STUDY DESIGN:A retrospective study. OBJECTIVE:To characterize subtype-specific gait patterns and neuromuscular adaptations in DSD using integrated 3D motion capture and surface electromyography (sEMG). BACKGROUND:Degenerative spinal diseases (DSD), including lumbar spinal stenosis (LSS), adult spinal deformity (ASD), and cervical spondylotic myelopathy (CSM), commonly impair gait in elderly patients. MATERIALS AND METHODS:In this retrospective cross-sectional study, 148 participants (31 ASD, 40 LSS, 35 CSM, 42 healthy controls) underwent gait analysis with a BTS motion capture system and sEMG assessment of erector spinae, multifidus, gluteus maximus, and rectus abdominis muscles. Spatiotemporal parameters, root mean square maximum (RMSmax) and median frequencies (MF) were compared across stance and swing phases. Nonparametric statistical analyses were performed with significance at P<0.05. RESULTS:The study included 106 patients with degenerative spinal diseases and 42 healthy elderly controls. A three-dimensional motion capture system and surface electromyography were used to synchronously analyze complete gait cycle parameters. The results showed that compared to the HC group, all three patient groups exhibited significantly reduced gait speed, lower step frequency, prolonged double-support time, increased step width, and increased asymmetry in lower limb gait parameters (P <0.001). sEMG analysis revealed that the ASD and LSS groups had increased RMSmax values and decreased MF (P <0.001). The asymmetry indices of bilateral muscles in all three patient groups were higher than those in the HC group (P <0.001), indicating compromised neuromuscular control related to disease-specific pathology. CONCLUSION:The study systematically revealed abnormal gait parameters and distinct activation patterns of core muscles in patients with degenerative spinal conditions, along with their underlying causes. Patients in the DSD group exhibited poorer bilateral lower limb gait stability and walking speed, with different muscle activation patterns due to varying causes. LEVEL OF EVIDENCE:Level IV.

BACKGROUND:Micro(nano)plastics (MNPs) are pervasive environmental contaminants, yet their presence in human cardiac tissue and their potential contribution to myocardial fibrosis remain unclear. We investigated whether myocardial MNP burden is associated with fibrosis severity in patients and evaluated mechanistic plausibility in mice. METHODS:Left atrial appendage tissues were collected from patients undergoing cardiac surgery (n=33). MNP burden and polymer composition were quantified by pyrolysis-gas chromatography/mass spectrometry, and fibrosis was quantified histologically. In mice, 100-nm or 1-µm polystyrene nanoplastics were administered by oral gavage in coexposure and sequential exposure protocols with isoprenaline. Cardiac function was assessed by echocardiography, and fibrosis was evaluated by histology and immunohistochemistry. Transcriptomics, metabolomics, and 16S ribosomal RNA sequencing were performed to identify pathways linked to MNP exposure. RESULTS:MNPs were detected in all human cardiac samples. Patients with high fibrosis exhibited higher total MNP levels than those with low fibrosis (171.74 [interquartile range [IQR], 158.18-202.39] versus 119.33 [IQR, 102.75-148.44] µg/g tissue; P=2.5×10-4), driven predominantly by elevated nanoplastics (122.83 [IQR, 100.10-149.06] versus 86.39 [IQR, 36.85-103.74] µg/g; P=0.010). Polystyrene and polyvinyl chloride were enriched in high-fibrosis tissues (polystyrene: P=3.3×10-4; polyvinyl chloride: P=0.002). Transcriptomics indicated activation of inflammatory and profibrotic pathways (TNF [tumor necrosis factor]/NF-κB [nuclear factor-κB], TGF-β [transforming growth factor-beta], and MAPK [mitogen-activated protein kinase]), supported by increased α-SMA (alpha-smooth muscle actin), COL1 (collagen I), and TGF-β1 immunostaining, while metabolomics suggested perturbations in lipid metabolism and mitochondrial function. In mice, polystyrene exposure exacerbated isoprenaline-induced systolic dysfunction and myocardial fibrosis in both experimental paradigms and recapitulated pathway signatures related to cell-matrix interactions. CONCLUSIONS:Myocardial MNP burden, particularly nanoplastics, is associated with greater fibrosis in humans, and experimental polystyrene exposure aggravates stress-induced myocardial remodeling in vivo. Multiomics analyses nominate inflammatory, ECM (extracellular matrix), and metabolic programs as candidate mediators of MNP-associated cardiotoxicity.

