To address the growing challenge of an increasing number of elderly lung cancer patients amidst China's aging population and to fill the gap in quality control standards for surgical treatment in this special population, this study aimed to develop a standardized surgical evaluation system for elderly lung cancer patients tailored to China's national conditions. The system was established through a literature review, integrated the pathophysiological characteristics of elderly patients, and was constructed following review, feedback, and revision by experts from multiple thoracic surgery centers. Employing a 100-point scoring system, it comprises three primary domains: physical infrastructure and geriatric adaptability foundational conditions (10 points); management level and perioperative care models (20 points); and technical proficiency and clinical outcomes (70 points). The system places a strong emphasis on geriatric adaptability, proposing specific, quantifiable indicators for age-friendly facility modifications, control of elderly-specific complications, multidisciplinary collaboration, and standardized perioperative management. It provides a convenient and measurable assessment tool for quality control in the surgical treatment of elderly lung cancer in China, which is expected to promote the standardization and homogenization of diagnosis and treatment.

Background/Aims: Liver transplantation (LT) following total hepatectomy is a life-saving treatment for hepatocellular carcinoma (HCC). The HCC recurrence after LT hinders the effectiveness of the procedure. The objective of this study is to develop a pre-operative risk stratification model based on a liquid biopsy. Methods: We conducted a comprehensive multi-omics study of 260 HCC patients from three centers, including clinical data, low-coverage whole-genome sequencing of cell-free DNA (cfDNA) from plasma, as well as whole-exome, single-nucleus RNA, and spatial transcriptomics from matched tumor and non-tumor tissues. Results: We identified cfDNA-derived copy number alteration (CNA) signatures associated with post-transplant recurrence. By integrating cfDNA-derived CNA profiles with single-cell transcriptomic data, we traced recurrence-associated cfDNA to a distinct subpopulation of malignant cells within the primary tumor. These cells were embedded in a pro-metastatic microenvironment of specialized endothelial subtypes and cancer-associated fibroblasts. Notably, most recurrence-associated lesions were detectable in cfDNA prior to liver transplantation (LT). Building on these insights, we developed the ZJU Criteria based on CNA fragments and tumor markers, a pre-LT risk prediction tool that integrates conventional clinical factors with cfDNA-derived CNA signatures, and validated it using internal and independent external cohorts. Conclusion Our findings suggest that post-transplant recurrence commonly originates from advanced subclones that emerge late during tumor evolution. The ZJU Criteria provides an accurate, non-invasive strategy that significantly improves pre-LT risk stratification and clinical decision-making for patients with HCC.

ObjectiveHepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. The main risk factors associated with HCC include viral hepatitis (B and/or C), alcohol abuse, and metabolic dysfunction-associated steatotic liver disease (MASLD), which progressively advance to liver fibrosis, cirrhosis, and ultimately evolve into HCC. Surgical resection represents the most effective treatment for HCC, while recent advances in immunotherapy, including immune checkpoint inhibitors and adoptive cell therapies, have provided improved treatment prospects for patients with unresectable HCC. However, the complex metabolic heterogeneity of HCC limits the therapeutic efficacy. Metabolic intermediates acyl-CoA not only provide energy and substrates for numerous biochemical reactions but also serve as donors for protein lysine acylation, a major class of post-translational modification (PTM). Therefore, a deeper understanding of the molecular mechanisms underlying protein lysine acylation and hepatocarcinogenesis is urgently needed. MethodsThe levels of protein lysine acylation and silence information regulator 5 (SIRT5) expression levels in clinical HCC samples were analyzed by Western blot. Quantitative malonylome and succinylome of HCC samples were analyzed by antibody-based affinity enrichment coupled with tandem mass spectrometry. The proliferation of HCC cells was analyzed with Cell Counting Kit-8 (CCK-8) assays, the apoptosis was quantified by Annexin V-FITC/propidium iodide (PI) staining coupled with flow cytometry, and the ability of cells to migrate was assayed by Transwell assays. The enzymatic activity of glutathione S-transferase Mu 1 (GSTM1) was quantified. Transgenic mice with hepatic overexpression of SIRT5 were constructed using CRISPR-Cas9, and primary hepatocarcinogenesis was induced by administration of diethylnitrosamine. ResultsWestern blot analysis indicated that the expression level of SIRT5 was elevated in clinical samples from HCC patients, and the levels of lysine malonylation, glutarylation, and succinylation were significantly reduced in HCC tissues. Knockout of SIRT5 in MHCC-97H and MHCC-97L hepatoma cells suppressed cell proliferation, and increased the percentage of apoptotic cells significantly. