Programmed surface platform orchestrates anti-bacterial ability and time-sequential bone healing for implant-associated infection.

Implant-associated infection (IAI) has become an intractable challenge in clinic. The healing of IAI is a complex physiological process involving a series of spatiotemporal connected events. However, existing titanium-based implants in clinic suffer from poor antibacterial effect and single function. Herein, a versatile surface platform based on the presentation of sequential function is developed. Fabrication of titania nanotubes and poly-γ-glutamic acid (γ-PGA) achieves the efficient incorporation of silver ions (Ag+) and the pH-sensitive release in response to acidic bone infection microenvironment. The optimized PGA/Ag platform exhibits satisfactory biocompatibility and converts macrophages from pro-inflammatory M1 to pro-healing M2 phenotype during the subsequent healing stage, which creates a beneficial osteoimmune microenvironment and promotes angio/osteogenesis. Furthermore, the PGA/Ag platform mediates osteoblast/osteoclast coupling through inhibiting CCL3/CCR1 signaling. These biological effects synergistically improve osseointegration under bacterial infection in vivo, matching the healing process of IAI. Overall, the novel integrated PGA/Ag surface platform proposed in this study fulfills function cascades under pathological state and shows great potential in IAI therapy.

Characteristic changes in astrocyte properties during astrocyte-to-neuron conversion induced by NeuroD1/Ascl1/Dlx2.

JOURNAL/nrgr/04.03/01300535-202506000-00030/figure1/v/2024-08-05T133530Z/r/image-tiff Direct in vivo conversion of astrocytes into functional new neurons induced by neural transcription factors has been recognized as a potential new therapeutic intervention for neural injury and degenerative disorders. However, a few recent studies have claimed that neural transcription factors cannot convert astrocytes into neurons, attributing the converted neurons to pre-existing neurons mis-expressing transgenes. In this study, we overexpressed three distinct neural transcription factors--NeuroD1, Ascl1, and Dlx2--in reactive astrocytes in mouse cortices subjected to stab injury, resulting in a series of significant changes in astrocyte properties. Initially, the three neural transcription factors were exclusively expressed in the nuclei of astrocytes. Over time, however, these astrocytes gradually adopted neuronal morphology, and the neural transcription factors was gradually observed in the nuclei of neuron-like cells instead of astrocytes. Furthermore, we noted that transcription factor-infected astrocytes showed a progressive decrease in the expression of astrocytic markers AQP4 (astrocyte endfeet signal), CX43 (gap junction signal), and S100ß. Importantly, none of these changes could be attributed to transgene leakage into pre-existing neurons. Therefore, our findings suggest that neural transcription factors such as NeuroD1, Ascl1, and Dlx2 can effectively convert reactive astrocytes into neurons in the adult mammalian brain.

Enhancement of PFAS stress tolerance and wastewater treatment efficiency by arbuscular mycorrhizal fungi in constructed wetlands.

This study aims to explore the effects of arbuscular mycorrhizal fungi (AMF) on the growth of Iris pseudacorus L. and treatment efficacy in constructed wetlands (CWs) subjected to stress from per-and poly-fluoroalkyl substances (PFASs). The findings reveal that PFASs exposure induces oxidative damage and inhibits the growth of I. pseudacorus. However, AMF symbiosis enhances plant tolerance to PFAS stress by modulating oxidative responses. AMF treatment not only promoted plant growth but also improved photosynthetic efficiency under PFAS exposure. Compared to non-AMF treatment, those with AMF treatment exhibited significantly increased levels of peroxidases and antioxidant enzymes, including peroxidase and superoxide dismutase, along with a notable reduction in lipid peroxidation. Additionally, AM symbiosis markedly enhanced the efficacy of CWs in the remediation of wastewater under PFASs-induced stress, with removal efficiencies for COD, TP, TN, and NH4+-N increasing by 19-34%, 67-180%, 106-137%, and 25-95%, respectively, compared to the AMF- treatments. In addition, the metabolic pathways of PFASs appeared to be influenced by their carbon chain length, with long-chain PFASs like perfluorooctanoic acid (PFOA) and perfluoro anionic acid (PFNA) exhibiting more complex pathways compared to short-chain PFASs such as perfluoro acetic acid (PFPeA), and perfluoro hexanoic acid (PFHpA). These results suggest that AMF-plant symbiosis can enhance plant resilience against PFAS-induced stress and improve the pollutant removal efficiency of CWs. This study highlights the significant potential of AMF in enhancing environmental remediation strategies, providing new insights for the more effective management of PFAS-contaminated ecosystems.