Cardiac fibrosis following myocardial infarction (MI) is a critical determinant of progressive cardiac dysfunction, yet the underlying mechanisms driving this pathological process remain incompletely understood. Elucidating these regulatory pathways holds profound implications for improving post-MI prognosis. Our prior work demonstrated that chronic intermittent hypoxia (CIH) exacerbates cardiac fibrosis while modulating the expression of long non-coding RNA (lncRNA) nonnmmut065573 (tentatively designated LncRNA-IH) in cardiac tissues. Herein, we sought to determine the role of LncRNA-IH in post-MI cardiac fibrosis and its underlying mechanisms. Using a C57BL/6 mouse model of MI, we established a mouse model with cardiac-specific overexpression of LncRNA-IH to evaluate post-MI cardiac fibrosis. In vitro, primary cardiac fibroblasts (MCF) and the PA12 cell line were subjected to LncRNA-IH overexpression or siRNA-mediated knockdown, and cell proliferation and migration were assessed. Transcriptomic profiling was performed to characterize LncRNA-IH-induced changes in cardiac gene expression and signaling pathways, aiming to elucidate the molecular mechanisms involved. Results showed that CIH significantly exacerbated post-MI cardiac fibrosis, and LncRNA-IH was predominantly localized to cardiac fibroblasts. Cardiac-specific overexpression of LncRNA-IH in MI mice markedly exacerbated post-MI cardiac dysfunction and fibrosis. In vitro, LncRNA-IH overexpression significantly enhanced the proliferation and migration capacities of primary cardiac fibroblasts and PA12 cells, whereas these effects were abrogated by LncRNA-IH knockdown. Transcriptomic analysis revealed that LncRNA-IH elicited significant alterations in cardiac gene expression profiles, specifically activating the TGF-β1 signaling pathway and upregulating the expression of its downstream target, ZEB1. Collectively, our findings indicate that LncRNA-IH promotes cardiac fibroblast proliferation and migration, thereby exacerbating post-MI cardiac remodeling, at least in part through activation of the TGF-β1 signaling pathway. This study identifies LncRNA-IH as a potential therapeutic target for mitigating post-MI cardiac fibrosis and preserving cardiac function.

Postoperative coronal malalignment (CM) is a prevalent complication following corrective surgery for degenerative lumbar scoliosis (DLS), particularly in lumbosacral (LS) curve-driven subtypes. This study aims to identify risk factors in this high-risk subgroup to enhance understanding of the condition and support the optimization of subtype-specific management strategies. A retrospective cohort analysis of 98 LS curve-driven DLS patients was conducted. Postoperative CM was defined as coronal balance distance (CBD) > 3 cm. A novel parameter, core offset distance (COD), was introduced to quantify the cumulative vertical displacement between the two most influential vertebral segments responsible for imbalance in the LS curve. Other coronal alignment measurements included thoracolumbar/lumbar (TL/L) curve Cobb angle, LS curve Cobb angle, upper instrumented vertebra tilt, L4 tilt, L5 tilt, pelvic obliquity, and CBD. Patient demographics and surgical parameters were also evaluated. Multivariate logistic regression was utilized to identify predictors of postoperative CM. Postoperative CM was observed in 35.7

