Diabetic cardiomyopathy （DCM） is one of the most common complications of diabetes mellitus and is a major threat to global health. As a key mechanism in the occurrence and progression of DCM， the inflammatory response persists throughout the entire course of the DCM. The Gaozhuo theory suggests that the basic pathogenesis of inflammatory injury in DCM is the Qi deficiency of spleen and kidney and Gaozhuo invasion， and divides the pathological process into three phases： Gaozhuo invasion， turbid heat damage to the channels， and turbid blood stasis and heat junction. Among them， the Qi deficiency of spleen and kidney and the endogenous formation of Gaozhuo represent the process of inflammatory factor formation induced by glucose metabolism disorders. Turbid heat damage to the channels refers to the process of myocardial inflammatory injury mediated by inflammatory factors， and turbid blood stasis and heat junction are the process of myocardial injury developing toward myocardial fibrosis and ventricular remodeling. As the disease continues to progress， it eventually develops into a depletion of the heart Yang， leading to the ultimate regression of heart failure. According to the theory of Gaozhuo， traditional Chinese medicine （TCM） should regulate inflammatory injury in DCM by strengthening the spleen and tonifying the kidney to address the root cause， and resolving dampness and lowering turbidity to treat the symptoms. If the turbidity has been stored for a long time and turns into heat， strengthening the spleen and tonifying the kidney， and clearing heat and resolving turbidity should be the therapy. If the turbidity， stasis， and heat are knotted in the heart and collaterals， strengthening the spleen and tonifying the kidney， and resolving stasis and lowering turbidity should be the therapy. TCM compounds and monomers can regulate the inflammatory response in DCM. TCM compounds can be divided into the categories for benefiting Qi to resolve turbidity， benefiting Qi and clearing heat to resolve turbidity， and benefiting Qi and activating blood to reduce turbidity. The compounds can inhibit upstream signals of inflammation and expression of inflammatory factors， improve the inflammatory damage to myocardium and blood vessels， myocardial fibrosis， and cardiac systole and diastole， and thus slow down the onset and progression of DCM.

Interferon regulatory factor 4 (IRF4) is a critical transcription factor that governs the differentiation of cluster of differentiation 4⁺ (CD4⁺) T cells. The pathogenesis and progression of psoriasis are primarily attributed to an immune imbalance stemming from the overproduction of interleukin-17A (IL-17A) by T lymphocytes. However, the role of IRF4 in psoriasis remains unexplored. In this study, we found that IRF4 activity is increased in the cutaneous lesions of patients with psoriasis in response to stimulation by IL-23A and IL-1β. This IRF4 elevation heightens its binding to the E1A binding protein p300 (EP300) promoter, triggering the transcription of downstream retinoic acid receptor-related orphan receptor-γt (RORγt) and increasing the secretion of IL-17A, thereby establishing the IL-1β/IL-23A-IRF4-EP300-RORC-IL-17A inflammatory cascade in psoriasis. The alleviation of imiquimod (IMQ)-induced psoriatic-like symptoms was achieved through the creation of a Irf4 ^-/- gene deletion mouse model and pharmacological inhibition using antisense oligonucleotides targeted for Irf4. This amelioration was accompanied by a decreased number of IL-17A-producing CD4⁺ T cells in the skin. The findings of this study suggest that IRF4 plays a crucial role in the promotion of inflammation and exacerbation of IMQ-induced psoriasiform dermatitis. Consequently, IRF4 targeting could be a promising therapeutic strategy.

For middle-aged and elderly patients with conditions such as spinal fractures and degenerative spinal diseases, spinal internal fixation is a core surgical procedure for reconstructing spinal stability, heavily relying on the biomechanical stability provided by pedicle screw systems. Whereas, these patients are often complicated by osteoporosis that can significantly compromise the stability of the bone-pedicle screw interface, leading to a marked increase in pedicle screw loosening and surgical failure rates. The bone cement-augmented pedicle screw technique, which involves injecting bone cement into the vertebral body or screw trajectory to optimize the mechanical properties of the bone-pedicle screw composite, has been proven to significantly enhance fixation strength and effectively prevent screw-related failures, thereby reducing the incidence of internal fixation failure in high-risk populations undergoing spinal fusion. However, the widespread clinical application of this technique has faced challenges such as inaccurate clinical decision-making (indication and contraindication selection), non-standardized operative practices, and insufficient awareness of complication prevention, resulting in considerable variability in clinical outcomes and even severe complications. To address this, Prof. Luo Fei from First Affiliated Hospital of Army Medical University initiated the project and the Chinese Association Orthopaedic Surgeons organized relevant experts to develop the Evidence-based clinical practice guideline for bone cement-augmented pedicle screw technique ( version 2025), based on current evidence. The guidelines put forward 8 recommendations regarding the clinical value, scope of application, and operational standards of the technique, aiming to provide evidence-based medical support and technical standardization for clinical decision-making.

