Henan Provincial Chest Hospital

To understand the current status and influencing factors of self-management ability in peritoneal dialysis (PD) patients. This study employed an interpretive sequential mixed-methods approach and followed the STROBE and CONDITION guidelines. From June 2024 to February 2025, convenience sampling was used to survey 507 PD patients from three tertiary hospitals. Quantitative data were collected using five scales. Concurrently,purposesampling was used to conduct semi-structured interviews with 13 patients until data saturation was reached. Quantitative data were analyzed using SPSS 26.0, and qualitative data were analyzed thematically using Nvivo15. The results were integrated to provide a comprehensive understanding. The quantitative results showed that PD patients had a self-management ability score of [55.00 (45.00, 60.00)] out of a possible 96, indicating a moderately low level. Multiple linear regression identified age, educational attainment, monthly household income, dialysis age, understanding of the disease, mastery of health education content, frequency of follow-up, and self-efficacy as significant influencing factors. The qualitative interviews identified two themes (obstructive and promoting factors) and nine sub-themes. The integration of results showed that qualitative findings confirmed and complemented the quantitative associations. The self-management ability of PD patients is moderately low. Medical staff should enhance the self-efficacy and social support of PD patients based on the influencing factors of their self-management ability, increase the frequency of follow-up, pay attention to PD patients with low education, advanced age and other types, strengthen training and monitoring for complications, and carry out targeted intervention to improve the self-management ability of PD patients.

Calcific aortic valve disease (CAVD) is driven by immune–metabolic dysregulation and osteogenic remodeling, yet actionable molecular targets remain limited. This study integrated multimodal computational analyses with experimental validation to identify functional biomarkers and therapeutic candidates. Single-nucleus RNA sequencing of human aortic valves was combined with CellChat, Monocle 3 and consensus NMF to define immune–stromal interactions and gene programs. A 10 gene classifier was developed using multi model machine learning and interpreted with SHAP. Cross cohort validation, immune deconvolution and network enrichment were applied. Network pharmacology, docking and 50 ns MD simulations were used to identify ligand candidates. Experimental validation was performed in human VICs using osteogenic stimulation, siRNA knockdown and small molecule treatments, followed by RT qPCR, Western blot, Alizarin Red S staining and ALP and proliferation assays. Computational analyses consistently prioritized HLA DRA and FTL as stable, high AUC biomarkers linked to macrophage rich and MHC II enriched microenvironments. Network analyses anchored HLA DRA to adaptive immunity and FTL to iron metabolic pathways. Docking and MD identified Chrysin, α Tocopherol, Colchicine and Diallyl trisulfide as structurally compatible ligands. In vitro, osteogenic stimulation markedly upregulated HLA DRA, FTL, RUNX2 and ALPL. siRNA knockdown of HLA DRA or FTL reduced mineral deposition, ALP activity and VIC proliferation. Predicted small molecule ligands decreased HLA DRA and FTL expression and attenuated calcification. HLA DRA and FTL function as immune–metabolic drivers of VIC osteogenic remodeling and represent viable therapeutic targets. This integrated systems to experimental framework highlights natural compound candidates with potential relevance for CAVD therapy. The study employed a stepwise multiomic workflow beginning with snRNA-seq of human calcified aortic valve tissue for cell-type clustering and ligand–receptor signaling inference. Monocle 3 trajectory reconstruction and cNMF gene-program extraction delineated dynamic transcriptional states and identified 12 pseudotime-associated genes. A machine-learning framework integrating 12 algorithms and SHAP interpretability analysis prioritized FTL, HLA-DRA, CXCL8, C1QA, and FTH1 as the top predictive markers. Functional enrichment, immune infiltration, and protein–protein interaction analyses revealed immune–metabolic cross-talk within the valve microenvironment. Subsequent network pharmacology and molecular docking integrated TCMBank screening, identifying Chrysin, α-Tocopherol, Colchicine, and Diallyl Trisulfide as high-affinity ligands targeting HLA-DRA and FTL. Docking and 50 ns MD simulations confirmed the dynamic stability of these interactions. Experimental validation was performed in human VICs using osteogenic stimulation, siRNA knockdown and small molecule treatments followed by RT qPCR, Western blot, Alizarin Red S staining and ALP and proliferation assays.

