ABSTRACT
Microplastics (MPs) in agricultural plastic film mulching system changes microbial functions and nutrient dynamics in soils. However, how biodegradable MPs impact the soil gross nitrogen (N) transformations and crop N uptake remain significantly unknown. In this study, we conducted a paired labeling 15N tracer experiment and microbial N-cycling gene analysis to investigate the dynamics and mechanisms of soil gross N transformation processes in soils amended with conventional (polyethylene, PE) and biodegradable (polybutylene adipate co-terephthalate, PBAT) MPs at concentrations of 0 %, 0.5 %, and 2 % (w/w). The biodegradable MPs-amended soils showed higher gross N mineralization rates (0.5-16 times) and plant N uptake rates (16-32 %) than soils without MPs (CK) and with conventional MPs. The MPs (both PE and PBAT) with high concentration (2 %) increased gross N mineralization rates compared to low concentration (0.5 %). Compare to CK, MPs decreased the soil gross nitrification rates, except for PBAT with 2 % concentration; while PE with 0.5 % concentration and PBAT with 2 % concentration increased but PBAT with 0.5 % concentration decreased the gross N immobilization rates significantly. The results indicated that there were both a concentration effect and a material effect of MPs on soil gross N transformations. Biodegradable MPs increased N-cycling gene abundance by 60-103 %; while there was no difference in the abundance of total N-cycling genes between soils without MPs and with conventional MPs. In summary, biodegradable MPs increased N cycling gene abundance by providing enriched nutrient substrates and enhancing microbial biomass, thereby promoting gross N transformation processes and maize N uptake in short-term. These findings provide insights into the potential consequences associated with the exposure of biodegradable MPs, particularly their impact on soil N cycling processes.
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OBJECTIVE: Inflammation plays an important role in epilepsy. There is evidence for the relationship between proinflammatory cytokines and epilepsy. We aimed to detect the serum levels of multiple cytokines in epilepsy patients, looking for biological indicators, and providing a theoretical basis for the clinical diagnosis, treatment, and prognosis of epilepsy. MATERIALS AND METHODS: In this study, 30 patients with drug-resistant epilepsy (DRE), 30 patients with well-controlled epilepsy (WCE), and 29 healthy controls (HC) were enrolled. Multi-proinflammatory cytokines were measured by LUMINX multi-factor detection. RESULTS: The levels of IL-1ß, IL-7, IL-12, and IL-17 were significantly elevated, and the levels of CX3CL1 and ITAC were significantly decreased in epilepsy patients compared with healthy controls. Furthermore, the level of IL-17 was significantly higher in the DRE group compared to WCE. We also found the ratio of IL-7/CX3CL discriminates accurately between patients and controls, with a ROC Area Under the Curve (AUC) of 0.963 (P<0.001). The levels of IL-1ß, IL-7, IL-12, and IL-17 in the DRE group were positively correlated with the National Hospital Seizure Severity Scale (NHS3) scores (IL-1ß, P = 0.029; IL-12, P = 0.039; IL-17, P = 0.004). IL-17 was positively correlated with seizure frequency (P = 0.050), while ITAC was negatively correlated with seizure frequency (P = 0.012) and Sudden Unexpected Death in Epilepsy-3 (SUDEP-3) scores (P = 0.023). CONCLUSIONS: IL-1ß, IL-12, and IL-17 may be used to predict seizure severity and the IL-7/CX3CL1 ratio may be a candidate biomarker for predicting epileptic seizures. While CX3CL1 and ITAC play anti-epileptic effects, ITAC may be used to assess the risk of SUDEP.
ABSTRACT
Oxidative stress has long been known as a pathogenic factor of ulcerative colitis. Superoxide dismutase (SOD) has been demonstrated to mitigate gut mucosal injury via combating oxidative stress. Herein, we developed SOD-loaded multivesicular liposomes (S-MVLs) as sustained-release depot for ulcerative colitis treatment. S-MVLs were spherical honeycomb-like particles with average particle size of 27.3 ± 5.4 µm and encapsulating efficiency of 78.7 ± 2.6â¯%. Moreover, the two-phase release profiles of SOD from S-MVLs were exhibited, that was, the burst release phase within 4â¯h and the sustained-release phase within 96â¯h. After intraperitoneally injecting S-MVLs, in situ retention time of SOD at bowel cavity extended by 4-fold in comparison with SOD solution. In vitro cells experiment showed that S-MVLs had the protective effect on LPS-treated RAW 264.7 cells via scavenging ROS and inhibiting pro-inflammatory cytokines production. S-MVLs ameliorated the body weight loss, DAI score and the colon shortening of colitis mice. Meanwhile, the colonic morphology and the epithelial barrier of colitis mice were effectively recovered after S-MVLs treatment. The therapeutic mechanism might be associated with polymerizing M1 macrophages to M2 phenotypes and alleviating oxidative stress. Collectively, multivesicular liposomes might be a promising sustained-release depot of SOD for ulcerative colitis treatments.
