animal model suffering acute myocardial ischemia and reperfusion, may worsen myocardial viability. As transient receptor potential vanilloid 1 (TRPV1) plays important roles in pain sensation and cardio-protection, we query whether opioids may exacerbate myocardial viability via interaction with TRPV1 activity in the pain relief. We found the co-expressions of TRPV1 and opioid μ, δ and κ receptors in adult rat cardiomyocytes. Intravenous injection of morphine (0.3 mg/kg) at 20 min after induction of myocardial ischemia, in the rat model of acute myocardial ischemia and reperfusion, induced significant reduction of phosphorylated TRPV1 (p-TRPV1) in the ventricular myocardium and increase in serum cardiac troponin I (cTnI), compared with the ischemia/reperfusion controls (all P < 0.05). The effects of morphine were completely reversed by selective opioid μ, δ and κ receptor antagonists. While significant upregulation of p-TRPV1 (P < 0.05) and improvement of ±dP/dt max (all P < 0.05) were detected in the animals giving the same dose of morphine before induction of myocardial ischemia. The changes in p-TRPV1 correlate with the alterations of cTnI (r = −0.5840, P = 0.0283) and ±dP/dt max (r = 0.8084, P = 0.0005 and r = −0.8133, P = 0.0004, respectively). The findings of this study may indicate that potentiation and attenuation of TRPV1 sensitivity correlate with the improvement of the cardiac performance and the aggravation of myocardial viability, respectively, by giving morphine before and during myocardial ischemia and reperfusion. [ABSTRACT FROM AUTHOR]

Ferrous iron (Fe2+) reduces the amount of external carbon source used for the denitrification of low-C/N wastewater. The effects of key operating parameters on the efficiency of ferrous-dependent autotrophic denitrification (FDAD) and the functioning mechanism of the microbiome can provide a regulatory strategy for improving the denitrification efficiency of low C/N wastewater. In this study, the response surface method (RSM) was used to explore the influence of four important parameters–the molar ratio of Fe2+ to NO 3 −-N (Fe/N), total organic carbon (TOC), the molar ratio of inorganic carbon to NO 3 −-N (IC/N) and sludge volume (SV, %)–on the FDAD efficiency. Functional prediction and molecular ecological networks based on high-throughputs sequencing techniques were used to explore changes in the structure, function, and biomarkers of the sludge microbial community. The results showed that Fe/N and TOC were the main parameters affecting FDAD efficiency. Higher concentrations of TOC and high Fe/N ratios provided more electron donors and improved denitrification efficiency, but weakened the importance of biomarkers (Rhodanobacter , Thermomonas , Comamonas , Thauera , Geothrix and unclassified genus of family Gallionellaceae) in the sludge ecological network. When Fe/N > 4, the denitrification efficiency fluctuated significantly. Functional prediction results indicated that genes that dominated N 2 O and NO reduction and the genes that dominated Fe2+ transport showed a slight decrease in abundance at high Fe/N levels. In light of these findings, we recommend the following optimization ranges of parameters: Fe/N (3.5–4); TOC/N (0.36–0.42); IC/N (3.5–4); and SV (approximately 35%). [Display omitted] • Fe/N, IC/N, SV, TOC effects on FDAD efficiency were explored. • TOC and Fe/N ratio are the most significant parameters affecting FDAD efficiency. • The biomarkers were Rhodanobacter, Thermomonas, Comamonas, Thauera in FDAD system. • TOC and Fe/N change the microbial community structure. • Both high Fe/N and high TOC/N weaken the importance of biomarkers in the ecological network. [ABSTRACT FROM AUTHOR]