HighlightsWhat are the main findings?Sinensetin is a citrus-derived flavone that consistently shows anti-inflammatory activities across models by suppressing inflammatory signaling and supporting antioxidant/autophagy programs.Across multiple cancers, sinensetin inhibits tumor-relevant signaling (including MKK6/P38 signaling), alongside emerging immune-related effects.What is the implication of the main finding?Multiple mechanisms support sinensetin as a multi-target lead for chemoprevention or adjunct therapy.Sinensetin, a polymethoxylated flavone abundant in citrus fruits, has been recognized for its broad biological activities and wide use in traditional medicine around the world. Emerging clinical evidence from flavonoid-enriched orange juice interventions indicates antioxidant and anti-inflammatory effects, aligning with extensive preclinical data. In this review, we explored in vitro and in vivo findings on the anti-inflammatory and anticancer actions of sinensetin and delineated the underlying cellular pathways, especially in terms of proposed targets for sinensetin. In inflammatory settings, sinensetin attenuates NF-κB activation, lowers pro-inflammatory cytokines (e.g., TNF-α, IL-6), and enhances antioxidant defenses, supporting its reported antioxidant, anti-bacterial, anti-viral, and anti-obesity properties. Across multiple tumor models, sinensetin suppresses oncogenic signaling—including β-catenin, PI3K/AKT, VEGF, NRF2, P53, and MKK6—concomitant with reduced proliferation, migration, and survival signaling. We further discuss emerging immunological effects, including modulation of innate immune cell activation and cytokine production, which may contribute to tumor microenvironment reprogramming and inflammation resolution. Together, these mechanistic insights position sinensetin as a promising lead for chemopreventive and adjunct therapeutic strategies. Our efforts aim to provide insights into the future translational development and clinical evaluation of sinensetin and its derivatives.

Postoperative nausea and vomiting (PONV) is a common complication of surgical procedures, especially of radical thoracoscopic lung cancer surgery, and causes patient discomfort, delays recovery, and increases healthcare costs. Penehyclidine hydrochloride (PHC), a novel anticholinergic agent, can potentially reduce surgery- and anesthesia-related adverse reactions such as PONV, possibly because of its selective M1 and M3 muscarinic receptor antagonism. The aim of this study is to investigate the efficacy and safety of PHC in reducing the incidence and severity of PONV after radical thoracoscopic lung cancer surgery. This single-center, prospective, double-blind, randomized controlled clinical trial will include 446 patients scheduled for radical thoracoscopic lung cancer surgery. Enrolled participants will be randomly assigned to a test or control group in a 1:1 ratio, with 223 patients in each group. The test group will receive an intravenous injection of 0.25mg PHC before anesthesia and an intravenous infusion of 0.25mg PHC within 48h after surgery, whereas the control group will receive normal saline instead of PHC. The primary outcome will be the incidence of PONV within 24h post-surgery. Secondary outcomes will include the incidence and severity of PONV within different time intervals (0-6, 6-12, and 12-24h post-surgery); surgeon and patient satisfaction levels at 48h post-surgery, rated using a visual analog scale; and the occurrence of dry mouth, dizziness, red face, dry skin, urinary retention, delirium, and hyperthermia within 48h post-surgery. An intention-to-treat analysis will be performed. We hypothesize that administration of intravenous PHC can reduce the incidence and severity of PONV and improve surgeon and patient satisfaction. The findings of this trial could have important implications for improving patient outcomes and optimizing postoperative care for patients who undergo radical thoracoscopic lung cancer surgery. This trial protocol was registered in the Chinese Clinical Trial Registry on April 19, 2024 (registration number: ChiCTR2400083262).

PurposeThe effect of esketamine on perioperative inflammatory factors and postoperative analgesic outcomes in patients with Obstructive sleep apnea syndrome (OSAS) remains unclear. This trial assesses whether 0.25 mg · kg− esketamine during general anesthesia can reduce the inflammatory level and relieve postoperative pain in OSAS patients.Patients and Methods96 adult patients with OSAS underwent palatopharyngoplasty under general anesthesia was included in our research. Following anesthetic introduction, subjects were randomized to either 0.25 mg · kg− esketamine (in 20mL solution; esketamine group) or an equivalent volume of saline (Control group). The primary result was the level of IL-6 and TNF-α before the infusion of esketamine, 40min, 4h, and 24h after the esketamine infusion. Secondary outcomes was NRS scores immediately after tracheal extubation, 4h after the infusion, postoperative day 1 (POD1), postoperative day 2 (POD 2) and postoperative day 7 (POD 7).ResultsThe esketamine group demonstrated significantly reduced IL-6 and TNF-α levels at 40 minutes post-infusion (P<0.001) and showed lower the numerical rating scale(NRS)scores with less rescue analgesia immediately after extubation (P<0.001) compared to the control group, despite prolonged extubation and post-anesthesia care unit (PACU) stay (P<0.001). Across POD1-2, the esketamine group maintained reduced NRS scores (P<0.001) and analgesic doses (P=0.021), higher quality of recovery-15 (QoR-15) scores and patient satisfaction scores (P<0.001) relative to control group. It is important to note that the significant differences in inflammatory markers and pain scores between groups were not sustained at the 24-hour assessment and on postoperative day 7, respectively, indicating transient effects.ConclusionIntraoperative infusion of 0.25 mg·kg− esketamine provided transient suppression of inflammatory responses and reduced early postoperative pain in OSAS patients. However, these benefits were exploratory and time-limited, and must be weighed against prolonged extubation and PACU stay.

