ObjectiveTo explore the mechanism of Xianfang Huomingyin （XFHMY） in the treatment of type Ⅲ prostatitis （CP/CPPS） through network pharmacology， molecular docking， and animal experiments. MethodsThe traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP） and the Swiss Target Prediction database were used to screen and sort out the active ingredients and corresponding targets of XFHMY. The potential therapeutic targets of CP/CPPS were collected from online databases， such as the Online Mendelian Inheritance in Man （OMIM）， GeneCards， and DisGeNET. The potential core targets of XFHMY for treating CP/CPPS were further screened by constructing a protein-protein interaction （PPI） network and performing topological analysis. Meanwhile， the DAVID database was chosen to perform enrichment analysis on the intersection targets. On this basis， the AutoDock software was used for molecular docking， and the data was subsequently imported into the GraphPad Prism 8 software to generate a heat map. SD rats were divided into seven groups： A blank group， a sham operation group， a model group， low-， medium-， and high-dose XFHMY groups （3.645， 7.29， 14.58 g·kg^-1）， and a tamsulosin hydrochloride group （0.018 mg·kg^-1）. Hematoxylin-eosin （HE） staining was used to evaluate the pathological changes in prostate tissue. The inflammatory factor indicators of rats in each group were detected via enzyme-linked immunosorbent assay （ELISA）. Real-time fluorescence quantitative reverse transcription polymerase chain reaction （Real-time PCR） and Western blot were used to evaluate the mRNA and protein expression levels of phosphatidylinositol 3-kinase （PI3K）， protein kinase B （Akt）， and nuclear transcription factor-κB （NF-κB） p65 in prostate tissue. ResultsThe HE staining showed no significant signs of inflammatory cell infiltration in the prostate of the sham operation group compared to the blank group， while the model group had significantly inflammatory cell infiltration. The ELISA results showed that compared to the blank group， TNF-α， IL-1β， and COX-2 in the sham operation group had no significant differences. However， they were significantly higher in the model group （P<0.01）， indicating successful CP/CPPS modeling in rats. Compared with the model group， the low-，medium-and high-dose XFHMY group and the tamsulosin hydrochloride group showed significant decreases in TNF-α， IL-1β， and COX-2 （P<0.05，P<0.01）. The Real-time PCR analysis revealed that compared to the model group， the low-dose XFHMY group had reduced Akt and NF-κB p65 mRNA expression（P<0.05，P<0.01）. In the medium-and high-dose XFHMY group and tamsulosin hydrochloride group， PI3K， Akt， and NF-κB p65 mRNA levels decreased significantly（P<0.05，P<0.01）. Western blot analysis showed that compared to the model group， the low-dose XFHMY group had lower p-NF-κB p65/NF-κB p65 （P<0.05）. The medium- and high-dose XFHMY group and the tamsulosin hydrochloride group showed significant decreases in p-PI3K/PI3K， p-Akt-ser473/Akt， p-Akt-thr308/Akt， and p-NF-κB p65/NF-κB p65 （P<0.01）. ConclusionXFHMY may exert therapeutic efficacy on CP/CPPS by inhibiting the PI3K/Akt/NF-κB signaling pathway and reducing inflammatory responses. Additionally， NF-κB activation may be related to the activation of ser473 and thr308 sites.