• Watershed land use led to spatial niche differentiation of AOA, AOB, and comammox. • Urban and agricultural land lowered AOA and comammox diversity, but promoted AOB. • Land use pressure simplified AOA and comammox networks, but complicated AOB. • Ammonia and C/N, TOM and pH were key drivers of AOB and comammox, respectively. River ecological health has been severely threatened by anthropogenic land-use pressures. Here, by combining remote sensing and molecular biology methods, we evaluated the impact of land-use activities on nitrification, a fundamental ecological process in rivers, which is conducted by ammonia-oxidising archaea (AOA) and ammonia-oxidising bacteria (AOB), or the newly discovered complete ammonia oxidisers (comammox). We explored the relationships of the abundance, activity, and diversity of AOA, AOB, and comammox in river sediments with land-use pressure by proposing a quantitative land use pattern index (LPI) over a 184 km continuum along the Beiyun River in North China. We found that comammox dominated nitrification in the forestry upstream (67.07 % in summer, 56.40 % in winter), while AOB became the major player in the urban middle (56.51 % in summer, 53.08 % in winter) and agricultural downstream reaches (62.98 % in summer, 50.74 % in winter). In addition, urban and agricultural land use lowered the α diversity of AOA and comammox, as well as simplified their co-occurrence networks, but promoted AOB diversity and complicated their networks. The structural equation model illustrated that the key drivers affecting the key taxa and activities were ammonia, and C/N for AOB, and total organic matter, and pH for comammox. We thus conclude that watershed urban and agricultural land use drive the niche differentiation of AOA, AOB, and comammox, specifically leading to a robust AOB community but weakened AOA and comammox communities. Our study connects the macro and micro worlds and provides a new paradigm for studying the variation in microbial communities as well as the potential ecological consequences under the increased anthropogenic land-use pressures in the Anthropocene. [Display omitted] [ABSTRACT FROM AUTHOR]

This study aims to compare the efficacy and safety of using overlapping low-profile visualized intraluminal support (LVIS) devices and flow diversion (FD) for the treatment of unruptured vertebral artery dissection (VAD) in the V3–V4 segments.The clinical and imaging data of 71 patients with unruptured VAD in the V3–V4 segments who underwent either dual LVIS stenting (d-LVIS group) or single FD stenting (FD group) at our center from September 2014 to December 2021 were retrospectively analyzed.Immediate postoperative angiography revealed no significant difference in the degree of occlusion between the two groups in treating vertebral artery dissecting aneurysms (with or without noncompact coiling). However, the d-LVIS group had significantly higher fluoroscopy exposure time and total radiation exposure dose compared to the FD group. During the perioperative period, two cases of pontine infarction and one case of acute thrombosis were encountered. One patient died from subarachnoid hemorrhage during the follow-up period. For dissecting the aneurysm, angiographic follow-up (8.56 ± 1.96 months) showed similar healing outcomes between the two groups (with or without noncompact coiling). However, seven patients (7/40, 17.5%) showed poor healing and one patient showed mild in-stent stenosis. For simple dissection, angiographic follow-up (8.78 ± 1.83 months) showed patent lumens in both groups, with all dissections healing well, and two patients having mild in-stent stenosis.Both methods could effectively treat unruptured VAD in V3–V4 segments. Nevertheless, simple FD implantation is relatively easier to perform and involves lower radiation exposure. [ABSTRACT FROM AUTHOR]

In computer vision, an important challenge to deep neural networks comes from adjusting the varying properties of different image domains. To study this problem, researchers have been investigating a practical setting in which the deep neural networks are trained on a labeled source domain and then transferred to an unlabeled or even unseen target domain. The major difficulty lies in the potential domain gap, which essentially arises from the overfitting in the source domain. Hence, it is important to introduce generalized priors to alleviate the issue. From this perspective, this paper presents a novel framework that forces visual features to align with domain-agnostic priors (DAP). Specifically, we study two kinds of priors, (i) language-guided embedding and (ii) class-level relationship, and we believe that more such priors can be constructed. Our framework, referred to as DAP, is evaluated on both unsupervised domain adaptation (UDA) and domain generalization (DG) where the target domain is unlabeled and even unseen, respectively. We use the standard benchmark that performs transfer semantic segmentation on synthesized datasets (i.e., GTAv and SYNTHIA) and a real dataset (i.e., Cityscapes). Experiments validate the effectiveness of DAP with competitive accuracy in all tasks. In particular, language-guided priors work sufficiently well for UDA, while class-level priors serve as useful complements for DG. The proposed frameworks shed light that domain transfer benefits from better proxies, possibly from other modalities. [ABSTRACT FROM AUTHOR]