Cerebral ischemia-reperfusion (I/R) injury triggers a cascade of neuroinflammatory responses and multiple forms of regulated cell death. PANoptosis, integrating pyroptosis, apoptosis, and necroptosis, has been implicated in inflammatory disorders, but its role in cerebral I/R remains unclear. This study explored the molecular profile and immune relevance of PANoptosis-related genes (PRGs) in rat I/R injury. A rat I/R model was established by transient middle cerebral artery occlusion (MCAO). Transcriptome sequencing identified differentially expressed genes (DEGs) using DESeq2, and PANoptosis-related DEGs (PR-DEGs) were obtained by intersecting with GeneCards-derived PRGs. Functional enrichment (GO, KEGG, Metascape, GSEA), weighted gene co-expression network analysis (WGCNA), and immune infiltration analyses were performed to uncover biological functions and immune features associated with PR-DEGs. Rats subjected to I/R injury showed significant infarction, neurological deficits, and increased TNF-α, IL-1β, and IL-10 expression, along with downregulated Bcl-2 and upregulated CD16 and iNOS, indicating strong inflammatory responses. A total of 51 PR-DEGs were identified, primarily enriched in inflammatory and immune signaling pathways such as TNF, NF-κB, and MAPK. WGCNA revealed the salmon module as most correlated with I/R injury, and hub genes including CASP8, STAT3 were identified. Correlation and immune infiltration analyses demonstrated strong associations between key PR-DEGs and pro-inflammatory immune cells, suggesting a close relationship between PANoptosis-associated gene expression patterns and immune dysregulation in I/R injury. Our findings suggest coordinated activation of PANoptosis-related signaling in cerebral I/R injury. CASP8 and STAT3 were identified as key PR-DEGs associated with I/R, providing a foundation for further mechanistic investigation. Transcriptomic profiling of the cerebral ischemia-reperfusion model identifies PANoptosis-related genes and reveals their role in driving inflammatory responses and immune dysregulation, highlighting PANoptosis as a key contributor to neuronal injury following ischemia-reperfusion.

Study Design. A retrospective study. Objective. To characterize subtype-specific gait patterns and neuromuscular adaptations in DSD using integrated 3D motion capture and surface electromyography (sEMG). Background. Degenerative spinal diseases (DSD), including lumbar spinal stenosis (LSS), adult spinal deformity (ASD), and cervical spondylotic myelopathy (CSM), commonly impair gait in elderly patients. Materials and Methods. In this retrospective cross-sectional study, 148 participants (31 ASD, 40 LSS, 35 CSM, 42 healthy controls) underwent gait analysis with a BTS motion capture system and sEMG assessment of erector spinae, multifidus, gluteus maximus, and rectus abdominis muscles. Spatiotemporal parameters, root mean square maximum (RMSmax) and median frequencies (MF) were compared across stance and swing phases. Nonparametric statistical analyses were performed with significance at P <0.05. Results. The study included 106 patients with degenerative spinal diseases and 42 healthy elderly controls. A three-dimensional motion capture system and surface electromyography were used to synchronously analyze complete gait cycle parameters. The results showed that compared to the HC group, all three patient groups exhibited significantly reduced gait speed, lower step frequency, prolonged double-support time, increased step width, and increased asymmetry in lower limb gait parameters ( P <0.001). sEMG analysis revealed that the ASD and LSS groups had increased RMSmax values and decreased MF ( P <0.001). The asymmetry indices of bilateral muscles in all three patient groups were higher than those in the HC group ( P <0.001), indicating compromised neuromuscular control related to disease-specific pathology. Conclusion. The study systematically revealed abnormal gait parameters and distinct activation patterns of core muscles in patients with degenerative spinal conditions, along with their underlying causes. Patients in the DSD group exhibited poorer bilateral lower limb gait stability and walking speed, with different muscle activation patterns due to varying causes. Level of Evidence. Level IV