ABSTRACT
Ulcerative colitis (UC) is a chronic bowel inflammatory disease affecting the colorectum. Epidermal growth factor (EGF) has been demonstrated to be effective to counteract UC. However, there exists the gastrointestinal challenges such as stomach acid, enzyme and bile salts for oral delivery of EGF. Herein, calcium alginate microsphere was prepared by the microfluidic technique to encapsulate EGF. The morphology of EGF-loaded microsphere (MS-EGF) was spherical and its average particle size was 80 ± 23 µm. The encapsulation efficiency of EGF was reaching to 93.8 % ± 1.6 %. In vitro release experiments showed that MS-EGF presented the good pH-sensitive properties, that was, it could effectively resist the gastric acid and small intestinal fluids, and undergone the rapid dissolution in the artificial colon fluid. In vitro cellular experiments demonstrated that the bioactivity of EGF was well preserved by microsphere. Moreover, in vivo murine colitis model showed that MS-EGF presented the obvious colitis alleviation. Furthermore, the colonic morphology of colitis mice was effectively recovered and the tight junction between the gut epithelium was obviously repaired. In conclusion, calcium alginate microsphere might be a promising vehicle of EGF for UC treatment.
Subject(s)
Alginates , Colitis, Ulcerative , Epidermal Growth Factor , Intestinal Mucosa , Microspheres , Animals , Alginates/chemistry , Alginates/administration & dosage , Colitis, Ulcerative/drug therapy , Epidermal Growth Factor/administration & dosage , Intestinal Mucosa/metabolism , Intestinal Mucosa/drug effects , Mice , Administration, Oral , Male , Drug Liberation , Humans , Particle Size , Colon/metabolism , Colon/drug effects , Colon/pathology , Drug Carriers/chemistry , Disease Models, Animal , Hexuronic Acids/chemistry , Hexuronic Acids/administration & dosageABSTRACT
Nanopore technology, re-fueled by two-dimensional (2D) materials such as graphene and MoS2, controls mass transport by allowing certain species while denying others at the nanoscale and has a wide application range in DNA sequencing, nano-power generation, and others. With their low transmembrane transport resistance and high permeability stemming from their ultrathin nature, crystalline 2D materials do not possess nanoscale holes naturally, thus requiring additional fabrication to create nanopores. Herein, we demonstrate that nanopores exist in amorphous monolayer carbon (AMC) grown at low temperatures. The size and density of nanopores can be tuned by the growth temperature, which was experimentally verified by atomic images and further corroborated by kinetic Monte Carlo simulation. Furthermore, AMC films with varied degrees of disorder (DOD) exhibit tunable transmembrane ionic conductance over two orders of magnitude when serving as nanopore membranes. This work demonstrates the DOD-tuned property in amorphous monolayer carbon and provides a new candidate for modern membrane science and technology.
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Trajectory tracking on a low-speed vehicle using the model predictive control (MPC) algorithm usually assumes a simple road terrain. This assumption does not correspond to the actual road situation, leading to low tracking accuracy. Therefore, a trajectory tracking method considering road curvature based on MPC is proposed in this paper. In this method, the controller can automatically switch between MPC types. Linear model predictive control (LMPC) is selected for small road curvatures, while nonlinear model predictive control (NMPC) is employed for large road curvatures. In addition, the NMPC algorithm in this work considers the effect of road curvature on tracking accuracy, making it suitable for tracking time-varying curvature roads. To verify the feasibility of the algorithm, simulation comparisons with the basic MPC model were carried out at different testing roads and vehicle longitudinal speeds. The results indicate that the method significantly improves trajectory tracking accuracy, all while ensuring real-time calculations. The intelligent switching capability of control models based on road curvature allows its application to track trajectories on arbitrarily complex roads.