Gait recognition is an important biometric technology that allows for the remote collection of stakeholders' characteristics, without requiring their explicit cooperation. It has gained considerable attention in the fields of criminal investigation and intelligent security. Previous studies have shown that local gait features can enhance gait recognition performance by improving robustness to disturbances. However, global gait features also play a crucial role in gait recognition. Many researchers have utilized convolutional operations to extract global features, but these operations tend to focus on features within the receptive field, neglecting those outside of it. Therefore, the potential of global gait features has not been fully explored. In this paper, we propose a gait recognition framework based on vision transformers, aiming to enhance the extraction of global gait features. We introduce an adaptive multi-frame global feature mapping (AMGM) method to address the challenge of inconsistent feature dimensions caused by variations in the number of gait frames when fusing global and local features. We evaluate our model on the latest datasets, and the experimental results demonstrate a significant breakthrough. Notably, our model achieves state-of-the-art recognition accuracy, particularly in scenarios where subjects are wearing coats. Additionally, our model achieves remarkable improvements in recognition accuracy through training with small sample sets. [ABSTRACT FROM AUTHOR]

[Display omitted] • The trends in anoxic P-take and dominant taxa abundance were highly similar. • High nitrite stress rapidly promoted the shift of the bacterial community state. • Shift of community state was mostly driven by low modularity and positive links. • OLB8 and Zoogloea functioned crucial roles in resisting nitrite to enhance P-uptake. • High nitrite inhibited the potential of carbon utilization and glycogen synthesis. Denitrifying phosphorus removal using nitrite as an electron acceptor is an innovative, resource-efficient approach for nitrogen and phosphorus removal. However, the inhibitory effects of nitrite on anoxic phosphorus uptake and process stability are unclear. This study investigated the total phosphorus removal performance under nitrite stress and analyzed microbiome responses in 186 sludge samples. The results indicated that the total phosphorus removal rates and dominant taxon abundance were highly similar under nitrite stress. High nitrite stress induced a community-state shift, leading to unstable dynamics and decreased total phosphorus removal. This shift resulted from increased species cooperation. Notably, the shared genera OLB8 and Zoogloea under non-inhibitory nitrite stress, suggesting their vital roles in mitigating nitrite stress by enhancing carbon and energy metabolism. The response patterns of these bacterial communities to high nitrite stress can guide the design and optimization of high-nitrogen wastewater reactors. [ABSTRACT FROM AUTHOR]

Ambient air pollution has been linked to an increased risk of various acute cardiovascular outcomes; however, its effects on hospital admissions for angina are yet to be evaluated. We conducted a time-stratified case-crossover study with conditional logistic regression models among 46,687 adults 60 years or older who were admitted to hospital for angina in Guangzhou, China during 2016–2019 to investigate the association of exposure to ambient particulate matter with an aerodynamic diameter ≤2.5 μm (PM 2.5), particulate matter with an aerodynamic diameter ≤10 μm (PM 10), sulfur dioxide (SO 2), nitrogen dioxide (NO 2), carbon monoxide (CO), and ozone (O 3) with hospital admissions for angina. Daily residential air pollutant exposures were extracted from a grid dataset. Each 10 μg/m3 increase of lag 0-day exposure to PM 10 , SO 2 , NO 2 , CO, and O 3 was significantly associated with a 0.80% (95% confidential interval: 0.32%, 1.28%), 4.04% (0.34%, 7.89%), 2.47% (1.81%, 3.12%), 0.13% (0.07%, 0.19%), and −0.38% (−0.74%, −0.01%) increase in odds of admission, respectively. The association for NO 2 exposure remained stable, while the associations for PM 10 , SO 2 , CO, and O 3 became insignificant with adjustment for other air pollutants. The association for NO 2 exposure was stronger in cool season. We estimated that up to 9.12% of angina admissions were attributable to NO 2 exposure. Our findings suggest that ambient NO 2 may trigger hospital admissions for angina in Chinese older adults, which highlights the importance to prevent angina by reducing individual NO 2 exposures. • Short-term exposure to ambient NO 2 was associated with an increased odds of angina admissions in older adults. • The association for NO 2 was stronger in cool season. • Reducing traffic-related air pollution may be helpful in preventing angina admissions. [ABSTRACT FROM AUTHOR]