Background:Severity assessment of human immunodeficiency virus (HIV)-associated Pneumocystis jirovecii pneumonia (PJP) is clinically important because arterial blood gas indices are standard but may not fully capture the heterogeneity of lung involvement on chest computed tomography (CT). We aimed to develop and internally validate a CT radiomics model for classifying severity in adults with confirmed HIV-associated PJP. Methods:This retrospective single-center study included 96 adult patients with confirmed HIV-associated PJP who underwent chest CT at presentation. Disease severity was classified as mild or moderate-to-severe according to room-air arterial blood gas criteria, with moderate-to-severe disease defined as arterial partial pressure of oxygen (PaO2) <70 mmHg or an alveolar-arterial oxygen gradient (A-aDO2) ≥35 mmHg. Clinical variables were retrospectively collected from medical records. Patients were randomly divided into training and test cohorts at a ratio of 7:3. Radiomics features were extracted from the bilateral lung parenchyma. After least absolute shrinkage and selection operator regression, features with non-zero coefficients were included in the final radiomics model. In parallel, a clinical logistic model incorporating serum lactate dehydrogenase, β-D-glucan, and CD4 count was developed in the training cohort and tested in the test cohort. Model performance was assessed using the area under the receiver operating characteristic curve (AUC) with 95% confidence intervals (CIs), calibration analysis, decision curve analysis, and pairwise DeLong test comparisons. Results:Of the 96 patients, 38 were classified as mild and 58 as moderate-to-severe. Patients with moderate-to-severe disease had a higher frequency of dyspnea, higher levels of inflammatory markers, and lower CD4 count. The final radiomics model included 10 features. In the training cohort, the radiomics model achieved an AUC of 0.92 (95% CI: 0.85-0.97), compared with 0.65 (95% CI: 0.51-0.78) for the clinical logistic model. In the test cohort, the radiomics model showed a numerically higher AUC of 0.89 (95% CI: 0.72-1.00), followed by the clinical logistic model at 0.84 (95% CI: 0.68-0.97). Using their respective classification thresholds, the radiomics model yielded a sensitivity of 0.778 (95% CI: 0.548-0.910) and a specificity of 0.818 (95% CI: 0.523-0.949) in the test cohort, while the clinical logistic model yielded a sensitivity of 0.722 (95% CI: 0.491-0.875) and a specificity of 0.909 (95% CI: 0.623-0.984). Pairwise DeLong tests in the test cohort showed no statistically significant difference between the radiomics model and the clinical logistic model. Conclusions:In this small single-center study, the CT radiomics model showed promising discrimination for severity classification in HIV-associated PJP, but these findings are preliminary and require external multicenter validation before clinical use.

BackgroundConcanavalin A (ConA)-induced acute hepatitis is a widely used murine model for studying immune-mediated liver injury, characterized by T-cell activation and pro-inflammatory cytokine production. Mesenchymal stem cells (MSCs) have shown promise in mitigating liver injury through immunomodulation, but the precise cellular and molecular mechanisms remain unclear. This study leverages single-cell RNA sequencing (scRNA-seq) to elucidate the role of MSCs in reshaping the hepatic immune microenvironment during acute liver injury.MethodsSingle-cell suspensions were isolated from liver tissues of ConA-induced acute hepatitis mice, with or without MSC treatment. ScRNA-seq libraries were generated using the 10× Genomics platform, and data were processed using Seurat for quality control, clustering, and cell-type annotation. Trajectory and pseudotime analysis were performed using Monocle 3 to model differentiation pathways. Ligand-receptor interactions were analyzed using CellChat to identify active signaling pathways. Key findings were further assessed in situ by multiplex immunohistochemistry (mIHC).ResultsMSC administration markedly alleviated ConA-induced acute liver injury. scRNA-seq analysis showed that the global hepatic cellular landscape remained largely dominated by the acute inflammatory challenge, whereas MSC treatment was associated with selective remodeling of specific immune compartments. In particular, MSC treatment reduced the proportions of MDSCs, Tregs, NK cells, and proliferating CD8+ T cells, while increasing monocyte-derived macrophages (MoMFs). Subclustering and pseudotime analyses revealed heterogeneous MoMF states distributed along distinct transcriptional branches, including inflammatory and tissue-remodeling-associated programs. Combined with the compositional changes, these findings suggest selective remodeling of MoMF states following MSC treatment rather than uniform suppression of all macrophage subsets. Cell–cell communication analysis further identified MoMFs as a major signaling hub, with complement-associated signaling emerging as a prominent communication module directed toward downstream MDSCs and NK cells. Consistently, mIHC showed increased CD206-associated macrophage staining and reduced CD86 signal in MSC-treated livers compared with ConA-treated livers.ConclusionMSCs ameliorate acute immune-mediated liver injury in association with selective remodeling of the hepatic immune microenvironment, particularly within the MoMF compartment. These findings support a model in which MSC treatment is linked to altered macrophage-state composition and MoMF-centered complement-associated communication during injury resolution, providing insight into the innate immune mechanisms underlying MSC-mediated hepatoprotection.

