Sertoli cells are the source of stem cell factor for spermatogenesis.

Several cell types have been proposed to create the required microenvironment for spermatogenesis. However, expression patterns of the key growth factors produced by these somatic cells have not been systematically studied and no such factor has been conditionally deleted from its primary source(s), raising the question of which cell type(s) are the physiological sources of these growth factors. Here, using single-cell RNA sequencing and a series of fluorescent reporter mice, we found that stem cell factor (Scf), one of the essential growth factors for spermatogenesis, was broadly expressed in testicular stromal cells, including Sertoli, endothelial, Leydig, smooth muscle and Tcf21-CreER+ stromal cells. Both undifferentiated and differentiating spermatogonia were associated with Scf-expressing Sertoli cells in the seminiferous tubule. Conditional deletion of Scf from Sertoli cells, but not any other Scf-expressing cells, blocked the differentiation of spermatogonia, leading to complete male infertility. Conditional overexpression of Scf in Sertoli cells, but not endothelial cells, significantly increased spermatogenesis. Our data reveal the importance of anatomical localization for Sertoli cells in regulating spermatogenesis and that SCF produced specifically by Sertoli cells is essential for spermatogenesis.

Preoxidation and Prilling Combined with Doping Strategy to Build High-Performance Recycling Spent LiFePO4 Materials.

Direct regeneration has gained much attention in LiFePO4 battery recycling due to its simplicity, ecofriendliness, and cost savings. However, the excess carbon residues from binder decomposition, conductive carbon, and coated carbon in spent LiFePO4 impair electrochemical performance of direct regenerated LiFePO4. Herein, we report a preoxidation and prilling collaborative doping strategy to restore spent LiFePO4 by direct regeneration. The excess carbon is effectively removed by preoxidation. At the same time, prilling not only reduces the size of the primary particles and shortens the diffusion distance of Li+ but also improves the tap density of the regenerated materials. Besides, the Li+ transmission of the regenerated LiFePO4 is further improved by Ti4+ doping. Compared with commercial LiFePO4, it has excellent low-temperature performance. The collaborative strategy provides a new insight into regenerating high-performance spent LiFePO4.

High-Entropy Configuration Strategy to Build High Performance Na-Ion Layered Oxide Cathodes Derived from Simple Techniques.

Layered transition metal oxides are commonly used as the cathode materials in sodium-ion batteries due to their low cost and easy manufacturing. However, the application is hindered by poor rate performance and complex phase transitions. To address these challenges, a new seven-component high-entropy layered oxide cathode material, O3-NaNi0.25Fe0.15Mn0.3Ti0.1Sn0.05Co0.05Li0.1O2 (HEO) has been developed. The entropy stabilization effect plays a crucial role in improving the performance of electrochemical systems and the stability of structures. The HEO exhibits a specific discharge capacity of 154.1 mA h g-1 at 0.1 C and 94.5 mA h g-1 at 7 C. In-situ and ex-situ XRD results demonstrate that the HEO effectively retards complex phase transitions. This work provides a high-entropy design for the storage materials with a high energy density. Meanwhile, it eliminates industry doubts about the performance of sodium ion layered oxide cathode materials.

Paternal genetic variants and risk of obstructive heart defects: A parent-of-origin approach.