The incidence of postoperative myocardial injury remains high as the underlying pathogenesis is still unknown. The dorsal root ganglion (DRG) neurons express transient receptor potential vanilloid 1 (TRPV1) and its downstream effector, calcitonin gene-related peptide (CGRP) participating in transmitting pain signals and cardiac protection. Opioids remain a mainstay therapeutic option for moderate-to-severe pain relief clinically, as a critical component of multimodal postoperative analgesia via intravenous and epidural delivery. Evidence indicates the interaction of opioids and TRPV1 activities in DRG neurons. Here, we verify the potential impairment of myocardial viability by epidural usage of opioids in postoperative analgesia. We found that large dose of epidural morphine (50 μg) significantly worsened the cardiac performance (+dP/dt max reduction by 11% and -dP/dt max elevation by 24%, all P < 0.001), the myocardial infarct size (morphine vs Control, 0.54 ± 0.09 IS/AAR vs. 0.23 ± 0.06 IS/AAR, P < 0.001) and reduced CGRP in the myocardium (morphine vs. Control, 9.34 ± 2.24 pg/mg vs. 21.23 ± 4.32 pg/mg, P < 0.001), while induced definite suppression of nociception in the postoperative animals. It was demonstrated that activation of μ-opioid receptor (μ-OPR) induced desensitization of TRPV1 by attenuating phosphorylation of the channel in the dorsal root ganglion neurons, via inhibiting the accumulation of cAMP. CGRP may attenuated the buildup of ROS and the reduction of mitochondrial membrane potential in cardiomyocytes induced by hypoxia/reoxygenation. The findings of this study indicate that epidurally giving large dose of μ-OPR agonist may aggravate myocardial injury by inhibiting the activity of TRPV1/CGRP pathway. • Impairing myocardial viability can be triggered by epidural injection morphine or DAMGO. • Opioid μ-receptor agonist desensitizes transient receptor potential vanilloid 1 (TRPV1). • Inhibition of TRPV1 reduces calcitonin gene-related peptide (CGRP) release from DRG neurons. • CGRP protects cardiomyocytes via stabilization of ROS, mitochondrial membrane potentials. [ABSTRACT FROM AUTHOR]

Recently, graph based hashing has gained much attention due to its effectiveness in multi-media retrieval. Although several graph embedding based works have been designed and achieved promising performance, there are still some issues that need to be further studied, including, (1) one significant drawback of graph embedding is its expensive memory and computation cost caused by the graph Laplacian matrix; (2) most pioneer works fail to fully explore the available class labels in training procedure, which generally makes them suffer from unsatisfactory retrieval performance. To overcome these drawbacks, we propose a simple yet effective supervised cross-media hashing scheme, termed Efficient Supervised Graph Embedding Hashing (ESGEH), which can simultaneously learn hash functions and discrete binary codes efficiently. Specifically, ESGEH leverages both class label based semantic embedding and graph embedding to generate a sharing semantic subspace, and class labels are also incorporated to minimize the quantization error for better approximating the generated binary codes. In order to reduce the computational sources, a well-designed intermediate terms decomposition is proposed to avoid explicitly computing the graph Laplacian matrix. Finally, an iterative discrete optimal algorithm is derived to solve above problem, and each subproblem can yield a closed-form solution. Extensive experimental results on four public datasets demonstrate the superiority of the proposed approach over several existing cross-media hashing methods in terms of both accuracy and efficiency. • The proposed method incorporates class labels not only to preserve the intra-modal and inter-modal similarities, but also to minimize the quantization error by a supervised iterative quantization algorithm, for improving the distinguishing capability of hash codes. • A well-designed intermediate terms decomposition is proposed for significantly reducing the computing complexity from O(n2) to O(n). • The experimental comparison results exhibits superior retrieval performance over existing popular methods. [ABSTRACT FROM AUTHOR]