Design of substation grounding grid in CFETR.

This paper aims to propose a method for the design of the substation grounding grid in China Fusion Engineering Test Reactor (CFETR). In order to evaluate the safety of the grounding grid, Electrical Transient Analysis Program (ETAP) was used to simulate the fault current, contact voltage, and step voltage, and the results are compared with theoretical calculations to verify the correctness of the design. This will help reduce faults caused by the defects of grounding grid This method is special in that the designed grounding grid not only meets the requirements of relevant standards, but also reduces the number of conductors. During the design process, factors such as voltage level, fault location, and soil resistivity were fully considered to adapt to different occasions. This method can also guide the design and renovation of grounding grids for other buildings in CFETR.

Second transplantation after kidney graft loss in primary hyperoxaluria type 2: a pedigree study and mutation analysis.

BACKGROUND: Primary hyperoxaluria type 2 (PH2) is a rare disorder caused by GRHPR mutations. Research on the mutation spectrum and pedigree of PH2 helps in comprehending its pathogenesis and clinical outcomes, guiding clinical diagnosis and treatment. METHODS: We report a case of PH2 with a three-generational pedigree. The GRHPR genotypes of the family members were confirmed by Sanger sequencing. Urine and blood samples were collected for biochemical analysis. Computational analysis was performed to assess the pathogenicity of the mutations. Cellular experiments based on site-directed mutagenesis were conducted to confirm the effect of mutations on GRHPR expression, activity, and subcellular localization. RESULTS: The proband underwent her first kidney transplantation in 2015, and experienced recurrent urinary tract infections and urolithiasis postoperatively. Graft failure occurred in 2018. Whole exome sequencing identified compound heterozygous GRHPR mutations p.G160E/p.P203Rfs*7. The patient underwent a second kidney transplantation in 2019 and maintained good graft function with urine dilution measures. Notably, her brother and sister carried the same mutations; however, only the proband progressed to renal failure. Computational analysis suggested that p.G160E reduced the affinity of GRHPR for coenzymes. Cellular experiments indicated that p.G160E reduced GRHPR activity (p < 0.001), whereas p.P203Rfs*7 not only suppressed expression (p < 0.001) and reduced activity (p < 0.001), but also facilitated protein aggregation. Based on our results, the variant p.G160E was classified as 'pathogenic' according to ACMG guidelines. CONCLUSIONS: Our findings suggest that treatment strategies for the long-term prevention of oxalate nephropathy should be developed for patients with PH2 receiving isolated kidney transplantation. Moreover, the pathogenicity of the compound heterozygous GRHPR mutations p.G160E/p.P203Rfs*7 was also validated.

Potential Anti-Obesity Effect of Hazel Leaf Extract in Mice and Network Pharmacology of Selected Polyphenols.

Background: Obesity is gradually becoming a widespread health problem, and treatment using natural compounds has seen an increasing trend. As a by-product of hazelnut, hazel leaf is usually disposed of as waste, but it is widely used in traditional and folk medicines around the world. Aim of this study: Based on previous studies, the effects of the regulation of lipid metabolism and the mechanism of hazel leaf polyphenol extraction obesity were investigated. Methods: In this study, a high-fat diet-fed mouse model of obesity and 3T3-L1 preadipocytes were established. The ameliorative effects of the hazel leaf polyphenol extract on obesity and the regulating lipid metabolisms were explored based on network pharmacology, gut microbiota, and molecular docking. Results: Network pharmacology showed that hazel leaf polyphenols may play a role by targeting key targets, including PPARγ, and regulating the PPAR signaling pathway. They significantly improved body weight gain, the liver index, and adiposity and lipid levels; regulated the gut microbiota and short-chain fatty acid contents; down-regulated the expression of lipid synthesis proteins SREBP1c, PPARγ, and C/EBP-α; and up-regulated the expression of p-AMPK in obese mice. They inhibited the differentiation of 3T3-L1 cells, and the expression of related proteins is consistent with the results in vivo. The molecular docking results indicated that gallic acid, quercetin-3-O-beta-D-glucopyranoside, quercetin, myricetin, and luteolin-7-O-glucoside in the hazel leaf polyphenol extract had strong binding activities with PPARγ, C/EBP-α, and AMPK. Conclusions: The results demonstrate that the hazel leaf polyphenol extract can improve obesity by regulating lipid metabolism, which provides a valuable basis for developing health products made from hazel leaf polyphenols in the future.