Benign central airway scar stenosis, a refractory complication of endobronchial tuberculosis and other inflammatory conditions, often leads to atelectasis, recurrent infections, and respiratory dysfunction. Traditional surgical interventions are associated with significant trauma and high restenosis rates. This case report describes a 28-year-old female with stenosing active tuberculosis of the left upper lobe bronchus, presenting with cough, high-grade fever, and lobar collapse. The patient underwent transbronchial needle knife electrocautery for precise scar tissue dissection, followed by sequential cryoablation to suppress granulomatous proliferation and balloon dilation for airway remodeling. After five interventional bronchoscopic procedures, complete luminal patency was achieved, with no recurrence observed during 8-month follow-up. Through this case demonstration and literature review, we highlight the clinical value of combined bronchoscopic techniques (high-frequency electrocautery, cryotherapy, and balloon dilation) in managing stenosing active tuberculosis and preventing complete bronchial occlusion, providing clinicians with a minimally invasive therapeutic alternative.

BackgroundCentral post-stroke pain (CPSP) is a debilitating neuropathic condition that significantly impairs quality of life and is challenging to manage. Salvia miltiorrhiza (Danshen), a traditional Chinese herb, has demonstrated efficacy against neuropathic pain, but its active analgesic components and underlying mechanisms remain unclear. This study investigated the therapeutic potential of Danshenol B, an active component of Danshen, in a CPSP mouse model, focusing on its mechanism of action via the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma isoform (PIK3CG)/NLR family pyrin domain-containing protein 3 (NLRP3) signaling pathway.MethodsA CPSP model was established in mice, and RNA sequencing of the ipsilateral ventral posterolateral thalamic nucleus/ventral posteromedial thalamic nucleus (VPL/VPM) was performed to identify differentially expressed genes (DEGs). Network pharmacology analysis linked these DEGs to known Danshen components, and molecular docking of 42 Danshen constituents was conducted to identify strong ligand-target interactions. Danshenol B was then administered (5, 10, 50 mg/kg) to CPSP mice to evaluate its analgesic effects, and thalamic PIK3CG and NLRP3 protein levels were measured to assess pathway involvement. Additionally, PIK3CG and NLRP3 expression were manipulated (via overexpression or knockdown) to determine their roles in CPSP and their regulatory relationship.ResultsIn the CPSP model, 409 DEGs were identified in the ipsilateral VPL/VPM. Network pharmacology revealed 21 Danshen-derived compounds potentially targeting 11 of these DEGs. Molecular docking highlighted Danshenol B as a top candidate, showing strong binding (-9.127 kcal/mol) to PIK3CG. In CPSP mice, Danshenol B (50 mg/kg) significantly alleviated CPSP and suppressed the PIK3CG/NLRP3 pathway. The overexpression of PIK3CG increased NLRP3 and negated the effects of Danshenol B, whereas its knockdown alleviated CPSP and reduced NLRP3. Notably, simultaneous overexpression of NLRP3 attenuated the analgesic effects induced by PIK3CG knockdown, further confirming that NLRP3 functions downstream of PIK3CG in mediating CPSP.ConclusionsDanshenol B alleviates CPSP in mice by suppressing the PIK3CG/NLRP3 signaling pathway, elucidating its analgesic mechanism and highlighting its potential as a novel therapeutic candidate for CPSP.