Previous research on risk factors for obstructive heart defects (OHDs) focused on maternal and infant genetic variants, prenatal environmental exposures, and their potential interaction effects. Less is known about the role of paternal genetic variants or environmental exposures and risk of OHDs. We examined parent-of-origin effects in transmission of alleles in the folate, homocysteine, or transsulfuration pathway genes on OHD occurrence in offspring. We used data on 569 families of liveborn infants with OHDs born between October 1997 and August 2008 from the National Birth Defects Prevention Study to conduct a family-based case-only study. Maternal, paternal, and infant DNA were genotyped using an Illumina Golden Gate custom single nucleotide polymorphism (SNP) panel. Relative risks (RR), 95% confidence interval (CI), and likelihood ratio tests from log-linear models were used to estimate the parent-of-origin effect of 877 SNPs in 60 candidate genes in the folate, homocysteine, and transsulfuration pathways on the risk of OHDs. Bonferroni correction was applied for multiple testing. We identified 3 SNPs in the transsulfuration pathway and 1 SNP in the folate pathway that were statistically significant after Bonferroni correction. Among infants who inherited paternally-derived copies of the G allele for rs6812588 in the RFC1 gene, the G allele for rs1762430 in the MGMT gene, and the A allele for rs9296695 and rs4712023 in the GSTA3 gene, RRs for OHD were 0.11 (95% CI: 0.04, 0.29, P = 9.16x10-7), 0.30 (95% CI: 0.17, 0.53, P = 9.80x10-6), 0.34 (95% CI: 0.20, 0.57, P = 2.28x10-5), and 0.34 (95% CI: 0.20, 0.58, P = 3.77x10-5), respectively, compared to infants who inherited maternally-derived copies of the same alleles. We observed statistically significant decreased risk of OHDs among infants who inherited paternal gene variants involved in folate and transsulfuration pathways.

Polystyrene nanoplastics aggravates lipopolysaccharide-induced apoptosis in mouse kidney cells by regulating IRE1/XBP1 endoplasmic reticulum stress pathway via oxidative stress.

Nanoplastics (NPs) pollution poses a huge threat to the ecosystem and has become one of the environmental pollutants that have attracted much attention. There is increasing evidence that both oxidative stress and endoplasmic reticulum stress (ERS) are associated with polystyrene nanoplastics (PS-NPs) exposure. Lipopolysaccharide (LPS) has been shown to induce apoptotic damage in various tissues, but whether PS-NPs can aggravate LPS-induced apoptosis in mouse kidneys through oxidative stress-regulated inositol-requiring enzyme 1 (IRE1)/X-box binding protein 1 (XBP1) ERS pathway remains unclear. In this study, based on the establishment of in vitro and in vivo PS-NPs and LPS exposure models alone and in combination in mice and HEK293 cells, the effects and mechanisms of PS-NPs on LPS-induced renal cell apoptosis were investigated. The results showed that PS-NPs could aggravate LPS-induced apoptosis. PS-NPs/LPS can induce ERS through oxidative stress, activate the IRE1/XBP1 pathway, and promote the expression of apoptosis markers (Caspase-3 and Caspase-12). Kidney oxidative stress, ERS, and apoptosis in PS-NPs + LPS combined exposure group were more severe than those in the single exposure group. Interestingly, 4-phenylbutyric acid-treated HEK293 cells inhibited the expression of the IRE1/XBP1 ERS pathway and apoptotic factors in the PS-NPs + LPS combined exposure group. N-acetyl-L-cysteine effectively blocked the activation of the IRE1/XBP1 ERS pathway, suggesting that PS-NPs-induced oxidative stress is an early event that triggers ERS. Collectively, these results confirmed that PS-NPs aggravated LPS-induced apoptosis through the oxidative stress-induced IRE1/XBP1 ERS pathway. Our study provides new insights into the health threats of PS-NPs exposed to mammals and humans.

The role of FUT8-catalyzed core fucosylation in Alzheimer's amyloid-ß oligomer-induced activation of human microglia.

Fucosylation, especially core fucosylation of N-glycans catalyzed by α1-6 fucosyltransferase (fucosyltransferase 8 or FUT8), plays an important role in regulating the peripheral immune system and inflammation. However, its role in microglial activation is poorly understood. Here we used human induced pluripotent stem cells-derived microglia (hiMG) as a model to study the role of FUT8-catalyzed core fucosylation in amyloid-ß oligomer (AßO)-induced microglial activation, in view of its significant relevance to the pathogenesis of Alzheimer's disease (AD). HiMG responded to AßO and lipopolysaccharides (LPS) with a pattern of pro-inflammatory activation as well as enhanced core fucosylation and FUT8 expression within 24 h. Furthermore, we found increased FUT8 expression in both human AD brains and microglia isolated from 5xFAD mice, a model of AD-like cerebral amyloidosis. Inhibition of fucosylation in AßO-stimulated hiMG reduced the induction of pro-inflammatory cytokines, suppressed the activation of p38MAPK, and rectified phagocytic deficits. Specific inhibition of FUT8 by siRNA-mediated knockdown also reduced AßO-induced pro-inflammatory cytokines. We further showed that p53 binds to the two consensus binding sites in the Fut8 promoter, and that p53 knockdown abolished FUT8 overexpression in AßO-activated hiMG. Taken together, our evidence supports that FUT8-catalyzed core fucosylation is a signaling pathway required for AßO-induced microglia activation and that FUT8 is a component of the p53 signaling cascade regulating microglial behavior. Because microglia are a key driver of AD pathogenesis, our results suggest that microglial FUT8 could be an anti-inflammatory therapeutic target for AD.