ABSTRACT
Nanoscale spatially controlled modulation of the properties of ferroelectrics via artificial domain pattering is crucial to their emerging optoelectronics applications. New patterning strategies to achieve high precision and efficiency and to link the resultant domain structures with device functionalities are being sought. Here, we present an epitaxial heterostructure of SrRuO3/PbTiO3/SrRuO3, wherein the domain configuration is delicately determined by the charge screening conditions in the SrRuO3 layer and the substrate strains. Chemical etching of the top SrRuO3 layer leads to a transition from in-plane a domains to out-of-plane c domains, accompanied by a giant (>105) modification in the second harmonic generation response. The modulation effect, coupled with the plasmonic resonance effect from SrRuO3, enables a highly flexible design of nonlinear optical devices, as demonstrated by a simulated split-ring resonator metasurface. This domain patterning strategy may be extended to more thin-film ferroelectric systems with domain stabilities amenable to electrostatic boundary conditions.
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BACKGROUND: Osteoarthritis (OA) is the most common degenerative joint disease worldwide. Further improving the current limited understanding of osteoarthritis has positive clinical value. METHODS: OA samples were collected from GEO database and endoplasmic reticulum related genes (ERRGs) were identified. The WGCNA network was further built to identify the crucial gene module. Based on the expression profiles of characteristic ERRGs, LASSO algorithm was used to select key factors according to the minimum λ value. Random forest (RF) algorithm was used to calculate the importance of ERRGs. Subsequently, overlapping genes based on LASSO and RF algorithms were identified as ERRGs-related diagnostic biomarkers. In addition, OA specimens were also collected and performed qRT-PCR quantitative analysis of selected ERRGs. RESULTS: We identified four ERRGs associated with OA risk assessment through machine learning methods, and verified the abnormal expressions of these screened markers in OA patients through in vitro experiments. The influence of selected markers on OA immune infiltration was also evaluated. CONCLUSIONS: Our results provide new evidence for the role of ER stress in the OA progression, as well as new markers and potential intervention targets for OA.
Subject(s)
Algorithms , Osteoarthritis , Humans , Endoplasmic Reticulum , Machine Learning , Osteoarthritis/diagnosis , Osteoarthritis/genetics , BiomarkersABSTRACT
Hepatitis B virus (HBV) may directly infect human podocytes (HPCs). However, the mechanism of direct infection is unclear. We found that HPCs express sodium taurocholate cotransporting polypeptide (NTCP), a specific receptor for HBV entry into hepatocytes. Thus, we investigated whether NTCP mediates HBV infection and damage in HPCs and further clarified the specific mechanism. We constructed shRNA-NTCP1,2, shRNA-NC, WT-NTCP, and MUT-NTCP and transfected them into HPCs. HPCs were infected with HBV, and HBV infection markers were detected by enzyme-linked immunosorbent assay (ELISA) and real-time quantitative PCR (RT-qPCR). The functional changes in HPCs were detected by Transwell migration and scratch assays, apoptosis was evaluated by flow cytometry (FCM), and podocytoskeletal proteins (nephrin, CD2AP, and synaptopodin) were determined by western blotting (WB). Compared with the control HPCs, HPCs infected with HBV showed increased levels of HBV infection markers and apoptosis along with decreased podocytoskeletal protein expressions, cell vitality, proliferation, and migration. Compared with the HPCs infected with HBV, the HPCs transfected with HBV + shRNA-NTCP, and HBV + MUT-NTCP showed decreased levels of HBV infection markers and apoptosis along with increased podocytoskeletal protein expressions, cell vitality, proliferation, and migration; the opposite effects were observed in the HPCs transfected with HBV + WT-NTCP. Overall, the changes to NTCP affected the susceptibility of HPCs to HBV and modulated HPC damage and repair. NTCP can mediate direct HBV infection and damage human podocytes, and the NTCP 157-165 locus is the main site of HBV entry. The findings provide a new target and theoretical basis for HBV-associated glomerulonephritis. IMPORTANCE: This study identified for the first time that sodium taurocholate cotransporting polypeptide (NTCP) can mediate HBV direct infection and damage to human podocytes, and the NTCP157-165 locus is the main HBV entry site. The findings provide theoretical support for the pathogenesis of direct infection of HBV with kidney tissue. The findings provide a new target and theoretical basis for the treatment of HBV-related glomerulonephritis (HBV-GN). Blocking NTCP is a new target for the treatment of HBV-GN. We found that tacrolimus, a calcineurin inhibitor that blocks NTCP, can effectively treat HBV-GN. This study also provides a theoretical basis for the effective and safe treatment of immunosuppressant tacrolimus for HBV-GN.