SynopsisHealth inequalities intensified, burden shifting to low-resource regions despite preventive advancements. HPV and screening rates diverged by SDI, highlighting coverage gaps. Screening and vaccination inversely linked to disease burden, underscoring critical efficacy. Innovative modeling exposed disparities, advocating SDI-stratified interventions.ObjectiveThis study analyzes global and regional cervical cancer trends (1990–2021) across different Socio-Demographic Index (SDI) levels, highlighting health inequalities, assessing the impact of HPV vaccination and screening, and modeling future trends. The findings aim to inform targeted prevention policies, reduce regional disparities, and promote global health equity.MethodsData were sourced from the Global Burden of Disease study 2021(GBD 2021), OECD, and WHO. The focus was on incidence and disability-adjusted life years (DALYs) of cervical cancer. Time trends were analyzed by SDI regions, alongside health inequality assessments. Correlation analyses examined links between screening rates, HPV vaccination coverage, and disease burden.ResultsFrom 1990 to 2021, global age-standardized incidence rate and age-standardized DALYs rates declined significantly, with estimated annual percentage changes (EAPC) of -0.54% (95% CI: -0.63 to -0.44) and − 1.27% (95% CI: -1.36 to -1.18). However, significant differences exist in specific patterns of change across SDI regions: exhibited an upward incidence trajectory. From 1990 to 2021, the burden of cervical cancer disease shifted from developed to less developed regions. Correlation analysis showed negative associations between screening rates and DALYs (r = -0.56, p < 0.01) and between vaccination coverage and incidence (r = -0.35, p < 0.01).ConclusionAlthough the global cervical cancer burden has decreased, significant regional disparities remain. Future policies should focus on tailored interventions, with low-resource regions strengthening healthcare infrastructure and implementing minimum effective preventive measures, while high-SDI regions shift to precision public health approaches. Policymakers must also incorporate culturally sensitive health education to address social barriers, challenge misconceptions, and empower communities, ultimately reducing preventable cervical cancer morbidity.

There is accumulating evidence linking the microbiome and cardiovascular diseases. Nevertheless, no existing studies have been conducted on atrial fibrillation (AF) and the oral microbiome. We collected and sequenced 245 AF tongue-coating samples and 26 AF samples after catheter ablation from Zhengzhou and Guangshan, China. We characterized tongue coating microbiome, constructed microbial classifiers in the discovery cohort, and verified their diagnostic potential in a cross-regional cohort. Tongue coating microbial richness and diversity were significantly increased in the AF group compared to the control group, indicating increased bacterial colonization. The classifiers based on four optimal tongue coating microbial markers achieved good diagnostic efficiency in AF cohorts, with area under the curve (AUC) of 99.10 and 98.62% in the discovery and validation cohorts, respectively, and 97.97% in the cross-regional cohort. Paroxysmal AF and persistent AF shared similar taxonomic features, but some specific differential bacteria acted in the AF progression. Moreover, the outcomes revealed that catheter ablation contributed to rehabilitating oral bacterial disorders. This was the first cross-sectional and longitudinal research of oral microbiome in AF patients and the alternations after catheter ablation, which offers promising new perspectives for AF clinical diagnosis and management.

O3 (ozone) is an environmental pollutant that can exacerbate inflammatory damage and contribute to respiratory diseases. However, the molecular mechanisms and potential targets for intervention in ozone-induced lung inflammatory injury are not yet known. To address this, our study exposed mice to 0.6 ppm and 1.0 ppm of O3 (3 h/d, 14 d), evaluating lung inflammation through histopathological examinations, lung function assessments, and analyses of white blood cells and inflammatory factors in BALF. Furthermore, we employed transcriptomic and non-targeted metabolomic approaches to decipher differentially expressed genes (DEGs) and metabolites in mouse lung tissue from the 1.0 ppm O3 exposure group. A comprehensive integration analysis of these omics data was conducted using Pearson correlation analysis. Finally, our findings show that ozone exposure indeed elicits pulmonary inflammation. Transcriptomic analysis identified 311 differentially expressed genes, predominantly implicated in circadian rhythm, IL-17 signaling pathway, and PPAR signaling. Meanwhile, metabolomic profiling revealed 41 differentially regulated metabolites, mainly associated with riboflavin metabolism, glutathione metabolism, and ABC transporter pathways. Integrated multi-omics analysis through Pearson correlation identified three key components (Pla2g10, O-phosphoethanolamine, and phosphorylcholine) showing significant enrichment in glycerophospholipid metabolism. Collectively, our findings suggest that glycerophospholipid metabolism may serve as potential therapeutic targets and diagnostic biomarkers for ozone-induced pulmonary inflammatory injury.