Aquaporin-1 Facilitates Macrophage M1 Polarization by Enhancing Glycolysis Through the Activation of HIF1α in Lipopolysaccharide-Induced Acute Kidney Injury.

This study aimed to investigate how aquaporin 1 (AQP1) modulates hypoxia-inducible factor-1α (HIF1α) to promote glycolysis and drive the M1 polarization of macrophages. Within 12 h post-treatment with LPS to induce acute kidney injury in rats, a significant upregulation of AQP1 and HIF1α protein levels was noted in serum and kidney tissues. This elevation corresponded with a decrease in blood glucose concentrations and an enhancement of glycolytic activity relative to the control group. Furthermore, there was a pronounced reduction in the circulating levels of the anti-inflammatory cytokine IL-10, accompanied by an upregulation in the levels of the pro-inflammatory cytokines IL-6 and TNF-α. The administration of an HIF1α inhibitor reversed these effects, which did not affect the production of AQP1 protein. In cellular assays, AQP1 knockdown mitigated the increase in HIF1α expression induced by LPS. Furthermore, the suppression of HIF1α with PX-478 led to decreased expression levels of Hexokinase 2 (HK2) and Lactate Dehydrogenase A (LDHA), indicating that AQP1 regulates glycolysis through HIF1α. M1 polarization of macrophages was reduced by AQP1 knockdown and was further diminished by the addition of an HIF1α inhibitor. Inhibition of the glycolytic process not only weakened M1 polarization but also promoted M2 polarization, thereby reducing the release of inflammatory cytokines. These findings provide a novel perspective for developing therapeutic strategies that target AQP1 and HIF1α, potentially improving the treatment of sepsis-associated AKI.

N6-methyladenosine-mediated upregulation of LNCAROD confers radioresistance in esophageal squamous cell carcinoma through stabilizing PARP1.

BACKGROUND: Radiotherapy is a primary therapeutic modality for esophageal squamous cell carcinoma (ESCC), but its effectiveness is still restricted due to the resistance of cancer cells to radiation. Long non-coding RNAs (lncRNAs) and N6-methyladenosine (m6A) have been shown to play significant roles in tumour radioresistance. However, the precise manifestation and role of m6A-modified lncRNAs in ESCC radioresistance remain unclear. METHODS: Bioinformatics analysis was conducted to identify m6A-modified lncRNAs implicated in the radioresistance of ESCC. A series of functional experiments were performed to investigate the function of LNCAROD in ESCC. Methylated RNA immunoprecipitation, chromatin isolation by RNA purification-mass spectrometry, RNA immunoprecipitation, and co-immunoprecipitation experiments were performed to explore the mechanism of m6A-mediated upregulation of LNCAROD expression and the downstream mechanism enhancing the radioresistance of ESCC. The efficacy of LNCAROD in vivo was assessed using murine xenograft models. RESULTS: Herein, we identified LNCAROD as a novel METTL3-mediated lncRNA that enhanced radioresistance in ESCC cells and was post-transcriptionally stabilised by YTHDC1. Moreover, we confirmed that LNCAROD prevented ubiquitin-proteasome degradation of PARP1 protein by facilitating PARP1-NPM1 interaction, thereby contributing to homologous recombination-mediated DNA double-strand breaks repair and enhancing the radiation resistance of ESCC cells. Silencing LNCAROD in a nude mouse model of ESCC in vivo resulted in slower tumour growth and increased radiosensitivity. CONCLUSION: Our findings enhance the understanding of m6A-modified lncRNA-driven machinery in ESCC radioresistance and underscore the significance of LNCAROD in this context, thereby contributing to the development of a potential therapeutic target for ESCC patients.

Disturbing microtubule-endoplasmic reticulum dynamics by gold nanoclusters for improved triple-negative breast cancer treatment.