Age-related changes in spine-pelvis sagittal alignment significantly impact spinal degeneration, yet their biomechanical correlations remain poorly understood. This study investigated whether spinal sagittal alignment exhibits distinct mechanical characteristics across different age groups. We developed parametric finite element models for five age groups (40–60 s, 60–65 s, 65–70 s, 70–75 s, and 75 over years) using radiological data from 625 adult volunteers. Models simulated upright posture based on trunk mass distribution. Overall sagittal range of motion (ROM) of the spine remained < 5° across all ages, transitioning from extension to flexion after 65 years. Vertebral ROM alternated between flexion (-1.46°) and extension (4.02°). Distal lumbar segments shifted from extension to flexion after 60, while pelvic rotation increased rearward with age. The trend in maximum matrix stress of the annulus fibrosus paralleled that of IDPs (0.09–0.31 MPa), while maximal fiber stress within the annulus fibrosus consistently increased with age across the five age models. Our study reveals that after 65, the spine’s overall sagittal ROM shifts from extension to flexion with age: age-related increases in IDPs, annulus matrix, and fiber stress lead distal lumbar rotation to transition from extension to flexion after 60 (initiating lumbar lordosis loss), while thoracic and pelvic rearward extension/rotation later sustain sagittal balance. Excluding age-related degenerative parameters may slightly underestimate inter-group stress differences, but does not alter the observed alignment-biomechanics trend, given the focus on sagittal alignment findings, enhancing understanding of age-related spinal biomechanics, and informing clinical management of degenerative spine conditions.

Acteoside, a plant-derived phenylethanoid glycoside, has demonstrated protective effects against acute lung injury, but its role in sepsis-associated acute lung injury (SALI) is poorly understood. Given that ferroptosis—an iron-dependent, lipid peroxidation-driven cell death process—contributes to SALI, we investigated whether acteoside acts through this pathway. Our results show that acteoside alleviated histological damage, pulmonary edema, and inflammatory cell infiltration in an LPS-induced SALI model. It reduced levels of inflammatory mediators (TNF-α, IL-6, IL-1β, IFN-β) and exerted potent anti-ferroptotic effects, marked by enhanced SOD/GSH activity, decreased iron, GSSG, 4-HNE, and MDA, and restored expression of SLC7A11, GPX4, Nrf2, ACSL4, TfR1, and PTGS2. In RAW264.7 cells, acteoside similarly inhibited inflammation and ferroptosis. Crucially, the ferroptosis inducer erastin counteracted acteoside's benefits, whereas the Nrf2 inhibitor ML385 blocked its anti-ferroptotic action, confirming that acteoside alleviates SALI by targeting ferroptosis via Nrf2 activation.

STUDY DESIGN:A retrospective analysis. OBJECTIVE:To explore the potential of radiomics as a novel bone assessment tool for early prediction of proximal junctional kyphosis (PJK) in adult spinal deformity (ASD). BACKGROUND:PJK is a prevalent complication following ASD surgery. Since impaired bone quality is a major risk factor, accurate preoperative bone assessment is crucial for early identification of high-risk patients. However, conventional metrics such as T-score, Hounsfield unit (HU) value, and vertebral bone quality (VBQ) score exhibit limitations in accuracy and reliability. METHODS:A total of 358 ASD patients were analyzed and randomly assigned to training and test sets (7:3). Radiomic features were extracted from lumbar CT and MRI scans to construct CT and MRI radiomics scores (CTRS/MRIRS). In parallel, T-score, HU value, and VBQ score were also evaluated. Univariable prediction models were first developed for each of the five bone metrics. Subsequently, multimodal models were constructed using the best-performing bone metric as the core variable, with additional selected clinical and radiographic parameters incorporated to further enhance predictive performance. Model performance was evaluated using AUROC, net reclassification improvement (NRI), and integrated discrimination improvement (IDI). RESULTS:Among univariable models, CTRS (AUROC=0.780) and T-score (AUROC=0.793) exhibited superior predictive performance compared to MRIRS (AUROC=0.694), HU value (AUROC=0.713), and VBQ score (AUROC=0.658). Multimodal models significantly outperformed their univariable counterparts (CTRS/T-score multimodal AUROC=0.880/0.885), with improved reclassification ability (CTRS univariable vs. multimodal: IDI=-0.2; T-score univariable vs. multimodal: NRI=-0.332, IDI=-0.247; all P <0.001). CONCLUSIONS:The CT-based radiomics score presents a promising alternative to conventional bone quality metrics for early prediction of PJK after ASD surgery. Integrating CTRS with clinical and radiographic factors further enhances predictive accuracy, providing a valuable framework for preoperative risk stratification. LEVEL OF EVIDENCE:III.

