Explore the vast range of titles available.

Objective To comprehensively evaluate the global, regional, and national burden of infective endocarditis (IE) from 2010 to 2021, and to project future trends. Methods This study utilized data from the Global Burden of Disease (GBD) Study 2021. Statistical methods, including joinpoint regression and the auto-regressive integrated moving average (ARIMA) model, were employed to analyze the prevalence, mortality, and disability-adjusted life years (DALYs) of IE, stratified by gender, age, and socio-demographic index (SDI). Result From 2010 to 2021, the global prevalence of IE increased by 40.1%, with a total of 421,667 cases reported in 2021. The age-standardized prevalence rate (ASPR) rose from 4.7 per 100,000 to 5.3 per 100,000. Although the number of deaths increased by 23.01% and DALYs rose by 13.26%, both the age-standardized death rate (ASDR) and the age-standardized DALYs rate exhibited slight declines. Significant regional disparities in ASPR were observed, with an overall increase correlated with higher SDI levels. Joinpoint regression analysis revealed that the average annual percentage change (AAPC) in ASPR, ASDR, and age-standardized DALYs rate during this period was 0.8 (0.6, 1.0), -1.1 (-1.7, -0.5), and -1.3 (-1.9, -0.7), respectively. Notably, predictions from the ARIMA model indicate that the ASPR for men is expected to continue rising over the next five years, while a decline is anticipated for women; however, both genders are projected to experience a decrease in ASDR. Conclusion Over the past decade, the ASPR of IE has been on a gradual increase, while the ASDR and the age-standardized DALY rate have slightly decreased. It is indicated that some progress has been achieved in the global disease management and treatment effectiveness of IE. Based on the increasing prevalence rate and the relatively high mortality rate, the burden of IE globally will still remain a major public health challenge in the future.

Metabolic - associated fatty liver disease (MAFLD) is a common hepatic disorder with increasing prevalence, and early detection remains inadequately achieved. This study aims to explore the relationship between the non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (NHHR) and MAFLD, and to establish a predictive model for MAFLD using NHHR as a key variable. All participants were selected from the NHANES cohort, spanning from 2017 to March 2020. Multiple linear regression models were employed to examine the relationship between the non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (NHHR) and the controlled attenuation parameter (CAP). To explore the non-linear association between NHHR and CAP, smooth curve fitting and restricted cubic splines (RCS) of the adjusted variables were utilized. Subgroup analyses were conducted to identify variations in the relationships between the independent and dependent variables across different populations. Finally, a metabolic - associated fatty liver disease (MAFLD) prediction model was developed using seven machine learning methods, including eXtreme Gradient Boosting (XGBoost), Light Gradient Boosting Machine (LightGBM), Multilayer Perceptron (MLP), Random Forest, Support Vector Machine (SVM), K-Nearest Neighbors (KNN), and logistic regression. The SHAP (SHapley Additive exPlanations) value was employed to interpret the importance of various features. Weighted multiple linear regression models revealed a significant positive correlation between the NHHR and the CAP (Beta =  7.42, 95% CI: 5.35-9.50, P <  0.001). Smooth curve fitting and RCS demonstrated a non-linear relationship between NHHR and CAP. Subgroup analyses indicated that this relationship was more pronounced in females. Among the seven machine learning predictive models incorporating NHHR, the XGBoost algorithm exhibited the highest predictive performance, with an area under the curve (AUC) of 0.828. Furthermore, NHHR was identified as the second most important feature in the SHAP analysis, following body mass index (BMI), highlighting its potential in predicting MAFLD. A significant positive correlation was identified between the NHHR and the CAP. The inclusion of NHHR in the XGBoost predictive model for MAFLD demonstrated robust predictive capability, providing a valuable tool for the early detection of MAFLD with considerable clinical application potential.

