The Second Nanning People's Hospital

The neural precursor cell expressed developmentally down-regulated protein 1 (NEDD1) is implicated in tumorigenesis, but its role in hepatocellular carcinoma (HCC) remains unclear. This study aims to explore the oncogenic role, regulatory mechanisms, and tumor microenvironment interactions of NEDD1 in HCC. Multi-omics analyses were performed using public datasets (TCGA, GEO) and in-house clinical samples. These included expression and survival analysis, epigenetic (DNA methylation) and post-translational (phosphorylation) profiling, functional pathway enrichment, and drug sensitivity prediction. Functional validation was conducted via NEDD1 knockdown in HCC cells and a subcutaneous xenograft model. The co-expression and spatial distribution of NEDD1 and its predicted partner MZT2B were investigated using single-cell (GSE140228) and spatial transcriptomic (HRA000437) datasets. NEDD1 was significantly overexpressed in HCC tissues and correlated with poor prognosis. Its overexpression was potentially linked to promoter hypomethylation and aberrant phosphorylation. NEDD1 knockdown suppressed HCC cell proliferation, migration, and tumor growth in vivo. Notably, NEDD1 expression positively correlated with immune checkpoint molecules (PD-1, CTLA-4), and low NEDD1 expression was associated with better predicted response to immunotherapy. Single-cell and spatial transcriptomics revealed that NEDD1 and MZT2B co-expression was highly enriched in specific macrophage subsets (e.g., APOE+) and exhibited cell context-dependent heterogeneity, suggesting they may constitute a dynamic functional module within the HCC microenvironment. This multi-omics study suggests NEDD1 as a potential prognostic biomarker and therapeutic target in HCC. We propose a novel model wherein the NEDD1-MZT2B module may operate in both tumor cells and immunosuppressive macrophages, potentially influencing disease progression and immunotherapy response.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-026-42505-z.

PurposeTo explore the clinical significance of the artificial intelligence (AI)-assisted three-dimensional (3D) planning system AI-HIP in total hip arthroplasty (THA) and evaluate its accuracy and efficacy in clinical practice.MethodsPreoperative planning was done using the AI-HIP system in the AI group and two-dimensional (2D) template measurements in the conventional group. The two groups were compared for postoperative radiographic results, perioperative monitoring indicators, and the degree of consistency between preoperative planning and actual implant size. Postoperative Harris scores, hip joint range of motion (ROM), and Barthel index were used to evaluate clinical effectiveness.ResultsNone of the patients who ultimately completed the 6-months follow-up experienced adverse events such as hip dislocation and infection during follow-up. Compared to the conventional group, the AI group had significantly higher Harris scores (P = 0.026), hip ROM (P = 0.018), Barthel index (P = 0.042) at 6 months postoperatively, and conformity rates of the acetabular (P = 0.001) and femoral components (P < 0.001) between intraoperative application of prosthesis model and preoperative planning. Additionally, the AI group had significantly shorter operation time (P = 0.041), less intraoperative blood loss (P = 0.012), and smaller discrepancy between bilateral acetabular offset (P = 0.032) and vertical distance of hip center of rotation (P = 0.011). However, no statistically significant intergroup differences were observed for the acetabular abduction angle, anteversion angle, femoral offset and leg length discrepancy.ConclusionPreoperative planning for THA using the AI-HIP system has a high accuracy rate and allows for effective reconstruction of the rotation center and acetabular offset, reduction of surgical time, and early recovery of joint function. Further research is needed to confirm its potential clinical value.Clinical Registration NumberChiCTR210004826, Date:28/03/2021, https://www.chictr.org.cn/showproj.html? proj=52846.

Abstract Objective The study aimed to evaluate the effectiveness of the Occupational Safety and Health Management System (OSHMS) in preventing and managing occupational blood-borne pathogen exposure (OBPE) among health workers (HWs), and to develop integrated strategies for improvement. Methods A qualitative study was conducted using semi-structured interviews with 55 HWs from a tertiary hospital in western China who had experienced OBPE in the preceding year. Data were collected via telephone and face-to-face interviews. Interviews were transcribed verbatim and analyzed thematically using NVivo 12.0. Results A total of 129 OBPE incidents were documented among 120 HWs in one year, with early-career staff at highest risk. Among the 55 participants, 47 reported at least one OBPE incident. Only 60% were aware of their immune status prior to exposure, and low hepatitis B vaccination coverage and serological testing awareness were noted. Psychological impacts included anxiety, stress, and sleep disorders, with 18 HWs experiencing significant mental distress. Current hospital measures included organizational management, training, cultural initiatives, and technological improvements. However, gaps were identified in reporting efficiency, psychological support accessibility, financial barriers to prophylaxis, low HBV vaccination and serological monitoring uptake, and inadequate follow-up compliance (70.11%). Suggestions included implementing standardized protocols, simplifying reporting procedures, enhancing psychological services, providing free vaccinations, and fostering a non-punitive safety culture. Conclusion OBPE remains a significant occupational hazard with multifaceted impacts. Despite some management advances, critical gaps persist in reporting, PEP access, routine monitoring, and psychological support. Effective mitigation requires a multidimensional strategy within a strengthened OSHMS. Further mixed-methods studies with larger samples are needed to inform sustainable national prevention guidelines.