Background:Lung cancer remains a leading cause of cancer-related mortality, with poor survival outcomes. Despite the widespread use of programmed cell death protein 1 (PD-1) blockade therapy, more than 70% of patients fail to benefit and might even develop adverse inflammatory responses. Clinical observations have shown that patients with high neutrophil levels experience worse outcomes following PD-1 blockade. However, the underlying mechanism remains elusive. This study aimed to investigate the impact of neutrophils on anti-PD-1 therapy in lung cancer. Methods:Clinical cohort analysis revealed that peripheral neutrophil levels correlated with survival and metastasis in non-small cell lung cancer (NSCLC) patients treated with PD-1 blockade. In this study, we established a subcutaneous Lewis lung carcinoma (LLC) mouse model, and depleted neutrophils by anti-Ly6G antibody with or without PD-1 blockade. Dynamic changes of peripheral immune cells (CD4+T cells, CD8+ T cells, macrophages, neutrophils, and myeloid-derived cells) in mice were examined by Flow cytometry during treatment, and cytokine levels were measured using Luminex multiplex assays. Results:Clinically, patients with high neutrophil counts exhibited significantly shorter progression-free survival (PFS) and overall survival (OS), and were more prone to distant organ metastases. In the mouse model, neutrophil depletion enhanced CD8+ T cell infiltration in tumor tissues and suppressed neutrophil-mediated interleukin (IL)-5, IL-6 and IL-17A inflammation, resulting in the inhibition of tumor growth. However, the combination of neutrophil depletion with PD-1 blockade paradoxically restored inflammatory cytokine production and increased myeloid-derived suppressor cell (MDSCs) infiltration, thereby compromising tumor suppression. Conclusions:Our observation shows that high neutrophil levels in cancer patients are associated with poorer prognosis and increased risk of distant metastasis. Depletion of neutrophils reshapes the tumor immune microenvironment, wherein excessive inflammatory cytokines drive resistance to PD-1 antibody therapy.

Introduction The gut microbiota plays a vital role in the progression of heart failure (HF), making it a potential strategy for treating HF. The Bacteroides genus has shown promising potential for treating HF. However, further research is needed to identify specific beneficial Bacteroides strains for treating HF and elucidate their potential mechanisms. Objectives This study aimed to elucidate the therapeutic effect and mechanism of Bacteroides strain on HF. Methods This study comprehensively used pharmacological evaluation, 16S rRNA genetic sequencing, short-chain fatty acid (SCFA) targeted metabolomics, transcriptome, and molecular biology methods to investigate the efficacy and mechanism of Bacteroides vulgatus (B. vulgatus) in the treatment of HF. Results We observed a significant decrease in the abundance of B. vulgatus in both HF patients and mice, and dysbiosis of the gut microbiota could cause cardiac dysfunction in mice. The administration of B. vulgatus to mice with HF significantly improved their cardiac function and significantly increased the levels of SCFAs, especially butyric acid. Meanwhile, we also observed a significant reduction in the level of butyric acid in the serum of HF patients, and the cardiac function of HF mice improved after the administration of butyric acid. Compared to patients with higher butyric acid level, patients with lower butyric acid level had a significantly increased incidence of endpoint events. Moreover, the transcriptome results revealed that B. vulgatus significantly regulated the mitogen-activated protein kinase (MAPK) pathway. After further molecular biology verification, B. vulgatus was confirmed to regulate the transforming growth factor-β1 (TGF-β1)/MAPK pathway in the heart through butyric acid, thereby exerting anti-HF effects. Conclusion This study provides evidence that B. vulgatus improves heart function by regulating SCFA metabolism and subsequently modulating the TGF-β1/MAPK pathway in myocardial tissue, confirming the potential therapeutic role of B. vulgatus in HF.