Subject(s)
Glomerulonephritis , Hepatitis B , Podocytes , Symporters , Humans , Hepatitis B virus/genetics , Tacrolimus/metabolism , Podocytes/metabolism , Organic Anion Transporters, Sodium-Dependent/genetics , Organic Anion Transporters, Sodium-Dependent/metabolism , RNA, Small InterferingABSTRACT
Biphasic glucose-stimulated insulin secretion (GSIS) is essential for blood glucose regulation, but a mechanistic model incorporating the recently identified islet ß cell heterogeneity remains elusive. Here, we show that insulin secretion is spatially and dynamically heterogeneous across the islet. Using a zinc-based fluorophore with spinning-disc confocal microscopy, we reveal that approximately 40% of islet cells, which we call readily releasable ß cells (RRßs), are responsible for 80% of insulin exocytosis events. Although glucose up to 18.2 mM fully mobilized RRßs to release insulin synchronously (first phase), even higher glucose concentrations enhanced the sustained secretion from these cells (second phase). Release-incompetent ß cells show similarities to RRßs in glucose-evoked Ca2+ transients but exhibit Ca2+-exocytosis coupling deficiency. A decreased number of RRßs and their altered secretory ability are associated with impaired GSIS progression in ob/ob mice. Our data reveal functional heterogeneity at the level of exocytosis among ß cells and identify RRßs as a subpopulation of ß cells that make a disproportionally large contribution to biphasic GSIS from mouse islets.
Subject(s)
Biphasic Insulins , Insulin-Secreting Cells , Mice , Animals , Insulin Secretion , Biphasic Insulins/metabolism , Glucose/pharmacology , Glucose/metabolism , Insulin-Secreting Cells/metabolism , Insulin/metabolism , Exocytosis/physiologyABSTRACT
INTRODUCTION: We aimed to determine the diagnostic criteria of myosteatosis in a Chinese population and investigate the effect of skeletal muscle abnormalities on the outcomes of cirrhotic patients. METHODS: Totally 911 volunteers were recruited to determine the diagnostic criteria and impact factors of myosteatosis, and 480 cirrhotic patients were enrolled to verify the value of muscle alterations for prognosis prediction and establish new noninvasive prognostic strategies. RESULTS: Multivariate analysis showed age, sex, weight, waist circumference, and biceps circumference had a remarkable influence on the L3 skeletal muscle density (L3-SMD). Based on the cut-off of a mean - 1.28 × SD among adults aged < 60 years, the diagnostic criteria for myosteatosis was L3-SMD < 38.93 Hu in males and L3-SMD < 32.82 Hu in females. Myosteatosis rather than sarcopenia has a close correlation with portal hypertension. The concurrence of sarcopenia and myosteatosis not only is associated with poor liver function but also evidently reduced the overall and liver transplantation-free survival of cirrhotic patients (p < 0.001). According to the stepwise Cox regression hazard model analysis, we established nomograms including TBil, albumin, history of HE, ascites grade, sarcopenia, and myosteatosis for easily determining survival probabilities in cirrhotic patients. The AUC is 0.874 (95% CI 0.800-0.949) for 6-month survival, 0.831 (95% CI 0.764-0.898) for 1-year survival, and 0.813 (95% CI 0.756-0.871) for 2-year survival prediction, respectively. CONCLUSIONS: This study provides evidence of the significant correlation between skeletal muscle alterations and poor outcomes of cirrhosis, and establishes valid and convenient nomograms incorporating musculoskeletal disorders for the prognostic prediction of liver cirrhosis. Further large-scale prospective studies are necessary to verify the value of the nomograms.