The observational association between cathepsin and Parkinson's disease (PD) has been partially explored in previous research. However, the causal relationship remains unclear. In this study, our objective is to investigate the causal link between cathepsin and PD using Mendelian randomization (MR) analysis and elucidate the underlying mechanisms governing their interaction. Utilizing bidirectional two-sample MR and multivariable MR, we systematically investigates the causal relationship between nine cathepsins and PD. The data pertaining to cathepsins were obtained from the Integrative Epidemiology Unit (IEU) Open GWAS Project, while data related to PD were sourced from versions R9 and R10 of the FinnGen database. The primary analytical method utilized was the inverse variance weighted (IVW), with MR analysis initially conducted using PD data from R9, complemented by a series of sensitivity analyses. Subsequently, replication analysis was performed on the R10 dataset, and meta-analysis were employed to merge the findings from both datasets. To explore potential mechanisms by which Cathepsins may impact PD, MR analyses were performed on significant Cathepsins with alpha-synuclein. MR analysis and colocalization analysis were conducted on expression quantitative trait loci (eQTL) data of gene related to alpha-synuclein with PD data. Forward MR analyses revealed more cathepsin B (CTSB) associated with less PD risk (OR = 0.898, 95%CI: 0.834-0.966,  = 0.004), while more cathepsin H (CTSH) (OR = 1.076, 95%CI: 1.007-1.149,  = 0.029) and more cathepsin S (CTSS) (OR = 1.076, 95%CI: 1.007-1.150,  = 0.030) associated with increasing PD risk. Meta-analyses validated these associations. Multivariate MR Results were consistent with those before adjustment. No significant results were observed in bidirectional MR analysis. In the investigation of the underlying mechanism, our findings demonstrate that CTSB significantly reduces the levels of alpha-synuclein (OR = 0.909, 95%CI: 0.841-0.983,  = 0.017). Concurrently, a genetically determined positive correlation between alpha-synuclein and PD is illuminated by both eQTL MR and colocalization analysis. In conclusion, this MR study yields robust evidence suggesting an association between elevated levels of CTSB and reduced PD risk, mediated by the downregulation of alpha-synuclein levels. Conversely, higher levels of CTSH and CTSS are associated with an increased risk of PD. These findings offer novel insights into the pathophysiological mechanisms of PD and identify potential drug targets for disease prevention and treatment warranting further clinical investigations.

Objective To assess the level of fear of disease progression (FoP) in patients with acute pancreatitis (AP) during early hospitalization and identify its influencing factors. Methods This cross-sectional study was conducted from March 2024 to June 2025 at a tertiary hospital in Xiamen, China. A total of 212 AP patients were recruited via convenience sampling. On the second day of admission, FoP was measured using the AP-FoP-Q-SF scale. Demographic, clinical, psychological, and self-reported symptom variables were also collected. Statistical analyses included descriptive statistics, chi-square or Mann–Whitney U tests, and multivariable binary logistic regression to identify factors associated with moderate-to-severe FoP (total score > 26). Results The prevalence of moderate-to-severe FoP was high at 59.4%, with a mean AP-FoP-Q-SF score of 26.78 ± 6.12. Item-level analysis showed that fears related to being a burden to family and disease worsening or recurrence were the most prominent concerns. Multivariable logistic regression analysis demonstrated that heavy financial burden (OR = 9.29, 95% CI: 2.65–32.66), alcohol use history (OR = 2.07, 95% CI: 1.07–4.02), and greater subjective weakness (OR = 1.21 per 1-point increase, 95% CI: 1.10–1.33) were associated with increased odds of moderate-to-severe FoP. Compared with patients aged 18–44 years, those aged 45–59 years had significantly lower odds of moderate-to-severe FoP (OR = 0.29, 95% CI: 0.14–0.59). Higher perceived social support was independently associated with reduced odds of moderate-to-severe FoP (OR = 0.97 per 1-point increase, 95% CI: 0.94–0.995). Conclusion A substantial proportion of patients experience clinically significant FoP at the onset of hospitalization for AP, with fears centered on familial burden and disease progression. Our cross-sectional analysis identified several factors independently associated with FoP, including socioeconomic strain, health behaviors, physical symptoms, and lower levels of social support. Early screening for FoP—which could prioritize younger patients, those with financial strain, alcohol use, lower social support, or pronounced weakness—may therefore be beneficial to facilitate timely psychosocial interventions.