Microtubules are highly dynamic structures, and their dynamic instability is indispensable for not only cell growth and movement, but also stress responses, such as endoplasmic reticulum (ER) stress. Docetaxel, a microtubule targeting agent (MTA), is the first-line drug for cancer treatment by simultaneously promoting microtubule dysregulation- and ER stress-induced cell death. However, it also causes adverse effects and drug resistance, especially in triple-negative breast cancer (TNBC) with a poor prognosis and high mortality rate. In this study, we developed a peptide-templated gold nanocluster, namely GA. GA significantly sensitizes TNBC cells to docetaxel, causing severe cell death. This effect is further validated by a 3D tumor spheroid model. Mechanistically, GA disrupted microtubule dynamic instability, meanwhile promoting PERK-mediated ER stress. Interestingly, ER stress inhibitors profoundly suppressed microtubule dysregulation, suggesting a retrograde regulation of ER stress on microtubules. In vivo, the combined administration of docetaxel and GA significantly suppresses tumor growth while docetaxel alone cannot. GA similarly elevated the level of caspases and PERK within tumors as in vitro. Importantly, GA treatment also profoundly promoted the production of anti-tumor inflammatory cytokines. Collectively, we developed an ER-microtubule regulatory nanomaterial that enhanced the therapeutic effect of docetaxel by elevating tumor cell death and anti-tumor cytokine production, providing a potential supplemental strategy for TNBC treatment.

Non-dietary exposure to phthalates in primary school children: Risk and correlation with anthropometric indices, cardiovascular and respiratory diseases.

Phthalates are endocrine disruptors of increasing concern for human health; however, previous studies have only assessed the association between internal exposure and human health. We aimed to assess the non-carcinogenic and carcinogenic risks of non-dietary exposure to phthalates in indoor environments among primary school children and their correlations with health indicators. A study involving 54 children was conducted in Jinan, Shandong Province, China. Questionnaires and health examinations were conducted, dust in hard-to-clean corners of students' classrooms and homes was collected, and airborne phthalates in the middle of classrooms and family living rooms were sampled. The gas-phase phthalate concentrations, individual exposure, and non-carcinogenic and carcinogenic risks were calculated. Associations were estimated using linear mixed models. The findings revealed that phthalates posed a non-carcinogenic risk to 7.4 % of the children and a moderate carcinogenic risk to 27.8 % of the children, with higher non-carcinogenic and carcinogenic risks to girls than to boys. Five phthalates were negatively correlated with body mass index, dimethyl phthalate and diethyl phthalate (DEP) were significantly correlated with waist circumference, and di-iso-butyl phthalate (DiBP) was negatively correlated with hip circumference. DiBP, di-n-butyl phthalate, and DEP, were significantly correlated with cardiovascular disease, DEP and di (2-n-butoxyethyl) phthalate were correlated with decreased lung function, and di-n-octyl phthalate influenced airway inflammation. The findings indicated that phthalate exposure may negatively impact children's health, thereby warranting further comprehensive research on the health effects of these chemicals.

NDUFS3 alleviates oxidative stress and ferroptosis in sepsis induced acute kidney injury through AMPK pathway.