Subject(s)
Sarcopenia , Male , Adult , Female , Humans , Sarcopenia/complications , Sarcopenia/diagnosis , Prospective Studies , Muscle, Skeletal/pathology , Liver Cirrhosis/pathology , Prognosis , Retrospective StudiesABSTRACT
The properties of two-dimensional (2D) van der Waals materials can be tuned through nanostructuring or controlled layer stacking, where interlayer hybridization induces exotic electronic states and transport phenomena. Here we describe a viable approach and underlying mechanism for the assisted self-assembly of twisted layer graphene. The process, which can be implemented in standard chemical vapour deposition growth, is best described by analogy to origami and kirigami with paper. It involves the controlled induction of wrinkle formation in single-layer graphene with subsequent wrinkle folding, tearing and re-growth. Inherent to the process is the formation of intertwined graphene spirals and conversion of the chiral angle of 1D wrinkles into a 2D twist angle of a 3D superlattice. The approach can be extended to other foldable 2D materials and facilitates the production of miniaturized electronic components, including capacitors, resistors, inductors and superconductors.
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BACKGROUND: Ferroptosis and lncRNAs both play crucial roles in cancers. But the roles of ferroptosis-related lncRNAs (FRLncs) in HBV-related HCC (HBV-HCC) remain ambiguous. METHODS: The gene expression profile and clinical data were originated from the Cancer Genome Atlas (TCGA) database. The risk signature was constructed by FRLncs based on the Cox regression analysis. The survival curve, Cox regression analysis, and time-dependent receiver operating characteristic (ROC) curve were adopted to verify the independence and reliability of the signature. A nomogram was established. Immune-infiltrating cells, immune functions, and checkpoints were analyzed. RESULTS: A risk signature composed of 7 FRLncs (LINC00942, AC131009.1, POLH-AS1, AC090772.3, MKLN1-AS, AC009403.1, AL031985.3) was constructed and divided HBV-HCC patients into high- and low-risk groups. Patients in the high-risk group showed a poor prognosis. The area under curves (AUC) of the signature for 1-, 3-, and 5-year was satisfactory. A nomogram composed of gender, stage, age, grade, and risk signature was established. The risk signature and nomogram displayed appreciable independence and reliability in HBV-HCC patients. The T-cell CD8 + , monocyte, and macrophage M1 were expressed differently significantly in HCC patients, while macrophage M2 showed an obvious difference in the HBV-HCC patients between the different risk groups. PDCD1 and CTL4 were expressed higher in the high-risk group of HCC patients. CONCLUSION: A 7-lncRNA signature was identified as a potential prognostic predictor for HBV-HCC patients. Immune therapy may be a promising strategy for HCC patients, especially HBV-HCC patients.
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Coronavirus disease 2019 (COVID-19) is a major disease that threatens human life and health. Its pathogenesis is complex and still not fully clarified. The clinical treatment is mainly supportive and lacks specific treatment methods. Acupuncture treatment can inhibit immune inflammatory reactions, neuroinflammatory reactions, oxidative stress levels, and hypothalamus-pituitary-adrenal (HPA) axis activity, improve lung function, and relieve migraine, fatigue, anxiety, and depression. However, whether acupuncture treatment is suitable for treating these symptoms in patients with COVID-19 still needs to be investigated. For this review, the literature was systematically searched for multiple databases to summarize the mechanisms of acupuncture treatment for COVID-19-related symptoms and complications. A complex network analysis of acupoints and symptoms was also performed to clarify acupoint selection in the acupuncture treatment of symptoms related to COVID-19. The evidence indicates that acupuncture can improve the respiratory, digestive, nervous, and mental and psychological symptoms related to COVID-19 by inhibiting immune inflammatory reactions, regulating intestinal flora, mitochondrial function, oxidative stress level, cardiomyocyte apoptosis, neurotransmitter release, and HPA axis activity, and alleviating basic diseases such as diseases of the vascular system. Acupuncture can improve various clinical and concomitant symptoms of COVID-19; however, its mechanism of action is complex and requires further study. Graphical abstract: http://links.lww.com/AHM/A54.