TERC haploid cell reprogramming: a novel therapeutic strategy for aplastic anemia.

The telomerase RNA component (TERC) gene plays an important role in telomerase-dependent extension and maintenance of the telomeres. In the event of TERC haploinsufficiency, telomere length is often affected; this, in turn, can result in the development of progeria-related diseases such as aplastic anemia (AA) and congenital keratosis. Cell reprogramming can reverse the differentiation process and can, therefore, transform cells into pluripotent stem cells with stronger differentiation and self-renewal abilities; further, cell reprograming can also extend the telomere length of these cells, which may be crucial in the diagnosis and treatment of telomere depletion diseases such as AA. In this study, we summarized the effects of TERC haploid cell reprogramming on telomere length and the correlation between this alteration and the pathogenesis of AA; by investigating the role of cell reprogramming in AA, we aimed to identify novel diagnostic indicators and therapeutic strategies for patients with AA.

ADEIP: an integrated platform of age-dependent expression and immune profiles across human tissues.

Gene expression and immune status in human tissues are changed with aging. There is a need to develop a comprehensive platform to explore the dynamics of age-related gene expression and immune profiles across tissues in genome-wide studies. Here, we collected RNA-Seq datasets from GTEx project, containing 16 704 samples from 30 major tissues in six age groups ranging from 20 to 79 years old. Dynamic gene expression along with aging were depicted and gene set enrichment analysis was performed among those age groups. Genes from 34 known immune function categories and immune cell compositions were investigated and compared among different age groups. Finally, we integrated all the results and developed a platform named ADEIP (http://gb.whu.edu.cn/ADEIP or http://geneyun.net/ADEIP), integrating the age-dependent gene expression and immune profiles across tissues. To demonstrate the usage of ADEIP, we applied two datasets: severe acute respiratory syndrome coronavirus 2 and human mesenchymal stem cells-assoicated genes. We also included the expression and immune dynamics of these genes in the platform. Collectively, ADEIP is a powerful platform for studying age-related immune regulation in organogenesis and other infectious or genetic diseases.

Precision Nutrition and Cardiovascular Disease Risk Reduction: the Promise of High-Density Lipoproteins.

PURPOSE OF REVIEW: Emerging evidence supports the promise of precision nutritional approaches for cardiovascular disease (CVD) prevention. Here, we discuss current findings from precision nutrition trials and studies reporting substantial inter-individual variability in responses to diets and dietary components relevant to CVD outcomes. We highlight examples where early precision nutrition research already points to actionable intervention targets tailored to an individual's biology and lifestyle. Finally, we make the case for high-density lipoproteins (HDL) as a compelling next generation target for precision nutrition aimed at CVD prevention. HDL possesses complex structural features including diverse protein components, lipids, size distribution, extensive glycosylation, and interacts with the gut microbiome, all of which influence HDL's anti-inflammatory, antioxidant, and cholesterol efflux properties. Elucidating the nuances of HDL structure and function at an individual level may unlock personalized dietary and lifestyle strategies to optimize HDL-mediated atheroprotection and reduce CVD risk. RECENT FINDINGS: Recent human studies have demonstrated that HDL particles are key players in the reduction of CVD risk. Our review highlights the role of HDL and the importance of personalized therapeutic approaches to improve their potential for reducing CVD risk. Factors such as diet, genetics, glycosylation, and gut microbiome interactions can modulate HDL structure and function at the individual level. We emphasize that fractionating HDL into size-based subclasses and measuring particle concentration are necessary to understand HDL biology and for developing the next generation of diagnostics and biomarkers. These discoveries underscore the need to move beyond a one-size-fits-all approach to HDL management. Precision nutrition strategies that account for personalized metabolic, genetic, and lifestyle data hold promise for optimizing HDL therapies and function to mitigate CVD risk more potently. While human studies show HDL play a key role in reducing CVD risk, recent findings indicate that factors such as diet, genetics, glycosylation, and gut microbes modulate HDL function at the individual level, underscoring the need for precision nutrition strategies that account for personalized variability to optimize HDL's potential for mitigating CVD risk.