Background Silicosis, caused by inhalation of silica (SiO₂) dust, remains the most prevalent occupational pneumoconiosis in China. While galectin-3 (Gal-3) is known to play pro-inflammatory and pro-fibrotic roles in various diseases, its specific mechanism in the pathogenesis of silicosis has not been fully clarified. Objective To investigate the role and underlying mechanisms of Gal-3 in silicosis using clinical samples of silicosis and a silicosis mouse model. Methods Lung nodule biopsy samples were collected from patients with stage III pneumoconiosis. Concurrently a silicosis mouse model was constructed via non-exposed tracheal intubation with instillation of a SiO₂ suspension. The expression levels of Gal-3 mRNA and protein in the lung tissues of the silicosis model mice were then detected using real-time quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC) staining. Single-cell transcriptomic sequencing (scRNA-seq) was performed on both human and murine lung samples to analyze the expression of the Gal-3-encoding gene Lgals3 across different cell types. In vitro, RAW264.7 macrophages were treated with varying concentrations of SiO₂ suspension for 24 h and 48 h; the expression levels of Gal-3 mRNA and protein were measured by RT-qPCR and Western blot. The Gal-3 inhibitor TD139 was used to intervene in the SiO₂-induced in vitro macrophage model, and Western blot was used to detect the intracellular expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and transforming growth factor-β1 (TGF-β1). Finally, mouse embryonic lung fibroblasts NIH/3T3 and Mlg2908 were treated with varying concentrations of recombinant mouse Gal-3 protein (rmGal-3) for 48 h, and Western blot was used to detect the expression of fibrosis markers [(Collagen I, Collagen III, Fibronectin, and α smooth muscle actin (α-SMA)] and proteins associated with the TGF-β1/Smads signaling pathway. Results RT-qPCR and IHC staining showed that both the gene and protein expression levels of Gal-3 were significantly elevated at all consecutive time points in the silicosis mouse model (P < 0.05). scRNA-seq revealed that Lgals3 was aberrantly highly expressed in lung tissues from pneumoconiosis patients and silicosis mouse models, with the highest expression observed in macrophages. After treatment of macrophages with different concentrations of SiO₂ for 24 h and 48 h, the mRNA and protein expression levels of Gal-3 were significantly upregulated compared with the control group (P < 0.05). Following TD139 intervention, the protein expression levels of IL-1β, TNF-α, and TGF-β1 in dust-exposed macrophages were markedly downregulated (P < 0.0001). After 48 h of stimulation with rmGal-3, the protein expression levels of Collagen I, Fibronectin, and α-SMA in mouse embryonic lung fibroblasts (NIH/3T3 and Mlg2908) were significantly increased in all treatment groups compared with the control group (P < 0.01). Moreover, Gal-3 treatment markedly upregulated TGF-β1 protein expression in Mlg2908 cells and enhanced the phosphorylation levels of Smad2 and Smad3 (P < 0.0001). Conclusion Gal-3 is abnormally expressed in silicotic lung tissues, which primarily originates from macrophages, and inhibition of Gal-3 suppresses SiO₂-induced inflammatory and pro-fibrotic responses. In addition, Gal-3 promotes fibroblast differentiation and extracellular matrix production by activating the TGF-β1/Smads signaling pathway.

Work serves as a critical means of obtaining resources, facilitating personal growth, realizing self-worth, and engaging in social interactions. However, work-related diseases pose significant threats to workers’ health and productivity, and impose considerable economic burdens. This article categorized work-related diseases into six major types, including musculoskeletal disorders, mental and behavioral disorders, cardiovascular and metabolic diseases, digestive system diseases, reproductive system diseases, and non-specific respiratory diseases, and summarized their risk factors, assessment methods, policy regulation, and prevention and control measures. Current research in this field predominantly relies on cross-sectional studies, which present limitations in causal inference and potential risks of bias. Future studies should expand sample sizes, optimize research designs, and establish multidimensional evaluation systems to comprehensively assess the health and economic impacts of work-related diseases. It is recommended to enhance the translation of research findings into practice, thereby providing a scientific basis for the occupational health protection system and promoting the well-being and sustainable development of the working population.