ObjectivePostherpetic neuralgia (PHN), a refractory neuropathic pain following herpes zoster reactivation, lacks clear central mechanisms for emerging therapies like short-term spinal cord stimulation (stSCS). This longitudinal study used multimodal neuroimaging to examine the effects of 14-day stSCS on brain function and white matter microstructure in PHN patients, and to identify neural correlates of clinical improvements.MethodsIn this longitudinal, single-arm, pre-post study, 17 PHN patients received 14 days of continuous stSCS. Clinical outcomes including pain intensity (Numeric Rating Scale, NRS), anxiety and depression (Hospital Anxiety and Depression Scale, HADS), and sleep quality (Pittsburgh Sleep Quality Index, PSQI), were assessed pre-stSCS and 3 days post-stSCS. Resting-state functional MRI (rs-fMRI) and Diffusion Tensor Imaging (DTI) data were acquired at both time points. Longitudinal changes in amplitude of low-frequency fluctuations (ALFF) and fractional ALFF (fALFF) were analyzed, alongside white matter integrity via TBSS and ROI analysis of key tracts.ResultsPost-stSCS, significant improvements occurred in all clinical outcomes (Wilcoxon signed-rank, all p < 0.001). Neuroimaging showed no DTI microstructural changes but significant fALFF increases in regions including the dorsal striatum. Notably, right medial orbitofrontal cortex (mOFC) fALFF increases correlated with NRS reductions (Spearman’s r = 0.71, FDR-corrected p = 0.036). Baseline cingulum integrity (lower FA, higher MD/RD) predicted greater striatal fALFF changes (r = ±0.75, FDR-corrected p < 0.02).ConclusionThese findings suggest that stSCS’s early clinical benefits in PHN are mediated by rapid functional reorganization rather than immediate microstructural changes. This reorganization appears prominent within fronto-striatal circuits: specifically, mOFC functional changes correlate with analgesia, while baseline cingulum integrity predicts subsequent striatal plasticity. This provides initial mechanistic insights into stSCS and suggest that baseline brain structure could be explored as a potential biomarker for treatment response, warranting validation in larger, controlled cohorts.

Microscopic polyangiitis (MPA), a severe antineutrophil cytoplasmic antibody associated vasculitis (ANCA-associated vasculitis, AAV), demonstrates strong clinical association with myeloperoxidase/perinuclear anti-neutrophilic cytoplasmic antibodies (MPO/P-ANCA). While genetic factors are known to contribute to MPA susceptibility, the potential roles of AKT signaling components remain incompletely characterized, with limited data available for AKT1 and even less for its homologous gene AKT2 in this specific disease context. This case-control analysis included 798 participants (202 MPA patients and 596 controls, the latter comprising 387 individuals from the 1,000 Genomes Project), with control groups pooled after confirmation of genetic homogeneity. Genotypes of seven single-nucleotidepolymorphisms (SNPs) (four in AKT1, three in AKT2) with divergent allele frequencies across populations were analyzed. Association analyses were conducted under multiple genetic models, with gene-level and set-based approaches employed to evaluate aggregate effects. Secondary analyses included haplotype reconstruction, SNP-SNP interaction testing, and functional characterization through expression quantitative trait locus (eQTL) mapping. Specific AKT1 variants (rs2498786 and rs1130233) demonstrated significant associations with reduced MPA risk, particularly in P-ANCA-positive patients. Gene-level analyses revealed a strong association for the AKT1 gene set (OR = 0.884, P=0.002) but not for AKT2. Haplotype analysis identified protective AKT1 haplotypes, while interaction testing revealed high-risk genotype combinations. eQTL analysis indicated that protective alleles correlate with enhanced AKT1 expression in immune-relevant tissues, suggesting a potential regulatory mechanism. AKT1 emerges from this study as a likely genetic contributor to MPA, with its influence potentially involving neutrophil regulatory functions and vascular maintenance. The consistent absence of association signals for AKT2 across all analytical approaches could be viewed as reinforcing the specificity of AKT1's involvement. These insights help refine the genetic architecture of MPA and position AKT1 signaling as a candidate pathway for future therapeutic exploration.