In recent years, ferroptosis has been found to play an important role in various acute kidney injury (AKI). However, relatively little research has been conducted on sepsis-induced acute kidney injury (SI-AKI). As an important trigger of ferroptosis, how mitochondrial damage plays a regulatory role in SI-AKI is still unclear. To explore the potential relationship between mitochondria and ferroptosis, we established a SI-AKI rat model by intraperitoneal injection of lipopolysaccharide (LPS). Transcriptome sequencing was used to detect changes in gene transcription levels in the control group, LPS 3 h group, LPS 6 h group and LPS 12 h group. The severity of kidney injury was determined based on serum creatinine (CRE), blood urea nitrogen (BUN), tissue HE staining, TUNEL staining and inflammatory factor levels. Cytoscape software was utilized to screen several mitochondria-related HUB genes, and NADH dehydrogenase [ubiquinone] ferrithionein 3 (NDUFS3) was selected for subsequent validation due to its novelty and feasibility. qRT-PCR, Western blot was employed to evaluate the expression of NDUFS3 in kidney tissues. GO enrichment analysis revealed that up-regulated genes in the LPS 12 h group were enriched in several cell death terms while down-regulated genes were enriched in lipid metabolic process and oxidation-reduction progress terms. Furthermore, Western blot, IHC, MDA, GSH and iron content levels were used to assess ferroptosis in the kidney tissue of the SI-AKI rats, dihydroethidium (DHE) assay and ATP kit were used to assess mitochondrial ROS levels and mitochondrial function. To further validate the function of NDUFS3, we constructed overexpression rats using hydrodynamic method by tail vein injection of pc DNA3.1-NDUFS3 overexpression plasmid. we utilized LPS to stimulate HK-2 cells and establish an in vitro model. We then overexpressed NDUFS3 using pcDNA 3.1. The overexpression of NDUFS3 was found to inhibit LPS-induced ferroptosis and mitochondrial damage in HK-2 cells, as evidenced by Western blot, MDA, GSH, divalent iron, ROS levels, Mitosox red, ATP content and transmission electron microscopy. Finally, the use of Compound C to inhibit AMPK in HK-2 cells demonstrated that NDUFS3 plays a protective role through the AMPK pathway. Therefore, our study supports the emerging role of NDUFS3 in SI-AKI, providing new potential mitochondria-related targets for the treatment of SI-AKI.

Co-Designing Remote Patient Monitoring Technologies for Inpatients: Systematic Review.

BACKGROUND: The co-design of health technology enables patient-centeredness and can help reduce barriers to technology use. OBJECTIVE: The study objectives were to identify what remote patient monitoring (RPM) technology has been co-designed for inpatients and how effective it is, to identify and describe the co-design approaches used to develop RPM technologies and in which contexts they emerge, and to identify and describe barriers and facilitators of the co-design process. METHODS: We conducted a systematic review of co-designed RPM technologies for inpatients or for the immediate postdischarge period and assessed (1) their effectiveness in improving health outcomes, (2) the co-design approaches used, and (3) barriers and facilitators to the co-design process. Eligible records included those involving stakeholders co-designing RPM technology for use in the inpatient setting or during the immediate postdischarge period. Searches were limited to the English language within the last 10 years. We searched MEDLINE, Embase, CINAHL, PsycInfo, and Science Citation Index (Web of Science) in April 2023. We used the Joanna Briggs Institute critical appraisal checklist for quasi-experimental studies and qualitative research. Findings are presented narratively. RESULTS: We screened 3334 reports, and 17 projects met the eligibility criteria. Interventions were designed for pre- and postsurgical monitoring (n=6), intensive care monitoring (n=2), posttransplant monitoring (n=3), rehabilitation (n=4), acute inpatients (n=1), and postpartum care (n=1). No projects evaluated the efficacy of their co-designed RPM technology. Three pilot studies reported clinical outcomes; their risk of bias was low to moderate. Pilot evaluations (11/17) also focused on nonclinical outcomes such as usability, usefulness, feasibility, and satisfaction. Common co-design approaches included needs assessment or ideation (16/17), prototyping (15/17), and pilot testing (11/17). The most commonly reported challenge to the co-design process was the generalizability of findings, closely followed by time and resource constraints and participant bias. Stakeholders' perceived value was the most frequently reported enabler of co-design. Other enablers included continued stakeholder engagement and methodological factors (ie, the use of flexible mixed method approaches and prototyping). CONCLUSIONS: Co-design methods can help enhance interventions' relevance, usability, and adoption. While included studies measured usability, satisfaction, and acceptability-critical factors for successful implementation and uptake-we could not determine the clinical effectiveness of co-designed RPM technologies. A stronger commitment to clinical evaluation is needed. Studies' use of diverse co-design approaches can foster stakeholder inclusivity, but greater standardization in co-design terminology is needed to improve the quality and consistency of co-design research.

Xenobiotic metabolism activity of gut microbiota from six marine species: Combined taxonomic, metagenomic, and in vitro transformation analysis.