Objective To screen key differentially expressed genes in head and neck squamous cell carcinoma(HNSCC)and analyze their prognostic value,based on biological information from gene expression omnibus(GEO)and the cancer genome atlas(TCGA)databases.Methods HNSCC mRNA expression data(GSE74530)were downloaded from the GEO database as a test dataset,and differentially expressed genes(DEGs)were identified.The biological function of DEGs in HNSCC was investigated by gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis.HNSCC mRNA expression data were obtained from the TCGA database as a validation dataset to preliminarily verify the expression of DEGs in HNSCC tissues and normal tissues.Seven up-regulated DEGs variants were analyzed using the cBioPortal database,and their effects on the survival of HNSCC patients were evaluated by the Kaplan-meier method and COX regression analysis.The co-expressed genes of ATP6V1C1 were analyzed by the cBioPortal database.Results A total of 1 432 differential genes were screened from HNSCC tissue and paracancerous tissue in the GSE74530 test dataset,among which 7 of the 10 most significant genes were up-regulated,respectively:MMP1,WDR66,PTPRZ1,TEAD4,RBM38,ATP6V1C1 and CBLB were downregulated by CGNL1,LOC100506990 and ADH1B.GO and KEGG enrichment analysis showed that HNSCC tissue differential genes were mainly enriched in lymphocyte migration and extracellular matrix regulation pathways.The TCGA dataset confirmed that 7 upregulated DEGs were highly expressed in HNSCC.cBioPortal analysis showed that the proportion of ATP6V1C1 gene changes was the highest among the 7 up-regulated genes,and the overall survival rate of patients with high expression of ATP6V1C1 gene decreased significantly.Correlation analysis showed that BIRC5 was the most closely related gene to ATP6V1C1.Conclusion MMP1,WDR66,PTPRZ1,TEAD4,RBM38,ATP6V1C1 and CBLB were highly expressed in HNSCC patients,among which ATP6V1C1 was the most significant,and its expression level was associated with poor prognosis in HNSCC patients.ATP6V1C1 is expected to be a biomarker for early diagnosis and prognosis of HNSCC,providing a new idea for clinical diagnosis and treatment.

Objective To screen key differentially expressed genes in head and neck squamous cell carcinoma(HNSCC)and analyze their prognostic value,based on biological information from gene expression omnibus(GEO)and the cancer genome atlas(TCGA)databases.Methods HNSCC mRNA expression data(GSE74530)were downloaded from the GEO database as a test dataset,and differentially expressed genes(DEGs)were identified.The biological function of DEGs in HNSCC was investigated by gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis.HNSCC mRNA expression data were obtained from the TCGA database as a validation dataset to preliminarily verify the expression of DEGs in HNSCC tissues and normal tissues.Seven up-regulated DEGs variants were analyzed using the cBioPortal database,and their effects on the survival of HNSCC patients were evaluated by the Kaplan-meier method and COX regression analysis.The co-expressed genes of ATP6V1C1 were analyzed by the cBioPortal database.Results A total of 1 432 differential genes were screened from HNSCC tissue and paracancerous tissue in the GSE74530 test dataset,among which 7 of the 10 most significant genes were up-regulated,respectively:MMP1,WDR66,PTPRZ1,TEAD4,RBM38,ATP6V1C1 and CBLB were downregulated by CGNL1,LOC100506990 and ADH1B.GO and KEGG enrichment analysis showed that HNSCC tissue differential genes were mainly enriched in lymphocyte migration and extracellular matrix regulation pathways.The TCGA dataset confirmed that 7 upregulated DEGs were highly expressed in HNSCC.cBioPortal analysis showed that the proportion of ATP6V1C1 gene changes was the highest among the 7 up-regulated genes,and the overall survival rate of patients with high expression of ATP6V1C1 gene decreased significantly.Correlation analysis showed that BIRC5 was the most closely related gene to ATP6V1C1.Conclusion MMP1,WDR66,PTPRZ1,TEAD4,RBM38,ATP6V1C1 and CBLB were highly expressed in HNSCC patients,among which ATP6V1C1 was the most significant,and its expression level was associated with poor prognosis in HNSCC patients.ATP6V1C1 is expected to be a biomarker for early diagnosis and prognosis of HNSCC,providing a new idea for clinical diagnosis and treatment.

For middle-aged and elderly patients with conditions such as spinal fractures and degenerative spinal diseases, spinal internal fixation is a core surgical procedure for reconstructing spinal stability, heavily relying on the biomechanical stability provided by pedicle screw systems. Whereas, these patients are often complicated by osteoporosis that can significantly compromise the stability of the bone-pedicle screw interface, leading to a marked increase in pedicle screw loosening and surgical failure rates. The bone cement-augmented pedicle screw technique, which involves injecting bone cement into the vertebral body or screw trajectory to optimize the mechanical properties of the bone-pedicle screw composite, has been proven to significantly enhance fixation strength and effectively prevent screw-related failures, thereby reducing the incidence of internal fixation failure in high-risk populations undergoing spinal fusion. However, the widespread clinical application of this technique has faced challenges such as inaccurate clinical decision-making (indication and contraindication selection), non-standardized operative practices, and insufficient awareness of complication prevention, resulting in considerable variability in clinical outcomes and even severe complications. To address this, Prof. Luo Fei from First Affiliated Hospital of Army Medical University initiated the project and the Chinese Association Orthopaedic Surgeons organized relevant experts to develop the Evidence-based clinical practice guideline for bone cement-augmented pedicle screw technique ( version 2025), based on current evidence. The guidelines put forward 8 recommendations regarding the clinical value, scope of application, and operational standards of the technique, aiming to provide evidence-based medical support and technical standardization for clinical decision-making.