Construction of a Preoxidation and Cation Doping Regeneration Strategy to Improve Rate Performance Recycling Spent LiFePO4 Materials.

Efficient recycling of spent lithium-ion batteries (LIBs) is significant for solving environmental problems and promoting resource conservation. Economical recycling of LiFePO4 (LFP) batteries is extremely challenging due to the inexpensive production of LFP. Herein, we report a preoxidation combine with cation doping regeneration strategy to regenerate spent LiFePO4 (SLFP) with severely deteriorated. The binder, conductive agent, and residual carbon in SLFP are effectively removed through preoxidation treatment, which lays the foundation for the uniform and stable regeneration of LFP. Mg2+ doping is adopted to promote the diffusion efficiency of lithium ions, reduces the charge-transfer impedance, and further improves the electrochemical performance of the regenerated LFP. The discharge capacity of SLFP with severe deterioration recovers successfully from 43.2 to 136.9 mA h g-1 at 0.5 C. Compared with traditional methods, this technology is simple, economical, and environment-friendly. It provided an efficient way for recycling SLFP materials.

Examining the Relationship Between Sleep Apnea Diagnosis and Suicide Risk in Veterans With Traumatic Brain Injury: A VA TBI Model Systems Study.

OBJECTIVE: Obstructive sleep apnea (OSA) is a common sleep disorder in people with traumatic brain injury (TBI). Although sleep disturbances have been associated with an increased risk of suicide compared with the general population, the relationship between OSA and suicide risk after TBI is not well documented. In this study, we hypothesized that OSA diagnosis would predict suicide risk in veterans with TBI. SETTING: Five Veterans Affairs (VA) Polytrauma Rehabilitation Centers. PARTICIPANTS: Participants were drawn from the VA TBI Model Systems study, with follow-up interviews at year 1 ( n = 392), year 2 ( n = 444), year 5 ( n = 498), or year 10 ( n = 252) post-TBI (7.8%-14.5% follow-up attrition). DESIGN: This was a retrospective analysis from observational data using logistic regression with repeated measurements. Suicide ideation and suicide attempts were examined as outcomes at each follow-up to evaluate the relationship between OSA and suicide risk after adjusting for other risk factors determined a priori via literature review. MAIN MEASURES: Suicidal ideation (Patient Health Questionnaire-9 item 9), suicide attempt during the past year (self-reported), and OSA diagnosis (self-reported). RESULTS: Contrary to study hypotheses, OSA diagnosis had no statistically significant association with suicide ideation or attempt after accounting for known predictors. However, greater depression symptoms, headache severity, and pre-TBI suicidal ideation and attempts predicted suicide risk at follow-up after accounting for other predictors. CONCLUSIONS: Results of this study did not support a relationship between OSA and suicide risk, possibly due to methodological limitations of OSA measurement. Future research on this topic should include objective measures of OSA severity and OSA treatment including adherence. Although suicide is a low base rate occurrence, the impact is disastrous and further research is needed to mitigate suicide risk.

Advancements in Research on Constructing Physiological and Pathological Liver Models and Their Applications Utilizing Bioprinting Technology.