The xenobiotic metabolism driven by the gut microbiota significantly regulates the bioavailability and toxic effects of environmental pollutants such as plasticizers on aquatic organisms. However, it is still unknown whether the gut microbiota can exhibit variable metabolic ability across host species and which functional bacteria and genes are involved in xenobiotic transformation. This study investigated the enriched gut microbiota community composition and diversity of in vitro enrichment cultures from 6 marine species, namely, yellowfin seabream (Acanthopagrus latus), thorn fish (Terapon jarbua), shortnose ponyfish (Leiognathus brevirostris), mussel (Perna viridis), prawn (Parapenaeopsis hungerfordi) and crab (Charybdis riversandersoni). Pseudomonadota, Bacteroidota and Bacillota were the dominant phyla and Enterobacter, Raoultella, Klebsiella, Dysgonomanas and Lactococcus were the dominant genera in the enriched flora according to 16S rRNA sequencing. Furthermore, the metagenomic results revealed that all enriched gut microbiota presented metabolic genes for carbohydrates, amino acids, lipids, and xenobiotics. In particular, the gut microbiota of yellowfin seabream had the highest abundance of glycoside hydrolase family genes and CYP450 enzyme genes. Klebsiella was identified as a common potential degrader of xenobiotic metabolism. In addition, the Biolog plate test system confirmed that the gut microbiota can metabolize various carbon sources and drive the xenobiotic transformation. According to AWCD analysis of community level physiological profiling (CLPP), yellowfin seabream > mussel > prawn > shortnose ponyfish > crab > thorn fish. The gut microbiota of yellowfin seabream presented a stronger metabolic profile of phthalates and bisphenol analogs which reflected by their AWCD results and concentration variations. Overall, our results demonstrated the diverse metabolic abilities of the gut microbiota from six marine organisms and their potential for altering of the fate of xenobiotics in the ecosystem on the basis of combined taxonomic, metagenomic, and in vitro transformation analysis.

Rapid on-site detection of echinococcosis and schistosomiasis based on RPA.

BACKGROUND: Echinococcosis and schistosomiasis, caused by parasitic worms, pose significant threats to millions of people in the world. Rapid and effective pathogen detection and epidemic control by public health authorities are urgently needed. OBJECTIVES: In this study, we aimed to develop rapid on-site detection method to detect echinococcosis and schistosomiasis. METHODS: Recombinase polymerase amplification (RPA) was utilised to examine its efficacy of detection of echinococcosis and schistosomiasis. FINDINGS: The detection probes for RPA were created through comparing parasitic genomes from international genomic data and the sequences generated by our group. We established an optimised RPA on-site testing platform, which significantly reduces the detection time (less than 30 min) and simplifies the operation (free of expensive equipment) as compared to traditional polymerase chain reaction (PCR) method. MAIN CONCLUSIONS: This RPA detection platform in our study for identifying echinococcosis or schistosomiasis pathogens would be greatly applicable for epidemic investigation, border screening, and early clinical diagnosis.

Urinary Concentrations of Organophosphate Flame-Retardant Metabolites in the US Population.

Importance: Organophosphate flame retardants (OPFRs) are an important group of pollutants associated with endocrine disorders, cancer, and nephrotoxicity. However, temporal trends in OPFR metabolite concentrations remain understudied. Objectives: To examine changes in urinary concentrations of OPFR metabolites among US children, youths, and adults from 2011 to 2020, and to evaluate whether sociodemographic factors were associated with variations in temporal trends. Design, Setting, and Participants: This population-based cross-sectional study used data from 4 US National Health and Nutrition Examination Survey (NHANES) cycles (2011-2012, 2013-2014, 2015-2016, and 2017-2020 [to March 2020 before the COVID-19 pandemic]). The study included children and youths (aged 6-19 years) and adults (aged ≥20 years) with valid urinary concentrations of the following OPFR metabolites: bis(2-chloroethyl) phosphate (BCEtP), bis(1-chloro-2-propyl) phosphate (BCPP), diphenyl phosphate (DPhP), and dibutyl phosphate (DBuP). Data analysis was performed between February and May 2024. Exposures: Calendar year and key sociodemographic subgroups (age, race and ethnicity, sex, educational attainment, and poverty-to-income ratio). Main Outcomes and Measures: The main outcome was urinary concentrations of OPFR metabolites among children, youths, and adults. Survey-weighted linear regression models were applied to estimate trends. Results: The study population of 10 549 NHANES participants included 3154 children and youths (mean [SE] age, 12.5 [0.1] years; 51.2% were male) and 7395 adults (mean [SE] age, 47.8 [0.4] years; 52.0% were women). Among children and youths, mean (95% CI) BCEtP concentrations decreased from 0.68 (0.60-0.77) µg/L in 2011-2012 to 0.41 (0.37-0.45) µg/L in 2017-2020 (P for trend < .001). Among adults, mean (95% CI) BCEtP concentrations decreased from 0.43 (0.37-0.50) µg/L in 2011-2012 to 0.29 (0.27-0.33) µg/L in 2017-2020 (P for trend < .001), and mean BCPP concentrations decreased from 0.15 (0.14-0.17) µg/L to 0.13 (0.12-0.14) µg/L (P for trend = .002). Parent level of educational attainment was associated with concentrations of BCPP and BCEtP among children and youths; however, no significant differences among adults were observed. Conclusions and Relevance: This study identified variations in temporal trends in urinary concentrations of OPFR metabolites among the US population from 2011 to 2020. In addition, substantial disparities in exposure levels persisted among children with different levels of parent educational attainment. These findings suggest that policy makers should consider socioeconomic factors to further reduce OPFR exposure and promote equity, ensuring a safe living environment for all individuals.