This study aims to assess the effectiveness of oblique lateral interbody fusion, which prioritizes the correction of core distance, in comparison to traditional posterior surgery, in patients with lumbosacral curve-driven degenerative lumbar scoliosis. This retrospective study analyzed consecutive patients with lumbosacral curve-driven degenerative lumbar scoliosis at a single institution from January 2019 to December 2023. The patients were divided into two groups: the traditional posterior approach group (n = 55) (Group T) and the prioritized core vertebral correction technology group (n = 52) (Group P-CV). Preoperative and postoperative data were analyzed using the SRS-22r score and imaging. To further illustrate the significance of prioritizing the core distance, a correlation analysis was conducted between the core distance and preoperative as well as postoperative coronal parameters. There was no significant difference in preoperative baseline data between two groups (P>0.05). Preoperative core distance was correlated with L4 tilt, L5 tilt, thoracolumbar Cobb, Aa, and CBD (P<0.05). Compared with Group T, intraoperative changes in core distance, change of core distance/preoperative core distance, CBD, Aa, and lumbosacral Cobb were greater in Group P-CV than in Group T. Similarly, postoperative CBD, Aa, L4 tilt, L5 tilt, core distance, and lumbosacral Cobb were smaller in Group P-CV than in Group T (P<0.05). The changes in core distance and core distance/preoperative core distance were correlated with postoperative CBD (-0.529, -0.771, P<0.05). Group P-CV had shorter operation time, less intraoperative blood loss, and fewer surgical segments (P<0.05). The core vertebrae of patients with lumbosacral curve-driven degenerative lumbar scoliosis can be identified by distance measurement. Oblique lateral interbody fusion with prioritized core vertebral correction technology can effectively prevent coronal imbalance after surgery, thereby improving the lumbosacral curve. This technique provides a safe and effective approach for treating lumbosacral curve-driven degenerative lumbar scoliosis.

Hypercholesterolemia is an independent risk factor for cardiovascular disease and lowering circulating levels of low-density lipoprotein cholesterol (LDL-C) can prevent and reduce cardiovascular events. MicroRNA-181d (miR-181d) can reduce the levels of triglycerides and cholesterol esters in cells. However, it is not known whether miR-181d-5p can lower levels of circulating LDL-C. Here, we generated two animal models of hypercholesterolemia to analyze the potential relationship between miR-181d-5p and LDL-C. In hypercholesterolemia model mice, adeno-associated virus (AAV)-mediated liver-directed overexpression of miR-181d-5p decreased the serum levels of cholesterol and LDL-C and the levels of cholesterol and triglyceride in the liver compared with control mice. Target Scan 8.0 indicated Proprotein convertase subtilisin/kexin type 9 (PCSK9) to be a possible target gene of miR-181d-5p, which was confirmed by in vitro experiments. miR-181d-5p could directly interact with both the PCSK9 3'-UTR and promoter to inhibit PCSK9 translation and transcription. Furthermore, Dil-LDL uptake assays in PCSK9 knockdown Huh7 cells demonstrated that miR-181d-5p promotion of LDL-C absorption was dependent on PCSK9. Collectively, our findings show that miR-181d-5p targets the PCSK9 3'-UTR to inhibit PCSK9 expression and to reduce serum LDL-C. miR-181d-5p is therefore a new therapeutic target for the development of anti-hypercholesterolemia drugs.