Background Silicosis, caused by inhalation of silica (SiO₂) dust, remains the most prevalent occupational pneumoconiosis in China. While galectin-3 (Gal-3) is known to play pro-inflammatory and pro-fibrotic roles in various diseases, its specific mechanism in the pathogenesis of silicosis has not been fully clarified. Objective To investigate the role and underlying mechanisms of Gal-3 in silicosis using clinical samples of silicosis and a silicosis mouse model. Methods Lung nodule biopsy samples were collected from patients with stage III pneumoconiosis. Concurrently a silicosis mouse model was constructed via non-exposed tracheal intubation with instillation of a SiO₂ suspension. The expression levels of Gal-3 mRNA and protein in the lung tissues of the silicosis model mice were then detected using real-time quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC) staining. Single-cell transcriptomic sequencing (scRNA-seq) was performed on both human and murine lung samples to analyze the expression of the Gal-3-encoding gene Lgals3 across different cell types. In vitro, RAW264.7 macrophages were treated with varying concentrations of SiO₂ suspension for 24 h and 48 h; the expression levels of Gal-3 mRNA and protein were measured by RT-qPCR and Western blot. The Gal-3 inhibitor TD139 was used to intervene in the SiO₂-induced in vitro macrophage model, and Western blot was used to detect the intracellular expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and transforming growth factor-β1 (TGF-β1). Finally, mouse embryonic lung fibroblasts NIH/3T3 and Mlg2908 were treated with varying concentrations of recombinant mouse Gal-3 protein (rmGal-3) for 48 h, and Western blot was used to detect the expression of fibrosis markers [(Collagen I, Collagen III, Fibronectin, and α smooth muscle actin (α-SMA)] and proteins associated with the TGF-β1/Smads signaling pathway. Results RT-qPCR and IHC staining showed that both the gene and protein expression levels of Gal-3 were significantly elevated at all consecutive time points in the silicosis mouse model (P < 0.05). scRNA-seq revealed that Lgals3 was aberrantly highly expressed in lung tissues from pneumoconiosis patients and silicosis mouse models, with the highest expression observed in macrophages. After treatment of macrophages with different concentrations of SiO₂ for 24 h and 48 h, the mRNA and protein expression levels of Gal-3 were significantly upregulated compared with the control group (P < 0.05). Following TD139 intervention, the protein expression levels of IL-1β, TNF-α, and TGF-β1 in dust-exposed macrophages were markedly downregulated (P < 0.0001). After 48 h of stimulation with rmGal-3, the protein expression levels of Collagen I, Fibronectin, and α-SMA in mouse embryonic lung fibroblasts (NIH/3T3 and Mlg2908) were significantly increased in all treatment groups compared with the control group (P < 0.01). Moreover, Gal-3 treatment markedly upregulated TGF-β1 protein expression in Mlg2908 cells and enhanced the phosphorylation levels of Smad2 and Smad3 (P < 0.0001). Conclusion Gal-3 is abnormally expressed in silicotic lung tissues, which primarily originates from macrophages, and inhibition of Gal-3 suppresses SiO₂-induced inflammatory and pro-fibrotic responses. In addition, Gal-3 promotes fibroblast differentiation and extracellular matrix production by activating the TGF-β1/Smads signaling pathway.

Objective To establish a DNA quantitation method based on dithiothreitol(DTT)-crystal vio-let.Methods DTT was used to decolorize crystal violet,mixed with different concentrations of λ-DNA and salmon sperm DNA standard samples or concentration standard samples,and the absorbance was read at 595 nm wavelength by microplate reader,and compared with the results of ultraviolet absorbance method.DTT-crystal violet method and ultraviolet absorbance method were used to compare the concentration of plasmid samples and the concentration of genomic DNA samples of cervical exfoliated cells.The protein tolerance of the two methods was assessed by simulating protein contaminants with bovine serum albumin(BSA).Results In the quantification of λ-DNA and salmon sperm DNA,the DTT-crystal violet method had a robust linear correlation between the absorbance at 595 nm and DNA concentration(r2＞0.95),and the measured concentrations of the standard samples were not significantly different from the theoretical concentrations of the prepared standard samples(P＞0.05).There was no significant difference in the concentration of plasmid samples measured by DTT-crystal violet method and ultraviolet absorption method(P＞0.05).The concen-tration of DNA samples from cervical exfoliated cells measured by ultraviolet absorption method was positive-ly correlated with that by DTT-crystal violet method(r=0.94,P＜0.01).The concentration of the standard sample containing BSA 1 μg/μL measured by ultraviolet absorption method was higher than that of the con-trol sample,and the difference was statistically significant(P＜0.01),whereas the DTT-crystal violet method was not significantly affected(P＞0.05).Conclusion DTT-crystal violet method has obvious advantages over the existing DNA quantitation method,and is suitable for DNA quantitative analysis in scientific research and clinic.

Hepatic encephalopathy is a difficult and critical disease with rapid progression and limited treatment methods in the field of liver disease， and it is urgently needed to make breakthroughs in its pathogenesis. Selection of appropriate prevention and treatment strategies is of great importance in delaying disease progression and reducing the incidence and mortality rates. This article reviews the theory of “turbid toxin pathogenesis” and related prevention and treatment strategies for hepatic encephalopathy in traditional Chinese medicine/Zhuang medicine， proposes a new theory of “turbid toxin pathogenesis”， analyzes the scientific connotations of “turbid”， “toxin”， and the theory of “turbid toxin pathogenesis”， and constructs the “four-step” prevention and treatment strategies for hepatic encephalopathy， thereby establishing the new clinical prevention and treatment regimen for hepatic encephalopathy represented by “four prescriptions and two techniques” and clarifying the effect mechanism and biological basis of core prescriptions and techniques in the prevention and treatment of hepatic encephalopathy， in order to provide a reference for the prevention and treatment of hepatic encephalopathy.