Development and Optimization of Thin-Lithium-Metal Anodes with a Lithium Lanthanum Titanate Stabilization Coating for Enhancement of Lithium-Sulfur Battery Performance.

Lithium-ion batteries are dominating high-energy-density energy storage for 30 years. However, their development approaches theoretical limits, spurring the development of lithium-sulfur cells that achieve high energy densities through reversible electrochemical conversion reactions. Nevertheless, the commercialization of lithium-sulfur cells is hindered by practical challenges associated primarily with the use of thick-lithium anodes, low-loading sulfur cathodes, and high electrolyte-to-sulfur ratios, which prevent realization of the cells' full potential in terms of electrochemical and material performance. To solve these extrinsic and intrinsic problems, the effect of lithium-metal thickness on the electrochemical behavior of lithium-sulfur cells with high-loading sulfur cathodes in lean-electrolyte configurations is investigated. Specifically, lithium lanthanum titanate (LLTO), a solid electrolyte, is utilized to form an ionically/electronically conductive coating to stabilize lithium-metal anodes, thereby enhancing their lithium-ion pathways and interfacial charge transfer. Electrochemical analyses reveal that an LLTO coating significantly reduces excessive reactions between lithium metal and an electrolyte, thereby minimizing lithium consumption and electrolyte depletion. Further, LLTO-stabilized lithium anodes improve lithium-sulfur cell performance, and most importantly, allow the fabrication of thin-lithium, high-loading-sulfur cells that open a pathway toward high-energy-density batteries.

Adaptive critic design for safety-optimal FTC of unknown nonlinear systems with asymmetric constrained-input.

Safe fault tolerant control is one of the key technologies to improve the reliability of dynamic complex nonlinear systems with limited inputs, which is hard to solve and definitely a great challenge to tackle. Thus the paper presents a novel safety-optimal FTC (Fault Tolerant Control) approach for a category of completely unknown nonlinear systems incorporating actuator fault and asymmetric constrained-input, which can guarantee the system's operation within a safe range while showcasing optimal performance. Firstly, a CBF (Control Barrier Function) is incorporated into the cost function to penalize unsafe behaviors, and then we translate the intractable safety-optimal FTC problem into a differential ZSG (Zero-Sum Game) problem by defining the control input and the actuator fault as two opposing sides. Secondly, a neural-network-based identifier is employed to reconstruct system dynamics using system data, and the resolution of handling asymmetric constrained-input with the introduced non-quadratic cost function is achieved through the design of an adaptive critic scheme, aiming to reduce computational expenses accordingly. Finally, through the theoretical stability analysis, it is demonstrated that all signals in the closed-loop system are consistently UUB (Uniformly Ultimately Bounded). Furthermore, the proposed method's effectiveness is also verified in the simulation experiments conducted on a model of a single-link robotic arm system with actuator failure. The result shows that the algorithm can fulfill the safety-optimal demand of fault tolerant control in fault system with asymmetric constrained-input.

Exact Ansatz of Fermion-Boson Systems for a Quantum Device.