This study aims to introduce a two-stage surgical procedure, namely oblique lateral interbody fusion (OLIF), for spinal disorders treatment. Furthermore, clinical outcomes and imaging results are analyzed between OLIF with posterior fixation and posterior lumbar interbody fusion (PLIF) with fixation for lumbosacral curve-driven degenerative lumbar scoliosis (DLS). 146 patients with type 2 DLS who underwent OLIF or PLIF between January 2019 and November 2023 were included. Spinal and pelvic parameters were measured using X-ray imaging before and after surgery. Clinical symptoms were assessed using Oswestry Disability Index (ODI) and visual analog scale (VAS). Operation time, intraoperative blood loss, surgical fixation segments, drainage tube indwelling time, and drainage volume were recorded. 70 patients underwent OLIF and 76 underwent PLIF. Preoperative and postoperative clinical symptoms remain the same (p > 0.05). OLIF group exhibited significantly less intraoperative blood loss, fewer fixation segments, shorter drainage tube retention time, and reduced drainage volume (p < 0.01). Additionally, improvements in coronal parameters, including coronal balance distance, were more pronounced in OLIF group with less potential postoperative coronal imbalance (p < 0.05). For type 2 DLS, two-stage surgery of OLIF with posterior fixation represents a more efficient surgical approach, reducing surgical fusion segments, causing less trauma and bleeding, and effectively avoiding postoperative coronal plane decompensation than traditional posterior surgery.

Microplastics are ubiquitous in the environment. Human body can be exposed to microplastics through inhalation and ingestion and some microplastics can enter the blood and accumulate in various tissues and organs throughout the body. Animal experiments have suggested that microplastics may promote atherosclerosis. However, data on microplastics in human arteries and clinical evidence supporting a link between microplastics and atherosclerosis are currently lacking. Pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS) was used in this study to detect microplastics in three types of human arteries: coronary and carotid arteries with atherosclerotic plaques, as well as the aorta without plaques. Microplastics were detected in all 17 arterial samples, with an average concentration of 118.66 ± 53.87 μg/g tissue. Four types of microplastics were identified: polyethylene terephthalate (PET, 73.70%), polyamide-66 (PA-66, 15.54%), polyvinyl chloride (PVC, 9.69%), and polyethylene (PE, 1.07%). Most importantly, the concentration of microplastics in arteries containing atherosclerotic plaques, both coronary arteries (156.50 ± 42.14 vs. 76.26 ± 14.86 μg/g tissue, P = 0.039), and carotid arteries (133.37 ± 60.52 vs. 76.26 ± 14.86 μg/g tissue, P = 0.015), was significantly higher than that in aortas which did not contain atherosclerotic plaques, suggesting that microplastics might be associated with atherosclerosis in humans. This study provides valuable data for further hazard assessments of microplastics on human cardiovascular health.

Background Cytokines are strongly associated with coronary artery disease (CAD); however, few studies have explored the relevance of cytokines in coronary chronic total occlusion (CTO). This study aimed to clarify the association of cytokines with CTO and its procedural outcomes. Methods A total of 526 patients with suspected CAD but not acute myocardial infarction were enrolled and divided into CTO (n = 122) and non-CTO (n = 404) groups based on coronary angiography. Furthermore, serum levels of 12 cytokines [Interleukin-1 beta (IL-1 beta), IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-17, tumor necrosis factor-alpha (TNF-alpha), interferon-alpha (IFN-alpha), and IFN-gamma] were measured for each patient. Results Patients with CTO had higher rates of male (P = 0.001), smoking (P = 0.014), and diabetes (P = 0.008); higher levels of IL-6 (P < 0.001), total triglycerides (P = 0.020), serum creatine (P = 0.001), and high-sensitivity troponin I (P = 0.001); and lower IL-4 (P < 0.001), total cholesterol (P = 0.027), and high-density lipoprotein cholesterol (HDL-C) (P < 0.001) levels compared to those without CTO. IL-4 (OR = 0.216, 95%CI:0.135-0.345, P < 0.001), IL-6 (OR = 1.248, 95%CI:1.165-1.337, P < 0.001), and HDL-C (OR = 0.047, 95%CI:0.010-0.221, P < 0.001) were identified as independent predictors of CTO. And good predictive performance (AUC = 0.876) for CTO, with a sensitivity of 81.96% and specificity of 81.19%, could be achieved by combining these three predictors. Furthermore, patients with procedural success had younger age (P = 0.004) and lower serum IL-6 levels (P = 0.039) compared to those with procedural failure, and IL-6 levels (OR = 0.962, 95%CI: 0.931-0.995, P = 0.023) were associated with procedural success. Conclusion IL-4, IL-6, and HDL-C levels were strongly associated with CTO, and IL-6 also linked to procedural outcomes of CTO. (c) 2023 Hellenic Society of Cardiology. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).