Allergen-specific immunotherapy（AIT） remains the only therapeutic approach with the potential to modify the natural course of allergic rhinitis（AR）. Nevertheless, considerable inter-individual variability exists in patients'responses to AIT. To facilitate more reliable assessment of treatment efficacy, the China Rhinopathy Research Cooperation Group（CRRCG） convened young and middle-aged nasal experts in China to formulate the present consensus. The recommended subjective outcome measures for AIT comprise symptom scores, medication scores, combined symptom and medication scores, quality-of-life assessments, evaluation of disease control, and assessment of comorbidities. Objective indicators may supplement these measures. Currently available objective approaches include skin prick testing, nasal provocation testing, and allergen exposure chambers. However, these methods remain constrained by practical limitations and are not yet appropriate for routine implementation in clinical efficacy evaluation. In addition, several biomarkers, including sIgE and the sIgE/tIgE ratio, sIgG4, serum IgE-blocking activity, IgA, cytokines and chemokines, as well as immune cell surface molecules and their functional activity, have been shown to have associations with AIT outcomes. While these biomarkers may complement subjective assessments, they are subject to significant limitations. Consequently, large-scale multicenter trials and real-world evidence are required to strengthen the evidence base. The present consensus underscores the necessity of integrating patients'subjective experiences with objective testing throughout the treatment process, thereby providing a more comprehensive and accurate framework for efficacy evaluation. Looking forward, future investigations should prioritize the incorporation of multi-omics data and artificial intelligence methodologies, which hold promise for overcoming current limitations in assessment strategies and for advancing both the standardization and personalization of AIT.
Humans ; Allergens/immunology* ; China ; Consensus ; Desensitization, Immunologic ; Immunoglobulin E ; Quality of Life ; Rhinitis, Allergic/therapy* ; Treatment Outcome ; East Asian People

Spine fracture and dislocation are common traumatic spinal conditions that often require surgical intervention due to compromised spinal stability. Surgical approaches include anterior, posterior, and combined anterior-posterior spinal procedures. According to the specific surgical requirements, patients may be placed in the prone position or repositioned between prone and supine positions during surgery. Intraoperative repositioning has become an essential step in patient positioning. However, during repositioning, patients with spinal fracture and dislocation are at increased risk for complications such as hemodynamic instability, nerve injury, and pressure injuries to the skin and soft tissue. Notably, due to the instability of the spinal cord, even minor manipulations can further exacerbate the damage, potentially leading to severe outcomes like paraplegia. Although the current clinical guidelines provide instructive recommendations for standard position, there remains no specific protocols for intraoperative repositioning in patients with spine fracture and dislocation. With a concern for the lack of clinical studies on positioning techniques, risk prevention, and operational norms for special patients, no applicable guidelines or standards are available. A consensus was required to provide clinical reference, meet the requirements of surgical treatment, and minimize the safety risks of patients caused by improper placement of positions. Professional Committee of Operating Room Nursing of Shaanxi Nursing Association organized experts in nursing management and operating room nursing from major hospitals across China to formulate Expert consensus on intraoperative repositioning for patients with spinal fracture and dislocation ( version 2025). The consensus provides 11 recommendations covering pre-repositioning preparation, intraoperative maneuvers, and post-repositioning observation, aiming to provide references for clinical standardization of the intraoperative repositioning process and protection of patients′ safety.