Objective Neutrophil extracellular traps (NETs) have been implicated in the pathogenesis of IgA vasculitis (IgAV), yet the NET-associated genes and their immune cell–specific contexts remain incompletely defined. This study aimed to exploratorily identify NET-associated candidate genes related to IgAV using an integrated multi-omics approach. Methods Peripheral-blood bulk transcriptomic data from IgAV patients and healthy controls were analyzed for differential expression. A curated set of 646 NET-associated genes was evaluated using gene set enrichment analysis (GSEA) and gene set variation analysis (GSVA). Differentially expressed genes, NET-related GSEA leading-edge genes, and transcriptome-wide association study (TWAS)–significant genes were intersected to prioritize candidate genes. Genetically supported associations with IgAV susceptibility were assessed using two-sample Mendelian randomization (MR), including cell-type–specific MR. Exploratory immune profiling and intercellular communication analyses were performed using single-sample GSEA and single-cell RNA sequencing (scRNA-seq). Results Five NET-associated candidate genes—AGER, TLR2, CXCR2, TEK, and THBD—were consistently prioritized across analyses. MR results indicated that genetically predicted higher expression of AGER, TLR2, and CXCR2 was associated with increased IgAV risk, whereas TEK and THBD showed inverse associations. Single-cell analyses suggested that these genes were mainly expressed in myeloid immune subsets, accompanied by elevated NETosis-related transcriptional signatures. Enhanced activity of immune-related signaling pathways, including MHC-I and MIF, was observed in IgAV samples. Conclusions This exploratory multi-omics study identified a set of NET-associated candidate genes showing consistent associations with IgAV. These findings provide a hypothesis-generating framework for understanding NET-related immune processes in IgAV and warrant further validation in larger cohorts and functional studies.

Complement C3 plays a prominent role in inflammatory processes, and its increase exacerbates ischemia reperfusion injury (IRI)-induced acute kidney injury (AKI). Infiltrated neutrophils can be stimulated to form neutrophil extracellular traps (NETs), leading to renal injury. However, the relationship between the increase of C3 and the release of NETs in AKI was not clear. Here we found that IRI in the mouse kidney leads to increased neutrophils infiltration and NET formation. Furthermore, neutrophils depletion by anti-Ly6G IgG (1A8) did not reduce C3 activation but reduced kidney injury and inflammation, indicating a link between neutrophils infiltration and renal tissue damage. Pretreatment with 1A8 suppressed ischemia-induced NET formation, proving that extracellular traps (ETs) in renal tissue were mainly derived from neutrophils. Renal ischemia injury also leads to increased expression of C3. Moreover, C3 KO mice (C3 KO) with IRI exhibited attenuated kidney damage and decreased neutrophils and NETs. In vitro , C3a primed neutrophils to form NETs, reflected by amorphous extracellular DNA structures that colocalized with CitH3 and MPO. These data reveal that C3 deficiency can ameliorate AKI by reducing the infiltration of neutrophils and the formation of NETs. Targeting C3 activation may be a new therapeutic strategy for alleviating the necroinflammation of NETs in AKI.

Background To establish a model of chronic renal fibrosis following acute kidney injury (AKI) in BALB/c mice and to observe the effect of AKI on podocyte injury and chronic fibrosis of the kidney. Additional aims included using the model to explore the role of podocyte injury in AKI and post-injury fibrosis. Methods Fifty BALB/C mice were randomly divided into control group (Ctr), sham group (sham), AKI 20 group (renal ischemia, 20 min reperfusion), AKI 30 group (renal ischemia, 30 min reperfusion) and AKI 40 group (renal ischemia, 40 min reperfusion). Mice serum and 24-h urine were collected on the 8th, 9th, 10th, 14th, and 28th days for urinary protein, serum creatinine (Scr) and blood urea nitrogen (BUN) analysis. HE staining, transmission electron microscopy (TEM), Masson staining, Q-PCR, Western Blot and immunohistochemistry were applied. Results Serum Scr and BUN levels across all AKI groups at the 9th day were significantly higher ( P  < 0.05) than controls, with higher reperfusion groups maintaining that increase up to 28 days ( P  < 0.05). Compared with Ctr group, the urinary protein of the AKI 40 group significantly rose on the 9th day ( P  < 0.05), normalizing immediately on the 10th day ( P  < 0.05). In contrast, the AKI 30 group rose significantly on the 14th day ( P  < 0.05) maintaining elevated levels for two weeks ( P  < 0.05). HE staining demonstrated ischemia-dependent renal tissue damage was aggravated in the mild to aggravated AKI groups. Mesangial proliferation, glomerulosclerosis, and tubulointerstitial pathology were also significantly increased in these groups ( P  < 0.05). Masson staining further showed that glomerular, renal tubular, and interstitial collagen were increased by ischemia in a time-dependent manner. Transmission EM additionally that podocytes of the mild to severe AKI groups displayed extensive fusion, exfoliation and GBM exposure. Synaptopodin, Nephrin, and CD2AP mRNA and protein expression demonstrated ischemic time-dependent decreases, while the TRPC6 was increased. There was a significant difference in the levels of Synaptopodin, Nephrin, CD2AP, and TRPC6 between the mild and severe AKI groups ( P  < 0.05). Conclusions 1) During the AKI process mice podocyte injury, proteinuria and the subsequent progression into chronic renal fibrosis is observed.2) Podocyte injury may be one of the causes of ischemia-reperfusion acute kidney injury and post-injury fibrosis.