In recent decades, significant progress has been made in liver tissue engineering through the use of 3D bioprinting technology. This technology offers the ability to create personalized biological structures with precise geometric design capabilities. The complex and multifaceted nature of liver diseases underscores the need for advanced technologies to accurately mimic the physiological and mechanical characteristics, as well as organ-level functions, of liver tissue in vitro. Bioprinting stands out as a superior option over traditional two-dimensional cell culture models and animal models due to its stronger biomimetic advantages. Through the use of bioprinting, it is possible to create liver tissue with a level of structural and functional complexity that more closely resembles the real organ, allowing for more accurate disease modeling and drug testing. As a result, it is a promising tool for restoring and replacing damaged tissue and organs in the field of liver tissue engineering and drug research. This article aims to present a comprehensive overview of the progress made in liver tissue engineering using bioprinting technology to provide valuable insights for researchers. The paper provides a detailed account of the history of liver tissue engineering, highlights the current 3D bioprinting methods and bioinks that are widely used, and accentuates the importance of existing in vitro liver tissue models based on 3D bioprinting and their biomedical applications. Additionally, the article explores the challenges faced by 3D bioprinting and predicts future trends in the field. The progress of 3D bioprinting technology is poised to bring new approaches to printing liver tissue in vitro, while offering powerful tools for drug development, testing, liver disease modeling, transplantation, and regeneration, which hold great academic and practical significance.

Innovative approach to identify multigenomic and environmental interactions associated with birth defects in family-based hybrid designs.

Genes, including those with transgenerational effects, work in concert with behavioral, environmental, and social factors via complex biological networks to determine human health. Understanding complex relationships between causal factors underlying human health is an essential step towards deciphering biological mechanisms. We propose a new analytical framework to investigate the interactions between maternal and offspring genetic variants or their surrogate single nucleotide polymorphisms (SNPs) and environmental factors using family-based hybrid study design. The proposed approach can analyze diverse genetic and environmental factors and accommodate samples from a variety of family units, including case/control-parental triads, and case/control-parental dyads, while minimizing potential bias introduced by population admixture. Comprehensive simulations demonstrated that our innovative approach outperformed the log-linear approach, the best available method for case-control family data. The proposed approach had greater statistical power and was capable to unbiasedly estimate the maternal and child genetic effects and the effects of environmental factors, while controlling the Type I error rate against population stratification. Using our newly developed approach, we analyzed the associations between maternal and fetal SNPs and obstructive and conotruncal heart defects, with adjustment for demographic and lifestyle factors and dietary supplements. Fourteen and 11 fetal SNPs were associated with obstructive and conotruncal heart defects, respectively. Twenty-seven and 17 maternal SNPs were associated with obstructive and conotruncal heart defects, respectively. In addition, maternal body mass index was a significant risk factor for obstructive defects. The proposed approach is a powerful tool for interrogating the etiological mechanism underlying complex traits.

Perivenous Stellate Cells Are the Main Source of Myofibroblasts and Cancer-Associated Fibroblasts Formed After Chronic Liver Injuries.

BACKGROUND AND AIMS: Studies of the identity and pathophysiology of fibrogenic HSCs have been hampered by a lack of genetic tools that permit specific and inducible fate-mapping of these cells in vivo. Here, by single-cell RNA sequencing of nonparenchymal cells from mouse liver, we identified transcription factor 21 (Tcf21) as a unique marker that restricted its expression to quiescent HSCs. APPROACH AND RESULTS: Tracing Tcf21+ cells by Tcf21-CreER (Cre-Estrogen Receptor fusion protein under the control of Tcf21 gene promoter) targeted ~10% of all HSCs, most of which were located at periportal and pericentral zones. These HSCs were quiescent under steady state but became activated on injuries, generating 62%-67% of all myofibroblasts in fibrotic livers and ~85% of all cancer-associated fibroblasts (CAFs) in liver tumors. Conditional deletion of Transforming Growth Factor Beta Receptor 2 (Tgfbr2) by Tcf21-CreER blocked HSC activation, compromised liver fibrosis, and inhibited liver tumor progression. CONCLUSIONS: In conclusion, Tcf21-CreER-targeted perivenous stellate cells are the main source of myofibroblasts and CAFs in chronically injured livers. TGF-ß signaling links HSC activation to liver fibrosis and tumorigenesis.