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Achieving both high efficiency and long-term stability is the key to the commercialization of perovskite solar cells (PSCs)1,2. However, the diversity of perovskite (ABX3) compositions and phases makes it challenging to fabricate high-quality films3-5. Perovskite formation relies on the reaction between AX and BX2, whereas most conventional methods for film-growth regulation are based solely on the interaction with the BX2 component. Herein, we demonstrate an alternative approach to modulate reaction kinetics by anion-π interaction between AX and hexafluorobenzene (HFB). Notably, these two approaches are independent but work together to establish 'dual-site regulation', which achieves a delicate control over the reaction between AX and BX2 without unwanted intermediates. The resultant formamidinium lead halides (FAPbI3) films exhibit fewer defects, redshifted absorption and high phase purity without detectable nanoscale δ phase. Consequently, we achieved PSCs with power conversion efficiency (PCE) up to 26.07% for a 0.08-cm2 device (25.8% certified) and 24.63% for a 1-cm2 device. The device also kept 94% of its initial PCE after maximum power point (MPP) tracking for 1,258 h under full-spectrum AM 1.5 G sunlight at 50 ± 5 °C. This method expands the range of chemical interactions that occur in perovskite precursors by exploring anion-π interactions and highlights the importance of the AX component as a new and effective working site to improved photovoltaic devices with high quality and phase purity.
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Satellite pose estimation plays a crucial role within the aerospace field, impacting satellite positioning, navigation, control, orbit design, on-orbit maintenance (OOM), and collision avoidance. However, the accuracy of vision-based pose estimation is severely constrained by the complex spatial environment, including variable solar illumination and the diffuse reflection of the Earth's background. To overcome these problems, we introduce a novel satellite pose estimation network, FilterformerPose, which uses a convolutional neural network (CNN) backbone for feature learning and extracts feature maps at various CNN layers. Subsequently, these maps are fed into distinct translation and orientation regression networks, effectively decoupling object translation and orientation information. Within the pose regression network, we have devised a filter-based transformer encoder model, named filterformer, and constructed a hypernetwork-like design based on the filter self-attention mechanism to effectively remove noise and generate adaptive weight information. The related experiments were conducted using the Unreal Rendered Spacecraft On-Orbit (URSO) dataset, yielding superior results compared to alternative methods. We also achieved better results in the camera pose localization task, indicating that FilterformerPose can be adapted to other computer vision downstream tasks.
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Microsatellite-stable colorectal cancer (MSS-CRC) is highly refractory to immunotherapy. Understanding tumor-intrinsic determinants of immunotherapy resistance is critical to improve MSS-CRC patient outcomes. Here, we demonstrate that high tumor expression of the core autophagy gene ATG16L1 is associated with poor clinical response to anti-PD-L1 therapy in KRAS-mutant tumors from IMblaze370 (NCT02788279), a large phase III clinical trial of atezolizumab (anti-PD-L1) in advanced metastatic MSS-CRC. Deletion of Atg16l1 in engineered murine colon cancer organoids inhibits tumor growth in primary (colon) and metastatic (liver and lung) niches in syngeneic female hosts, primarily due to increased sensitivity to IFN-γ-mediated immune pressure. ATG16L1 deficiency enhances programmed cell death of colon cancer organoids induced by IFN-γ and TNF, thus increasing their sensitivity to host immunity. In parallel, ATG16L1 deficiency reduces tumor stem-like populations in vivo independently of adaptive immune pressure. This work reveals autophagy as a clinically relevant mechanism of immune evasion and tumor fitness in MSS-CRC and provides a rationale for autophagy inhibition to boost immunotherapy responses in the clinic.
Subject(s)
Colonic Neoplasms , Colorectal Neoplasms , Animals , Female , Humans , Mice , Autophagy/genetics , Autophagy-Related Proteins/genetics , Colorectal Neoplasms/drug therapy , Colorectal Neoplasms/genetics , Genes, Regulator , Liver , Clinical Trials, Phase III as TopicABSTRACT
After being ingested and entering the human stomach, Helicobacter pylori (H. pylori) adopts several effective strategies to adhere to and colonize the gastric mucosa and move to different regions of the stomach to obtain more nutrients and escape from the harsher environments of the stomach, leading to acute infection and chronic gastritis, which is the basis of malignant gastric tumors. The endoscopic manifestations and pathological features of H. pylori infection are diverse and vary with the duration of infection. In this review, we describe the endoscopic manifestations of each stage of H. pylori gastritis and then reveal the potential mechanisms of bacterial intragastric colonization and migration from the perspective of endoscopists to provide direction for future research on the effective therapy and management of H. pylori infection.