We present an exact Ansatz for the eigenstate problem of mixed fermion-boson systems that can be implemented on quantum devices. Based on a generalization of the electronic contracted Schrödinger equation (CSE), our approach guides a trial wave function to the ground state of any arbitrary mixed Hamiltonian by directly measuring residuals of the mixed CSE on a quantum device. Unlike density functional and coupled cluster theories applied to electron-phonon or electron-photon systems, the accuracy of our approach is not limited by the unknown exchange-correlation functional or the uncontrolled form of the exponential Ansatz. To test the performance of the method, we study the Tavis-Cummings model, commonly used in polaritonic quantum chemistry. Our results demonstrate that the CSE is a powerful tool in the development of quantum algorithms for solving general fermion-boson many-body problems.

Cross-subject emotion recognition in brain-computer interface based on frequency band attention graph convolutional adversarial neural networks.

BACKGROUND: Emotion is an important area in neuroscience. Cross-subject emotion recognition based on electroencephalogram (EEG) data is challenging due to physiological differences between subjects. Domain gap, which refers to the different distributions of EEG data at different subjects, has attracted great attention for cross-subject emotion recognition. COMPARISON WITH EXISTING METHODS: This study focuses on narrowing the domain gap between subjects through the emotional frequency bands and the relationship information between EEG channels. Emotional frequency band features represent the energy distribution of EEG data in different frequency ranges, while relationship information between EEG channels provides spatial distribution information about EEG data. NEW METHOD: To achieve this, this paper proposes a model called the Frequency Band Attention Graph convolutional Adversarial neural Network (FBAGAN). This model includes three components: a feature extractor, a classifier, and a discriminator. The feature extractor consists of a layer with a frequency band attention mechanism and a graph convolutional neural network. The mechanism effectively extracts frequency band information by assigning weights and Graph Convolutional Networks can extract relationship information between EEG channels by modeling the graph structure. The discriminator then helps minimize the gap in the frequency information and relationship information between the source and target domains, improving the model's ability to generalize. RESULTS: The FBAGAN model is extensively tested on the SEED, SEED-IV, and DEAP datasets. The accuracy and standard deviation scores are 88.17% and 4.88, respectively, on the SEED dataset, and 77.35% and 3.72 on the SEED-IV dataset. On the DEAP dataset, the model achieves 69.64% for Arousal and 65.18% for Valence. These results outperform most existing models. CONCLUSIONS: The experiments indicate that FBAGAN effectively addresses the challenges of transferring EEG channel domain and frequency band domain, leading to improved performance.

Causal associations between constipation and pan-cancer: a bidirectional Mendelian randomization study.

Objective: Observational studies have suggested a potential association between constipation and several cancers. However, the causal relationship between constipation and cancer remains unclear. The purpose of this study is to explore the potential causal relationship between constipation and pan-cancer using Mendelian Randomization (MR) methods. Methods: We performed a bidirectional MR analysis using publicly available summary data from Genome-Wide Association Studies (GWAS) statistics. The Inverse Variance Weighted (IVW) method was used as the main analysis method. We also used four MR methods: MR-Egger, Weighted Median, MR-PRESSO and MR.RAPS. Simultaneously, MR-Egger regression, Cochran's Q test and MR-PRESSO Global test were used to estimate the pleiotropy and heterogeneity of SNPs. In addition, we performed "leave-one-out" analyses" to avoid bias caused by horizontal pleiotropy of individual SNPs. Results: MR analysis revealed a potential causal association between constipation and the risk of colorectal cancer (CRC) [IVW (OR= 1.0021 (1.0003, 1.0039), P= 0.0234)], lung cancer (LC) [IVW (OR=1.0955 (1.0134, 1.1843), P=0.0218)], Oral cavity and pharyngeal cancer (OPC) [IVW (OR=1.4068 (1.0070, 1.9652), P=0.0454)], and Pancreatic cancer (PC) [IVW (OR=1.5580 (1.0659, 2.2773), P=0.0221)]. In addition, we explored causal relationships between constipation and 12 other types of cancers, including gastric cancer, esophageal cancer, skin melanoma and so on. All five methods yielded no evidence of a causal association between constipation and the risk of these cancer types. In the reverse MR analysis, there was no evidence of a causal association between cancer and the risk of constipation for all five methods. Conclusion: Our bidirectional MR study suggests a potential relationship between constipation and an increased risk of CRC, LC OPC and PC. The underlying mechanisms behind these associations will need to be explored in future experimental studies.