Background The positive impacts of work engagement among specialist nurses on retention, organizational commitment, and quality of care are well-documented. However, there is a lack of research on the specific differences in work engagement among specialist nurses. Therefore, the purpose of this study is to assess the level of work engagement among specialist nurses in China and identify its influencing factors. Methods A descriptive cross-sectional study was conducted in China from April to July, 2023, with 724 nurses selected from 22 hospitals through convenience sampling involved. The survey was conducted by using self-administered general information questionnaires and work engagement scales. Questionnaire Star was employed as the online data collection tool. The collected data was analyzed by using descriptive statistics and stepwise regression analysis to draw meaningful conclusions from the study. Results Among specialist nurses in Xiamen, China, who had a response rate of 97.10%, an average work engagement score is 140.35 (SD=18.17), with the highest score for the work attitude at 4.65 (SD=0.52) and the lowest score for the work recognition at 4.09 (SD=0.85). It was shown through regression analysis that factors such as career satisfaction, involvement in challenging case discussions, marital status, gender, presence of promotion advantage and title accounted for 14.5% of the total variance in the model and were significant explanatory variables that could predict work engagement. Conclusion It is shown that specialist nurses in Xiamen, China have a high level of work engagement. It is imperative for nursing managers to prioritize the work engagement of specialist nurses, provide the specialist nurses with ample development opportunities and room for growth, and effectively promote the overall development of specialist nurses by improving work engagement in various aspects.

The mechanisms underlying the progression of chronic kidney disease (CKD) following acute kidney injury (AKI) remain poorly understood. Senescent cells induce maladaptive repair have been identified as a significant contributor to CKD subsequent to AKI. The purpose of this study was to investigate the correlations between kidney fibrosis after unilateral ischemia injury and cellular senescence and explored the potential therapeutic effect of GM6001 on AKI to CKD transition. The study revealed a progressive increase in both fibrosis and matrix metalloproteinase 9 (MMP9) expression, peaking approximately 14 days following unilateral ischemic injury, indicating a pivotal role of MMP9 in the pathogenesis of renal fibrosis. Additionally, the research identified an elevation in markers of renal senescence over time, including SA-β-gal, P53, P21, and P16. Treatment with GM6001 demonstrated a significant reduction in both fibrosis and senescence, evidenced by decreased MMP9 expression and associated fibrotic markers, alongside improvements in cellular senescence indicators. studies further substantiated these findings, as GM6001 effectively inhibited MMP9 expression in TGF-β-stimulated HK-2 cells, reinforcing its antifibrotic and antisenescent properties and highlighting its potential as a therapeutic intervention for renal fibrosis. The study provided compelling evidence on the role of MMP9 in the progression of renal fibrosis and the transition from AKI to CKD. The early activation of MMP9 and its association with fibrosis highlighted its potential as a therapeutic target. GM6001, through its inhibition of MMP9, offered a promising avenue for reducing both fibrosis and cellular senescence, suggesting its potential utility in ameliorating CKD.

Periodic microscale array structures play an important role in diverse applications involving photonic crystals and diffraction gratings. A polarized holographic lithography system is proposed for patterning high-uniformity microscale two-dimensional crossed-grating structures with periodic tunability. Orthogonal two-axis Lloyd’s mirror interference and polarization modulation produce three sub-beams, enabling the formation of two-dimensional crossed-grating patterns with wavelength-comparable periods by a single exposure. The two-dimensional-pattern period can also be flexibly tuned by adjusting the interferometer spatial positioning. Polarization states of three sub-beams, defining the uniformity of the interference fringes, are modulated at their initial-polarization states based on a strict full polarization tracing model in a three-dimensional space. A polarization modulation model is established considering two conditions of eliminating the unexpected interference and providing the desired identical interference intensities. The proposed system is a promising approach for fabricating high-uniformity two-dimensional crossed gratings with a relatively large grating period range of 500–1500 nm. Moreover, our rapid and stable approach for patterning period-tunable two-dimensional-array microstructures with high uniformity could be applicable to other multibeam interference lithography techniques.