Protein S-palmitoylation is a reversible post-translational modification of lipids that regulates protein localization, stability and protein-protein interactions. The thioesterification of palmitate to internal cysteine residues is catalyzed by palmitoyltransferase, while the removal of palmitate is mainly catalyzed by acyl-protein thioesterase. The S-palmitoylation of some tumor-related proteins is abnormally altered in tumor, which is closely related to the biological processes such as tumor cell proliferation, invasion, metastasis, drug resistance and immune response. Furtherly, exploring the characteristics of protein S-palmitoy-lation and its role in tumor progression could deliver new ideas in targeting protein S-palmitoylation for tumor therapy.

Objective:To explore the correlation between c-myc and glutaminase(GLS)and glutamine synthase(GS)in oral epider-moid carcinoma cells in animal models.Methods:Immunohistochemistry was used to detect the expression of c-myc,GLS and GS in clinical samples of oral cancer.KB cell model with stable and high expression of c-myc was established and verified,then the KB cells were transplanted into nude mice to establish mouse tumorigenic models.The cells and nude mouse models were respectively diveded into 3 groups(n=6):normal cotnrol,empty vector and c-myc overexpression groups.The tumor growth was observed.The expression of c-myc,GLS and GS in the cells and the tumor samples was detected by immunohistochemistry.Results:c-myc,GLS and GS were highly expressed in clinical samples of oral cancer.In the cells of c-myc overexpression group c-myc mRNA expression level was sig-nificantly higher than that of empty vector control group.The tumorigenic models were formed in all nude mice of the groups,and the volume and weight of the c-myc overexpression group increased more significantly(P＜0.01),in the c-myc overexpression group c-myc was overexpressed,the expression of GLS and GS was significantly higher than that in the other 2 groups.Conclusion:c-myc is highly expressed in oral cancer,and may up-regulate GLS and GS expression.

With the aging of population, the elderly (≥65 years old) cancer patients have become one of the main populations for cancer care. For inoperable locally advanced head and neck squamous carcinomas, cisplatin-based concurrent chemoradiotherapy is the first-line choice. Several large clinical studies have shown that patients under 70 years of age can still benefit from concurrent chemoradiotherapy, while it should be cautious to apply chemotherapy to patients aged 70-80 years. For elderly patients who are intolerant to cisplatin, carboplatin or other regimens with less gastrointestinal and renal toxicity should be considered. Although anti-epidermal growth factor receptor (EGFR) monoclonal antibodies combined with radiotherapy has been proved to be more effective than radiotherapy alone in total patient population, age-subgroup analysis showed limited benefit in elderly patients. The safety of immune checkpoint inhibitors in elderly patients has been validated and those with high programmed death ligand-1 (PD-L1) expression may benefit from concurrent or neoadjuvant immunotherapy, however, high-level evidence is still lacking. For patients older than 80 years, radiotherapy alone may be superior to concurrent chemoradiotherapy, and hypofractionated radiotherapy for palliative purposes can be safely used in this population.

Chang-Kang-Fang (CKF) formula, a Traditional Chinese Medicine (TCM) prescription, has been widely used for the treatment of irritable bowel syndrome (IBS). However, its potential material basis and underlying mechanism remain elusive. Therefore, this study employed an integrated approach that combined ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q/TOF-MS) with network pharmacology to systematically characterize the phytochemical components and metabolites of CKF, as well as elucidating its underlying mechanism. Through this comprehensive analysis, a total of 150 components were identified or tentatively characterized within the CKF formula. Notably, six N-acetyldopamine oligomers from CicadaePeriostracum and eight resin glycosides from Cuscutae Semen were characterized in this formula for the first time. Meanwhile, 149 xenobiotics (58 prototypes and 91 metabolites) were detected in plasma, urine, feces, brain, and intestinal contents, and the in vivo metabolic pathways of resin glycosides were elaborated for the first time. Furthermore, network pharmacology and molecular docking analyses revealed that alkaloids, flavonoids, chromones, monoterpenes, N-acetyldopamine dimers, p-hydroxycinnamic acid, and Cus-3/isomer might be responsible for the beneficial effects of CKF in treating IBS, and CASP8, MARK14, PIK3C, PIK3R1, TLR4, and TNF may be its potential targets. These discoveries offer a comprehensive understanding of the potential material basis and clarify the underlying mechanism of the CKF formula in treating IBS, facilitating the broader application of CKF in the field of medicine.
Humans ; Tandem Mass Spectrometry/methods* ; Irritable Bowel Syndrome/drug therapy* ; Molecular Docking Simulation ; Drugs, Chinese Herbal/chemistry* ; Glycosides ; Chromatography, High Pressure Liquid/methods*