Performance analysis of a spatial diversity coherent free-space optical communication system based on optimal branch block phase correction.

Coherent optical communication systems have high receiver sensitivities, high spectral efficiencies, and high-capacity information transmission, which are widely used in free-space optical communications. However, atmospheric turbulence affects the power budget of coherent receiving systems. Diversity can effectively suppress atmospheric turbulence, but relative phase differences caused by phase asynchrony degrade the performances of diversity systems. Hence, spatial diversity reception based on optimal branch block phase correction is proposed herein and verified through simulations and experiments to improve diversity gain and reduce the complexity and outage probability of diversity systems effectively. This scheme is promising for application to high-speed low Earth orbit satellite-to-ground communications.

A three-stage design for allergen immunotherapy trials.

BACKGROUND: Clinical trials of allergen immunotherapy (AIT) may require up to 5 years to complete. These lengthy trials may be complicated by high and potentially differential dropouts, especially among participants who perceive that they are receiving placebo. We propose a three-stage design in which the placebo group in Stage 1 crosses over to receive active treatment in Stage 2. In Stage 3, AIT is discontinued to determine whether benefit is maintained post-treatment. We apply inferential statistics to support the three-stage design for clinical trials to determine clinical efficacy, treatment response over time, and sustained response to AIT. METHODS: The proposed framework constitutes a series of hypothesis tests for comparing treatment responses at the end of each stage. A simulation study was performed to illustrate the statistical properties under varying statistical missing mechanisms and effect sizes. RESULTS: The statistical properties in terms of bias and statistical power were consistent with what are expected from conventional analyses. Specifically, the extent of bias depended on the missing mechanism and magnitude. The statistical powers were largely driven by effect and sample sizes as well as prespecified success margins. As an illustration, assuming relative treatment differences of 25% and stagewise dropout rate of 15%, a sample size of 200 per group may achieve 93% power to demonstrate a treatment effect and 60% power to demonstrate a maintained response post-treatment. CONCLUSIONS: Inferential statistics support our proposed study design for evaluating benefits of AIT over time and inform clinical understanding and decisions.

Conditional power in vaccine trials with seasonal variations.

Conditional power (CP) is widely used in clinical trial monitoring to quantify the evidence for futility stopping or sample size adaptation during the trial. When planning an interim analysis in vaccine trials for seasonal infectious diseases, CPs calculated under the hypothesized or currently estimated effect sizes may not truly reflect future data due to seasonal variations in disease incidence and/or vaccine efficacy (VE). Relying on these estimates alone could lead to erroneous decisions. Therefore, we carried out simulation studies to investigate the use of seven different choices for the drift parameter in computing CP or predictive power (PP) in end-of-season interim analysis. Our simulations showed that, when used to inform futility stopping, CP under the hypothesized effect and a weighted PP under a normal prior distribution appear to outperform others in terms of the overall type II error rate. All CPs and PPs considered in this study resulted in comparable powers and expected sample sizes when used to inform sample size adaptation. The performance of either CP or PP largely depends on the extent to which the chosen drift parameter or the prior distribution of the drift parameter matches the remainder of the trial. Weighted CP/PP tends to be less sensitive to settings where observed data and emerging data in future seasons differ substantially as they incorporate both current estimate and future variations. Therefore, weighted strategies deserve further exploration and perhaps increased usage in guiding trial operations because they are more robust to inaccuracies in prediction. In summary, for vaccine trials with seasonal variations, a decision on trial operations should be guided by a careful consideration of plausible CPs and PPs calculated under reasonable assumptions leveraging the data, prior hypotheses, and new evidence on clinical relevance.

Health Conditions Among Special Operations Forces Versus Conventional Military Service Members: A VA TBI Model Systems Study.