Objective To investigate whether exposure pathways influence the distribution pattern and toxicity of polystyrene nanoplastics(PSNPs)in hepatic cells.Methods Male C57BL/6J wild-type healthy mice aged 6 to 8 weeks old and weighed 18 to 22 g were administered with PSNPs via gavage or tail vein injection.Then,we tracked PSNPs distribution in the major organs of mice via an in vivo imaging system(IVIS).After that,we analyzed the cellular accumulation patterns in hepatic cell subpopulations(hepatocytes and Kupffer cells)using immunofluorescence and transmission electron microscopy(TEM).300 nm PSNPs were administered via gastric gavage or tail vein injection,and 70 nm PSNPs were injected via the portal vein.The cellular localization of PSNPs in the liver was analyzed using immunofluorescence.Subsequently,using AML-12 cells,a normal mouse liver cell line,as the parenchymal hepatocyte model,the uptake of PSNPs in AML-12 cells was analyzed by confocal laser scanning microscope(CLSM).Flow cytometry was performed to observe and quantify PSNPs uptake,and to analyze the underlying endocytosis mechanisms.IVIS was used to analyze PSNPs uptake features in vivo.Finally,using mouse macrophage line RAW264.7 as a Kupffer cell model and AML-12 cells as a parenchymal hepatocyte model,the cell-type-specific toxic effects induced by 100 μg/ml PSNPs were examined through transcriptomics and metabolomics analyses.Results IVIS revealed predominant hepatic accumulation of PSNPs regardless of exposure pathways via intragastric gavage or tail vein injection.Immunofluorescence/TEM demonstrated exposure pathway-dependent cellular distribution:intragastric PSNPs were localized mainly in hepatocytes,while intravenous PSNPs were accumulated in Kupffer cells.Changes in particle size(300 nm vs.70 nm)did not alter the cellular distribution pattern,while 70 nm PSNPs injected via the portal vein accumulated in Kupffer cells,which suggested that the cell-type-specific distribution of PSNPs in the liver was independent of PSNPs size and might be related to the transport of PSNPs in the gastrointestinal tract.Flow cytometry showed that PSNPs uptake by AML-12 was time-dependent and that the underlying endocytosis mechanism involved pathways mediated by clathrin(P<0.000 1),macropinocytosis(P=0.002 6),and lipid rafts(P<0.000 1).Findings on PSNPs distribution in blood revealed that the uptake of PSNPs by hepatocytes exhibited a rate saturation phenomenon.Multi-omics analysis identified distinct toxicity patterns:PSNPs disrupted lipid metabolism and neurotransmitter homeostasis in AML-12 cells and induced inflammation and oxidative stress in Kupffer cells.Conclusion Exposure pathways mediate the hepatic cell-type-specific distribution of PSNPs,thereby altering the downstream toxicological consequences induced by exposure to PSNPs.

Objective To explore the effects of modified prone ventilation combined with bronchoscopic alveolar lavage on respiratory mechanics and hemodynamics in children with Acute Respiratory Distress Syndrome(ARDS),as well as to evaluate the clinical treatment efficacy.Methods A total of 96 ARDS children receiving mechanical ventilation treatment in the emergency intensive care unit of Kunming Children's Hospital from January 2021 to December 2023 were selected and randomly assigned into three groups:Group A(prone ventilation group,n=32),Group B(modified prone ventilation group,n=32),and Group C(modified prone ventilation combined with bronchoscopic alveolar lavage group,n=32).The changes in the following parameters before and after treatment among the three groups were compared:oxygenation indicators:arterial oxygen partial pressure(PaO2),arterial oxygenation index(PaO2/FiO2);respiratory mechanics indicators:lung compliance,mean airway pressure,plateau airway pressure,and total airway resistance;hemodynamic indicators:cardiac output,cardiac index,systemic vascular resistance index,and mean arterial pressure;clinical efficacy indicators time to disappearance of rales,mechanical ventilation duration,and length of hospital stay;and incidence of complications:arrhythmia,airway obstruction,pressure injuries,total incidence of catheter dislodgment,and gastric content reflux.Results The oxygenation indicators in Group C after treatment were superior to those in Groups A and B(P<0.05).The respiratory mechanics indicators in Group C after treatment were also better than those in Groups A and B(P<0.05).In terms of hemodynamics,there were no statistically significant differences in cardiac output,cardiac index,and mean arterial pressure among Groups A,B,and C after treatment(P>0.05).However,the SVRI in Group C was better than that in Groups A and B(P<0.05).Curative effect for Group C were also better than those for Groups A and B(P<0.05).The incidence of complications in Group C showed no significant difference compared to Groups A and B(P>0.05).Conclusion The modified prone ventilation combined with bronchoscopic alveolar lavage treatment scheme demonstrates better therapeutic effects compared to traditional treatment methods,significantly improving oxygenation and respiratory mechanics indicators as well as the systemic vascular resistance index in children,and is worthy of clinical promotion.