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the differentially malonylome and succinylome of HCC samples revealed significant enrichment in two major classes of biological processes: core energy metabolism (e.g., glycolysis/gluconeogenesis, tricarboxylic acid metabolic process, fatty acid beta oxidation) and detoxification and oxidative stress response (e.g., response to toxic substance, chemical carcinogenesis, reactive oxygen species (ROS)). SIRT5 removes malonylation from lysine residues in GSTM1 and restores its detoxification activity, which is crucial for the survival of hepatocytes under stressed conditions. More importantly, in vivo experiment indicated that hepatic-specific overexpression of SIRT5 in mice accelerated diethylnitrosamine-induced liver fibrosis and hepatocarcinogenesis, indicating the critical role of SIRT5 in HCC progression. ConclusionThis study highlights the previously unrecognized SIRT5-GSTM1 axis as a key regulator in hepatocarcinogenesis, and suggests a potential target for the treatment of patients with HCC.

Aberrant activation of glycolysis represents a key metabolic mechanism underlying the initiation and progression of nasal inflammation. Allergic rhinitis, chronic rhinosinusitis, and vasomotor rhinitis exhibit distinct etiologies, yet all are characterized by inflammatory responses, impaired epithelial barrier function, and neurovascular dysregulation, in which glycolytic metabolic reprogramming acts as a central hub connecting immunometabolism and inflammatory regulation.Recent evidence indicates that glycolysis-dependent activation of immune cells provides the essential energy basis for inflammatory onset. In dendritic cells, eosinophils, mast cells, and Th2 cells, the expression of key glycolytic enzymes including HK2, PKM2, and LDHA is upregulated, thereby promoting cellular activation and proinflammatory cytokine release via the mTOR-HIF-1α signaling axis. Notably, the metabolic reprogramming of eosinophils prolongs their survival and enhances the release of cytotoxic granules, while in mast cells, enhanced glycolysis facilitates IgE-mediated degranulation and histamine release. Furthermore, glycolysis also influences the Th17/Treg balance, with enhanced glycolytic flux promoting Th17 differentiation and contributing to the heterogeneous inflammatory profiles observed across different rhinitis subtypes.As a central metabolite, lactate contributes to the formation of a metabolism-inflammation vicious cycle through multiple mechanisms. Lactate acidifies the local microenvironment to activate TRPV1 channels and facilitate neuropeptide release, mediates immune cell chemotaxis through GPR81, and regulates gene expression via histone lactylation, thereby sustaining proinflammatory gene transcription. These lactate-mediated processes collectively amplify local inflammation and contribute to the persistence of nasal symptoms.Glycolytic reprogramming in epithelial cells is modulated by the EGF/EGFR pathway, and its dysregulation may result in disrupted tight junctions, abnormal goblet cell hyperplasia, and subsequent tissue remodeling. Substance P and calcitonin gene-related peptide released from sensory neurons, in conjunction with metabolic products, synergistically maintain persistent inflammatory stimulation by activating mast cells, forming a neuro-immune-metabolic regulatory network that drives disease chronicity.From a therapeutic perspective, glycolytic inhibitors such as 2-deoxyglucose, FX11, and 3-bromopyruvate exert anti-inflammatory effects by targeting key enzymes including HK2 and LDHA, each with distinct mechanisms: 2-DG competitively inhibits hexokinase, FX11 selectively targets LDHA to reduce lactate production, and 3-BrPA modulates multiple glycolytic enzymes. Moreover, traditional Chinese medicine formulas, monomeric active components, and small-molecule compounds have shown promising potential in alleviating nasal inflammation by regulating the mTOR-HIF-1α axis, exerting antioxidant effects, and modulating endoplasmic reticulum stress pathways. The multi-target characteristics of these natural products offer advantages in addressing the complex pathophysiology of nasal inflammatory diseases.Despite these advances, several challenges remain. The non-selective inhibition of glycolysis may interfere with epithelial repair and mucosal regeneration, leading to delayed wound healing. Technical limitations in dynamic metabolic monitoring and sampling precision hinder the accurate assessment of local nasal metabolism. Furthermore, current animal models, which predominantly rely on acute stimulation protocols, inadequately recapitulate the chronic tissue remodeling processes characteristic of human rhinitis.This review systematically summarizes glycolysis as a common metabolic node shared by different rhinitis subtypes, offering a novel theoretical basis for the development of precision therapeutic strategies targeting metabolic reprogramming.