OBJECTIVE: To examine traumatic brain injury (TBI) characteristics and comorbid medical profiles of Special Operations Forces (SOF) Active Duty Service Member/Veterans (ADSM/Vs) and contrast them with conventional military personnel. SETTING: The 5 Veterans Affairs (VA) Polytrauma Rehabilitation Centers. PARTICIPANTS: A subset of participants in the VA TBI Model Systems multicenter longitudinal study with known SOF status. These included 157 participants who identified as SOF personnel (average age = 41.8 years; 96% male, 81% active duty), and 365 who identified as Conventional Forces personnel (average age = 37.4 years; 92% male, 30% active duty). DESIGN: Retrospective analysis of prospective cohort, cross-sectional. MAIN MEASURES: The Health Comorbidities Interview. RESULTS: SOF personnel were more likely to have deployed to a combat zone, had more years of active duty service, and were more likely active duty at time of TBI. SOF personnel were more likely to have had mild TBI (vs moderate/severe) and their TBI caused by violent mechanism. SOF personnel had a higher number of comorbidities, with more diagnoses of chronic pain, osteoarthritis, hyperlipidemia, hip fractures, and obstructive sleep apnea. CONCLUSION: SOF personnel are at a higher risk for multimorbidity after TBI. Current rehabilitation practices should incorporate early screening and treatment of common conditions in this population, while future practices may benefit from a focus on prevention.

Polystyrene nanoplastics exacerbated lipopolysaccharide-induced necroptosis and inflammation via the ROS/MAPK pathway in mice spleen.

Plastics are novel environmental pollutants with potential threats to the ecosystem. At least 5.25 trillion plastic particles in the environment, of which nanoplastics are <100 nm in diameter. Polystyrene nanoplastics (PS-NPs) exposure damaged the spleen's immune function. Lipopolysaccharide (LPS) induced other toxicants to damage cells and organs, triggering inflammation. However, the mechanism of PS-NPs aggravated LPS-induced spleen injury remains unclear. In this study, the PS-NPs or/and LPS mice exposure model was replicated by intraperitoneal injection of PS-NPs or/and LPS, and PS-NPs or/and LPS were exposed to RAW264.7 cells. The histopathological and ultrastructural changes of the mice spleen were observed by H&E staining and transmission electron microscope. Western Blot, qRT-PCR, and fluorescent probes staining were used to detect reactive oxygen species (ROS), oxidative stress indicators, inflammatory factors, and necroptosis-related indicators in mice spleen and RAW264.7 cells. The results showed that PS-NPs or LPS induced oxidative stress, activated the MAPK pathway, and eventually caused necroptosis and inflammation in mice spleen and RAW264.7 cells. Compared with the single treatment group, the changes in PS-NPs + LPS group were more obvious. Furthermore, ROS inhibitor N-Acetyl-L-cysteine (NAC) significantly inhibited the activation of the mitogen-activated protein kinase (MAPK) signaling pathway caused by co-treatment of PS-NPs and LPS, reducing necroptosis and inflammation. The results demonstrated that PS-NPs promoted LPS-induced spleen necroptosis and inflammation in mice through the ROS/MAPK pathway. This study increases the data on the damage of PS-NPs to the organism and expands the research ideas and clues.

A Novel Fault Diagnosis Method of Rolling Bearing Based on Integrated Vision Transformer Model.

In order to improve the diagnosis accuracy and generalization of bearing faults, an integrated vision transformer (ViT) model based on wavelet transform and the soft voting method is proposed in this paper. Firstly, the discrete wavelet transform (DWT) was utilized to decompose the vibration signal into the subsignals in the different frequency bands, and then these different subsignals were transformed into a time-frequency representation (TFR) map by the continuous wavelet transform (CWT) method. Secondly, the TFR maps were input with respective to the multiple individual ViT models for preliminary diagnosis analysis. Finally, the final diagnosis decision was obtained by using the soft voting method to fuse all the preliminary diagnosis results. Through multifaceted diagnosis tests of rolling bearings on different datasets, the diagnosis results demonstrate that the proposed integrated ViT model based on the soft voting method can diagnose the different fault categories and fault severities of bearings accurately, and has a higher diagnostic accuracy and generalization ability by comparison analysis with integrated CNN and individual ViT.