Objective: To elucidate the biological basis of traditional Chinese medicine (TCM) syndromes from the perspective of “same syndrome, different diseases” in patients with chronic hepatitis B (CHB), liver cirrhosis (LC), and hepatocellular carcinoma (HCC), thereby providing a complementary approach for the diagnosis and treatment of chronic liver diseases (CLD). Methods: To investigate the dynamic characteristics of TCM syndromes in CLD, transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) was performed from patients with CHB, LC, or HCC presenting with three TCM syndromes: liver gallbladder dampness heat syndrome (LGDHS), liver depression spleen deficiency syndrome (LDSDS), and liver kidney Yin deficiency syndrome (LKYDS). These participants were recruited at Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine between August 1, 2018 and December 31, 2021. Differentially expressed genes (DEGs) were identified using the random variance model (RVM) F test with false discovery rate (FDR) correction. Principal component analysis (PCA) and unsupervised hierarchical clustering were applied to visualize sample grouping. Dynamic network biomarkers (DNB) analysis was employed to detect critical transition stages during syndrome evolution, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses to characterize the functional roles and pathway involvement of the DNB members. Random forest (RF) analysis and the area under the receiver operating characteristic (ROC) curves (AUC) were used to rank the importance of candidate genes. External validation was performed using microarray data from an independent CLD cohort (GSE89377) and RNA-seq data from The Cancer Genome Atlas Liver Hepatocellular Carcinoma (TCGA-LIHC) dataset. Additionally, reverse transcription quantitative polymerase chain reaction (RT-qPCR) was performed on an independent cohort of LC patients to validate the expression levels of the candidate genes. Results: The study included a total of 132 participants. DNB analysis identified LDSDS stage as a critical tipping point during TCM syndrome evolution across CHB, LC, and HCC. The phosphoinositide 3-kinase/protein kinase B (PI3K-AKT) signaling pathway was consistently enriched in the DNB analysis across all three types of CLD, suggesting its potential involvement in the critical transition of TCM syndromes. Among the 24 core DNB members of the PI3K-AKT pathway, four genes—integrin subunit beta 1 (ITGB1), collagen type IV alpha 1 chain (COL4A1), collagen type IV alpha 2 chain (COL4A2), and DNA damage inducible transcript 3 (DDIT3)—were identified by RF analysis (Gini score > 1) and ROC analysis. ROC analysis demonstrated high discriminative ability for distinguishing LGDHS from LKYDS in CHB patients, with AUC of 0.7891 for ITGB1, 0.7070 for COL4A1, 0.7148 for COL4A2, and 0.8945 for DDIT3. In the independent CLD cohort (GSE89377), all four genes showed significant stepwise upregulation from normal to CHB, LC, and HCC (all P < 0.05). In the TCGA-LIHC dataset, their expression progressively increased with tumor stage. RT-qPCR validation in an independent LC cohort (30 LGDHS vs. 30 LKYDS) confirmed that ITGB1, COL4A2, and DDIT3 were significantly upregulated in LKYDS compared with LGDHS (P = 0.0152, 0.0186, and 0.0247, respectively), whereas COL4A1 showed a non-significant upward trend (P = 0.1201). Conclusion This study introduces a novel approach to understanding the molecular features underlying TCM syndrome evolution in CLD. The PI3K-AKT pathway and four identified genes (ITGB1, COL4A1, COL4A2, and DDIT3) play crucial roles in the transition from excess (LGDHS) to deficiency (LKYDS) via the critical LDSDS stage. These findings offer potential quantitative biomarkers and therapeutic targets for TCM syndrome differentiation and may help arrest syndrome progression in CLD.

AIM:To investigate the expression characteristics of TRIM 27 in human nasopharyngeal carcinoma tissues, nasopharyngeal carcinoma 5-8F cells and NP69 cells, and to observe the effect of TRIM27 on the proliferation, in-vasion and migration of 5-8F cells.METHODS:The levels of TRIM27 in the nasopharyngeal carcinoma tissues and normal nasopharyngeal epithelial tissues were observed by the method of immunohistochemistry .The mRNA and protein levels of TRIM27 in the 5-8F cells and NP69 cells were determined by real-time PCR and Western blot .TRIM27 siRNA was trans-fected into the 5-8F cells with Lipofectamine 2000.The relative mRNA expression of TRIM27 was detected by real-time PCR.The relative protein expression of TRIM 27 was detected by Western blot .The cell proliferation was analyzed by CCK-8 assay and cell colony formation assay .The change of cell invasion was examined by Matrigel invasion assay .The change of cell migration were examined by wound healing assay .RESULTS:The results of immunohistochemistry showed that the protein expression of TRIM27 in the nasopharyngeal carcinoma tissues was obviously higher than that in the normal nasopha -ryngeal epithelial tissues .The results of real-time PCR and Western blot showed that the mRNA and protein levels of TRIM27 in the 5-8F cells were obviously higher than those in the NP69 cells.The abilities of proliferation, invasion and migration in the 5-8F cells were significantly suppressed after TRIM27 gene silencing ( P <0.05).CONCLUSION:TRIM27 acts as a oncogene in the 5-8F nasopharygeal carcinoma cells .The abilities of proliferation , invasion and migration are significantly suppressed after TRIM27 gene silencing in the 5-8F cells.

The computer three-dimensional reconstruction of serial sections is an important research area in the world at precent. In this paper, we combine the computer graphics, image processing and biomedical techniques to reconstruct the stereo model of intra-glandular lymphatics, veins, arteries and duets with the serial semithin sections of human submandibular gland.