ObjectiveTo investigate the effect of bone morphogenetic protein 3 （BMP3） on the expression of inflammatory factors and joint damage in adjuvant arthritis （AA） induced by Freund′s complete adjuvant （FCA） in rats. MethodsThe AIA model was established in SD rats by intradermal injection of FCA into the toes of the left hind limb， and BMP3 overexpressing adenovirus （Ad-BMP3） or control adenovirus （Ad-NC） was injected in situ into the knee joint cavity on day 8 after modeling. Subsequently， HE staining was used to observe the histopathological changes in the synovium， immunohistochemistry was used to detect the expression of BMP3 in the synovium， and ELISA was used to analyze the expression levels of IL-6， IL-1β and TNF-α in the serum. Primary fibroblast-like synoviocytes （FLS） were isolated from AIA rats， the expression of BMP3 in FLS was knocked down or overexpressed， and Western blot and qRT-PCR were used to detect the expression levels of BMP3 and inflammatory factors in FLS. ResultsHE staining confirmed the successful establishment of the AIA model. Compared with normal rats， AIA rats showed decreased BMP3 expression in synovial tissue. Knockdown of BMP3 promoted the protein expression of inflammatory factors （IL-6， IL-1β， IL-17A， TNF-α） and the mRNA expression of chemokines ［C-C motif chemokine ligand 2 （CCL2）， C-C motif chemokine ligand 3 （CCL3）， Vascular Cell Adhesion Molecule-1 （VCAM-1）］ in FLS. In contrast， overexpression of BMP3 suppressed the expression of these inflammatory factors and chemokines. Intra-articular injection of BMP3-overexpressing adenovirus in AIA rats upregulated BMP3 expression in synovial tissue and inhibited synovial inflammation and bone erosion. ConclusionBMP3 suppresses the production of inflammatory factors and chemokines in FLS， thereby alleviating synovial hyperplasia and bone erosion in arthritis.

ObjectiveTo observe the effectiveness and safety of Xingeng No.Ⅱ Granules （心梗2号颗粒剂） in preventing and treating left ventricular remodeling in patients with qi deficiency and blood stasis syndrome following percutaneous coronary intervention （PCI） for ST-segment elevation myocardial infarction （STEMI）. MethodsIn this randomized controlled trial， patients with qi deficiency and blood stasis syndrome after PCI for STEMI were randomly assigned to treatment group and control group at a 1∶1 ratio， with 66 patients in each group. In the control group， patients only received conventional western medicine after surgery， while the treatment group additionally received the granules （8 g per dose， twice daily）， for a treatment duration of 8 weeks in both groups. The primary outcome was the incidence of left ventricular remodeling within 6 months after surgery. The secondary outcomes were the incidence of major adverse cardiovascular and cerebrovascular events （MACCE） within 6 months， all-cause mortality， stent thrombosis， BARC Ⅲ and V bleeding events， rehospitalization due to acute heart failure， and severe complications of STEMI. Traditional Chinese medicine （TCM） syndrome scores at 1 day and 1， 2， and 6 months after surgery was evaluated. Adverse events during the study were recorded to evaluate safety. ResultsSix cases dropped out from both the treatment group and the control group. The full analysis set （FAS） analysis showed that the incidence of left ventricular remodeling in the treatment group was 16.67% （11/66）， significantly lower than 40.91% （27/66） in the control group （P=0.004）. The per protocol set （PPS） analysis also showed lower incidence of left ventricular remodeling in the treatment group （20.37%， 11/54） than in the control group （49.09%， 27/55） with significant difference （P=0.002）. Within 6 month after surgery， 0 patients in the treatment group and 4 out of 60 patients （6.67%） in the control group were readmitted to hospital for acute heart failure， with significantly higher rate in the control group （P=0.042）. Neither group of patients experienced recurrent myocardial infarction， target vessel revascularization， in-stent thrombosis， or severe complications of STEMI. There was no statistically significant difference between groups in the incidence of stroke， cardiovascular mortality， all-cause mortality， BARC Ⅲ and V bleeding events （P＞0.05）. At 1 day after surgery， there was no statistically significant difference in TCM syndrome score between the groups （P＞0.05）； while 1， 2 and 6 months after surgery， TCM syndrome score in the treatment group was significantly lower than that in the control group （P＜0.05）. Analysis of the safety dataset （SS） showed that the incidence of adverse events in the treatment group was 7.41% （4/60）， while in the control group it was 16.36% （9/57）， showing no statistically significant difference （P = 0.117）. ConclusionIn addition to conventional western medicine， Xingeng No.Ⅱ Granules can reduce the incidence of left ventricular remodeling and the incidence of rehospitalization due to acute heart failure in STEMI patients with qi deficiency and blood stasis syndrome after PCI， with good safety profile.

ObjectiveTo evaluate the feasibility of various strength levels of deep learning image reconstruction （DLIR） algorithms for improving non-contrast abdominal CT image quality at ultra-low radiation doses， by comparing ultra-low-dose DLIR images with low-dose filtered back projection （FBP） images. MethodsA prospective collection of 85 patients undergoing non-contrast abdominal CT scans was performed， and a self-controlled study method was employed to conduct low-dose （LD） group and ultra-low-dose （ULD） group scans. The LD group used a noise index of 10 and employed FBP for image reconstruction （LD-FBP group）. The ULD group used a noise index of 30 and employed DLIR at different levels （low， medium， high）， resulting in three subgroups of reconstructed images： ULD-DLIR-L， ULD-DLIR-M， and ULD-DLIR-H. For each group， CT values， standard devia-tion （SD）， signal-to-noise ratio （SNR）， and contrast-to-noise ratio （CNR） were measured and calculated for the liver， spleen， kidneys， aorta， psoas major， and subcutaneous fat. Effective dose （ED） was also recorded. Two radiologists independently performed subjective evaluations of image quality using a 5-point scale. ResultsCompared with the LD-FBP group， the ULD-DLIR-L group showed significantly lower SNR and CNR values in the liver， spleen， kidneys， aorta， and psoas major （P<0.001）， while the ULD-DLIR-H group exhibited significantly higher values （P<0.001）. The difference of SNR and CNR values for the ULD-DLIR-M group showed no statistically significant difference. For subjective evaluation， the scores of the ULD-DLIR-L and ULD-DLIR-M groups were lower than those of the LD-FBP group， while there was no statistically significant difference in scores between the ULD-DLIR-H group and the LD-FBP group. The ED value of the ULD group was approximately 88% lower than that of the LD group. ConclusionCompared with the LD-FBP group， the ULD-DLIR-H group significantly reduces SD values while increasing SNR and CNR values， effectively improving the image quality of non-contrast abdominal CT scans.